hjeltfoundations

When Time Meets Decay: Uncovering the Links Between Circadian Rhythms and Pancreatic Health

Wed, 22 Apr 2026 12:33:41 GMT

Giorgia Katsioudi,

Hjelt Grant Holder 2026,

University of Geneva.

Disruptions in our circadian rhythms, the internal biological clocks that regulate vital metabolic processes are linked to T2D pathogenesis. Peripheral clocks are located in almost all organs of the human body, including the pancreas that regulates the rhythmic secretion of insulin. Modern stressors like chronic shift work, irregular sleep patterns, or jet lag, cause a chronic hormonal misalignment, which significantly elevates the risk of developing metabolic diseases.

Nonsense-mediated mRNA decay (NMD), a cellular mechanism that degrades certain mRNA molecules, regulates which genes are expressed under different conditions and potentially at different times of day. Our preliminary research shows that NMD is rhythmic in pancreatic cells and is important for normal pancreatic function. In this project, we will use a new mouse model that specifically blocks NMD in insulin-producing pancreatic β-cells to study how the interaction between NMD and the body's internal clock regulates insulin secretion and glucose metabolism. We will also examine these processes in human islets from healthy and T2D donors.

By uncovering the molecular links between circadian rhythms, mRNA decay, and pancreatic function, this research may improve our understanding of how internal clocks regulate insulin production and offer insights relevant to T2D development and prevention.

Allan and Bo Hjelt Art Foundation Partners with Circus & Dance Finland

Wed, 10 Dec 2025 16:04:30 GMT

The Allan and Bo Hjelt Art Foundation and Circus & Dance Finland have established a collaboration that brings international circus expertise to Finland. Through this partnership, Swedish circus director Tilde Björfors will visit Helsinki in January 2026 as part of an initiative to foster cross-border dialogue within the performing arts sector.

In September 2025, Circus & Dance Finland submitted a cooperation proposal to the Allan and Bo Hjelt Art Foundation, requesting support to invite four international guests to Finland. These visits were planned in connection with two events: the Moving in November Festival (6–16 November 2025) and the Hurjaruuth Winter Circus (10 December 2025 – 25 January 2026). The collaboration has brought together international guests with Finnish circus and dance professionals. As an ending to this collaboration, a Morning Coffee event is put together in January with Tilde Björfors.

Morning Coffee with Tilde Björfors

On 16 January 2026, Circus & Dance Finland will host a morning coffee event with Tilde Björfors at the Cable Factory in Helsinki. The gathering offers Finnish circus professionals an opportunity to engage with one of Scandinavia's leading circus directors.

During the event, Björfors will share insights from her career as a circus director, artistic leader, and researcher. Her perspectives on creating interdisciplinary work, navigating international collaborations, and developing artistic vision will provide learning opportunities for Finnish practitioners.

The Allan and Bo Hjelt Art Foundation has financed this visit, enabling Finnish circus professionals to access international expertise and perspectives. Such encounters benefit individual practitioners and contribute to the development of Finland's circus sector.

Circus & Dance Finland

Circus & Dance Finland serves as the national information center for circus and dance in Finland. Operating from the Cable Factory in Helsinki, the organization provides services to professionals and audiences, including performance calendars, databases, professional resources, and international networking opportunities.

The organization's work includes maintaining databases of Finnish circus and dance companies, facilitating international collaborations and tours, and organizing professional development opportunities for artists and practitioners. Through projects such as Performing HEL and Ice Hot, Circus & Dance Finland strengthens the position of Finnish performing arts internationally.

Tilde Björfors

Tilde Björfors is a Swedish artist and innovator whose career spans multiple dimensions of circus arts. As a director, artistic leader, playwright, and researcher, she works with circus as her primary artistic language, which she integrates into collaborations with diverse art forms.

Björfors's work includes collaborations with Scandinavian cultural institutions. Her production "Borders" (2015) was created with Malmö City Theatre and Cirkus Cirkör, while "God's Disobedient Rib" (2020) involved the Royal Dramatic Theatre in Stockholm. "Satyagraha" (2016-2018) toured internationally to venues including BAM in New York City and Copenhagen Opera Festival. Other productions include "Inside Out" (2008-2011), "Limits" (2016-2019), "Circus Days and Nights" (2021) at Malmö Opera House, and "Pippi at the Circus" (2022-2023).

ERMP1, a new gatekeeper in diabetic kidney diseas?

Thu, 07 Aug 2025 10:09:15 GMT

Monika Gjorgijeva Ducros,

Hjelt Grant Holder 2025,

University of Geneva.

Background
Diabetic kidney disease (DKD) is a serious complication of diabetes characterized by progressive renal dysfunction due to chronic hyperglycemia. AI showed upregulation of endoplasmic reticulum metallopeptidase 1 (ERMP1), a mediator of ER stress, in renal samples from patients with DKD. Collectively, the data suggest a protective role for ERMP1 in DKD. We aim to elucidate the interplay between renal cells with or without ERMP1 in vivo. We will use kidney-specific ERMP1 knockout mice fed either standard diet or a diabetogenic diet to induce DKD.

Around 403.000 patients per year are diagnosed with renal carcinomas worldwide. Renal carcinomas are promoted by several factors such as obesity/diabetes, chronic kidney disease, smoking, toxin exposure, genetic predispositions and high blood pressure. This diverse array of risk factors leads to very strong differences in terms of tumor morphology, mutational profile and metabolic status and testifies for the need to deepen our understanding of the pathological processes involved in this disease in order to develop novel therapeutic approaches to fight renal cancer.

Dr Gjorgjieva’s research aims therefore at deciphering the different molecular mechanisms involved in the incidence and progression of renal cancer .

She is working on the development of an in vivo model of renal carcinoma that better mimics the pathology observed in humans and might open new therapeutic avenues.

June 2025 | "ODDfest 2025" in Helsinki

Wed, 21 May 2025 14:46:42 GMT

6-7 June 2025, ODDfest will take place in central Helsinki. The festival brings together art, business, and society through a two-day program focused on creativity and innovation. This year, the Bo and Allan Hjelt Art Foundation is partnering with ODDfest to support a keynote appearance by American professor Arthur C. Brooks.

Transcriptional regulation of human islet development and function

Thu, 15 May 2025 07:10:54 GMT

Isabella Artner,

Hjelt Grant Holder 2025,

Lund University.

Transcriptional regulation of human islet development and function

Background

Type 2 diabetes affects around 400 million people worldwide and is caused by the pancreas not producing enough insulin due to issues with β-cells (the insulin-producing cells). More than 250 genes have been linked to type 2 diabetes, many of which are active in the pancreas. This suggests that problems with how the insulin-producing β-cells and other cells in the pancreas (like α-cells) function, as well as how the cells are organized, play a key role in the development of the disease.

Hypothesis

Through animal studies, we have discovered that the MafB transcription factor is crucial for the proper function and development of islet cells in the pancreas. Additionally, we've identified the transcription factors AUTS2 and ETV1 as targets of MafB and we propose that these factors regulate molecular processes that are critical to islet cell function.

Methods

We plan to use human islets to study hormone secretion and employ embryonic stem (ES) cell differentiation models to explore how the transcription factors AUTS2 and ETV1 regulate islet development and function.

Results

Our preliminary results show that ETV1 and AUTS2 regulate several proteins that are essential for islet function and we have found that variants in the AUTS2 and ETV1 genes are critical for the expression of these genes in islets.

Conclusions

Our results will identify key proteins that are important for islet function and are affected in type 2 diabetic patients.

Importance

By understanding the mechanisms behind β-cell differentiation and islet function, we can advance efforts to create functional β-cells from stem cells for transplantation. This knowledge will also help us better understand the causes of type 2 diabetes and improve strategies for treating the disease.

ACSL1 and β-Cell Function: A Novel Pathway in the Pathophysiology of Type 2 Diabetes

Wed, 26 Feb 2025 14:45:15 GMT

Sevda Gheibi,

Hjelt Grant Holder 2025,

Lund University.

ACSL1 and β-Cell Function: A Novel Pathway in the Pathophysiology of Type 2 Diabetes

Background

Type 2 diabetes (T2D) is a growing global health problem. While much research has focused on how insulin and glucose interact, the role of fatty acids in diabetes is less understood.

Hypothesis

Our research suggests that a protein called ACSL1 is important for insulin production in the pancreas. ACSL1 helps process fatty acids in cells, and we believe it plays a key role in keeping insulin-producing cells healthy and functioning properly.

Methods

We studied genetic data from 26,000 individuals and found that ACSL1 may affect diabetes risk. In lab experiments, we tested how turning ACSL1 “on” or “off” in pancreatic cells influences insulin production, energy use, and cell health. We also studied mice lacking ACSL1 in their insulin-producing cells and are using stem cells from diabetes patients to understand how ACSL1 affects human cells.

Results

When ACSL1 was turned off, insulin production decreased, and the cells struggled to generate energy properly. Mice without ACSL1 in their pancreatic cells had higher blood sugar and lower insulin levels. In diabetes-like conditions, ACSL1 levels naturally increased, helping cells produce more insulin.

Conclusions

ACSL1 is essential for insulin production and energy balance in pancreatic cells. Genetic differences in ACSL1 may influence a person’s risk of developing diabetes.

Importance

By understanding how ACSL1 functions, we may find new ways to predict who is at risk for diabetes before they develop high blood sugar. This research could also lead to new treatments that improve insulin production and prevent diabetes progression.

Therapeutic potential of S100A10 Inhibition in Hepatic Insulin Resistance, MASLD and Type 2 Diabetes

Thu, 16 Jan 2025 08:10:29 GMT

Etienne Delangre,

Hjelt Grant Holder 2024,

University of Geneva.

Therapeutic potential of S100A10 Inhibition in Hepatic Insulin Resistance, MASLD and Type 2 Diabetes

Background

Obesity is a major risk factor for the development of Metabolic dysfunction Associated Steatotic Liver Disease (MASLD), affecting one quarter of the global population worldwide. It initiates with ectopic fat accumulation in the liver (steatosis) and can progress toward steatohepatitis (inflammation and fibrosis). Steatosis promotes insulin-resistance, a key event in the development of Type 2 Diabetes (T2D).

In this context, our recent findings underscored a role for the protein S100A10 in MASLD development and thus, in T2D. As S100A10 can be released in the circulation upon damages, it has been shown that S100A10 can trigger deleterious effects on other cells through autocrine, paracrine or endocrine effect.

Hypothesis

Based on our preliminary data, we suggested that intra-cellular and secreted fraction of S100A10 in the liver have different outcomes on MASLD, insulin resistance and T2D.

Methods

In our laboratory, we recently implemented the utilization of Human Liver Organoids (HLOs), derived from embryonic stem cells, and composed of the main cell types of the liver. Using the HLOs we recapitulate MASLD formation and aim to better define the appropriate therapeutic strategy to target S100A10. In order to hamper the intra-cellular activity of S100A10 we use a pharmacological inhibitor, whereas the extra-cellular actions are investigated with recombinant S100A10 and neutralizing antibodies.

Results

We optimized MASLD formation in the HLOs, in which we recapitulated different steps of the disease formation. Our preliminary data showed a regulation of steatosis by the extra-cellular fraction of S100A10 while it did not contribute to fibrosis development. On the contrary, targeting intra-cellular S100A10 with pharmacological inhibitor rescued fibrosis without affecting steatosis.

Conclusions

We discovered specific functions of S100A10 within and outside of the cell, driving liver disease progression.

Importance

The findings of this study pave the way for further investigations of the proper contribution of intra-cellular versus secreted S100A10 in order to design relevant therapeutic approaches. By targeting circulating S100A10 with a neutralizing antibody, we might reduce lipid accumulation in the liver. Besides, we might also improve the functionality of other organs involved in the regulation of glucose homeostasis, which we are currently investigating.

Towards Personalized Medicine: Unraveling Biomarkers in Gestational Diabetes for Predicting Diabetes Subtypes and Prevention

Mon, 16 Dec 2024 14:47:38 GMT

Rashmi B. Prasad ,

Hjelt Grant Holder 2024,

Lund University.

Towards Personalized Medicine: Unraveling Biomarkers in Gestational Diabetes for Predicting Diabetes Subtypes and Prevention

Gestational diabetes mellitus is transient hyperglycemia during pregnancy that can have negative consequences for the mother and the child in both the short and long term. GDM shares many similarities with type 2 diabetes (T2D). Gestational diabetes mellitus (GDM), like type 2 diabetes (T2D), does not look the same for everyone. Different people can experience it in different ways because it can result from a mix of factors like genetics, lifestyle, or hormonal changes during pregnancy. This variation in how it manifests is called "heterogeneous presentation." It means that the symptoms, severity, and underlying causes can vary widely from person to person. The specific goals of the project focus on understanding the genetic basis of GDM as well as carefully analyzing the heterogeneity of the disease.

We will investigate whether a previous occurrence of GDM can predict predisposition to diabetes and risk of complications. Furthermore, we will identify gene expression networks for the subtypes, which will provide valuable clues to the underlying pathophysiology, as well as identify biomarkers specific to the subtypes in question. With this, we aim to be able to create a web resource for the prediction of GDM to facilitate individual-based treatments.

It has been shown that women with GDM as well as their offspring have a high risk of developing T2D later in life. GDM creates an "overnutrition environment" in the womb, which can alter fetal programming and make them more vulnerable to cardiovascular disease and diabetes later in life. We will therefore also investigate signs of fetal programming in the offspring of mothers with GDM. The overall goal is to identify women at high risk of developing T2D, in order to tailor "personal" treatment and individualized care.

Diabetes Research Grants for 2025: Welcome to Apply

Sun, 20 Oct 2024 14:07:34 GMT

Application period begins today!

The Diabetes Foundation: The application period for next year’s research grants is 20 October to 15 December. Research grants are awarded to applicants at the Medical Faculties of Lund University, Sweden and Geneva University, Switzerland.

October 27, 2024 | "For the love of Italy – the connection between Allan Hjelt and the Aalto's"

Fri, 18 Oct 2024 08:29:29 GMT

Two expert presentations at Helsinki Book Fair on Aino and Alvar Aalto's Italian connections

Exhibition in Åbo: feb 3 – June 6 2024 | "More than just oldsters"

Thu, 30 May 2024 13:19:35 GMT

"More than just oldsters"

The exhibition More than just oldsters presents the art that has been donated to the Åbo Akademi University Foundation, as well as its donators.

The exhibition opens February 3 ^rd 2024. The last time the Foundation’s donated art collection was presented was over 30 years ago in Turku Art Museum.

Upcoming event: May 25, 2024 | "Play for creativity" - The Hjelt Talk in cooperation with Circus Helsinki

Fri, 03 May 2024 10:32:22 GMT

Circus educators Lena Kruit & Rieke Hambach From MeerManege in Kiel, Germany

The benefit of play in creating a good atmosphere and how it is linked to Education for Sustainable Development (ESD)

This spring we have the pleasure to invite two circus educators Lena Kruit and Rieke Hambach from MeerManege in Kiel, Germany to give an inspiring Hjelt talk, demonstrating the importance of play for creativity, the benefit of play in creating a good atmosphere and how it is linked to Education for Sustainable Development ESD.

Lena Kruit and Rieke Hambach will show us the ESD goals and how games and circus arts can help to achieve them – and why playing and 'acting like children' can help us from time to time in all kinds of situations. This playful and interactive session will be followed by two festival performances with a short break for coffee and savoury snacks between the performances. The Hjelt Talk is organised in cooperation with Circus Helsinki.

Time: Saturday 25 May 2024 from 12:15 to 15:30
Venue: Circus Helsinki, Suvilahti, Sörnäisten rantatie 22, Helsinki, Finland

The two performances:
Circus Helsinki's Elokuu (August) is a stagnant place between the new and the old. Hot summer and Helsinki, the Elokuu performance glides and lingers in the heat. On stage there are pyramids, aerial acrobatics, foot juggling and dance acrobatics to Finnish music. (Duration approx. 20 min).

Norrköpings Cirkus & Varietés Circus Fantastica is a joyful and colourful traditional circus performance with fantastic circus tricks. On stage, you will see dazzling human pyramids, jump rope acrobatics, unicycles, juggling, and much more. (Duration approx. 40 min).

Leveraging discordancy between obesity and type 2 diabetes to target insulin resistance

Thu, 07 Mar 2024 14:04:53 GMT

Sebastian Kalamajski,

Hjelt Grant Holder 2024,

Lund University.

Leveraging discordancy between obesity and type 2 diabetes to target insulin resistance

Background

Obesity is often associated with type 2 diabetes, but it does not always lead to metabolic disorders. This interesting phenomenon is called discordant diabesity, and its causes are unclear. Investigating those causes could reveal the mechanisms that protect against type 2 diabetes despite obesity.

Hypothesis

We hypothesize that common genetic variation, modulating the expression of specific genes, contributes to discordant diabesity. We also hypothesize that the function of these genes is closely related to metabolic traits.

Methods

In our recent study, we have found that the expression of a gene named DNAH10 in adipose tissue associates with the genetic variation linked to discordant diabesity. To identify the genetic variants that cause the altered gene expression we will use CRISPR-mediated allele editing. To elucidate the role of DNAH10 in adipocytes we will investigate the allele-edited or DNAH10-knockout cells for adipogenic differentiation potential, transcriptome and metabolome profile, insulin resistance, and the function of primary cilia, to which we have localized the DNAH10 gene product.

Results

Our project aims to find the causal genetic variant that alters the expression of DNAH10 and to demonstrate the mechanism through which DNAH10 confers, at least to a certain extent, protection against metabolic disorders. We hope this can lead to novel drug target candidates against insulin resistance.

Conclusions

Our project combines the epidemiological findings with experimental science to find novel approaches for investigating metabolic disorders. We aim to define the clinically relevant function of common genetic variation, and eventually leverage that knowledge to find novel druggable molecular targets to treat insulin resistance.

Lund University presents three Hjelt researchers

Tue, 05 Sep 2023 15:21:53 GMT

Jiangming Sun, Emma Ahlqvist and Sabrina Ruhrmann have each been awarded a project grant of 47,500 euro by the Hjelt Diabetes Foundation.

Today, three of our grant holders in the Diabetes foundation for 2023 are presented in an article on the Lund University Diabetes Center website. Read more at the LUDC web site .

March 22, 2023 | Italo-Finlandese Success Stories - Design Talk with Leonardo Ferragamo

Wed, 17 May 2023 08:51:55 GMT

Leonardo Ferragamo
Italo-Finlandese Success Stories

Allan and Bo Hjelt Art Foundation had the great honour to welcome Mr. Leonardo Ferragamo, Chairman of Nautor Swan, to give an inspirational design talk on Finnish-Italian collaboration in Helsinki in March.

A Swan is a Swan

Over the years, the passion for yachts, racing and the sea has been a great source of inspiration for Mr. Ferragamo. Therefore, it was not surprising to learn that the first Finnish design product that he bought was a Swan yacht.

Mr. Ferragamo gave an inspirational speech of what led him to transform Nautor into a world leading yacht brand. The talk was followed by a discussion with the Finnish journalist Mr. Peter Nyman about the fusion of Finnish craftsmanship and Italian design and how the two worlds have found a common expression in the Nautor Swan products.

Design Ambassador for the Italian Design Day 2023 in Helsinki

Leonardo Ferragamo is Chairman of Nautor Swan, Honorary Consul of Finland in Florence for the regions of Tuscany and Umbria. He is engaged in the renowned Italian fashion house Salvatore Ferragamo. As a Design Ambassador for the Italian Design Day 2023 in Helsinki, he visited The Design Museum Helsinki on 22 March 2023 to give a design talk around Finnish-Italian collaboration.

The Italian Design Day is an initiative to celebrate Italian design, supported by the Ministry of Foreign Affairs of Italy. The global theme for the event in 2023 is “The quality that illuminates. The energy of design for people and the environment”.

Allan and Bo Hjelt Art Foundation would like to express our gratitude to Mr. Leonardo Ferragamo, the Embassy of Italy and the Italian Institute of Culture in Helsinki, and the Design Museum Helsinki for joining us in encouraging future Italo-Finlandese success stories and for making the Italian Design Day 2023 in Helsinki a memorable event.

Epigenetic Editing - a way to a personalized treatment approach in type 2 diabetes (T2D)

Tue, 21 Mar 2023 10:24:27 GMT

Sabrina Ruhrmann,

Hjelt Grant Holder 2023,

Lund University.

Epigenetic Editing - a way to a personalized treatment approach in type 2diabetes (T2D)

The number of people affected by diabetes is rapidly increasing worldwide. Type 2 diabetes (T2D) largely contributes to this increase and individuals with T2D usually face high blood sugar levels. To balance our blood sugar level the hormone Insulin is necessary and Insulin target tissues like muscles need to be able to take up glucose in response to Insulin. Overweight

and no physical exercise can lead to insulin resistance (where the uptake of glucose is not any longer possible e.g. in our muscles) and almost all individuals with T2D show Insulin resistance.

Our DNA only explains a small proportion of how T2D is passed on from parents to their children (also described as the so called “missing heritability”). Given the crucial role of diet and physical exercise in the development of T2D, mechanisms mediating the interaction of those factors with our genes should be of particular importance when trying to explain how T2D develops.

Epigenetic mechanisms fulfil this criterion. Epigenetics is the study of how e.g. the environment and/or our behavior can affect the expression of our genes without changing our DNA. The fact that epigenetic changes do not change our DNA unlike genetic changes gives us the opportunity to “correct“ them.

We are here trying to discover epigenetic changes that cause T2D. We will create small molecules called guideRNAs (gRNAs) that will help us to search for those epigenetic changes using the so called inactivated gene scissor system, CRISPR-dCas9. We will further try to also 'correct' these epigenetic changes to explore if epigenetic mechanisms may be targeted for a more patient specific treatment of T2D in the future.

April 27 , 2022 | Pre-War Rolls-Royce Motor Cars with a Finnish connection

Mon, 07 Nov 2022 08:06:05 GMT

Sir John Stuttard
Pre-War Rolls-Royce Motor Cars with a Finnish connection

Time: Wed, April 27 ^th 2022 at 5 pm
Venue: Handelsgilletin juhlasali, Kasarminkatu 40, 2. krs., Helsinki
Lecture in English.

Sir John Stuttard has had a long association with Finland, prominent Finnish companies and Rolls-Royce-motor cars. A chartered accountant, and former Lord Mayor of London, he holds a MA in Economics.

Starting in 1983, working with the firm Salmi, Virkunnen & Helenius, he assisted Finnish companies establish operations in other countries, list their shares on overseas Stock Exchanges, acquire and sell businesses and help them prepare annual reports using best international practice. These companies included Amer, Metsäliitto, Metsä-Serla, Metso, Nokia, Nordea, Outokumpu, Pohjola, Rauma-Repola and Stora-Enso.

He was also, for many years, Chairman of the Finnish-British Chamber of Commerce in the UK and is now one of its two Life Presidents. For his services to Finnish companies, he was awarded the honour of Commander of the Order of the Lion of Finland, as well as the Silver Medal of Helsinki. He has spent much time in Finland on business and, socially, with friends. In 1987 he completed the 78 kilometre cross-country skiing marathon, Reppu-Finlandia, from Hämeenlinna to Lahti.

In 1989 he acquired his first pre-WWII Rolls-Royce, a 1934 20/25 Barker Sports Saloon which, in 1997, he drove from Beijing to Paris in a rally lasting six weeks, travelling 16,000 kilometres across the world through rugged terrain. He has also owned other old Rolls-Royce cars and his family now has a 1921 Silver Ghost Harrison All Weather Tourer which was owned originally by the Maharaja of Porbandar.

For nine years, he was Chairman of The 20-Ghost Club, the oldest Rolls-Royce club in the world, and is now a Vice-President. In his recent book, “Pre-War Rolls-Royce Motor Cars with a Finnish connection”, he traces fascinating stories of Rolls-Royce-motor cars and their Finnish owners.

Year: 2022

Diabetes Research Grants for 2023: Welcome to Apply

Wed, 19 Oct 2022 14:07:21 GMT

Application period begins today!

The Diabetes Foundation: The application period for next year’s research grants is 19 October to 15 December. Research grants are awarded to applicants at the Medical Faculties of Lund University, Sweden and Geneva University, Switzerland. Read more/apply

Lund University presents three Hjelt researchers

Thu, 08 Sep 2022 14:30:58 GMT

Anja Schmidt-Christensen, Rodrigo Cataldo and Sebastian Kalamajski have each been awarded a project grant of 47,500 euro by the Hjelt Diabetes Foundation.

Today, three of our grant holders in the Diabetes foundation for 2022 are presented in an article on the Lund University Diabetes Center website. Read more at the LUDC web site .

April 27, Upcoming event: Rolls-Royce Motor Cars with a Finnish connection

Thu, 31 Mar 2022 08:41:05 GMT

Fascinating stories of Pre-War Rolls-Royce-motor cars and their Finnish owners

Sir John Stuttard, former Lord Mayor of London, has had a long association with Finland, prominent Finnish companies and Rolls-Royce-motor cars. In his recent book, “Pre-War Rolls-Royce Motor Cars with a Finnish connection”, he traces fascinating stories of Rolls-Royce-motor cars and their Finnish owners.

Time: Wed, April 27 ^th 2022 at 5 pm

Venue: Handelsgilletin juhlasali, Kasarminkatu 40, 2. krs., Helsinki

Lecture in English.

Due to limited seats available, pre-registration is required to art@hjeltfoundations.org .

Welcome!

Congratulations!

Fri, 04 Mar 2022 10:44:51 GMT

Our Grant Holders 2022

The Diabetes Foundation: Four scientists have been awarded the Hjelt Research Grant for 2022: Luis Rodrigo Cataldo Bascunan, Anja Schmidt-Christensen and Sebastian Kalamajski, Lund University Diabetes Centre, and Monika Gjorgijeva Ducros, University of Geneva Faculty of Medicine Diabetes Centre. Read more

Human liver organoids to investigate the role of miR-149 in obesity-associated hepatic insulin resistance

Fri, 04 Mar 2022 08:16:44 GMT

Monika Gjorgijeva Ducros,

Hjelt Grant Holder 2022,

University of Geneva.

Background
MicroRNAs (miRNAs) are critical gene expression regulators involved in mRNA decay or translation inhibition. MiRNAs play an important role in various physiological processes and therefore, deregulation of their expression/activity has been associated with the development of metabolic disorders.

Obesity and the metabolic syndrome represent key etiological conditions that predispose to the development of insulin resistance (IR), Type 2 Diabetes (T2D) and non-alcoholic fatty liver disease (NAFLD). Increasing evidence indicate that miRNA deregulation contributes to the development of these diseases. In this context, our recent findings highlighted a strong induction of miR-149 in the liver of various models of IR, T2D and NAFLD, suggesting an important role of this miRNA in these metabolic disorders.

Hypothesis

Based on our preliminary results, we hypothesize that the increase in hepatic mir-149 in IR/T2D/NAFLD conditions can favor these pathologies. We will therefore investigate i) the pathophysiological role and pre-clinical relevance of miR-149 upregulation in IR/T2D/NAFLD and ii) which miR-149 target genes are involved in this process.

Methods
To investigate the role of miR-149 in IR/T2D/NAFLD, we are using human liver organoids (HLOs). HLOs are obtained by inducing differentiation of human progenitor cells into different hepatic cell types (hepatocytes, Kuppfer cells, stellate cells) that form functional structures. These organoids respond to insulin stimulation in the same manner as human liver. Moreover, they develop hepatic steatosis under high-fat/high sugar conditions and can undergo inflammation when stimulated with cytokines. Finally, HLOs are an extremely relevant experimental model as they allow us to avoid animal experimentation protocols.

Therefore, we will modulate the expression of miR-149 in HLOs via synthetic nucleotides and/ or viral vectors and we will analyze the molecular responses in HLO under various metabolic / inflammatory stimuli. We will further identify miR-149 target genes involved in IR/T2D/NAFLD and we will validate their relevance in public human datasets.

Results

Our preliminary data suggest a pertinent role for miR-149 upregulation in the induction of steatosis in vitro in currently used hepatic cell lines, as well as in HLO. We have also observed that alteration of miR-149 levels has a striking effect on hepatic glucose and lipid metabolism, implying a functional role for this miRNA in IR/T2D/NAFLD.

Conclusion
This project should allow us to better understand the role of miR-149 in hepatic IR, and more generally in obesity-associated disorders of the hepatic lipid/glucose metabolism. We will identify novel target genes of miR-149 contributing to IR/T2D/NAFLD and the fine-tuning metabolic regulation in the liver in pathophysiological conditions. Our investigations should provide key evidence and proof-of-concept about the potential of miR-149 and its targets as new biomarkers for IR/T2D as well as the therapeutic potential of targeting this miRNA to counteract and/or to alleviate IR/T2D development.

Importance
Modulation of miR-149 represents a promising therapeutic strategy by targeting numerous genes at once. Therefore, miR-149 modulation could represent a multi-targeting approach relevant and pertinent for multifactorial disorders such as obesity, IR/T2D/NAFLD. A significant and innovative aspect of this proposal is the development and use of genetically engineered functional HLOs in which hepatic steatosis, inflammation and IR can be reproduced. HLOs have the potential of replacing animal experimentation, thereby alleviating important ethical issues related to the use of laboratory mice for pre-clinical research.

EPDR1, a novel human batokine regulating β cell metabolism and function

Tue, 01 Mar 2022 08:11:01 GMT

Rodrigo Cataldo,

Hjelt Grant Holder 2022,

Lund University.

Background

The role of beta cells is to sense glucose and response by releasing insulin to maintain glucose homeostasis. Consequently, the loss of beta cell function is the main culprit of type 2 diabetes development.

Ependymin-related protein 1 (EPDR1) was recently identified as a protein released by the human brown adipose tissue, where it plays a role in regulating thermogenesis, a protective metabolic process that transform stored fat into heat. It was suggested that EPDR1 may act as a novel hormone regulating whole-body energy metabolism.
Apart of this, the biological role of EPDR1 is poorly known.
I have identified that human beta cells also produce EPDR1 protein and that its expression is upregulated in pancreatic islets from Type 2 diabetes vs. non diabetic donors and that its expression is associated to beta cell function.

Hypothesis
Based on the data obtained so far, I believe that EPDR1 expression in beta cells may increase in response to the metabolic stress caused by overfeeding in obese people to, in a compensatory fashion, restore glucose metabolism and maintain beta cell function.

Methods

I aim to apply a cutting-edge methodology, Metabolic Flux Analysis (MFA), which is based in fueling beta cells with labeled energy substrates and then quantify the rate of different metabolic pathways underlying insulin secretion. With this method we plan to elucidate the mechanism of action for EPDR1 in regulating beta cell function.

I also plan to study animals that lack EPDR1, make them obese (to mimic metabolic stress in obese people) and test beta cell function (in vitro) and glucose tolerance (in vivo) to understand the role of EPDR1 in beta cell function and glucose homeostasis.

Results
I have so far conducted some in vitro experiments and found that treatment of beta cells with EPDR1 protein increases insulin secretion whereas silencing EPDR1 expression reduces insulin secretion.
I have performed metabolomics experiments and found that silencing EPDR1 expression in beta cells alter the levels of glucose-derived metabolites in different relevant pathways associated to insulin secretion.

Conclusions
I have found that EPDR1 is required to maintain normal human beta cell function.
EDPR1 regulates glucose metabolism by increasing coupling of glycolysis and mitochondrial function in beta cells.

Importance
The proposed research project will help to elucidate the role of EPDR1 for beta cell function and glucose homeostasis and to deepen the knowledge of molecular mechanisms of EPDR1 to regulate beta cell metabolism and function.
We have also identified genetic variants associated to EPDR1 expression in human beta cells and function and this study will also explore the potential of these genetic variants to make advances of precision medicine in Type 2 diabetes.
Finally, if we confirm the positive effects of EPDR1 protein for human beta cell function and glucose homeostasis, EPDR1 could become a target to develop treatments for obese people to prevent progress to T2D.

Effects of PPARGC1A gene polymorphism on metabolism and obesity

Tue, 08 Feb 2022 08:22:52 GMT

Sebastian Kalamajski,

Hjelt Grant Holder 2022,

Lund University.

Background
Our health relies on a proper balance between energy intake, storage, and expenditure. To accomplish that, a number of genes act as responders to the continuously changing calorie intake, and can direct our fat cells to either store or degrade the calories, depending on our needs. One of those genes is called PPARGC1A, and an estimated 43% of the people globally carry a genetic variant of PPARGC1A that associates with obesity and diabetes. Our goal is to investigate whether this variant not merely correlates, but causes changes in fat cells that make them more or less responsive to calorie intake. Why this is of concern is that a disturbed fat storage capacity leads to insulin resistance and diabetes. In the end, our aim is to create guidelines for precision medicine treatment of obesity and diabetes, based on what genetic variants the individuals are carrying in their DNA.

Hypothesis
We think the genetic variant in the PPARGC1A gene somehow alters the production and/or degradation of the protein (called PGC-1alpha), which in turn would affect how fast a cell can respond to calorie intake or fasting. This would effectively change how much fat is being stored or removed from a fat cell, and would help predict the effect of the genetic variants on obesity and diabetes.

Methods
We can genomically edit fat cells for the different genetic variants using CRISPR-Cas9 toolkit. The edited cells are then analyzed for their specialized fat cell properties, including capacity to store and release fat under different environmental changes, including calorie restriction or cold exposure. Our results will later guide us in the design of clinical studies where we can assess the combined influence of the different environmental factors and genetic variation on e.g. weight loss.

Results
We have genomically edited several cell populations for the obesity-associated genetic variant of PPARGC1A. We have also generated cells that allow us to follow the turnover of the PGC-1alpha protein over time, under different environmental conditions. So far, we have observed rather dramatic effects of one of the genetic variants on the fat cell lipid storage capacity, and also a clear effect of the variant on PGC-1alpha protein stability.

Conclusions
To this end, we have observed clear causal effects of the genetic variants in the PPARGC1A gene on the produced PGC-1alpha protein stability, and on overall fat cell properties. More studies are underway with regards to the effects of different environmental factors and PPARGC1A variants on the fat cell lipid storage and release.

Importance
Almost half of the human population is carrying a genetic variant in PPARGC1A that seems to cause profound effects on fat cell capacity of storing or releasing lipids. This information could guide future precision medicine-based treatments of obesity and diabetes.

Synchrotron X-ray micro-CT imaging for resolving complex 3D structural changes in the kidney

Tue, 08 Feb 2022 08:15:09 GMT

Anja Schmidt-Christensen,

Hjelt Grant Holder 2022,

Lund University.

Synchrotron X-ray micro-CT imaging for resolving complex 3D structural changes in the kidney:
a missing piece of information needed to understand and potentially predict DKD progression and response to treatment

Diabetic Kidney Disease (DKD) is a common complication of diabetes, and is characterized by a gradual loss in kidney function, eventually leading to end-stage renal disease which requires dialysis or kidney transplantation. The kidney is a very important organ for continued good health because it acts as a filter to extract waste and excess water from blood.

The visualization of complex renal 3D functional units with micrometer precision and early microstructural changes in DKD may help redefine the way DKD is understood and treated. Here we use high-resolution Synchrotron X-ray micro-CT to image biopsies from both patients with DKD and animal models, to get a better understanding of how adaptive morphological and functional changes in the chronically diseased kidney develop.

The working principle of the X-ray imaging we use is not any different from that used in common medical radiology known as CT scan, however synchrotron light – is unique!

A Synchrotron source is about a hundred billion times brighter than a hospital X-ray source and can therefore provide us with more detailed information related to injuries and/or diseases of the kidneys. With this technique we can finally resolve complex 3D microstructures with a mesoscale window and potentially uncover local structure-specific alterations in disease or after drug treatment that could otherwise be missed in 2D histology.

The biography of Allan Hjelt and a new TV documentary in Finnish

Fri, 05 Nov 2021 09:41:28 GMT

The biography "Allan Hjelt – Entreprenör i brytningstider", published in Swedish in 2020, is now available in Finnish. In this biography, written by Maria Ekman, we meet a man who built an empire, lost almost everything, – and started all over again. It tells the story of a successful Finland-Swedish entrepreneur, patron of the arts, honorary consul and Finland’s trade negotiator for military equipment and support in the midst of World War II.

”Allan Hjelt - murrosvaiheiden liikemies” is translated into Finnish by writer and editor Marjo Uusikylä. It is available in bookstores in Helsinki, and in your online bookstore.

Publisher: Mistake Media.

ISBN 9789527188194

A tribute to his late father

The half-hour documentary of Allan Hjelt premiered on Finnish AlfaTV on 27 October 2021. It is shown as a part of the series ”Merkit” (Brands) that explores the history, present, values and future of brands .

In the documentary, Bo Hjelt, the son of Allan Hjelt, tells about his childhood memories of his father and how the biography has brought new information of A llan Hjelt to the fore. Maria Ekman, the writer of Allan Hjelt’s biography, presents important places for Consul Hjelt in Helsinki, such as Villa Hjelt and Keskuskatu, the street that transformed the city centre of Helsinki hundred years ago in the 1920’s .

View the episode: Merkit , Kausi 2: 3/10 Producer: Mistake Media. (in Finnish)

Diabetes Research Grants for 2022: Welcome to Apply

Tue, 19 Oct 2021 14:48:07 GMT

Application period begins today!

Lund University presents three Hjelt researchers

Tue, 12 Oct 2021 08:59:46 GMT

Ola Hansson, Karl Bacos and Malin Fex have been awarded 45 000 euros each for their research projects

Today, three of our grant holders in the Diabetes foundation are presented in an article on the Lund University Diabetes Center website. Read more at the LUDC web site .

A golden leaf to the Diabetes Foundation

Mon, 23 Aug 2021 12:34:33 GMT

A golden leaf to the Diabetes Foundation from Lund University

We are proud and happy for the Foundation's new golden leaf in the research tree at The Faculty of Medicine at Lund University. A golden leaf is the Faculty's way to thank organisations, foundations and private individuals for their cooperation and support. Read more at the Lund University web site .

Taking advantage of nature’s own experiment to identify novel pharmacological targets to improve muscle health

Tue, 17 Aug 2021 07:54:10 GMT

Ola Hansson,

Hjelt Grant Holder 2021,

Lund University.

When we eat a meal, the pancreas secretes insulin to signal that energy is plenty and should be harvested. High insulin means that energy stores should not be used but replenished. If a person has type 2 diabetes, this system is not functioning properly. We talk about the two hallmarks of type 2 diabetes, i.e. (1) decreased insulin secretion from the pancreas and (2) decreased insulin sensitivity of target tissues like fat, muscle and the liver. This leads to abnormally high blood glucose levels, which is the definition of diabetes. The largest user of glucose in the body is by far skeletal muscle. When we get older our muscles are getting less and less sensitive to insulin, but this can be counteracted by physical exercise. Today we have ways to pharmacologically stimulate the pancreas to enhance insulin secretion, but unfortunately after many years of research, still no drug to enhance insulin sensitivity specifically targeting skeletal muscle. Reasons for this lack of success could be many, but differences in muscle function and metabolism between humans and model organisms commonly used in research is probably contributing. The aim of this project is to use novel methods to finally identify pharmacological targets to specifically increase muscle insulin sensitivity.

We will test two different approaches. In aim I, we will take advantage of naturally occurring rare mutations that may change muscle insulin sensitivity in humans. By sequencing the DNA of ~10.000 individuals, we have already identified one such candidate in the MSS51 gene. A mutation carried by 139 individuals. This gene is only activated in skeletal muscle and has previously been linked to diabetes in rodent studies. We will now invite mutation carriers and measure their insulin sensitivity. Muscle stem cells will be isolated from biopsies to study how insulin sensitivity may be influenced by MSS51. With this study we will be able to test if MSS51 is associated with diabetes also in humans. In aim II we will investigate if a biological mechanism called splicing may be used to develop a completely new type of drugs to increase muscle insulin sensitivity. Taken together, this project will explore new approaches to elucidate the underlying mechanisms of insulin sensitivity in humans with the goal of identifying novel pharmacological targets to improve muscle health.

Exploring the association of melatonin with type 2 diabetes risk and islet cell function

Thu, 22 Apr 2021 07:39:34 GMT

Malin Fex,

Hjelt Grant Holder 2021,

Lund University.

Metabolism of nutrients in our body is regulated mainly by two hormones; insulin and glucagon. These hormones are secreted from beta and alpha-cells respectively, that are located in small spherical dense cell clusters, termed islets of Langerhans, in the pancreas. Type 2 diabetes (T2D) is a disease resulting from a combination of reduced circulating insulin and a decline in the action of the hormone in peripheral tissues. This results in increased blood glucose levels, a perturbation that over time becomes life-threatening. In addition, glucagon secretion from alpha cells becomes dysregulated in T2D and this contributes even further to high blood glucose concentrations. Therefore, understanding how both these cell types and their hormones act are essential to understand the disease.

The causes of T2D are pleiotropic (e.g., a combination of genetic predisposition and life style), where obesity and a sedentary life style are considered as the main risk factors. Our research aims to understand how genetic risk is associated with T2D and how dysfunction of insulin- and glucagon-producing cells is connected to these events. More specifically, we aim to understand the underlying molecular mechanisms of genetic variants that cause disease under certain conditions. One such gene variant currently studied by us is located in a gene encoding a receptor protein that mediates signals of the hormone melatonin (a molecule that binds melatonin – called melatonin receptor 1B (MTNR1B)). Melatonin is a hormone secreted from the pineal gland in the brain and it regulates sleep and wake patterns in humans. Melatonin can bind and signal via two melatonin receptors, the MTNR1B or the MTNR1A. In addition to regulating sleep-wake cycles, melatonin is involved in regulating the body’s energy demand. Furthermore, the receptors binding melatonin are present on beta and alpha cells. As such, the how and when of melatonin signaling in the insulin- and glucagon-producing cells is of great importance for understanding how T2D evolves.

To understand the properties of melatonin signaling in beta and alpha cells, we will use patient-specific human induced pluripotent stem cells (hiPSCs), which are differentiated to alpha- and beta-like cells. A small skin biopsy (2mm) is taken from the arm of the individuals included in the study. These skin cells are reprogrammed by adding specific factors that reprogram skin cells to stem cells, the hiPSCs. hiPSCs have the capacity to become almost any cell type if treated with the right factors. The past two years, our research team has refined this technique, and we are now able to make beta- and alpha-like cells from human skin cells. This is a tremendous opportunity for our studies, as we now can investigate specific diabetes genes from humans in a cell culture dish. We will utilize skin biopsies from patients with T2D that carry the MTNR1B risk variant, as well healthy individuals that do not carry this variant. The next steps involve so called “genetic scissors” to change the risk variant in the MTNR1B gene to a non-risk variant in the hiPSCs. In addition, we will create cells where we completely delete/knock out the two melatonin receptors. This will enable us to study regulation of insulin and glucagon secretion in our genetically modified beta and alpha like cells.

Presently, we have differentiated skin cells from seven individuals to commence functional studies of beta- and alpha-like cells, by high resolution microscopy techniques. We have utilized genetic scissors to modify the risk variant of MTNR1B to non-risk variants in cells from two patients and confirmed that they are viable and functional. Our next steps are to create beta- and alpha-like cells that completely lack the two receptors for melatonin (MTNR1B and MTNR1A) to even further understand the role of melatonin in regulating insulin and glucagon secreting cells, as well as to more fully understand the genetic contribution of the MTNR1B variant in the disease. We strongly believe that our studies will deepen our understanding of how T2D evolves. Additionally, our models can be utilized, not only to determine genetic influence and the role of melatonin in T2D, but the cell models we create will allow for screening of pharmacological compounds targeting melatonin signaling. This information can in turn be utilized to provide novel precision medicine tools and thus innovative therapeutic strategies to combat T2D.

Restoring circadian rhythmicity in metabolic organs: role of inter-organ circadian desynchrony in the pathogenesis of type 2 diabetes

Mon, 08 Mar 2021 09:49:11 GMT

Volodymyr Petrenko,

Hjelt Grant Holder 2021,

University of Geneva.

The circadian clock system (from Latin “circa diem”, about a day) allows most of the organisms on Earth to anticipate periodical changes of geophysical time. Nearly all the cells in our body comprise molecular clocks that regulate and adjust metabolic functions to a 24-hour cycle of day-night changes. Increasing evidence indicates that misalignment between external stimuli and internal clocks stemming from irregular working schedules, frequent time zone changes, or ageing, have a significant impact on the development of metabolic diseases in human beings, including type 2 diabetes (T2D). Importantly, the organism needs a functional coupling between clocks that are located in different organs in order to function as a whole. Hence, inter-organ circadian desynchrony may also perturb glucose homeostasis. Transplantation of metabolic organs carrying functional clocks to the host with dysfunctional oscillators (associated with aging and/or metabolic disease) represents a model of such inter-organ circadian misalignment due to circadian autonomy of the graft. We hypothesize that circadian autonomy of metabolic organs from rest of the body clocks may lead to circadian misalignment between metabolic tissues, contributing to the pathogenesis of T2D, including post-transplant diabetes mellitus (PTDM).

In this project we aim at evaluating the effect of restoring functionality of molecular clocks in organ-specific manner in otherwise arrhythmic mice on glucose metabolism. By restoring oscillators in liver, kidney, or in insulin-producing cells of pancreatic islets we shall identify the impact of circadian autonomy in each of these tissues on whole-body glucose homeostasis. Given that transplantation is currently an important option to treat many types of metabolic organs failure, the molecular clock autonomy of the transplanted graft should be considered in these transplantations. Establishing the role of graft’s clock on glucose metabolism of the host will provide a novel clinically important information on the pathogenesis of PTDM. Additionally, we aim to unravel interplay between the proinflammatory cytokines and clocks operative in human endocrine pancreas to better understand the pathogenesis of T2D upon systemic (including transplant-associated) or pancreatic islet-derived inflammation. The data generated in this study, funded by Hjelt Foundation, will contribute to further understanding the molecular link between peripheral clocks and glucose metabolism in the context of T2D development, and will prove to be of utmost scientific and clinical relevance.

Obesity, type 2 diabetes and epigenetics in the islets of Langerhans – from genome-wide analysis to functional validation

Tue, 02 Mar 2021 14:09:11 GMT

Karl Bacos,

Hjelt grant holder 2021,

Lund University.

Epigenetic modifications regulate gene activity in our cells. For example, they help make sure that the gene for insulin is active in insulin producing cells, but inactive in cells where insulin is not needed. This is a dynamic system and changes to it can be induced by both internal and external factors, such as our age and sex, or our diet and exercise habits. We have shown that different risk factors for Type 2 diabetes (T2D) influence epigenetic patterns in the so-called islets of Langerhans, small cell clusters in the pancreas which contain insulin producing cells. These epigenetic changes in turn impair insulin secretion and can thereby contribute to the development of T2D. Obesity, perhaps the strongest T2D risk factor of them all, is associated with increased nutrient levels in blood. Exposing islets of Langerhans to increased nutrient levels in culture dishes for only 48h leads to detrimental epigenetic changes. In real life obesity often persist for years, or even decades, but the effect of obesity on epigenetics in the islets of Langerhans has not been studied. Based on these findings we hypothesized that obesity leads to epigenetic changes that in turn increase the risk for T2D.

Our current data supports this hypothesis. We have identified epigenetic changes that occur in islets of Langerhans from obese individuals and mimicking these changes in cultured insulin producing cells leads to impaired insulin secretion. The funds from the Hjelt foundation will be used for two main research tracks. The first is to identify the mechanism by which these epigenetic changes alter insulin secretion. The second is to use cutting-edge techniques for epigenetic editing to reverse the detrimental epigenetic changes in “sick” cells to improve cellular function. And vice versa, we want to induce the detrimental changes in “healthy” cells to impair cell function. This will provide direct evidence that the epigenetic changes we identify are causing cellular dysfunction and disease.

This project may reveal cellular targets for novel T2D therapeutics. As the changes we identify occur in individuals that are non-diabetic, but at high risk for disease, these targets could potentially be hit even to prevent development of the disease.

New book in Swedish: "Allan Hjelt – Entreprenör i brytningstider"

Fri, 08 Jan 2021 08:06:17 GMT

Allan Hjelt – Entreprenör i brytningstider

Allan Hjelt (1885-1945), Bo Hjelt's father, was a successful businessman whose life and career are strongly linked to Finnish industry, the redesign of central Helsinki, the patronage of Finnish leading artists, designers and architects and the acquisition of munitions during both the Winter War and the Continuation War. In this biography we meet a man who built an empire, lost almost everything and started again.
The book is available in bookstores in Helsinki, and in your online bookstore.
ISBN: 9789526943305
The book will be released in Finnish in September 2021.

World Diabetes Day

Tue, 17 Nov 2020 13:50:41 GMT

Hjelt Lecture on Diabetes

The Diabetes Foundation: The World Diabetes Day raises awareness of a condition that millions of people all around the world live with every day. The Lund University Diabetes Center together with Medeon Science Park Malmö and the patient organizations in Skåne presented a digital program on Saturday 14th. The Hjelt Lecure was held by our Grant Holder Karin Stenkula at LUDC.

The Hjelt Interior at the Alvar Aalto Museum in Jyväskylä, Finland

Tue, 10 Nov 2020 13:46:04 GMT

The Hjelt Interior
at The Alvar Aalto Museum in Jyväskylä, Finland

The furniture donation from the Allan and Bo Hjelt Art Foundation made it possible to create Artek's 1940s interior for the Alvar Aalto Museum's permanent exhibition.

The donation includes two safari chairs and two upholstered dining room chairs that were exclusively designed for Allan Hjelt’s official residence as one of the first major private commissions received by Artek, a renowned Finnish furniture company founded in 1935.

The Hjelt interior will be on display until the end of 2020.

Visit the Alvar Aalto Museum

Diabetes Research Grants for 2021: Welcome to Apply

Thu, 15 Oct 2020 13:05:34 GMT

Application period begins today!

The Diabetes Foundation: The application period for next year’s research grants is 15 October to 1 December. Research grants are awarded to applicants at the Medical Faculties of Lund University, Sweden and Geneva University, Switzerland. Read more/apply

Hjelt Talk cancelled

Thu, 02 Apr 2020 12:20:46 GMT

Hjelt Talk cancelled

Allan and Bo Hjelt Foundation has decided to cancel The Hjelt Talk in May 2020 to keep everyone safe. We will let you know the new date for the next talk in November 2020 as soon as we can. Read more about our previous lectures

Type 2 diabetes is a complex multifactorial disease

Wed, 01 Apr 2020 10:14:21 GMT

Daniel Oropeza

Hjelt grant holder 2020

University of Geneva

Type 2 diabetes is a complex multifactorial disease in which a pathological combination of metabolic and genetic factors severely affects the normally exquisite control of blood glucose levels performed by our metabolic organs. There are two highly specialized endocrine cells in the pancreas that secrete hormones that can abruptly change blood glucose levels: the insulin-secreting beta cells and the glucagon-secreting alpha cells. These perplexing cells have diametrically opposed functions: insulin is secreted at high blood glucose levels to promote efficient glucose absorption into our organs while glucagon is secreted at low blood glucose levels to trigger release of glucose from our organs. The delicate balance in secretion of insulin and glucagon forms the basis through which our bodies maintain healthy blood glucose levels at all times.

Various cellular mechanisms control the function of alpha and beta cells, including the fine-tuning of hormone production and secretion in response to subtle changes in the environment, which are sensed through the metabolism of the nutrients circulating in our blood. Unfortunately, for the most part, these basic mechanisms are still poorly understood because of the difficulty in analyzing human alpha and beta cells due to their anatomical configuration and low abundance in our body. In particular, there is very little information regarding how do human alpha cells metabolize sugars, lipids and amino acids. Recently, in our laboratory we have developed novel methods that allow us to efficiently isolate numerous human alpha and beta cells and perform many different types of experiments and analyses. Using these new techniques, we will perform a comprehensive characterization of the metabolism of human beta and alpha cells to understand how they react to the changing metabolic status that is a hallmark of type 2 diabetes.

In addition, we believe that the different ways alpha and beta cells metabolize nutrients to generate new metabolic molecules is intimately linked to how they control the activation or inhibition of specific genes that help to define the key differences between these two cell types. Like for example the decision to whether produce glucagon or insulin as a hormone. Thus, to better understand this process, we will also study how does the metabolism of alpha and beta cells impact the activity of genes that maintain their key diametrically-opposed cellular and physiological differences.

The results from our experiments will generate important and basic information about the key role of metabolism in human pancreatic alpha and beta cell biology, which will be highly relevant to understand how Type 2 Diabetes develops given the strong link between the disease and metabolic dysregulation.

Precision diabetes in paediatrics: screening of molecular and functional effects of new gene variants

Wed, 01 Apr 2020 10:04:35 GMT

Rodolphe Dusaulcy

Hjelt grant holder 2020

University of Geneva

Diabetes is defined by chronic hyperglycemia which may lead to dangerous complications. Type 2 diabetes and type 1 diabetes are the best known forms. Type 2 is often associated with obesity, while type 1 is an autoimmune disease where the immune system destroys the insulin-producing pancreatic beta cells. The form of diabetes studied here is called “monogenic”, and is caused by a mutation in a single gene. These monogenic diabetes forms represent up to 4% of diabetes cases in pediatric populations and are characterized by alteration of beta cell function and or beta cell mass reduction.

Our objective is to identify and validate new genes and mutations responsible for monogenic diabetes. We previously sequenced over 400 genes potentially implicated in diabetes in a population of children with a suspicion of monogenic diabetes. We thereby identified a series of sequence variants in novel and known genes that constitute potential new monogenic diabetes genes and variants.

We hypothesize that these variants may reduce the capability of beta cells to adapt and resist to stressors such as fat and sugar excess or inflammatory mediators. We propose to study in vitro, in human and mouse beta cells, the specific impact of the identified genes and variants. On one hand, we will silence the expression of target genes and, on the other hand, reproduce in vitro the variants observed in diabetic children. To do that, we plan to use a new technology, called the Crispr/Cas9 system, to reproduce the sequence variants in beta cells. Then, we will study the consequences of these gene defects at molecular and functional level by assessing the impact on insulin production and release, cell proliferation and survival.

We believe that this project will be helpful for diabetic children and will allow a better understanding of disease development, adaptation and personalization of the treatments as well as the potential development of new therapeutic strategies.

Creating A Human Disease-In-A-Dish Model Of Diabetes By Genetically Engineering iPSCs Using CRISPR/Cas9

Wed, 01 Apr 2020 09:42:45 GMT

Sebastian Kalamajski

Hjelt grant holder 2020

Lund University

Type II diabetes is associated with several physiological shortcomings in our organism, one of which is the inability of our tissues to respond to insulin. Also, the insulin-producing beta cells in pancreas can lose their insulin secretion capacity, which further complicates the matter, and contributes to elevated blood glucose. It is now known that a few hundred common human genetic variants may influence the capacity of beta cells to produce and secrete insulin. However, in many cases we lack a definitive proof that these genetic variants directly contribute to, and not merely associate with diabetes. To solve this puzzle, in our research we intend to combine the latest advances in genomic editing and in human stem cell technology to uncover how common human genetic variation can jeopardize an efficient insulin production or secretion in pancreatic beta cells.

One of the hypotheses we intend to test is that a specific human genetic variation influences how the beta cell responds to melatonin. Melatonin is a sleep-related hormone that should shut down insulin secretion during fasting, i.e. when we sleep and not want our blood glucose to decrease too much. On the other hand, too much shutdown of insulin secretion by melatonin could create excessively low blood insulin levels when we need it, perhaps after an evening meal. In previous studies scientists have identified genetic variation in a gene called MTNR1B that appears to determine the levels of insulin secretion in the presence of melatonin. The response of the beta cell to melatonin, depending on what type of genetic variant in the MTNR1B gene it carries, may therefore be a potential contributing factor to diabetes.

To test the above hypothesis we need to establish cell lines that have exactly the same genomic sequence, except for the one variation in the MTNR1B gene. We intend to accomplish this using genomic editing technology called CRISPR/Cas9, which we’ll utilize on human stem cells donated by people that carry the MTNR1B gene variant often found in type 2 diabetes patients. We will attempt to switch the cells’ genetic code to one that is associated with lower risk of diabetes, and then evaluate how these stem cells develop into mature insulin-producing beta cells, and how these cells’ insulin secretion is affected by melatonin. Using this strategy we will be able to dissect the contribution of particular genetic variants to the central role of beta cells, which is providing our tissues with insulin.

Our study also carries a secondary aim – once the above-described technologies become established we will be able to study the effects of other human genetic variants on the biology of beta cells in a much more reliable way than has so far been possible. We hope that combining the latest genomic editing with stem cell technologies will result in new knowledge of type 2 diabetes genetics, and create new perspectives on personalized diabetes medicine.

Effect of having low or high salivary amylase copy number on postprandial response to different starch doses

Wed, 01 Apr 2020 09:37:33 GMT

Emily Sonestedt

Hjelt grant holder 2020

Lund University

Genetic factors can influence our ability to digest carbohydrates. The gene encoding for salivary α-amylase, AMY1, has gathered attention in recent years due to the extensive copy number variation (when sections of the genome are repeated in various numbers in different individuals). Individuals with few copies of the AMY1 gene have lower levels of salivary amylase and may have difficulty digesting starch into glucose. We have in a study comprising 19 subjects found a higher postprandial (after eating) glycemia in those with high AMY1 copy number compared to those with low copy number. We now intend to examine the postprandial response to two different starch doses in 60 individuals with low or high AMY1 copy number. Including outcomes such as breath analysis, microbiota and metabolites such as sugars, lipids, amino and organic acids, would give us a more detailed insight into the effect of AMY1 copy number on starch digestion and glucose metabolism. Participants will be recruited from the Malmö Offspring Study by genotype-based recall. We will also examine whether AMY1 copy number is associated with microbiota composition and metabolites among approximately 1500 individuals from the cohort to further understand the metabolic profile of those with low and high copy number. Because high postprandial glycemia is a risk factor for type 2 diabetes, this research project will hopefully contribute to more personalized prevention strategies in which glucose intolerance could be reduced by recommending specific starch intakes depending on the AMY1 copy number.

EHD2: a novel candidate essential for lipid transport and overall glucose homeostasis

Wed, 01 Apr 2020 09:12:09 GMT

Karin Stenkula

Hjelt grant holder 2020

Lund University

Obesity is one of the main risk factors behind type 2 diabetes and cardiovascular diseases. Both obesity and type 2 diabetes are characterized by an insulin resistance, which means that even though insulin is released into the blood, it does not stimulate uptake of fat and glucose into the cells. This results in elevated blood glucose levels, which can develop into type 2 diabetes. Still, it is not known how an increased fat tissue mass is linked with onset of these diseases.

Recently, the protein EHD2 was shown to promote both insulin sensitivity and fat cell function. In the present proposal, we hypothesize that EHD2 is central for regulating uptake of both glucose and fat from the blood. To test our hypothesis, we will apply a variety of cell biology- and microscopy techniques to monitor cellular insulin response, and nutritional uptake. To specifically address the role of EHD2 for these processes, we will analyze fat cells isolated from both normal, wild-type mice and a recently established mouse model lacking EHD2.

Possibly, knowledge of how EHD2 contributes to maintain intact fat cell function can result in new strategies to improve insulin sensitivity and lipid storage capacity in fat cells. This will be useful to both prevent and improve adipocyte dysfunction, with beneficial effects on whole-body glucose homeostasis.

Nov 20, 2019 | Amateur, Autodidact, and Beginner’s Luck: The Making of an Aesthete

Mon, 04 Nov 2019 13:57:18 GMT

Mitchell Owens
Amateur, Autodidact, and Beginner’s Luck: The Making of an Aesthete

Time: Wed, Nov 20th 2019 at 4 pm – 5.30 pm
Venue: Design Museum Helsinki, Korkeavuorenkatu 23 Högbergsgatan
Lecture in English.  Free entry. No registrations.  Please note, that the seats are limited.
Welcome!

Renowned journalist and Decorative Arts Editor of Architectural Digest (AD) Mitchell Owens will be speaking at the Design Museum on Wednesday, November 20th. Owens is an editor, reporter, curator, and scholar whose subjects range from architecture and design to social history and popular culture.

In his talk at Design Museum Helsinki he will address his relationship with Finnish design and architecture, and how it has impacted him over the years.

Scandinavian design has been a passion of Owens’s for many years. The very first design piece he ever owned was Alvar Aalto’s Savoy vase, which he describes to be ’brilliant, yet so very, very modest design’.

In his lecture Amateur, Autodidact, and Beginner’s Luck: The Making of an Aesthete Owens also gives insight into his career: how he became interested in design and became a design writer.

The lecture is organized in collaboration with Design Museum Helsinki and the Museum of Finnish Architecture , courtesy of Allan and Bo Hjelt Art Foundation.

Mitchell Owens :
Owens is currently working as the Decorative Arts Editor of Architectural Digest. In addition, he has written to other publications, among them The New York Times, The New York Times Style Magazine, Travel + Leisure, House Beautiful and The World of Interiors. Up until 2012 also wrote a blog called An Aesthete’s Lament, which was called “charmingly bizarre” by The New York Times Book Review and “one of the best style blogs on the web” by ELLE Decoration. In 2017, Mitchell Owens received an honorary Doctor of Fine Arts degree from the New York School of Interior Design.

Mitchell Owens lives in Cooperstown, New York, with his husband and two daughters. His next book, A More Interesting Life, is a biography of style icon Pauline de Rothschild.

Year: 2019

Application period begins today!

Tue, 15 Oct 2019 12:59:40 GMT

Application period begins today!

Aril 9–10, 2019 | The End (and Ends) of Photo Criticism

Tue, 09 Apr 2019 12:44:23 GMT

A. D. Coleman
The End (and Ends) of Photo Criticism

Time: 9 and 10 April 2019
Venues: Turun Taidehalli and Yrkeshögskolan Arcada

Titled “The End (and Ends) of Photo Criticism” , the lecture addressed Coleman’s professional experiences over the past half-century, changes in the field of photography during that period, and the shifting situation of photography criticism across those decades.

Celebrating his 50th year as a critic, historian and curator

Currently celebrating his 50th year as a critic, historian, and curator of photography and photo-based art, Allan Douglass Coleman has published 8 books and more than 2 500 essays on photography and related subjects. Formerly a columnist for the Village Voice, the New York Times, and the New York Observer, Coleman has contributed to ARTnews, Art On Paper, Technology Review, Juliet Art Magazine (Italy), European Photography (Germany), La Fotografia (Spain), and Art Today (China). His work has been translated into 21 languages and published in 31 countries.

Coleman received the Culture Prize of the German Photographic Society in 2002, the first critic of photography ever so honored. In 2010 he received the J Dudley Johnston Award from the Royal Photographic Society (U.K.) for “sustained excellence in writing about photography.” And in 2014 he received the Society for Photographic Education’s Insight Award for lifetime contribution to the field.

His widely-read blog “Photocritic International” appears at photocritic.com. Since 2005, exhibitions that he has curated have opened at museums, galleries, and festivals in Canada, China, Finland, Hong Kong, Italy, Rumania, Slovakia, Spain, Taiwan, and the U.S.

The talks were organised by Smidiga övergångar i Svenskfinland Development Project at Yrkesinstitutet Prakticum , in co-operation with Arcada University of Applied Sciences, The Museum of Finnish Photography, Photographic Centre Peri, Arts Academy – Turku University of Applied Sciences and Allan and Bo Hjelt Art Foundation.

Alternate History and Poetry Performance
Coleman’s presentation “Alternate History: Robert Capa on D-Day”, was followed by a poetry performance at Club F5.6 Lavaklubi at The Finnish National Theatre in Helsinki on April 9, 2019.

A major leap forward for the understanding of beta cells in T2D

Mon, 01 Apr 2019 08:56:34 GMT

Nils Wierup

Hjelt grant holder 2019

Lund University

The pancreatic islets are key regulators of blood sugar and it is well established that islet dysfunction is the final culprit in type 2 diabetes (T2D). However, the exact mechanisms explaining what fails in the islets in T2D are not known. Studies aiming to understand this have been difficult to pursue due to the complex cellular composition of the islets. The islets are composed of at least 5 cell types and it has not previously been possible to study what fails in T2D in each cell type at a time. This has been made possible thanks to new technology (single-cell RNA-sequencing) that enables measurement of the expression of all genes in a single cell.

We have used single-cell RNA-sequencing on cells from patients with T2D as well as healthy subjects. This way we identified numerous genes with altered expression levels in T2D in each of the 5 islet cell types. We anticipated that these genes would represent at least to some extent the already experimentally proven disease mechanisms of T2D. But this was not the case. Guided by this fact we decided to instead assess alterations in entire genetic programs between T2D and healthy cells. To this end we created a novel analysis algorithm.

When this algorithm was employed to the data set, we found the absolute majority of the biological processes and genes known to be affected in T2D beta cells. We also identified several less well studied processes, as well as numerous genes without a known role in beta cell function. Thereafter we tested the function of a large number of such genes with previously unknown function in beta cells. We found that the absolute majority of them were regulators of insulin secretion or production. Thus our approach can accurately pinpoint both known and unknown T2D disease mechanisms. This is a major leap forward for the understanding of the altered characteristics of beta cells in T2D, and will promote development of T2D therapeutics.

Recycling within the beta cell

Sun, 31 Mar 2019 22:00:00 GMT

Ben King

Hjelt grant holder 2019

Lund University

Beta cells are protein-producing factories that secrete insulin in response to increased blood sugar. Insulin acts on cells all around the body, causing muscle, fat and liver cells to take up sugar, therefore controlling blood glucose levels. During diabetes development, the body becomes resistant to the action of insulin, and so beta cells increase insulin production to compensate. This puts beta cells under increased stress, worsened by local inflammation and other pressures.

Autophagy is a process by which cells can relieve stress, by recycling damaged cellular machinery and disposing of misfolded and aggregated proteins. Autophagy can be a beneficial process for beta cell survival. We have been investigating C3, a protein that is highly expressed in human pancreatic islets. We found that pancreatic islets from human donors with diabetes produced higher levels of the C3 protein, than islets from diabetic patients. When we removed the C3 gene from beta cells grown in the lab, preventing them from producing the C3 protein, we found that autophagy no longer worked properly. These cells were therefore more vulnerable to cell death when faced with stress.

C3 is usually released from cells into the blood, but we have found that C3 exists within beta cells, where it interacts with an autophagy protein called ATG16L1. We are therefore investigating exactly how C3 exists inside cells, and how it regulates autophagy. This involves basic studies of cellular biology and increases our understanding of this otherwise well-studied protein. We are also developing new mouse models to investigate the specific role of C3 in beta cells during diabetes development, to assess the contribution of this protein to beta cell function and survival, with the hope that this will reveal new mechanisms that can be targeted by future therapeutics.

Precision medicine in Type 2 Diabetes

Sun, 31 Mar 2019 22:00:00 GMT

Grant Holder 2019

Rashmi Prasad

Lund University

Type 2 diabetes (T2D) is the fastest growing global epidemic with worldwide prevalence estimates of 382 million people living with diabetes in 2013 and 592 million by 2035. T2D is caused by a complex interplay of genetic and environmental factors. While T2D has shown strong heritability, variants discovered through case control based GWAS studies have only been able to explain a small proportion (~15%) of the heritability. In the current proposal, we aim to use novel approaches to identify this undetermined component of heritability, referred to as missing heritability, of T2D.

It has been observed that T2D is seen more often in offspring of T2D mothers rather than fathers. This could be attributed to parent-of-origin effects, wherein the phenotypic effect of the allele depends on its parental origin; Therefore, a preferred maternal or paternal transmission of risk genotypes is observed, accompanied by differential epigenetic programming (where the DNA code is unchanged but the reading is affected by environmental factors) of paternal and maternal alleles and gene expression discordance. This could also relate to fetal programming during the intrauterine period. Conventional GWAS studies using case-control design could miss such effects.

We will here use global genetic, epigenetic and transcriptomic data from large family cohorts to identify such effects. Subsequently, we will explore whether these loci affect gene expression in a parent of origin manner in relevant adult and fetal tissues – pancreas, liver, kidney, muscle, adipose tissue, placenta and cord blood to understand their role in fetal programming and development as well as relationship to diabetes in later life.

Another source of missing heritability could be de novo mutations. An estimated 70 new mutations arise in the human diploid genome each generation. The role of de novo mutations in diabetes has however been largely unexplored, mostly because of lack of family materials. We will, in this project also investigate de novo mutations as well as their parental specific transmissions and association with diabetes.

New genetic risk variants can help us understand the biology of the disease and point to new mechanisms that lead to disease development.

Can epigenetic factors explain the positive effect of exercise on human metabolism?

Sun, 31 Mar 2019 22:00:00 GMT

Hjelt Grant Holder 2019

Tina Rönn

Lund University

We all know that exercise is good for human health, but still metabolic diseases including type 2 diabetes increase worldwide, partly due to a sedentary lifestyle and unhealthy diets. With this study, we aim to find epigenetic mechanisms that can explain the beneficial effects of exercise and how it differs between individuals. Eventually, this may lead to new treatment strategies for type 2 diabetic patients.

Epigenetic factors include chemical modifications to our genome, that regulates what genes that should be turned on or off at a given time. While the DNA sequence is constant in all cell types, the epigenome is dynamic and gives the different tissues of the human body its own characteristics and also allow the body to respond to external influences. Thereby, epigenetic factors can be seen as a link between the environment and our genes, and understanding this regulation is important for understanding disease development. This knowledge will also be important for future drug development, with targets that could be modified to mimic or inhibit environmental influences on the epigenome and thereby turn on or off gene activity.

To start with, this project will focus on identifying epigenetic mechanisms responsible for the beneficial effects of exercise. For this, advanced mathematical methods will be developed to integrate genome-wide epigenetic factors with genetic factors and gene activity, in human skeletal muscle and adipose tissue from individuals participating in an exercise intervention. This information will be related to physiological parameters, such as age, BMI, glucose and insulin levels in the blood, and physical fitness. Secondly, this study aims to identify epigenetic markers in blood that mirrors the changes in muscle or fat after regular exercise, and that predict the response to exercise.

Overall, the proposed project has the potential to generate novel targets of importance for future prediction, prevention and treatment of metabolic disorders including type 2 diabetes.

Lipidomic signatures of obesity and type 2 diabetes in humans: connection to circadian rhythm perturbations

Thu, 28 Feb 2019 23:00:00 GMT

Hjelt grant holder 2019

Ursula Loizides-Mangold

University of Geneva

The worldwide increase in obesity and type 2 diabetes represents one of today’s biggest health challenges. Moreover, disruption of our body clock due to rotational shift work, jet lag and aging has additional negative effects on metabolism and contributes to the development of obesity and type 2 diabetes. In this project we will analyze the contribution of lipid (fat) metabolism to the development of obesity and diabetes and investigate, which role the biological clock plays in this context.

Fat molecules (lipids) are part of cell membranes, which are thin layers of lipids that form the boundary of living cells and internal cell compartments. Alternatively, lipids are also stored inside the cell in form of lipid droplets. This storage capacity is in particular important for adipose (fat) cells where lipid droplets serve as the main long-term energy store. Overall, there are thousands of distinct lipids in our body cells and lipidomics studies all of them and their relationships. In this project we will analyze the lipid composition of human skeletal muscle, adipose tissue and blood from lean, obese and type 2 diabetic human individuals and will search for differences between patient groups. Furthermore, we will analyze the effect of the biological clock on lipids found in human adipose tissue. We have recently discovered that levels of various types of lipids that are present in our muscle cell membranes vary during the day and could demonstrate that our biological clock is controlling these rhythms. In this project we will now investigate whether these lipid molecules are also rhythmic in human adipose cells and whether these oscillations are controlled by the body clock. Moreover, we will analyze if adipose cells produce signaling proteins (adipokines) in a rhythmic manner and whether their secretion is disturbed if the biological clock is not functional. Taken together, the findings of this study will allow us to identify, which lipid pathways are affected by obesity and type 2 diabetes and will hopefully lead to novel therapeutic approaches for diabetic patients. Moreover, the results of this project will also prepare the way for the identification of new biological markers for type 2 diabetes.

November 21, 22, 2018 | Humanitarian Architecture – Disasters, Development and Design Responsibility

Wed, 21 Nov 2018 14:02:26 GMT

Esther Charlesworth
Humanitarian Architecture – Disasters, Development and Design Responsibility

Humanitarian Architecture – Disasters, Development and Design Responsibility

Time: 21 and 22 November 2018
Venues: Museum of Finnish Architecture, Helsinki and Migration Institute of Finland, Turku

Esther Charlesworth is a Professor in the School of Architecture and Design at RMIT University and Director of the Humanitarian Architecture Research Lab [HARB].

‘Humanitarian Architecture’ is a collective belief that through a consultative process of spatial problem solving, the design profession can contribute in a significant way to the complex challenge of rebuilding a city and its community, following the event of a natural disaster.

Esther Charlesworth’s lecture explored her journey into humanitarian architecture over the last two decades and explored how she has merged theory and practice during her career in the establishment of Australia’s first design not for profit agency – Architects Without Frontiers.

Professor Charlesworth is the founding Director of Architects without Frontiers (AWF). Since 2002, AWF has undertaken over 42 health, education and social infrastructure projects in 12 countries for vulnerable communities, and has been described by ABC radio broadcaster Phillip Adams as ‘destined to develop into one of the greater forces of good on this battered planet ’ .

At RMIT, Charlesworth is the Academic Director of Master of Disaster, Design and Development degree [MoDDD]. Since 1990 she has worked in the public and private sectors of architecture and urban design in Melbourne, Sydney, New York, Boston and has published seven books on the theme of social justice and architecture, including: ‘Divided Cities ‘ (2009), ‘Humanitarian Architecture ’ (2014) and ‘Sustainable Housing Reconstruction ’ (2015).

The lectures were organised by the Department of Architecture at Aalto University School of Arts, Design and Architecture and the Museum of Finnish Architecture as part of the Interplay of Cultures program, and in collaboration with the Migration Institute of Finland and the Allan and Bo Hjelt Art Foundation.

Can architecture build a better world?

Interplay of Cultures – the Museum of Finnish Architecture’s leading autumn exhibition – celebrates the 25th anniversary of education in global sustainability and humanitarian development at Aalto University, while also raising concern regarding the current state of world affairs.

The exhibition Interplay of Cultures is on until February 24, 2019 at the Museum of Finnish Architecture.

May 28, 2018 | Benjamin Hayes, Florence Lam and Toshiko Mori

Mon, 28 May 2018 13:34:00 GMT

Benjamin Hayes, Florence Lam and Toshiko Mori
Säynätsalo Talks | Rethinking Säynätsalo Town Hall

Time: 28 May 2018 at 15.00

Venue: Säynätsalo Town Hall, Council Chamber, Säynätsalo

In the fall of 2017, eleven Master of Architecture students from the Harvard University Graduate School of Design travelled to Finland with professor Toshiko Mori , to conduct research on the Säynätsalo Town Hall and the work of Alvar Aalto.

They spent the semester contemplating the future role of a town hall that had lost its original programmatic and symbolic functions due to the redistricting of regional townships.

In these talks professor Toshiko Mori discussed the working process and key findings of the architecture studio. Florence Lam and Benjamin Hayes , Master’s Students in Architecture, presented their fresh views on the future of the Säynätsalo Town Hall.

The Rethinking Säynätsalo Town Hall talks included a poster exhibition at the Säynätsalo Town Hall .

Detailed program

Facebook: Säynätsalo Talks

The Talks are organised by Hjelt Art Foundation in collaboration with Alvar Aalto Foundation , Artek , City of Jyväskylä and Tavolo Bianco Oy.

Artek Talks Rethinking Säynätsalo Town Hall by Harvard University Graduate School of Design

Time: May 29, 2018

Venue: Artek Helsinki Store, Helsinki

Professor Toshiko Mori discussed the working process and key findings of the architecture studio. Florence Lam and Benjamin Hayes , Master’s Students in Architecture, presented their fresh views on the future of the Säynätsalo Town Hall.

Opening of the Rethinking Säynätsalo Town Hall exhibition. The exhibition will be on display at the Artek Helsinki Store until mid-June.

New ways to combat deterioration of the aging islet cells

Sat, 31 Mar 2018 22:00:00 GMT

Hjelt grant holder 2018

Enming Zhang

Lund University

Could rejuvenating treatment reverse diabetes?

The risk of type 2-diabetes tends to increase following the process of aging. Could there be a way to rejuvenate old insulin producing cells and restore its capacity? In a new project funded by the Hjelt Foundation, researcher Enming Zhang will study the anti-diabetic effects of GDF11, a protein that has lately been widely discussed for its anti-aging qualities.

GDF11 (Growth differentiation factor 11) has been identified as a rejuvenating factor that can reverse aging in muscles, heart and nerve cells in rodents. In 2014, GDF11 was described as a life extension factor in some publications based on the results of experiments with mice. The findings were chosen as the ”scientific breakthrough of the year” by the scientifical journal Science. Later studies have questioned these findings but still…

– There is a debate about the functions of GDF11- anti-aging or pro-aging. Here we would like to just call GDF11 a circulating factor in the blood, and we would like to study its anti-diabetic effects, says Enmin Zhang.

The role of GDF11 in protection against type-2 diabetes is unknown.

– The aim of our study is to find new ways to combat deterioration of the aging islet in the pancreas that contains the insulin producing cells. We hypothesize that this is a cause to impairments in both insulin sensing and the capacity for insulin secretion.

Could it be that high levels of GDF11 is good and low levels is bad…?

– We would say that low level is bad for blood glucose control, but we don’t know if high level is good. As a part of this project we will try to figure out how to stimulate GDF11 production in a diabetic model.

Preliminary data show that GDF11 expression is suppressed in type-2 diabetic islets from human donors.

– Our main proposal is that GDF11 is capable of reprograming aged human islet cells or insulin targeting cells towards a juvenile state, and thereby reinstalling a series of cell functions e.g. insulin secretion, metabolism and insulin sensitivity.

The project will proceed in two steps. First they aim to explore the rejuvenating effect of GDF11 on aged diabetic islets in rodents and humans, and then they intend to investigate the signaling pathways in the aged cell when stimulating with the rejuvenating substans, GDF11.

– We hope this study will bridge the gap for finding use of GDF11 in the treatment of the aging-related component of type-2 diabetes, Enming Zhang ends.

The impact of Nicotinamide Riboside on alpha and beta pancreatic cells function

Sat, 31 Mar 2018 22:00:00 GMT

Hjelt grant holder 2018

Karim Gariani

University of Geneva

Can vitamin injections boost insulin production?

In type 2-diabetes the function of the beta cells is disordered resulting in an unmet need for insulin. Could an addition of vitamin B3 help and restore the function by boosting energy to the cells? Karim Gariani at Geneva University wants to find out.

Type 2-diabetes is a condition when our beta cells fail to produce or secrete enough insulin, or if other cells in our body can’t assimilate the hormone – which causes an even greater demand for insulin from the beta cells.

In order to increase the capacity of the beta cells to produce insulin, Karim Gariani want to study the mechanisms in the mitochondria inside the cells.

The mitochondria play an important roll in every cell in our body. They are considered to be the powerhouse of the cells as they produce energy in the form of ATP. A way to increase ATP could be to increase the amount of a molecule called NAD+ which is involved in various cellular processes and has shown to induce mitochondrial biogenesis and improve mitochondrial homeostasis.

The beta cells are located in islets in the pancreas, and so are alpha cells that produce glucagon, a hormone which in contrary to insulin increase the blood sugar level.

– As observed for beta cells, mitochondria are also known to play a key role in control of glucagon secretion. We thus postulate that modulation of mitochondria activity through NAD+ levels may impact the secretion of insulin and glucagon through direct effect on pancreatic alpha and beta cells, says Karim Gariani.

His plan is to assess the impact of Nicotinamide Riboside on alpha and beta cells function using an in vitro and in vivo approach. Nicotinamide Riboside is a natural vitamin B3 derivative and has showed to elevate NAD+ in mice and humans without any adverse effect detected so far.

– This study will hopefully help to better understand the potential role of NAD+ in pancreatic islets and pave the way for new therapeutic approach for type 2 diabetes.

Nicotine and beta cell function in health and disease

Sat, 31 Mar 2018 22:00:00 GMT

Hjelt grant holder 2018

Isabella Artner

Lund university

Why smoking and diabetes is a bad combination

Smoking is one of the biggest risk factors for developing type 2-diabetes. It is known to raise blood sugar levels and increase the risk for serious complications. The underlying mechanisms remain unknown, but Isabella Artner at Lund University aims to find out.

People who smoke are 30-40 percent more likely to develop type 2-diabetes than non smokers. People with any type of diabetes have more difficulties controlling their blood sugar levels than non smokers. Smokers with diabetes have higher risks for serious complications, including heart and kidney disease, poor blood flow in the legs and feet that can lead to infections and ulcers, retinopathy (an eye disease that can cause blindness) and neuropathy (damaged nerves to the arms and legs that causes numbness, pain, weakness, and poor coordination).

The benefits of quitting smoking are thus huge.

Nicotine is the addictive substance in cigarettes and chewing tobacco. Research has shown that nicotine decreases insulin sensitivity in muscles and fat tissue, but also reduces the function of insulin producing beta cells in the pancreas. However the mechanisms underlying nicotine’s effect on the beta cell have not been determined yet.

– Our earlier results show that nicotine reduces insulin release from beta cells and affects beta cell development during early life in animal models. We aim to determine the signaling pathways activated by nicotine in beta cells and to study the effect of nicotine exposure in healthy and overweight animal models, Isabella Artner says.

Next step would be to investigate if the mechanisms are the same in humans.

– Understanding how nicotine influences beta cell function in diabetes development is of considerable clinical interest since smoking and tobacco use are still common in Scandinavia and the rest of the world. Nicotine treatment is widely used as smoking cessation treatment.

"Molecular crosstalk between the liver and pancreatic β-cells during early diabetic stages"

Sat, 31 Mar 2018 22:00:00 GMT

Hjelt grant holder 2018

Cecilia Jiménez Sánchez

University of Geneva

The liver appears to be sensitive to early decline of insulin production during the early stages of type 2-diabetes. By using cutting-edge techniques Cecilia Jiménez Sánchez, University of Geneva, will study the communication between liver cells and insulin producing beta cells in an attempt to find new biomarkers that predicts the development of the disease.

– It is not possible to assess functional beta cells due to its location in the pancreas, so an identification of sensitive and robust biomarkers in blood to identify early pre-diabetic stages is of major importance of diabetes prevention, she says.

The biological mechanisms that lead to type 2-diabetes often involve so called insulin resistance, which elevates the amount of insulin required to maintain normal blood glucose levels. The beta cells, located in islets in the pancreas, that produce insulin are able to temporarily adapt to this milieu by increasing their cell mass and insulin secretion, but eventually evolve to beta cell failure, promoting the diabetic state.

The liver appears to be sensitive to asymptomatic early decline of functional beta cell mass in a pre-diabetic stage. The associated key challenge raised by this observation is identification of the molecules signaling from the pancreatic islet when they start to lose their beta cells as a primary event, to the liver; and potentially the other way round.

– It could be that unidentified molecules released by the islets can trigger changes in metabolism of the liver, indicating there is an inter-organ crosstalk from islets to the liver, and vice versa during early diabetes stages, says Cecilia Jiménez Sánchez.

Cecilia Jiménez Sánchez will use a special mouse model which progressively develops dysfunction and death of beta cells that ultimately results in the spontaneous and gradual development of diabetes – and cutting-edge techniques such as transcriptomics and proteomics. This will enable studies of gene activity, how the genes affect other genes in the beta cells and the liver cells, and as proteins produced as a result of this activity.

– Identification of novel mechanisms and key molecules, will potentially open new routes of tissue signaling and provide novel insights into the progression of this metabolic disorder.

November 8 and 9, 2017 | Eero Lundén

Wed, 08 Nov 2017 14:40:43 GMT

Eero Lundén
Architecture in the Future in Cities – Towards New

Time: November 8 and 9, 2017

Venues: The Museum of Finnish Architecture, Helsinki and Brinkkala Mansion, Turku

What is the role of art in exploring the possibilities of new buildings? Can museums shape the way we experience art? Can architecture add to the learning experience in schools? What will the cities of the future look like? How can architects and citizens together shape our future cities?

Designing a museum or a school is an exciting architectural challenge. In this talk the Finnish architect Eero Lundén outlined some of the architectural challenges in designing public buildings, transport hubs and visions for cities, described his methods and working processes, and provided examples of architecture and urban design for the future within and beyond Finland.

Eero Lundén (b.1982) is an architect FRSA and the founder of Lundén Architecture Company based in Helsinki. The office is focused on researching the possibilities of new technologies and cross-disciplinary cooperation in creating new visionary buildings and urban environments.

The talks were organised in collaboration with the Museum of Finnish Architecture and the Bryggman Institute .

May 23, 2017 | Mikkel Bogh

Tue, 23 May 2017 13:46:10 GMT

Mikkel Bogh
Towards the Unbound Museum

Time: May 23, 2017

Venue: Ateneum Hall, Ateneum Art Museum, Helsinki

The digitised museum has opened up an experimental space not defined by architecture and opening hours and more or less undefined by curatorial perspectives.

But what are the challenges of the thus unbound museum in terms of curatorial authority as well as in terms of finances and legal issues?

What do we risk losing by giving almost unlimited access to digitized collections? What can be gained? And how far do we want to go towards the unbound museum?

Dr. Mikkel Bogh , art historian and director of Statens Museum for Kunst SMK in Copenhagen, gave an inspiring talk on the challenges and gains towards the unbound museum.

This talk took as a starting point experiences with open access and strategic developments such as the newly launched project SMK Open at Statens Museum for Kunst. The talk was organised in collaboration with Ateneum Art Museum and Hjelt Art Foundation.

Life without insulin: Testing the anti-diabetic role of a candidate involved in inflammation

Fri, 31 Mar 2017 22:00:00 GMT

Hjelt grant holder 2017

Sanda Ljubicic och Giorgio Ramadori

University of Geneva

– Identification of novel mechanisms and key molecules, will potentially open new routes of tissue signaling and provide novel insights into the progression of this metabolic disorder.

Blocking aberrant cell surface mitochondrial VDAC1 is associated with restoration of insulin secretion in diabetes

Fri, 31 Mar 2017 22:00:00 GMT

Hjelt grant holder 2017

Albert Salehi

Lund university

The information that will emanate from this project would have great impact on the prevention of T2D in view of the years of dysregulated blood glucose control preceding the outbreak of the disease.

A hallmark of type 2 diabetes is decreased insulin secretion and a loss of functional beta-cells, leading to dysregulation of blood glucose control. The elevated average blood glucose concentrations consequently exert harmful effects on the insulin secreting beta-cells, so called glucotoxicity. Since beta-cell mitochondria play a central role in the coupling of glucose metabolism to insulin secretion, their dysfunction has been implicated in the defective hormone release in type 2-diabetes. A key regulator of mitochondrial function is the voltage-dependent anion channel 1 (VDAC1), a multi-functional protein located on the outer mitochondrial membrane (OMM) mediating the fluxes of nucleotides and metabolites across the OMM. Changes in the VDAC1 or VDAC2 function have been related to impaired mitochondrial metabolism and apoptosis. The present project aims to identify the mechanisms underlying pancreatic beta-cell dysfunction during episodes of glucotoxicity and to dissect the complex signaling network involved in hyperglycemia-induced beta-cell dysfunction in human islets and also in relevant animal models of type 2 diabetes.

New Epigenetic Targets for Diabetic Kidney Disease Prediction

Fri, 31 Mar 2017 22:00:00 GMT

Hjelt grant holder 2017

Yang De Marinis

Lund university

Diabetic kidney disease affects almost 30 percent of diabetic patients and is a prime reason for kidney function loss. High blood glucose may contribute to diabetic kidney disease progression, and several studies including my previous publications have shown that diabetic kidney disease development may involve glucose-triggered epigenetic changes, which will be the focus of this project.

Epigenetic changes may occur via modifications on the histone proteins, around which the DNA strand winds and packs into chromosome structure. Based on our previous research, we suggest that glucose may modify histones on various locations, leading to changes in DNA packaging structure, and consequently affects gene activity that contributes to diabetic kidney disease development. Here we will make detailed analysis on histone modifications in blood from diabetic patients with Diabetic kidney disease, and associate these changes to diabetic kidney disease risk.

This study will hopefully contribute to better understanding of diabetic kidney disease pathogenesis. The epigenetic markers in blood identified in this project may be used as predictive biomarkers for diabetic kidney disease. Once validated, patients can be screened by simple blood tests for presence of these markers without invasive biopsy procedures. Patients at high diabetic kidney disease risk can be thereby identified to allow intensified therapy to prevent diabetic kidney disease.

New markers and therapeutic targets to prevent cardiovascular events

Fri, 31 Mar 2017 22:00:00 GMT

Hjelt grant holder 2017

Andreas Edsfeldt

Lund university

The risk of dying from cardiovascular disease is increased among individuals with type 2-diabetes. Type 2-diabetes is increasing fast and considering the high risk to suffer from a cardiovascular event it is crucial to increase our knowledge regarding atherosclerosis in type 2-diabetes. Through the identification of biological differences in type 2-diabetes we aim to find markers and therapeutic targets to prevent cardiovascular events.

The risk of suffering from cardiovascular events as myocardial infarction and stroke is increased for individuals with type 2-diabetes. These complications are commonly caused by ruptures of vulnerable atherosclerotic plaques, located in the large arteries. The cause of the increased risk to suffer from a vulnerable plaque rupture among individuals with type 2-diabetes remains unknown.

We recently showed that atherosclerotic plaques from individuals with type 2-diabetes have signs of an impaired arterial tissue repair as a potential cause of the high risk for a plaque rupture.

We aim to identify if the impaired tissue repair might be caused by a defect inflammatory resolution and clearance of dead cells, two important steps in tissue healing and regeneration.

By characterizing the role of these processes in the arterial wall we further aim to assess if they might be possible to trace in blood as biomarkers or by imaging to identify high risk individuals.

November 16 and 17, 2016 | Gudmar Olovson

Wed, 16 Nov 2016 14:54:41 GMT

Gudmar Olovson
Mitt liv i skulptur

Time: November 16 and 17, 2016

Venues: The National Museum of Finland, Helsinki and Humanisticum, Turku

The renowned Swedish sculptor Mr. Gudmar Olovson , gave two talks about his life and sculpting in Swedish with the title “Mitt liv i skulptur”.

Gudmar Olovson (1936-2017) was born in Boden, Sweden. He grew up in Stockholm where he received his training at the Royal Academy of Fine Arts. After spending time in Florence and Rome, Gudmar Olovson moved to Paris in 1960, where he established his atelier. His many well-known sculpted portraits include those of Carl XVI Gustaf King of Sweden, Crown Princess Victoria of Sweden, Pope John Paul II, Charles de Gaulle and Ingrid Bergman. He received a number of international awards for his art.

The seminars were a collaboration between The National Museum of Finland, Åbo Akademi University Foundation and Hjelt Art Foundation.

May 12, 2016 | Kent Bloomer

Thu, 12 May 2016 13:58:40 GMT

Kent Bloomer
Art Approaching Science and Religion

Time: May 12, 2016

Venue: Sibelius Museum, Turku

As part of the Hjelt Lecture series Mr. Kent Bloomer , Founder of Bloomer Studio and Professor at the Faculty of Architecture at Yale attended the symposium Art Approaching Religion and Science.

Professor Bloomer presented his timeless approach on ornaments, both historically and how they translate into the modern society and architecture.

PPARγ signaling in bone cells controls glucose homeostasis implications in diabetes and osteoporosis

Thu, 31 Mar 2016 22:00:00 GMT

Hjelt grant holder 2016

Dr Nicolas Bonnet

University of Geneva

Type 2 diabetes mellitus (T2DM) and osteoporosis are two major disorders which prevalence increases with aging and is predicted to worsen in the coming years. Preclinical investigations suggest common mechanisms implicated in the pathogenesis of both disorders. Recent evidence has established that there is a clear link between glucose and bone metabolism. The emergence of bone as an endocrine regulator has led to the re-evaluation of the role of bone cells in the development of metabolic diseases such as T2DM.

The grant generously provided by the Hjelt Foundation will be used to clarify how bone cell can contribute in the regulation of glucose homeostasis. We already provide evidence that in mice that lack the gene encoding the transcription factor PPARγ in specific bone cells (osteocytes, Ocy-Pparγ-/-) exhibit an increase in energy expenditure and an improvement in glucose homeostasis, in addition to a better bone strength.

This project aims to further elucidate the mechanisms by which PPARγ expression in bone cells regulates energy metabolism. First, we will investigate if under high fat diet Ocy-Pparγ-/- mice are protected against bone fragility, fat accumulation, steatotic livers and the development of insulin resistance all associated with obesity. Second, we will elucidate which insulin sensitizing bone derived hormone exerts these metabolic effects.

In the future, the group of Pr Ferrari, in which Dr Nicolas Bonnet is conducting this research, will try to identify other bone-derived factors able to regulate glycemia. As a proof of concept this research can be quickly validated in humans by investigating GERICO cohort currently composed of 1000 retired workers who have been followed up for more than 6 years with assessments of risk of incident diabetes according to insulin sensitizing bone derived hormone.

Stimulate adhesion-signaling to enhance insulin secretion and β-cell survival

Thu, 31 Mar 2016 22:00:00 GMT

Hjelt grant holder 2016

Dr. Caroline Arous

University of Geneva

Subtitle: A better adhesion of beta-cells for a better insulin secretion and survival

Proposed by: Dr. Caroline Arous, Dept. of Cell Physiology and Metabolism, University of Geneva.

Type 2 Diabetes (T2D) is characterized by the death of insulin-producing pancreatic β-cells, which affects insulin secretion, leading to an impairment of glucose homeostasis. β-cells are localized within the islet of Langerhans inside the pancreatic tissue. In addition to the β-cells, pancreatic islets contain also a network or scaffold of fibrous or sheet like extracellular structures, also called extracellular matrix (ECM) to which β-cells are attached, and which supports their secretory function, in so far non-understood ways. In T2D, this ECM scaffold is modified or reduced and could therefore be involved or responsible for β-cell dysfunctions. β-cells are linked to the ECM via cell-surface receptors called β1-integrins. These receptors can regulate many cellular functions such as survival and insulin secretion in β-cells, but it is not known whether their function is affected by high glucose levels found in diabetic individuals. The goal of our project is to determine how different types of ECM affect β1-integrin-mediated secretion of insulin and β-cell survival, and to study how the context of T2D is impairing the function of the β1-integrin receptor. Our preliminary results propose that β1-integrin activity is affected by high glucose concentration (for example during hyperglycemia), resulting in reduced cell survival, but also in a change in the deposition and organization of the ECM scaffold. By understanding the glucose-mediated effect, we hope to provide new information how the tissue architecture and β-cell function is affected in T2D and how the function of the β1-integrin receptor can be improved.

Generating a detailed map of human islet metabolism and its relation to insulin secretion

Thu, 31 Mar 2016 22:00:00 GMT

Hjelt grant holder 2016

Peter Spégel

Lund university

Metabolism in the pancreatic β-cells, located in the pancreatic islets of Langerhans, controls secretion of insulin, which in turn regulates metabolism in peripheral tissues. Hence, if metabolism in these cells is perturbed, insulin secretion will be insufficient and diabetes may evolve. Investigation of metabolism is challenging, as it involves thousands of reactions, producing hundreds of different substances from even a simple sugar. During recent years, novel analytical techniques have been established that allow for measurement of hundreds of metabolites in cultured, mainly rodent, β-cells that are available at sufficiently large quantities. However, cultured cells differ from their primary counterparts and differences also exist between rodents and humans. We are now establishing new highly sensitive analytical platforms that will allow for these analyses in small quantities of isolated human islets. With these platforms we intend to generate a detailed map of human islet metabolism and its relation to insulin secretion. Moreover, we intend to examine alterations in metabolism elicited by altered circulating levels of nutrients associated with pre-diabetes, characterizing the early phase of β-cell failure.

Dissection of the molecular mechanisms of glucose-stimulated hormone secretion during OGTT using GWAS

Thu, 31 Mar 2016 22:00:00 GMT

Foto: Johan Bävman

Hjelt grant holder 2016

Emma Ahlqvist

Lund university

The hormones secreted in response to an oral glucose tolerance test (OGTT) are central players in regulating blood glucose. Insulin and glucagon are secreted in response to high and low glucose respectively and regulate glucose uptake and release in peripheral tissues, keeping blood glucose at healthy levels. The two incretin hormones GIP and GLP-1 are secreted by cells in the intestine in response to nutrient stimulation and have insulin-stimulating capacity as well as numerous other functions in the metabolic and cardiovascular systems. By using genome-wide association studies (GWAS) we have identified a number of genetic variants that affect the levels of GIP, GLP-1 and glucagon in blood, both in the fasting state and after an oral glucose tolerance test. The aim of this project is to identify the genes that mediate the effect of the genetic variants and to functionally characterize the involved cellular mechanisms. We will do this by genetic analysis of related traits in different human cohorts, by studying the expression of candidate genes in relevant tissues and by exploring the function of candidate genes in cell lines, animal models and human tissue. This way, we hope to identify genes and cellular pathways involved in hormone secretion and inactivation that are potential therapeutic targets for treatment of type 2 diabetes and obesity.

May 16, 2015 | Ying Gao

Sat, 16 May 2015 14:04:30 GMT

Gereon Sievernich
Exhibiting Ai Weiwei

Time: May 16 and 17, 2015

Venues: Bukowskis, Helsinki and Sibelius museum, Turku

During a lecture professor Ying Gao engaged the audience wearable technology and interactive fashion, giving a chance to reflect on fashion in another way. A work can be activated by the sound of a voice, the stimulus of a gaze, a flash of light bringing the garment into definition.

May 16, 2015 | Gereon Sievernich

Sat, 16 May 2015 14:02:24 GMT

Gereon Sievernich
Exhibiting Ai Weiwei

Time: May 16, 2015

Venue: HAM (Helsinki Art Museum), Helsinki

Presenting his personal view on the man behind the artist Ai Weiwei, Gereon Sievernich , Director of the Martin-Groupius-Bau in Berlin, gave the audience a wide perspective on the work Weiwei have produced over the years and how the political climate of China and the rest of the world have affected the artist Ai Weiwei.

Possible mechanisms behind insulin resistance to be mapped

Tue, 31 Mar 2015 22:00:00 GMT

Hjelt grant holder 2015

Olga Göransson

Lund university

During 2014, Olga Göransson’s group of researchers described the role of the hitherto unknown protein SIK2 in adipose cells from rats and mice. With the support of the Hjelt Foundation, they are now able to go further and investigate whether there is a link between SIK2 and the incidence of insulin resistance in humans.

Diabetes is an increasing among the population, health problem, which is partly due to insensitivity to the blood-sugar lowering hormone insulin (insulinhjelt_project report resistance). The disease is very strongly linked to obesity. Insulin resistance means that the cells’ ability of cells to react to insulin is reduced. Consequently, the cells are unable to absorb energy from nutrients in the blood after a meal. Many overweight people develop insulin resistance, but the reason for this has not been established. Not Furthermore, not all overweight people develop type 2 diabetes either. However, it is clear that disrupted adipose tissue function is an underlying cause of insulin resistance.

“To understand why obesity leads to insulin resistance in certain individuals, it is important to find out which mechanisms control the function of adipose cells and investigate the differences between sufferers and non-sufferers,” says Olga Göransson, who leads a group of researchers focusing on protein phosphorylation (a process that regulates cell activity).

Present in adipose tissue

SIK2 is a protein that primarily occurs in adipose tissue, the main function of which is primarily to store fat formed from fatty acids and sugar from the blood. Olga Göransson and her colleagues previously showed that SIK2 is required for an adipose cells to be able to absorb take up glucose, i.e. sugar, from the blood. By reducing the quantity of SIK2 in rats and mice, they showed that the level of a glucose transporter, GLUT4, was reduced.

“With our partners in Stockholm, we have also studied SIK2 in humans and our preliminary results show that the quantity of SIK2 is dramatically reduced in adipose tissue from insulin-resistant individuals.”

Investigating the link

The questions they are asking themselves now are: does SIK2 affect cells’ the sensitivity of cells to insulin? Can SIK2 itself be regulated by insulin? Can a change in the quantity of SIK2 lead to the biological response to insulin and thus the function of adipose cells being affected?

“We will test whether there is a causal connection between reduced SIK2 and the incidence of insulin resistance in human adipose cells, and thus reduced ability to store fat,” says Olga Göransson.

Sara Liedholm

A step towards customised treatment for type 2 diabetes

Tue, 31 Mar 2015 22:00:00 GMT

Hjelt grant holder 2015

Petter Storm

Lund university

How we react to a medicine may depend on our genes. Petter Storm, a bioinformatician at Lund University Diabetes Centre, is searching for new markers that show which medicine is most suitable for individual patients.The overall objective of the research for which Petter Storm was granted EUR 50,000 by the Hjelt Foundation is to identify genetic markers that can be used to understand or explain responses to pharmaceutical treatment of type 2 diabetes.

hjelt_projectreport“One response, for example, is the absence of any blood-sugar lowering effect of a medicine. Another might be adverse reactions,” says Petter Storm. There are currently around ten different pharmaceutical classes for diabetes with completely different mechanisms of action. The ability to use a simple test to decide which medicine will be most beneficial for a patient would save the patient a lot of suffering.

Adverse reactions

The most common medicine for type 2 diabetes, metformin, is one example. Nearly a quarter of patients suffer adverse reactions such as vomiting and diarrhoea. The group of sulphonylurea preparations are another example, where certain diabetics have an excellent response because they have mutations in a particular gene.

Doctors and patients currently have to work towards the right dose and the right medicine by trial and error.

“However, we believe that are genetic explanations for intolerance to a specific medicine,” says Petter Storm.

This would imply a completely new approach to prescribing diabetes medicines and is one of the objectives of customised treatment of diabetes for the research project ANDIS (Alla Nya diabetiker i Skåne – All New Diabetics in Skåne). ANDIS started in 2008 and monitors just over 10,000 people who have contracted diabetes in Skåne.

Analysing genetic material

In ANDIS, the researchers will now analyse the genetic material, the DNA, of all participants.

“We will also extract all the prescription data, i.e. information on the diabetes and diabetes-related medicines (for example for complications such as cardiovascular disease) they have been prescribed in the past five years,” says Petter Storm.

Using information on HbA1C (the long-term average blood sugar level) for each participant, the researchers can monitor the progression of the disease.

“By comparing those who have had adverse reactions with those who had none, and those who responded well to treatment with those who did not, we hope to be able to find genetic markers to explain the differences.”

Complications

Before the entire ANDIS puzzle has been completed, the ANDIS researchers also hope to find genetic markers for complications such as cardiovascular disease or damage to eyes, nerves and kidneys.

“As the participants in ANDIS will be monitored for a long period of time, they will gradually develop various complications. This will allow us to compare those who suffer a certain complication with those who do not,” says Petter Storm.

Markers that indicate the risk of developing a specific complication will allow preventive treatment to be started in good time.

“The great thing about ANDIS is that the longer it lasts, the more data we will collect, giving us an even better basis for future research,” says Petter Storm.

Sara Liedholm

The molecular mechanisms of the circadian clockwork and their roles in metabolism regulation and the etiology of diseases such as diabetes and cancer

Tue, 31 Mar 2015 22:00:00 GMT

Hjelt grant holder 2015

Charna Dibner

University of Geneva

New insights into the circadian clock and type 2 diabetes. Charna Dibner is the head of a recently established research group in the Division of Endocrinology, Diabetes, Hypertension and Nutrition, Geneva University Hospital and recipient of a grant of CHF 50,000 from the Hjelt Foundation. Charna Dibner undertook her PhD in the field of neurological development, and her postdoc in the field of mammalian circadian clocks. The circadian clockwork is a biochemical mechanism that oscillates with a period of exactly 24 hours when it receives daily corrective signals from the environment, primarily daylight and darkness.

“I came across papers on the circadian clock by Professor Ueli Schibler, my postdoctoral supervisor, and found the subject captivating. It’s quite amazing how universal this mechanism is. It has become increasingly clear that the circadian clock is functional in nearly every cell, and impacts critically on most aspects of physiology and behaviour,” she says.

The role in metabolism

Charna Dibner’s laboratory investigates the molecular mechanisms of the circadian clockwork and their roles in metabolism regulation and the etiology of diseases such as diabetes and cancer. This is a recent subject not even a decade old. What is quite intuitive in the discovery of the connection between the clock and metabolism is that certain bodily tasks should not occur at the same time. During catabolic and anabolic processes, such as eating, for example, we need to digest food and then store any unused energy within the body; this should not happen simultaneously. One of the obvious functions of the clock is temporarily segregating opposite metabolic processes to make our body more economical.

“Our long-term goal is to clarify the relationship between the circadian clock and metabolism and its effect on physiological conditions, and on obesity and type 2 diabetes. We are also focusing on the relationship between the circadian clock and cancer progression,” Charna Dibner says.

Severe consequences

Most, if not all, metabolic processes are subject to diurnal oscillations and, conversely, daily feeding-fasting rhythms are the dominant timing cues in the synchronisation of circadian clocks in peripheral organs. The disruption of circadian physiology imposed by social constraints on many human subjects, such as the chronic ‘social jetlag’ phenomenon, can have severe consequences on their health conditions. Concomitant with increasing sleep deficit and irregular mealtimes, there is a worldwide rise in the incidence of metabolic disorders and type 2 diabetes, and both biological and epidemiological studies suggest a direct link between lifestyle and these metabolic disorders.

However, the genetic and biochemical connections between circadian clocks and metabolic disorders are still poorly understood in humans. It is therefore of utmost scientific and clinical importance to provide further insights into the emerging connection between the circadian oscillator function and the etiology of obesity and type 2 diabetes. If we succeed in establishing a molecular link between the circadian clock and these metabolic disorders, modulating the oscillator could be considered to be a new potential therapeutic avenue.

Sara Liedholm

Characterizing some specific neuron populations, which play a crucial role in the control of body weight, food intake and glucose metabolism under different situations

Tue, 31 Mar 2015 22:00:00 GMT

Hjelt grant holder 2015

Jordi Altirriba

University of Geneva

– The grant generously received from the Hjelt Foundation will be used to characterize some specific neuron populations, which play a crucial role in the control of body weight, food intake and glucose metabolism under different situations (normal, obesity and diabetes) and to describe how they are modified in response to an oxytocin treatment, which has been demonstrated to be useful for treating obesity. In the future, the group of Prof. Françoise Rohner-Jeanrenaud, in which Jordi Altirriba is currently integrated, will try to perform a clinical trial involving diabetic patients in order to validate its utility as a diabetes treatment.

Note: For his project Jordi Altirriba was granted EUR 50,000 from The Hjelt Foundation.

Sara Liedholm

October 21, 2014 | Wim Pijbes and Berndt Arell

Tue, 21 Oct 2014 14:06:48 GMT

Wim Pijbes and Berndt Arell
Reinventing the museum

Time: October 21, 2014

Venue: Ateneum Hall, Ateneum Art Museum

How can museums become visitor-friendly and modern, yet stay true to their architectural heritage?

In our quickly-changing society National Museum’s continue to be an important constant in the lives of art and history lovers. But the National Museums have to stay in touch with their time, and are therefore affected to change. Renovation is essential to ensure perfect conditions for delicate art pieces, but also to keep attracting visitors.

General Director of Rijksmuseum in Amsterdam, Mr. Wim Pijbes , and General Director of the Swedish National Museum in Stockholm Mr. Berndt Arell gave us their view on renovating historical sites and on how to keep up with changes in society at two of the most important National Galleries in Europe.

May 22, 2014 | Hans Barnekow

Thu, 22 May 2014 14:09:38 GMT

Hans Barnekow
I Stalins Skugga. Finland 1944–1952

Time: May 22, 2014

Venue: Bukowskis, Helsinki

The Swedish Filmmaker, Director and Producer Hans Barnekow (1944-2016) introduced his documentary film I Stalins Skugga. Finland 1944–1952 (2002). Mr. Barnekow was renowned for his documentaries focusing on Swedish and Finnish history.

A seminar and screening in a collaboration with Bukowskis and Svenska Klubben.

Does Micu2 control insulin secretion? – A role in health and disease

Mon, 31 Mar 2014 22:00:00 GMT

Hjelt grant holder 2014

Dr. Annika Bagge

Lund university

In Type 2 diabetes glucose-stimulated insulin secretion (GSIS) is impaired. In β-cells, GSIS is tightly coupled to the metabolism of glucose, which ultimately results in a rise in intra-cellular calcium (Ca2+) levels activating the insulin-secretion-mechanism. Ca2+ is also taken up by the mitochondria through the Mitochondrial Calcium Uniporter complex (MCU-complex). This Ca2+-uptake as well as the MCU-complex have been shown to be important for GSIS, but the function of mitochondrial Ca2+ is still not fully understood. Micu2 was recently identified in mouse liver as a subunit of the MCU-complex functioning as a gate-keeper for mitochondrial Ca2+-uptake. However, The fact that a genetic variation in the Micu2 gene affects beta-cell function and insulin secretion in humans suggests that Micu2 has an important function in β-cells. The project aims at elucidating the function of Micu2 in pancreatic β-cells by studying the metabolic effects of removing and/or adding Micu2 in cultured β-cells. In addition, we will examine the pathophysiological role of Micu2 in mice in which Micu2 is genetically deleted. The project should lead to better understanding of the role of the MCU-complex as well as Ca2+ signaling in β-cells, and ultimately lead to improved understanding, prevention and treatment of T2D.

Characterization of non-coding RNAs in the pancreatic islets of Langerhans and identification of circulating RNAs as blood-based biomarkers in type-2 diabetes and associated complications

Mon, 31 Mar 2014 22:00:00 GMT

Hjelt grant holder 2014

Dr. Jonathan Esguerra

Lund university

Dr. Jonathan Esguerra, “Characterization of non-coding RNAs in the pancreatic islets of Langerhans and identification of circulating RNAs as blood-based biomarkers in type-2 diabetes and associated complications” (€ 25 000):

The complexity of diabetes as a disease necessitates novel therapeutic and diagnostic avenues. An emerging trend in pharmacology is RNA-based therapeutics targeting non-coding RNA genes (ncRNA), i.e. genes which do not code for proteins but rather transcribe functional RNA molecules as the final gene product. However, the potential of using such approach in diabetes may not be fully realized until the roles of ncRNA genes in glucose homeostasis are reasonably elucidated. Recent studies have also shown the presence of stable RNAs circulating in the blood after tissue injuries. Because many transcripts are expressed in cell-type enriched manner, it should be possible to monitor the progress of specific cellular damage by measuring RNAs which has leaked into the bloodstream. In micro- and macro-vascular diabetic complications, cellular damage in affected tissues remains undetected until major pathophysiological symptoms are already manifested. This proposal has the following aims: i) establish the global ncRNA landscape in the pancreatic islets with RNA sequencing, ii) elucidate the roles of emerging ncRNA genes in glucagon and insulin secretion, and iii) investigate the potential of circulating RNAs as blood-based biomarkers in predicting the onset of diabetes, as well as monitoring the progression of its various complications. Identification of ncRNA genes important for glucose homoeostasis will bring additional arsenal in diabetes therapy, while early monitoring of the disease via blood-based RNA biomarkers will significantly improve personalised diabetes treatment.

Zinc transporter ZnT8 and type 2 diabetes

Mon, 31 Mar 2014 22:00:00 GMT

Hjelt grant holder 2014

Dr. Jens Lagerstedt

Lund university

Dr. Jens Lagerstedt, “Zinc transporter ZnT8 and type 2 diabetes” (€ 50 000):

Understanding the causative factors in type 2 diabetes may provide possibilities to intervene and revert the progression of the disease at an early stage. Much effort is therefore put into investigating the environmental and genetic factors contributing to the disease. As part of this, genome-wide association studies (GWAS) have successfully identified several genes linked to type 2 diabetes. One of those, the SLC30A8 gene, encodes a zinc transporter, the ZnT8 protein, that resides in the membrane of insulin storage vesicles and shuttles zinc ions to the interior, or lumen, of the vesicles. Lumenal zinc is important as it helps in packaging and storage of the insulin produced.

The genetic variation that links the SLC30A8 gene to type 2 diabetes results in an amino acid substitution in the ZnT8 protein. It has generally been assumed that the risk variant is associated with decreased functionality. However, recent findings describe loss-of-function variants to be associated with reduced incidence of type 2 diabetes. While these findings challenge the established view, they also provide new possibilities to assess the role of the ZnT8 protein in beta cell function and type 2 diabetes risk. With the generous support from the Hjelt foundation we can now explore the cellular and molecular mechanisms of the ZnT8 variants, and thereby hopefully be able to explain their involvement in the etiology of type 2 diabetes.

microRNA-21 in obesity, insulin resistance and diabetes

Mon, 31 Mar 2014 22:00:00 GMT

Hjelt grant holder 2014

Prof. Michelangelo Foti

University of Geneva

“miRNA-21 in obesity, insulin resistance and diabetes” (CHF 37 000):

Obesity has reached pandemic proportions and represents an important risk factor for metabolic liver diseases and diabetes. Recent studies have put emphasis on the critical role of a special class of small molecules, called microRNAs, in insulin resistance, hepatic diseases and diabetes. Among these microRNAs microRNA-21 is significantly deregulated with obesity and diabetes in peripheral organs such as the liver and the adipose tissue. These recent findings suggest that microRNA-21 may play an important role in these metabolic diseases. This hypothesis is further supported by our preliminary studies showing that microRNA-21 is an important factor involved in hepatic metabolic disorders occurring in obese mice.

The goal of this project is to investigate the prophylactic and therapeutic benefits of microRNA-21 targeting using genetic and pharmaceutical tools in order to prevent liver metabolic disorders and insulin resistance in obese mice. In parallel, the molecular mechanisms by which microRNA-21 promotes the development of liver diseases and insulin resistance with obesity will be investigated.

These studies should provide important insights into the therapeutic potential of targeting microRNA-21 to alleviate obesity-associated liver diseases, insulin resistance and diabetes. In addition, this project should also permit the pinpointing of new and potentially other drug susceptable molecules contributing to the development of insulin resistance and diabetes with obesity.

Decipher single-cell transcriptomes of human pancreatic islets in non-diabetic and diabetic individuals (CHF 63 000)

Mon, 31 Mar 2014 22:00:00 GMT

Hjelt grant holder 2014

Dr. Christelle Borel

University of Geneva

Our research project aims to achieve a full characterization of all human islet cells including, but not exclusive to, insulin producing cells in non-diabetic and type 2 diabetic patients.

We developed a specific, cutting-edge methodology, named “single-cell RNA sequencing “, that enables whole transcriptome sequencing of hundreds of single cells. Practically, human pancreatic islets are prepared and enzymatically dissociated. Viable islet cells are individually captured into microscopic chambers using a microfluidic system. Expression levels of all detectable genes are measured by RNA-sequencing technology using a next generation sequencer.

By characterizing individual islet cells in non-diabetic and diabetic patients, we will be able to decipher the identities of islet cells based on their transcriptome, understand the pancreas function more deeply and reveal any candidate genes in relation to type 2 diabetes.

The ultimate goal of our research program is a better understanding of the pathological process of type 2 diabetes using single-cell functional genomics.

October 15 and 16, 2013 | Stephanie Ansari and Tatyana Franck

Tue, 15 Oct 2013 14:13:05 GMT

Stephanie Ansari and Tatyana Franck
Picasso at Work: Through the Lens of David Douglas Duncan

Time: October 15 and 16, 2013

Venues: Arken, Åbo Akademi, Turku and Ateneum Art Museum, Helsinki

In 1956, American photojournalist David Douglas Duncan (b. 1916) met Pablo Picasso. Through his lens, Duncan followed one of the world’s most famous artists and became a close friend and companion. The photographer took thousands of photos of Picasso at work and at play, thus becoming one of the greatest witnesses of the artist.

Duncan’s work was presented by curators Stephanie Ansari and Tatyana Franck in the exhibition Picasso at work: Through the lens of David Douglas Duncan. The exhibition has amazed thousands of visitors in Museo Picasso Málaga in Spain, Kunstmuseum Pablo Picasso Münster in Germany, and La Piscine, Musée d’Art et d’Industrie André Diligent de Roubaix in France, revealing Picasso’s sources of inspiration and explaining the creative process behind some of his most well-known works.

During a 90-minute lecture, Ansari and Franck engaged in a dialogue with Duncan’s photographs and the works of Pablo Picasso, giving the audience a chance to reflect on Picasso’s extraordinary life and artistic process.

The seminars were a collaboration between Åbo Akademi University Foundation, Ateneum Art Museum and Hjelt Art Foundation.

May 15 and 16, 2013 | Kigge Hvid

Wed, 15 May 2013 14:24:00 GMT

Kigge Hvid
Design to Improve Life and the Global Mega trends towards 2020 “Me & We – how the creative process itself is changing.”

Time: May 15 and 16, 2013

Venues: The Aalto University and Kiasma, Helsinki

Kigge Hvid is the CEO and founder of the the non-profit organization INDEX: Design to Improve Life®. She is a influental person in the Danish design field and has been a frequent panelist at eg. World Economic Forum in Davos and has also served as a member of the Forum’s Global Agenda Council on Design.

Kigge Hvid is the recipient of an honorary doctorate in 2006 by the Art Center College of Design in Pasadena, California, and the Design leadership award which is organized by the Commerce and Economic Development Bureau of the Hong Kong SAR Government along with the Hong Kong Design Centre. Index: Design to Improve Life works toward a more sustainable world through inspiring design innovations and concepts – developing them, testing them and implementing them in our everyday life. The INDEX: award is the biggest – and most important – design award in the world.

The seminars were a collaboration between Aalto University, Museum of Contemporary Art Kiasma and Hjelt Art Foundation.

Mechanisms whereby genetic variation in the TCF7L2 gene causes diabetes: novel targets for anti-diabetic therapy?

Sun, 31 Mar 2013 22:00:00 GMT

Hjelt grant holder 2013

Ola Hansson

Lund university

Mechanisms whereby genetic variation in the TCF7L2 gene causes diabetes: novel targets for anti-diabetic therapy?

In recent years, researchers have discovered around 70 genetic risk variants for diabetes, but still TCF7L2, known as the diabetes gene, is the gene that carries with it the largest risk of developing type 2 diabetes. Using a new method called exon skipping, Ola Hansson at Lund University Diabetes Centre (LUDC) wants to learn more about TCF7L2 by studying new ways of delaying the onset of type 2 diabetes in animal trials.

Ola Hansson at LUDC is one of four researchers that have been awarded a grant of half a million Swedish kronor from the Hjelt Foundation. “It’s confirmation that we’re doing good work and that we’re on the right track. It’s a prestigious grant and I’m happy to have been awarded it in competition with other good projects”, he says.

Exon skipping is a process that restores the production of a certain protein using short RNA strings, almost like a ’molecular plaster’. The method was developed to treat muscle dystrophy, which is caused by a fault in a gene that carries the instructions for the muscular protein dystrophin. In the same way, Ola Hansson now wants to examine if it is possible to repair, or restore, damaged or mutated functions within TCF7L2.

TCF7L2 is a so-called transcription factor. This means that the protein governs the activity of several other genes. “If you manipulate TCF7L2, which other genes are regulated?” Ola Hansson asks. As with many risk genes for type 2 diabetes, TCF7L2 is linked to decreased beta cell function. The pancreatic beta cells secrete insulin, which helps the body’s cells to absorb glucose from the blood. If the pancreas stops producing insulin or if the number of beta cells decreases, the person develops type 2 diabetes over time.

When beta cell function decreases, but before too many of the cells have died, it is possible to change lifestyle behaviours and thereby delay or prevent the onset of type 2 diabetes. “With better diet and improved exercise habits, combined with other treatment, it’s possible to change this to increased insulin secretion. We would also like to find out why the beta cells die. If we can find out why, perhaps we can find a way to delay the onset or even reverse the process”, says Ola Hansson.

Ola Hansson is a biologist. His research group consists of Yuedan Zhou from China, who has a biomedical degree, Nikolay Oskolkov from Russia, who is a theoretical physicist, and Peter Osmark from Denmark, who is a protein chemist. In previous studies, they have studied the gene in different human tissues: in fat, muscles, the islets of Langerhans (where insulin is produced), and in blood, and described which variants of the gene there is and how they are expressed. The group deduced that there are four different variants of the TCF7L2 gene that dominate in the islets of Langerhans. What the group is now looking for are the molecular mechanisms behind the altered expression and what this leads to, and if you can correct it by using exon skipping. The group is now testing their hypothesis on animal models in collaboration with a research group based in Chicago. “We will inject mice with exon skipping RNA in order to correct the imbalance of the different variants of TCF7L2,” explains Ola Hansson.

Owing to the fact that researchers at LUDC have access to insulin producing cells from deceased donors, he believes they are on the right track. “We know that what we’re examining in the cell systems is relevant to humans. It will be exciting to see what the trials on the animal models show, as they are more similar to the human situation,” he concludes.

Sara Liedholm

New anti-diabetic treatments through gene network analysis

Sun, 31 Mar 2013 22:00:00 GMT

Hjelt grant holder 2013

Anders Rosengren

Lund university

New anti-diabetic treatments through gene network analysis

Using a simple blood sample, it is now possible to identify people at risk of developing type 2 diabetes in the future. In a new project, Anders Rosengren, researcher at Lund University Diabetes Centre and physician at Skåne University Hospital in Malmö, has identified a new risk protein for type 2 diabetes.

Anders Rosengren is one of four researchers who was awarded 50 000 euro from the Hjelt Foundation in 2012. Together with his PhD student Taman Mahdi, Anders Rosengren discovered that the protein SFRP4 constitutes a link between inflammation and decreased insulin release. The team was also able to establish that people who will develop type 2 diabetes in the future have an increased level of the specific protein in their blood, something that can be ascertained using a simple blood test. The results were published in Cell Metabolism in the autumn of 2012.

– Our aim is to move ahead using the findings relating to SFRP4 and see if it’s possible to modify the inflammatory process by blocking the protein, and later develop custom-made drugs, explains Anders Rosengren.

– In previous studies, it has been possible to see that when diabetes-related inflammation is modified, blood glucose regulation is improved. It’s not entirely clear how this works, but we believe that if we can target SFRP4 more specifically we may be able to eliminate certain side effects and at the same time achieve more targeted treatment, says Anders Rosengren.

Thanks to the grant from the Hjelt Foundation he will also be able to use a new method to search for drugs with a certain effect. Instead of studying one drug, or one substance, and it’s influence on a specific gene at a time, the team will be able to utilize the large amounts of data available in order to identify gene expressions and genetic factors.

– All drugs have side-effects from the target protein that you really want to influence, but by using this method you establish from the start how they affect different genes and you can use the entire spectrum of effects for a specific drug. This is a much more efficient way of identifying new candidate drugs, explains Anders Rosengren. One drug that has been found this way and which will be studied is a substance which occurs naturally in broccoli and cauliflower.

The project will run during 2013 and Anders Rosengren is happy about the support from the Hjelt Foundation that has made it possible to carry out the research.

– It’s always nice with grants from private funds where people are excited about the research. It means that we feel even more motivated to offer something in return, he concludes.

Sara Liedholm

Role of FGF21 in NAFLD-associated hepatic insulin resistance

Sun, 31 Mar 2013 22:00:00 GMT

Hjelt grant holder 2013

Dr. François Jornayvaz

University of Geneva

Dr. François Jornayvaz, MD, Service of Endocrinology, Diabetes, Hypertension and Nutrition, Geneva University Hospitals, received a subsidy for the project entitled “Role of FGF21 in NAFLD-associated hepatic insulin resistance”. Obesity leads to insulin resistance in the liver and other organs. Liver insulin resistance is associated with non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disorder. The project aims at evaluating the circulating protein fibroblast growth factor-21 (FGF21) on improvement of insulin action in the liver. The effects of FGF21 on various lipids in the liver of obese mice will be studied. The mechanism of action of FGF21 will also be elucidated in immortalized liver cells with special focus on the oxidation (degradation) of lipids by the mitochondria, the power generators of the cell. Finally, liver biopsies from healthy and obese subjects will be examined for the relationship between content of FGF21 and various lipid types. The project should validate the usefulness of FGF21 for the treatment of obesity and type 2 diabetes.

The Hjelt Foundation Interview with Dr. François Jornayvaz:

Obesity is rapidly rising worldwide and is associated with diseases such as nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes. NAFLD is now the most prevalent chronic liver disease, affecting approximately 1 out of 4 individuals, and is strongly associated with hepatic insulin resistance.

Fibroblast growth factor 21 (FGF21) is an endocrine factor mainly acting in the liver. FGF21 improves insulin sensitivity in animal models of insulin resistance and is gaining interest as a therapeutic agent. However, its exact mechanisms of action, particularly on hepatic insulin resistance, remain largely unknown.

François Jornayvaz from Geneva University recieved 20 000 Euro from the Hjelt Foundation. The aim of his project is to study the mechanisms by which FGF21 improves hepatic insulin resistance in NAFLD. The main hypothesis is that FGF21 decreases hepatic lipid content, mostly lipid intermediates involved in the development of hepatic insulin resistance, i.e. diacylglycerol and ceramide. We also hypothesize that this decrease in hepatic lipid content might be secondary to an FGF21-mediated improvement in hepatic mitochondrial oxidative function.

This project will help understand the role of FGF21 in NAFLD-associated hepatic insulin resistance in vitro but also in vivo in mice and humans. The suggested experiments will also provide cellular mechanisms by which FGF21 improves NAFLD and insulin sensitivity when injected in a rodent model of insulin resistance, more specifically in, but not limited to the liver. This is highly relevant given the potential use of this endocrine factor as a therapeutic agent in the future in humans in the treatment of insulin resistant states such as NAFLD, obesity or type 2 diabetes. Given the high and ever increasing prevalence of these major health problems, and despite numerous treatments available, there is still a need to better understand their pathogenesis in order to develop targeted therapeutic molecules. If FGF21 is found to improve hepatic mitochondrial function, these studies might also open new perspectives in the field of mitochondrial related diseases such as Alzheimer’s disease and cardiovascular diseases.

This is a translational project, meaning that we will first use hepatic cell lines (from human liver cancer) and study the effect of FGF21 on these cells, notably on mitochondrial function. This is important, as mitochondria are involved in lipid oxidation. We will also study mice that have fatty livers secondary to dietary interventions. We will assess different lipid metabolites in these livers, mostly those associated with insulin resistance, which is a key step in the development of type 2 diabetes. We hope that FGF21 will ameliorate NAFLD and hepatic insulin resistance in these conditions. If true, this opens perspectives in humans in the treatment of NAFLD, but also for other diseases associated with insulin resistance, such as type 2 diabetes and obesity. Finally, we plan to set up a liver biopsies bank from patients with NAFLD, but also from healthy patients, in order to better understand how insulin resistance and type 2 diabetes develop in the presence of NAFLD.

What is your long term goal?

– As a physician, I am always patient-oriented in my research. Studies in cells and animals are necessary for some research aspects such as mechanisms comprehension, but my long-term goal is to better identify cellular targets that could be used in the treatment of type 2 diabetes in humans.

What is your personal driving force?

– Diabetes is a difficult disease. It is chronic and you have to think about it every day. Although lots of medications are available, we still miss efficient, safe and global molecules to better control diabetes. I therefore think that just prescribing drugs is not enough and I would like to contribute to a better understanding of this complex disease in order to find specific treatment targets. However, I also think that prevention is the key, i.e. notably avoiding obesity by eating a healthy diet and having regular physical activity. Unfortunately, type 2 diabetes is not only an environmental disease and has a genetic component. You cannot fight your genes and sometimes even if you do your best in term of lifestyle interventions to avoid diabetes, this will not be enough. By seeing all diabetes related complications in the clinic, I couldn’t just renew prescriptions or assist without power to the unfortunate fate of some patients. I therefore decided to be part of the scene and engaged into research. My patients are my best inspiration to develop and improve my research.

Sara Liedholm

Insulin sensitivity in specific skeletal muscle fibre

Sun, 31 Mar 2013 22:00:00 GMT

Hjelt grant holder 2013

Dr. Karim Bouzakri

University of Geneva

PhD, Dept of Genetic Medicine and Development, University of Geneva, received a subsidy for the project entitled “Molecular and genetic basis for differential insulin sensitivity in skeletal muscle cells from healthy subjects and individuals with type 2 diabetes”. In Type 2 diabetes, not only insulin secretion but also glucose uptake by skeletal muscle and other insulin actions are impaired. Muscle represents the quantitatively most important insulin target tissue. The project aims at defining how the effects of insulin are inhibited by studying cell cultures established from muscle biopsies of type 2 diabetic patients and healthy controls. In particular, the three subtypes of muscle fibers will be examined for changes in genetic and epigenetic characteristics as well as insulin signaling parameters. It is hoped that the results will help to develop therapy improving the biological action of insulin in those muscle fiber types most affected by diabetes.

– One of my goal is to understand the molecular basis for altered insulin sensitivity in specific skeletal muscle fibre types in control and type 2 diabetic patients, says Karim Bouzakri, researcher at Geneva University who received 50 000 Euro from the Hjelt Foundation.

– I have hypothesis and demonstrated that human skeletal muscle secrete different pattern of myokines regarding their insulin sensitivity. These myokines have therefore a bimodal impact on beta-cells functions and proliferation regarding them muscle type origin.

– To this end, I plan to identify target secreted and release by skeletal muscle from different fibres isolated from control and Type 2 diabetic patients. We are using new approach to identify either protein or epigenetic modification in order to understand the differences in insulin sensitivity.

What is your long term goal?

– I hope to be able to pursue my line of research as I did since I have started my PhD. In fact, I am in turning point in my carrier, as I will have to set up my own laboratory in the next coming years.

What is your personal driving force?

– I have been starting working on diabetes and insulin resistance when I was a master student. In this time several person from my family (included my Father) have been diagnostic with T2D. I have been the first witness of this terrible disease, which deeply killed all my family with all the know complications (Kidney failure, stroke, blindness, amputation…). Therefore, I have been interesting to understand how this disease can progress so rapidly with a broad panel of horrible complication. That is why, I am working on insulin resistance and Type 2 Diabetes mellitus since my master.

Sara Liedholm

Toshiko Mori and Marika Wachtmeister

Sun, 01 Jan 2012 15:28:00 GMT

Toshiko Mori and Marika Wachtmeister
Designing for a Sustainable Future

Venues: The Aalto University and Kiasma, Helsinki

Toshiko Mori Principal at Toshiko Mori Architect. She established the firm in New York City in 1981. The firm has been noted for its intelligent approach to historical context, ecologically sensitive strategies, and innovative use of materials, creatively integrating design and technology. Current work includes projects for New York City’s Department of Design and Construction and for the Department of Parks and Recreation, institutional projects for Syracuse University and Brown University, a master plan for New York University, as well as residences in New York, Massachusetts, Taiwan and Mongolia.

Mori also recently designed the Eleanor and Wilson Greatbatch Pavilion, the Visitor Center at Frank Lloyd Wrights Darwin D. Martin House Complex and the Syracuse Center of Excellence in Environmental and Energy Innovations, Syracuse, New York.

Toshiko Mori was chair of the Department of Architecture at Harvard from 2002 to 2008. She has been a visiting faculty member at Columbia University and Yale University, where she was the Eero Saarinen Visiting Professor in 1992.

Marika Wachtmeister is the Founder of Open Art Museum at Wanås Slott, Sweden. Wachtmeister was a lawyer. However, as she lived at Wanås Slott (Castle) she had the idea of inviting contemporary artists to a place in the countryside in a part of Sweden lacking contemporary art. This was at a time when many artists found it difficult to place their sculptures and installations. Her purpose was to invigorate Wanås and broaden local interest in contemporary art.

The Foundation was established by Marika Wachtmeister in 1987. In 2011 the Wanås Foundation took a step into the future and introduced new leadership by Elisabeth Millqvist, Artistic Director, and Mattias Givell, Project Director. Together they share the management responsibilities and continue to strengthen the international profile of contemporary art at Wanås. The permanent collection of the Wanås Foundation consists of nearly 50 outdoor installations and sculptures.

The seminar was a collaboration between Aalto University, Sitra and Hjelt Art Foundation.

April 4, 2011 | Dr Sebastian Storz

Mon, 04 Apr 2011 14:35:54 GMT

Dr Sebastian Storz
Dresden – the total Destruction of the Historic Centre and its Reconstruction

Time: April 4, 2011

Venues: The Aalto University and Ateneum Art Museum, Helsinki and Åbo Akademi University, Turku

The historic center of Dresden was completely destroyed in 1945, close to the very end of World War II. The architectural heritage had been extinguished. Now after 66 years, the center of Dresden is still under rebuilding.

In his lecture, Dr. Sebastian Storz did not only look back at the rebuilding phase of Dresden, but also emphasized the questions that any urban reconstruction work has to deal with. These questions are linked to buildings and environments, and consider factors that give a modern building or an urban environment the quality to attract inhabitants.

Dr Sebastian Storz is an architect and a historian of architecture and Director of Forum für Baukultur, Dresden. He is also a founder member of MusAA, Museo Architettura Arte. MusAA is an architectural institute established in the earthquake area of L’Aquila, Italy, by a German-Italian cooperation project to help with future reconstruction work.

Epigenetic changes in diabetic nephropathy (DN)

Thu, 31 Mar 2011 22:00:00 GMT

Hjelt grant holder 2011

Dr. Mengyin Cai

Lund university

Dr. Mengyin Cai, PhD, received a postdoctoral fellowship from the Foundation February 2011 to December 2012. Dr. Cai obtained her PhD in Sun Yat-sen University, China, working on “molecular mechanism on lamin C deficiency related lypodystrophic diabetes”. She started her Hjelt Foundation-funded funded project in Prof. Leif Groop’s group, focusing on epigenetic changes in diabetic nephropathy (DN). DN is one of the most devastating diabetic complications and the leading cause of renal failure in developed countries. Although hyperglycemia represents the most important risk factor for development of diabetic vascular complications, not all hyperglycemic patients seem to be at equal risk. Based upon observations in two large studies on T1D and T2D, DCCT and UKPD, the term “metabolic memory” was introduced to describe the long term effects of initial good or poor metabolic control for protection of or susceptibility to diabetic complications in both T1D and T2D. While genetic factors have been suggested to contribute to DN susceptibility in addition to the elevated glucose, results from genetic studies have thus far been disappointing. It suggests other factors modify an indivdual’s susceptibility to develop complications. One possible reason could be epigenetic mechanism including histone modifications. Dr. Cai’s project tested effect of glucose on expression of two proinflammatory genes, thioredoxin-interacting protein (TXNIP) and ostepontin (OPN), which both have been ascribed a role in the pathogenesis of DN in cell lines and animal models. She found that hyperglycemia induced active TXNIP and OPN genes expression, increased H3K9 acetylation (activating histone marks) and reduced H3K27 trimethylation (H3K27me3) (inactivating histone marks) in normal human mesangial cells. In a diabetes-prone mouse model (a mouse model with knock-in of a human mutation in the Sur-1 gene), she further identified the more coordinated changes in histone marks, TXNIP and OPN genes expression in kidneys in response to the longer exposure to hyperglycemia. These results demonstrate the impact of glucose on histone modifications, which contributes to two proinflammatory genes: TXNIP and OPN expression may be association with development of DN. The research data is included in a manuscript to soon be submitted.

Evaluating the green tea flavonoid epigallocatechin-3-gallate (EGCG) as a model substance for the treatment of type 2 diabetes

Thu, 31 Mar 2011 22:00:00 GMT

Hjelt grant holder 2011

Dr. Shirin Pournourmohammadi

University of Geneva

Dr. Shirin Pournourmohammadi, PhD, received a senior postdoctoral fellowship from the Foundation February 2011 to February 2013. Dr. Pournourmohammadi obtained her PhD in pharmacology/ toxicology in Tehran University, Iran, spending the last year of her thesis work in Professor P. Maechler’s group, University of Geneva. Thereafter, she was first assistant professor in pharmacology, Kerman University, Iran; subsequently associate professor, University Kebangsaan Malaysia, Kuala Lumpur, Malaysia. The funded project conducted in Prof. Maechler’s group, aimed at evaluating the green tea flavonoid epigallocatechin-3-gallate (EGCG) as a model substance for the treatment of type 2 diabetes. Dr. Pournourmohammadi could demonstrate that EGCG inhibited glucose-stimulated insulin secretion by blocking the mitochondrial enzyme glutamate dehydrogenase. This enzyme generates the metabolic coupling factor glutamate and its genetic ablation inhibits glucose-stimulated insulin secretion. EGCG was without effect in the ablated mouse islets, proving that the compound acts by blocking glutamate dehydrogenase. The studies established a link between inhibition of glutamate dehydrogenase and stimulation of the energy-sensing enzyme adenosine monophosphate kinase (AMPK). Indeed, EGCG activated AMPK both in insulin producing beta cells and in muscle cells, where it exerted an insulin-like enhancement of glucose uptake. It is proposed that EGCG like-compounds could be used in the treatment of type 2 diabetes in patients with overweight, displaying increased insulin secretion and decreased insulin action in muscle and other insulin target tissues.

Mikael Storåkers and Henrik Åberg

Sun, 02 Jan 2011 15:42:56 GMT

Mikael Storåkers and Henrik Åberg
Bukowskis – an arena for art and antiques lovers

Venues: Åbo Akademi University, Turku, The Swedish School of Economics and Ateneum Art Museum, Helsinki

Mr. Mikael Storåkers , General Manager for Bukowskis Auction House, Stockholm, and Head of Bukowskis Group, visited Åbo Akademi and described the company’s history and the work to build the business taking account of both tradition and the changes on the art market. In Helsinki he gave a most interesting lecture for the students at the Swedish School of Economics about how to rebuild a proud traditional name and logo in order to increase interest in the auction world for a new public.

The audience of Ateneum got an interesting insight into the auction business from Mr. Henrik Åberg , Head of Department at Bukowskis.

October 11, 2010 | Louise Neri

Mon, 11 Oct 2010 14:50:04 GMT

Louise Neri
Commercial contemporary galleries in today’s art world and market

Time: October 11, 2010 in Helsinki

Venues: Aalto University and Museum of Contemporary Art Kiasma, Helsinki; Åbo Akademi University, Turku

Who wields power in today’s art market? Who will be the next big artist? Who sets the prices? What roles do galleries, museums andauction houses play?

Louise Neri , Director of International Affairs for the world’s largest privately owned international gallery Gagosian in New York, gave her views on these questions. Neri spoke from her own experience about the role the commercial contemporary galleries play on today’s art world and market.

In 2006 Louise Neri joined The Gagosian Gallery, the world’s largest privately owned international art gallery. For ten years before this she was the U.S. Editor of Parkett magazine and also co-curated the 1997 Whitney Biennial and 1998 Sao Paulo Biennial. After moving back to Europe in 2002 she curated exhibition programs and festival programs in London and Frankfurt.

Neri works principally on artist acquisitions, programming of exhibitions and publications, sales, consulting, research and development, and communications.

In Finland she held three lectures on the role that commercial contemporary galleries play in today’s art world and market. In a rapidly changing art world, where the lines between public and private are increasingly blurred, Gagosian has in many ways by-passed and surpassed the power once wielded by major museums and auction houses.

This lecture is organised with the cooperation of the Kiasma Foundation and Hjelt Art Foundation.

The role of the amino acid glutamate in insulin and glucagon secretion

Tue, 31 Mar 2009 22:00:00 GMT

Hjelt grant holder 2009

Dr. Nicole Burkhardt-Feldmann

University of Geneva

Dr. Nicole Burkhardt-Feldmann, PhD, received a postdoctoral fellowship from the Foundation from February to August 2009. During this time, she finished her project on the role of the amino acid glutamate in insulin and glucagon secretion. The amino acid is formed from glucose both in pancreatic islet beta and alpha cells, secreting respectively the blood glucose-lowering hormone insulin and the glucose-raising hormone glucagon. The results show that glutamate clearly acts as an intracellular messenger molecule, essential for glucose-stimulated insulin secretion. In contrast, under conditions in which glucose stimulates glucagon secretion, glutamate is not involved in the release mechanism. These results substantiate the hypothesis that glutamate is an intracellular mediator in the action of glucose on insulin secretion in the beta cell. The selective implication of glutamate makes this signaling pathway an interesting target for the development of new drugs for type 2 diabetes, in which insulin secretion is deficient.

Identification of genetic susceptibility loci associated with diabetic nephropathy (DN) in Europeans

Tue, 31 Mar 2009 22:00:00 GMT

Hjelt grant holder 2009

Dr. Tarunveer Singh Ahluwalia

Lund university

Dr. Tarunveer Singh Ahluwalia, PhD, received the postdoctoral fellowship from the Bo and Kerstin Hjelt Foundation for two years (March 2009 to February 2011). He holds a Master’s degree in Biotechnology from Panjab University, Chandigarh, India and was awarded his PhD degree at the Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India on his work titled “Functional Genomic Approaches to study the influence of genetic factors on the development of diabetic nephropathy”.

He started his Hjelt Foundation-funded project under the guidance of Prof. Leif Groop at the prestigious Lund University Diabetes Centre, Malmo, Sweden, focusing on identification of genetic susceptibility loci associated with diabetic nephropathy (DN) in Europeans.

DN is one of the most severe complications of type 1 and type 2 diabetes mellitus, and the leading cause of end-stage renal disease (ESRD) and renal replacement therapy. DN results from a complex interaction between genetic susceptibility and the diabetic environment characterised by poor glycaemic control and hypertension. About 35% of type 2 diabetic patients develop diabetic nephropathy. Familial clustering has been reported supporting the presence of a genetic component.

Based on these facts Dr. Ahluwalia initiated some projects: a) Carnosinase Dipeptidase (CNDP1 and CNDP2) variants and risk of DN: Among one of the loci identified in linkage scans chromosome 18q harboring CNDP1 and CNDP2 genes is a locus associating with DN. The former encodes a dipeptidase that hydrolyses the substrate L-carnosine (β-alanyl-L-histidine) specifically, while CNDP2 encodes a non-specific dipeptidase. Carnosine has been ascribed a protective role in diabetic nephropathy, since it serves as a scavenger of oxygen radicals and thus can inhibit formation of AGEs. Against this background, Dr. Ahluwalia tested whether there is an association between genetic variants (single nucleotide polymorphisms, SNPs) in the CNDP locus and DN in a large population of patients with type 2 diabetes from southern Sweden (Scania Diabetes Registry). He identified two SNPs (rs7577 in CNDP2 and rs2346061 in CNDP1) in the regulatory regions associating with risk of DN where rs7577 was also associated with an altered kidney function particularly in women [1].

b) Uromodulin gene (UMOD) variant and DN: Dr. Ahluwalia also tested the association of a genetic variant (rs13333226) in the UMOD gene which encodes the most common protein in human urine and risk of DN. This variant was previously identified to be associated with hypertension and chronic kidney disease in a genome wide association setting but had never been tested for association with DN. He found this variant to be associated with DN among the Swedish population [2].

c) He was involved in a couple of other projects where he contributed as a co-author. His first contribution involved in writing a review on the genetics of type 2 diabetes published in the year 2011 [3]. d) Another project where he was a co-author and contributed in data research and analysis was focussed on evaluating the effects of common genetic variants associated with type 2 diabetes and glycemic traits on alpha and beta-cell function and insulin action in humans. [4].In addition to these Dr. Ahluwalia has also contributed to another project still under finalization with the ENGAGE consortia.

hjeltfoundations

When Time Meets Decay: Uncovering the Links Between Circadian Rhythms and Pancreatic Health

Allan and Bo Hjelt Art Foundation Partners with Circus & Dance Finland

Morning Coffee with Tilde Björfors

Circus & Dance Finland

Tilde Björfors

ERMP1, a new gatekeeper in diabetic kidney diseas?

June 2025 | "ODDfest 2025" in Helsinki

Transcriptional regulation of human islet development and function

Transcriptional regulation of human islet development and function

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Hypothesis

Methods

Results

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Importance

ACSL1 and β-Cell Function: A Novel Pathway in the Pathophysiology of Type 2 Diabetes

ACSL1 and β-Cell Function: A Novel Pathway in the Pathophysiology of Type 2 Diabetes

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Hypothesis

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Therapeutic potential of S100A10 Inhibition in Hepatic Insulin Resistance, MASLD and Type 2 Diabetes

Therapeutic potential of S100A10 Inhibition in Hepatic Insulin Resistance, MASLD and Type 2 Diabetes

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Hypothesis

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Towards Personalized Medicine: Unraveling Biomarkers in Gestational Diabetes for Predicting Diabetes Subtypes and Prevention

Towards Personalized Medicine: Unraveling Biomarkers in Gestational Diabetes for Predicting Diabetes Subtypes and Prevention

Diabetes Research Grants for 2025: Welcome to Apply

Application period begins today!

October 27, 2024 | "For the love of Italy – the connection between Allan Hjelt and the Aalto's"

Two expert presentations at Helsinki Book Fair on Aino and Alvar Aalto's Italian connections

Exhibition in Åbo: feb 3 – June 6 2024 | "More than just oldsters"

"More than just oldsters"

Upcoming event: May 25, 2024 | "Play for creativity" - The Hjelt Talk in cooperation with Circus Helsinki

Circus educators Lena Kruit & Rieke Hambach From MeerManege in Kiel, Germany

Leveraging discordancy between obesity and type 2 diabetes to target insulin resistance

Leveraging discordancy between obesity and type 2 diabetes to target insulin resistance

Background

Hypothesis

Methods

Results

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Lund University presents three Hjelt researchers

Jiangming Sun, Emma Ahlqvist and Sabrina Ruhrmann have each been awarded a project grant of 47,500 euro by the Hjelt Diabetes Foundation.

March 22, 2023 | Italo-Finlandese Success Stories - Design Talk with Leonardo Ferragamo

Leonardo Ferragamo Italo-Finlandese Success Stories

Epigenetic Editing - a way to a personalized treatment approach in type 2 diabetes (T2D)

Epigenetic Editing - a way to a personalized treatment approach in type 2diabetes (T2D)

April 27 , 2022 | Pre-War Rolls-Royce Motor Cars with a Finnish connection

Sir John Stuttard Pre-War Rolls-Royce Motor Cars with a Finnish connection

Diabetes Research Grants for 2023: Welcome to Apply

Application period begins today!

Lund University presents three Hjelt researchers

Anja Schmidt-Christensen, Rodrigo Cataldo and Sebastian Kalamajski have each been awarded a project grant of 47,500 euro by the Hjelt Diabetes Foundation.

April 27, Upcoming event: Rolls-Royce Motor Cars with a Finnish connection

Fascinating stories of Pre-War Rolls-Royce-motor cars and their Finnish owners

Congratulations!

Our Grant Holders 2022

Human liver organoids to investigate the role of miR-149 in obesity-associated hepatic insulin resistance

EPDR1, a novel human batokine regulating β cell metabolism and function

Effects of PPARGC1A gene polymorphism on metabolism and obesity

Synchrotron X-ray micro-CT imaging for resolving complex 3D structural changes in the kidney

The biography of Allan Hjelt and a new TV documentary in Finnish

A tribute to his late father

Diabetes Research Grants for 2022: Welcome to Apply

Application period begins today!

Lund University presents three Hjelt researchers

Ola Hansson, Karl Bacos and Malin Fex have been awarded 45 000 euros each for their research projects

A golden leaf to the Diabetes Foundation

A golden leaf to the Diabetes Foundation from Lund University

Taking advantage of nature’s own experiment to identify novel pharmacological targets to improve muscle health

Exploring the association of melatonin with type 2 diabetes risk and islet cell function

Restoring circadian rhythmicity in metabolic organs: role of inter-organ circadian desynchrony in the pathogenesis of type 2 diabetes

Leonardo Ferragamo
Italo-Finlandese Success Stories

Sir John Stuttard
Pre-War Rolls-Royce Motor Cars with a Finnish connection

The Hjelt Interior
at The Alvar Aalto Museum in Jyväskylä, Finland

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Amateur, Autodidact, and Beginner’s Luck: The Making of an Aesthete

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The End (and Ends) of Photo Criticism

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Humanitarian Architecture – Disasters, Development and Design Responsibility

Benjamin Hayes, Florence Lam and Toshiko Mori
Säynätsalo Talks | Rethinking Säynätsalo Town Hall

Eero Lundén
Architecture in the Future in Cities – Towards New

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Towards the Unbound Museum

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Mitt liv i skulptur

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Art Approaching Science and Religion

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Exhibiting Ai Weiwei

Gereon Sievernich
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I Stalins Skugga. Finland 1944–1952