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Molecular Biology


Cell Division: Image: The Institute of Cancer Research, London


Patients’ Own Cells Could Be the Key to Treating Crohn’s Disease













|| February 18: 2019: University of Manchester News || ά. A new technique, using patients’ own modified cells to treat Crohn’s Disease has been proven to be effective in experiments, using human cells. A clinical trial of the treatment is expected to start in the next six months. Researchers at the NIHR Guy’s and St Thomas’ Bio-medical Research Centre:BRC developed the technique by studying white blood cells, taken from patients, who have Crohn’s Disease and comparing them to cells of healthy people.

Their findings allowed cell therapy specialists in the BRC to develop a treatment, involving taking patients’ cells and growing them in a special culture so that they behave more like cells from healthy people. The research, published in the journal Gastroenterology, shows that this technique is effective in human cells, meaning it is ready for use in a clinical trial. The proposed Tribute Trial will test whether the treatment is safe and effective for treating Crohn’s Disease.  Crohn’s Disease is a lifelong condition, in which, parts of the digestive system become severely inflamed, causing a range of symptoms, such as, diarrhoea, stomach aches, tiredness and weight loss.

Its causes are unknown but, the immune system is known to play a part. The often debilitating condition is estimated to affect around 620,000 people in the UK. Professor Graham Lord, from the University of Manchester, led the Study. The research was carried out while he was Director of the NIHR Guy’s and St Thomas’ BRC and a Consultant Nephrologist at Guy’s and St Thomas’.  He is now Vice President and Dean of the Faculty of Biology, Medicine and Health at the University of Manchester.

Professor Lord said, “This is the next frontier in cell therapy, as we’re going beyond treating the symptoms of Crohn’s Disease and trying to reset the immune system to address the condition.

It’s a real home-grown treatment in the sense that we started with observing cells and tissues, donated by patients at Guy’s and St Thomas’, have developed a treatment and are now starting to undertake trials, all at the Trust. It shows how central patients are to research, helping to create a treatment, that, might, help thousands more people.”“

Ms Rachel Sawyer, Communications Manager, who is 50 and lives in Anerley in south east London, was diagnosed with Crohn's Disease in 2,000 and treated at Guy's and St Thomas'. Although, her condition is now under control, she supports other people, who have Crohn's.

Ms Sawyer said, "One of the worst things for me was the unpredictability, particularly, around needing the toilet in a hurry. Having Crohn's completely re-routes your daily life and makes it hard to do the normal things most of us take for granted like going out socially or taking public transport. Even, now, the fear of it is never really far from my mind.

Another difficult thing is the stigma associated with bowel disease. It's difficult to talk and be open about it, even, with family and friends. I found life very isolating and challenging at times and that's something so many people with Crohn's experience, regardless of whether they were diagnosed years ago or last month. For people diagnosed young, it can impact on the formative years of their life. Anything, that could help people with Crohn's have the confidence to go out and get back to being the people they were destined to be, would be a game-changer."

The researchers found that specialised white blood cells, called, regulatory T-cells from Crohn’s patients produced less of a gut-specific protein, called, integrin α4β7 than regulatory T-cells from healthy people. Working with the specialists at the NIHR Guy’s and St Thomas’ BRC’s Advanced Therapies Manufacturing Platform, they developed a cell therapy technique based on these findings.

This technique involves developing cells from the Crohn’s Disease patients with a molecule, called, RAR568, which restores healthy levels of integrin α4β7. The cells are, then, given back to patients by intravenous infusion.

Dr Peter Irving, a Consultant Gastro-enterologist and Co-author on the Paper, said, “While the treatments available for Crohn’s Disease have increased over recent years, they only work in some patients. In addition, the treatments have, potentially, serious side effects in some patients. This research paves the way for a trial of using patients’ own cells to treat their Crohn’s Disease and we look forward to offering people the chance to take part in the very near future.”

The research was supported by the National Institute for Health Research:NIHR through the NIHR Guy’s and St Thomas’ Biomedical Research Centre and the Medical Research Council. Additional support was provided by Litwin IBD Pioneers Funding Programme at the Crohn’s and Colitis Foundation, the Freemason’s Grand Charity and the Rosetree’s Trust.:::ω.

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New Research Finds Hope in the Treatment of Type One Diabetes With Pancreatic Islets Transplant: Short Anti-Rejection Therapy Protects Transplants in Diabetic Animals



|| February 06: 2019: Karolinska Institutet News || ά. Transplanted pancreatic islets in diabetic animals can survive for a long period of time, if, the animals are treated with short anti-rejection therapy around the time of the transplant. This has been shown by researchers at Karolinska Institutet, Sweden and the Diabetes Research Institute, University of Miami Miller School of Medicine, USA, in a new study, published in the scientific journal Diabetologia. The results, might, have a significant impact on clinical islet transplantation in the treatment of Type One Diabetes.

Transplantation of pancreatic islets, with their insulin-secreting cells, is a promising therapy for Type One Diabetes. However, one complication is this that anti-rejection therapy, in the form of generalised immune suppression, is required to ensure the survival and functioning of the transplanted islets by preventing the immune system from attacking the transplants. It is well known that extended use of generalised immune suppression, might, have serious side effects, that harm the transplanted patient.

Moreover, immune attack against the transplanted islets can, still, occur, despite continued immune suppression. Therefore, the transplantation field has been looking for new ways to ensure the long-term survival and functioning of transplanted islets with little or, even, no immune suppression.

This new Study demonstrates the potential for achieving long-term survival and function of transplanted pancreatic islets with short-term anti-rejection therapy around the time of the transplant. In transplanted mice and monkeys, this strategy resulted in immune tolerance, that enabled survival of the transplanted islets long after the anti-rejection treatment was stopped.

“These findings support the establishment of immune tolerance towards the transplanted islets and, thereby, their long-term protection from an immune attack in the transplanted patient after stopping the use of anti-rejection therapy.” says the First Author of the paper, Dr Midhat H Abdulreda at the Diabetes Research Institute.

This new way of achieving immune tolerance, might, minimise the need for life-long immune suppression, which raises hope for an effective treatment of Type One Diabetes with fewer side effects. “If, these findings are repeated in humans, this approach, may, serve as a game changer and positively impact on the success of islet transplantation for future treatment of Type One Diabetes.” says the Senior Author of the paper, Professor Per-Olof Berggren at the Department of Molecular Medicine and Surgery and Rolf Luft Research Centre for Diabetes and Endocrinology at Karolinska Institutet.

The research was supported by funds from the Diabetes Research Institute Foundation:DRIF and the Diabetes Wellness Foundation and by grants from the Stanley J Glaser Foundation Research Award, the NIH:NIDDK:NIAID, the Swedish Diabetes Association Fund, the Swedish Research Council, Novo Nordisk Foundation, the Family Erling-Persson Foundation, the Strategic Research Programme in Diabetes at Karolinska Institutet, the Knut and Alice Wallenberg Foundation, Skandia Insurance Company Ltd, the Diabetes and Wellness Foundation, the Berth von Kantzow Foundation  and the Stichting af Jochnick Foundation.

Professor Per-Olof Berggren is the Co-founder and the CEO of Biocrine, an unlisted bio-tech company, that is using the approach of cell transplant in the anterior chamber of the eye as a research tool. Mr Midhat H Abdulreda is a Consultant for the same company.

The Paper: Operational immune tolerance towards transplanted allogeneic pancreatic islets in mice and a non-human primate: Midhat H Abdulreda, Dora M Berman, Alexander Shishido, Christopher Martin, Maged Hossameldin, Ashley Tschiggfrie, Luis F Hernandez, Ana Hernandez, Camillo Ricordi, Jean-Marie Parel, Ewa Jankowska-Gan, William J. Burlingham, Esdras A Arrieta-Quintero, Victor L Perez, Norma S Kenyon, Per-Olof Berggren: Published in Diabetologia: The journal of the European Association for the Study of Diabetes: Online January31: 2019

Caption: Professor Per-Olof Berggren: Image: Stefan Zimmerman:::ω.

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Molecular Profiling for Very Early Lung Cancer Detection



|| January 24: 2019: UCL News || ά. The world’s first genetic sequencing of pre-cancerous lung lesions could pave the way for very early detection and new treatments, reports a new Study, led by UCL researchers. Before lung cancer develops, pre-cancerous lesions are found in the airway but, only, half of these will, actually, become lung cancer, while others will disappear or remain benign without becoming harmful. Under the microscope, the lesions look the same, making it difficult to know which lesions to treat.

In this study, published in Nature Medicine, researchers have, for the first time, discovered the differences between the lesions, that will become invasive and those, that are harmless and they can, accurately, predict which lesions will become cancerous. “Our study helps to understand the earliest stages of lung cancer development, by figuring out what’s going on inside these cells, even, before they become cancerous.” said the Study’s Lead Author, Professor Sam Janes, UCL Division of Medicine and University College London Hospitals, UCLH.

“Using this information, we, may be, able to develop screening tests and new treatments, that could stop cancer in its tracks.” The researchers were studying biopsies of pre-invasive lung cancer lesions of patients, who were seen at UCLH. They conducted tests, including, gene expression profiling, methylation profiling and whole-genome DNA sequencing on 129 biopsy samples from 85 patients.

On average, the patients were followed up for over five years post-biopsy, to see which patients developed lung squamous cell carcinoma, one of the two most common sub-types of lung cancer. The research team identified differences in genomic features, such as, mutations, gene expression and chromosomal instability, finding enough differences, that they could predict with near-perfect accuracy, which lesions would develop into cancer by checking the lesion’s molecular profile.

By identifying which pre-cancerous lesions are harmful, the researchers say that clinicians could decide whether or not to offer a patient surgery at a much earlier stage of the disease than is currently possible, while saving others with benign lesions from unnecessary surgeries.

Pre-cancerous lesions are detected by bronchoscopy, a minimally invasive test, that is, often, done on people with chronic cough or a history of lung cancer. There is no consensus on treatment for pre-cancerous lung lesions; in some countries, patients with such lesions undergo surgery, while elsewhere, patients are monitored and, only, treated, if, clear signs of cancer appear.

While bronchoscopy isn’t offered to everyone at risk of lung cancer, the researchers say that their findings could help to develop a simpler blood test to pick up the same molecular signals, that are linked to early cancer development. ‘’If, we can use this new understanding of cancer development to create new diagnostic tests, it, may, one day, be invaluable in picking up cancer early, enabling people to access treatment much earlier in the disease process.” said Dr Adam Pennycuick, UCL Division of Medicine, one of the Study’s authors.

The Study could, also, help lead to new treatments. Some of the genes, that are expressed differently in lesions, that will become cancerous, have previously been identified as potential drivers of lung cancer. “We are now continuing our research to further understand how these genes are driving cancer progression and to see which ones could be targeted by new drug treatments.” said Dr Vitor Teixeira, one of the authors of the Study, UCL Division of Medicine.

The Study involved researchers at UCL Division of Medicine, UCL Cancer Insititute, UCLH, Wellcome Sanger Institute, Boston University, The Francis Crick Institute, Cancer Research UK Cambridge Institute and University of St Andrews and was supported by Wellcome, Rosetrees Trust, Roy Castle Lung Cancer Foundation, Welton Trust, Garfield Weston Trust, Stoneygate Trust, UCLH Charitable Foundation, Cancer Research UK, Stand Up to Cancer and the University College London Hospitals National Institute for Health Research Biomedical Research Centre.:::ω.

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New Research Sheds Light on the Evolution of Metabolism



|| January 09: 2019: University of Helsinki News || ά. Researchers at the University of Helsinki have found out that the ability to use sugar as food varies strongly between closely related species and identified the genetic basis of this variation. Diet choice of animal species is highly variable. Some are specialists feeding only on one food source, such as, a sugar-rich fruit or protein-rich meat. Other species, like humans, are generalists, that can feed on different kinds of food sources. Because of these differences, animal species ingest different amounts of macronutrients, like carbohydrates and amino acids.

It is conceivable that the metabolism has to match the diet choice of each species. However, we understand poorly the evolution of animal metabolism, what the underlying genetic changes are and how these changes define the optimal nutrient composition for a given species. The research group led by Associate Professor Ville Hietakangas at the University of Helsinki have studied the evolution of metabolism by using two very closely related fruit fly species. The first one of them is a generalist, Drosophila Simulans, which feeds on varying fruits and vegetables, which, typically, contain a high amount of sugars.

The second one is Drosophila Sechellia, which has specialised to feed on one fruit, Noni, Morinda Citrifolia, which has low sugar content. “We found pretty dramatic metabolic differences between these species. D. Sechellia larvae, that are not exposed to sugar in nature, were not able to grow when placed on a sugar-rich diet, while D. Simulans had no problems handling dietary sugar.” Explains Mr Hietakangas.

The close relatedness of the fruit fly species allowed the scientists to interbreed the species, to make hybrids, that were largely genetically like D. Sechellia but contained those genomic regions of D. Simulans, that were needed for sugar tolerance.

“The ability to analyse hybrid animals was the key advantage of our study. This way we could not only rely on correlating the findings but were able to identify genetic changes, that were causally important.

We, also, could tell that sugar tolerance comes with a cost. D. Simulans and the sugar tolerant hybrids survived poorly on a low nutrient diet. This suggests that D. Sechellia has evolved to survive on a low nutrient environment, which has required rewiring the metabolism in a way that has made feeding on high sugar impossible.” says Mr Hietakangas.

This study opens up many interesting questions, also, related to humans. In the future, it will be interesting to explore whether human populations, that have different dietary histories, for example, experiencing extremely limited nutrition for many generations, may, respond differently to modern diets rich in sugars. 

The Paper: Natural variation in sugar tolerance associates with changes in signaling and mitochondrial ribosome biogenesis: Richard G Melvin, Nicole Lamichane, Essi Havula, Krista Kokki, Charles Soeder, Corbin D Jones, Ville Hietakangas: eLife:::ω.

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It’s Like a Photograph in Which All Movement IS Frozen in Time: New Method Shows the Cell Development




|| August 15: 2018: Karolinska Institutet News || ά. Researchers at Karolinska Institutet and Harvard Medical School report in the journal Nature that they have developed a technique for capturing dynamic processes in individual cells. Apart from studying disease processes, the method can be used to observe, in detail, how specialised cells are formed during embryonic development. The body is composed of specialised cells, that give each organ its unique function. The brain, for instance, is made up of hundreds of different kinds of neurons, while the kidneys have specialised cells for filtering blood and the heart muscle cells have a built-in pacemaker function.

Organs are formed as the embryo develops through a process of gradual specialisation. The fertilised egg divides and as more cells are formed they start to take on more specific functions. Similar processes are, also, found in tumours, which, gradually, develop into a kind of organ with blood vessels and supporting cells, that help the tumour grow. What determines the unique function of each cell is the specific genes, that are active within it. In neurons, for example, genes are activated, that control electrical signals, while muscle cells use genes for motor proteins.

In recent years, Swedish and international researchers have developed methods for mapping the cellular composition of complex tissues by studying the gene activity of individual cells. The downside of these methods is that they are destructive. Measuring gene activity of individual cells involves destroying the cells so that their content can be analysed, which makes it difficult to study dynamic processes.

“It’s like a photograph in which all movement is frozen in time.” says Professor Sten Linnarsson at the Department of Medical Biochemistry and Biophysics, Karolinska Institutet and one of the Researchers, who led the study. “We’ve now developed a new method, that measures not only genetic activity but, also, changes in this activity in individual cells. You can compare this to a photo captured with a long exposure, which results in motion blur: stationary objects are sharp while objects in motion are blurred. Objects moving quickly are blurrier and the direction of movement is revealed by the direction of blur.”

The new method exploits the fact that when genes are activated, a series of RNA molecules are formed in a certain order. By separating out these molecules, the researchers can work out, if, a gene has, just, been activated or, if, for example, it is about to be switched off. 

“This new method allows us to observe in detail how specialised cell types are formed in the embryo, including, the human embryo.” says Professor Linnarsson. “It can, also, be used to study dynamic disease processes, such as, tumour formation, wound healing and the immune system.”

The study was conducted in close collaboration with Peter Kharchenko from Harvard Medical School in the USA and with contributions from several other groups. It was financed with grants from the Swedish Foundation for Strategic Research:SSF, the Knut and Alice Wallenberg Foundation, the Erling-Persson Family Foundation, the Wellcome Trust, the Centre for Innovative Medicine:CIMED, the Swedish Research Council, the European Research Council, the Swedish Brain Fund, the Ming Wai Lau Centre for Reparative Medicine, the Swedish Cancer Society, Karolinska Institutet and the USA’s National Institutes of Health:NIH and National Science Foundation:NSF.

The Paper: RNA velocity of single cells: Gioele La Manno, Ruslan Soldatov, Amit Zeisel, Emelie Braun, Hannah Hochgerner, Viktor Petukhov, Katja Lidschreiber, Maria E. Kastriti, Peter Lönnerberg, Alessandro Furlan, Jean Fan, Lars E. Borm, Zehua Liu, David van Bruggen, Jimin Guo, Erik Sundström, Gonçalo Castelo-Branco, Patrick Cramer, Igor Adameyko, Sten Linnarsson, Peter V. Kharchenko: Nature: Online: August 08:2018 :::ω.

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New Research Find Way to Reverse Key Aspects of Human Cell Ageing by New Compounds




|| August 12: 2018: University of Exeter News || ά. New research breakthrough made in reversing the key aspects of human cell ageing could be the ‘basis for a new generation of anti-degeneration drugs’. This reversal is achieved by new compounds developed at the University of Exeter in this research. In a laboratory study of endothelial cells, which line the inside of blood vessels, researchers tested compounds designed to target the mitochondria, called, the power stations of cells. In the samples used in the study, the number of senescent cells, older cells, that have deteriorated and stopped dividing, was reduced by up to 50%.

The research team, also, identified two splicing factors, a component of cells, that play a key role in when and how endothelial cells become senescent. The findings raise the possibility of future treatments not only for blood vessels, which become stiffer as they age, raising the risk of problems, including, heart attacks and strokes but, also, for other cells. “As human bodies age, they accumulate old, senescent cells, that do not function as well as younger cells.” said Professor Lorna Harries, of the University of Exeter Medical School. The compounds developed at Exeter have the potential to tweak the mechanisms by which this ageing of cells happens.

We used to think age-related diseases like cancer, dementia and diabetes each had a unique cause but they, actually, track back to one or two common mechanisms. This research focuses on one of these mechanisms and the findings with our compounds have potentially opened up the way for new therapeutic approaches in the future. This, may, well, be the basis for a new generation of anti-degenerative drugs.”

Professor Harries said that the goal was to help people stay healthier for longer. “This is about health span and quality of life, rather than merely extending lifespan.”

In a paper published last year, the research team demonstrated a new way to rejuvenate old cells in the laboratory. However, the new research looked at precisely targeting and rejuvenating mitochondria in old cells. Each one of our genes is capable of making more than one product and splicing factors are the genes, that make the decision about which of these products are made.

In this new work, using specific new chemicals, the researchers were able to very specifically target two splicing factors, SRSF2 or HNRNPD, that play a key role in determining how and why our cells change with advancing age.

“Nearly half of the aged cells we tested showed signs of rejuvenating into young cell models.” said Professor Harries. The researchers tested three different compounds, all developed at the University of Exeter and found each produced a 40-50% drop in the number of senescent blood vessel cells.

The compounds in question, AP39, AP123 and RT01, have been designed by the researchers to selectively deliver minute quantities of the gas hydrogen sulfide to the mitochondria in cells and help the old or damaged cells to generate the ‘energy’ needed for survival and to reduce senescence.

“Our compounds provide mitochondria in cells with an alternative fuel to help them function properly.” said Professor Matt Whiteman, also, from the University of Exeter. “Many disease states can essentially be viewed as accelerated ageing and keeping mitochondria healthy helps either prevent or, in many cases, using animal models, reverse this.

Our current study shows that splicing factors play a key role in determining how our compounds work.” The research was funded by Dunhill Medical Trust and the Medical Research Council.

The Paper: Published in the journal Aging, is entitled: “Mitochondria-targeted hydrogen sulfide attenuates endothelial senescence by selective induction of splicing factors HNRNPD and SRSF2. :::ω.

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New Research Sheds Light on the Effects of In-Vitro Fertilisation on Embryonic Growth

|| June 24: 2018: University of Helsinki News: Päivi Lehtinen Writing || ά. In vitro fertilisation affects the regulatory region of genes, essential for placental and embryonic growth, as well as, the birth weight. This new study suggests that the effects depend on genetic variation inherited from the parents. This information could be useful in development of assisted reproduction technologies. It is known that in vitro fertilisation:IVF, can affect the size of the new-borns. Children derived from fresh embryo transfer have smaller birth weight and, surprisingly, children derived from frozen embryo transfer have, subtly, higher birth weight in average.

In the study conducted by University of Helsinki, Helsinki University Hospital and University of Tartu, the researchers looked for mechanisms by how the IVF can alter the embryonic growth. More than three percent of new-borns are derived from IVF treatments currently in Finland. 86 couples with IVF derived pregnancies and 157 couples with spontaneous pregnancies as controls were recruited for this study. IVF samples were divided in two groups depending on whether the embryos were transferred in utero fresh after fertilisation or after they were frozen and thawed before the transfer.

The regulation region of two growth genes, insulin-like growth factor two and H19, was examined. A common genetic variation in this region has been associated with different amount of epigenetic marks depending on which variants an individual has inherited from the parents.

DNA methylation, the most well-known epigenetic mark, was investigated in this study. These methyl groups bind to the DNA strand and affect the gene function.

“We divided the placentas in genotypes according to the variants, which the new-borns had inherited and we observed that the effect of IVF on the epigenetic marks depends on the genotype.” Says Adjunct Professor Nina Kaminen-Ahola, the Leader of the research team at the University of Helsinki.

Furthermore, the birth weight and placental weight, as well as, the head circumference of new-borns, which were derived from fresh embryo transfer, were smaller only in one particular genotype. Also, the new-borns with this genotype, who were derived from frozen embryo transfer, were significantly heavier.

“This work together with our previous work about the effects of prenatal alcohol exposure on embryonic development, reveals a genotype-specific effects of environmental factors.” Says Professor Kaminen-Ahola. “As far as I know, this is the first genetic factor, which has been associated with the phenotype of IVF-derived new-borns.

This single nucleotide polymorphism locates in the binding site of a regulatory protein and, thus, could affect the binding of the protein, as well as, gene function in altered environmental conditions. However, the effect of this variation on the regulation of these growth genes should be examined by functional studies.”

Professor Kaminen-Ahola emphasizes that these changes are not dangerous and IVF treatments are safe. “Low birth weight has been associated with increased risk for heart and vascular diseases and, therefore, it is necessary to understand the mechanisms underlying it to develop the IVF methods.

In the future, this could be a part of personalised medicine and help to target the sources of health care system more specifically.”
Research Group of Environmental Epigenetics: Children born with the help of fertility treatments are, generally, healthy. Comparisons with children conceived spontaneously without treatments indicate that they have a slightly higher risk of premature birth and low birth weight.

Several studies have connected fertility treatment methods to changes in the epigenome that regulates gene function in the placenta or cord blood. However, the results have been conflicting, and no extensive follow-up studies have been conducted.

In order to investigate the potential effects of fertility treatments, Dr Nina Kaminen-Ahola has launched an extensive study based on samples gathered at birth and follow-up data.

“The purpose of our study is to find whether fertility treatment methods alter the epigenome and whether such changes can affect the health and development of the individual.” Professor Kaminen-Ahola says. “In addition, we study whether there are differences between various fertility treatment methods and how these methods could be developed further.”

For more information, contact: Dr. Nina Kaminen-Ahola, PhD, University of Helsinki: Tel. +358 50 4482768: email: nina.kaminen at
The Paper: rs10732516 polymorphism at the IGF2/H19 locus associates with genotype-specific effects on placental DNA methylation and birth weight of newborns conceived by assisted reproductive technology: Heidi Marjonen, Pauliina Auvinen, Hanna Kahila, Olga Tšuiko, Sulev Kõks, Airi Tiirats, Triin Viltrop, Timo Tuuri, Viveca Söderström-Anttila, Anne-Maria Suikkari, Andres Salumets, Aila Tiitinen and Nina Kaminen-Ahola: Clinical Epigenetics:::ω.

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Research Identifies New and Unconventional Type of Immune Cell Capable of Fighting Viral Infections

|| May 10: 2018: University of Birmingham News || ά. Research led by the University of Birmingham has identified a new unconventional type of immune cell capable of fighting viral infections. The study, published in Nature Communications and carried out in collaboration with the Academic Medical Centre, Netherlands and Skolkovo Institute of Science and Technology, Russia, focussed on T-cells, that control our immune system. Specifically, the research has defined a subset of ‘unconventional V-delta-2 lymphocytes’, which are a type of Gamma Delta T-cell, an ancient class of immune cells, that has been relatively poorly understood.

The new findings establish that this subtype is not only present at birth but persists in adults at low levels and can increase in numbers massively during virus infections. The researchers examined how this subtype of T-cells responded to a virus infection, called, cytomegalovirus. They found that when these T-cells detected signs of the virus infection they both increased in numbers and became ‘licensed to kill’. Lead Author Dr Martin Davey, of the University of Birmingham’s Institute of Immunology and Immunotherapy, said, “These cells can clearly adapt to some key challenges, that life throws at them.

Upon viral infection, they change from harmless precursors into what appear to be ruthless killers. They can, then, access tissues, where, we believe, they detect and destroy virally infected target cells.”

The results build on previous work from the same research group, published last month in Trends in Immunology, which, also, suggests that many gamma delta T-cells, that control our immune system can adapt in the face of infectious challenges.

The research team is now trying to better understand the scenarios, when these unconventional killer T-cells are most important and how to harness them to advance treatments to fight viral infections.

Dr Davey said, “We think, these cells contribute to defence against viral infection in the liver, a site, which is exposed to many potentially dangerous infectious diseases.

They, may, also, be, particularly, important, when other aspects of our immune system are not working at full strength, such as, in newborn babies but, also, in transplant patients, who are taking immuno-suppressive drugs to prevent organ rejection. In these scenarios, boosting the activity of these cells could prove beneficial to patients and we are now starting to explore how to do that.” ::: ω.

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Regine Humanics Foundation Begins Its Journey Today: The Humanion Is Now A Regine Humanics Foundation Publication

|| April 06: 2018 || ά. The Humanion was first published on September 24, 2015 and has been run, since that day, on a complete voluntary basis without any 'formal' or 'constituted' manner or form and, it was run on as a Human Enterprise, which is an idea of Humanics, in which, ownership is replaced by belongingship and, thus, in a Humanical Society, no one owns anything but everyone belongs to the whole as the whole belongs to everyone lawfully and equally and, it neither believes in nor makes money but human utilities, needs, aspirations, creativity, imagination and dreams are served without money, where everyone works and creates for all others as all others create and work for all others, thus, bringing in meaning and purpose to life along with it come natural justice, equality and liberty, that establish a true civilisation within the Rule of Law. And in one word, this system of human affairs management is called, Humanics and a society that runs itself in humanics is called a humanical society. Today, we have begun the process of 'constituting' this Human Enterprise, which does not exist in the current system, but the next closest thing to it, that exists in the UK Law is Social Enterprise. Therefore, today, Friday, April 06, 2018, we are beginning Regine Humanics Foundation, that is the 'Agency', that will lead, run, manage and develop everything, that The Humanion has been trying to do.

Regine Humanics Foundation is established by the Thinker, Author, Poet, Novelist, Playwright, Editor of The Humanion, Festival Director of London Poetry Festival and a Humanicsxian: hu: maa: neek: tian: One, that believes in, lives and exists by Humanics, Mr Munayem Mayenin, of London, England, United Kingdom. Mr Mayenin says, ''Humanics is a vision; people, may, call it, utopia, we, call it our Humanicsovicsopia; Humanics. Humanics is our philosophy, our faith, our conviction, our resolution, our way of existing, thinking, being and doing: to seek and try to do so in the determination that all we must do and be is to exist to advance the human condition. People, readers and agencies and organisations, from all across England, Scotland, Northern Ireland, Wales and the whole of the United Kingdom and Australasia, Africa, Asia, Europe, North and South America, from all walks and strata of life, have supported our endeavours, supported The Humanion and The Humanion Team, who volunteered their time to run things, since the beginning of The Humanion and long before that, when other things, that are now part of The Foundation, were developing. Nothing has changed in terms of the nature and value of what we have been seeking to do.''

''But the founding of The Foundation brings it all in a solid foundation so that we can keep on building this 'vision' so that it keeps on going regardless of who come to take the vision-mission of The Foundation forward. The Foundation runs along with time and along with the flowing humanity. This is the dream, this is the vision, this the hope in founding this Foundation. And, in this, we hope and invite all our readers, supporters, well wishers and all agencies and organisations to support our endeavours to build something, a Human Enterprise, which we are in the process of registering as a Social Enterprise, as a Community Interest Company, working for the common good of the one and common humanity. No one makes or takes profit out of The Foundation, which now runs The Humanion and everything else, that is part of it. The Foundation, once registered, will have an Asset Lock, which means that in any event, should The Foundation dissolve itself, all its existing assets shall go to a similar Social Enterprise. Therefore, we invite everyone to support The Foundation, support The Humanion in whatever way they can. And, there are endless number of ways people and organisations can support The Foundation and The Humanion.'' ::: ω.

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Advance Made Towards Personalised Medicine in the Approach to Treating Bowel Cancer


|| March 23: 2018: Queen's University Belfast News || ά. Researchers from Queen’s have demonstrated, for the first time, how molecular analysis of clinical trial biopsy samples can be used to help clinicians identify the key changes, that occur in an individual patient’s bowel or colorectal tumour. It is thought that this ‘personalised medicine’ approach could, ultimately, improve the prognosis and quality of life for bowel cancer patients. The Queen’s led study, in collaboration with the University of Turin, University of Oxford, the University of Leeds and a number of clinical trial centres across the UK, demonstrates how personalised medicine can be successfully used to help improve outcomes in ongoing clinical trials.

For clinicians, identifying which bowel cancer patients are likely to respond to different types of treatment can be, particularly, challenging. Dr Philip Dunne, Senior Research Fellow from the Centre for Cancer Research and Cell Biology at Queen’s and an author on the study, explains,  “There are, approximately, 01.4 million cases of bowel cancer diagnosed annually worldwide, with 41,000 cases in the UK each year. A number of treatment options are available but mortality rates remain high, with bowel cancer the second most common cause of cancer death in the UK. “In order to develop better treatments for individual patients, we, must, first, understand the biology of that person’s tumour; this is the basis of personalised medicine in cancer.

Advances in molecular and genetic analysis in the past 10 years have markedly improved our biological understanding of colorectal cancer, although, this increased knowledge it is yet to, significantly, change standard patient care. This study highlights how we can begin to use this new understanding developed in research laboratories, to identify the biology underlying an individual patient’s tumour in the clinic; the ‘bench-to-bedside’ approach.”

The research study has been published in the Journal of Pathology. Dr Matthew Alderdice, a Postdoctoral Fellow on the project and First Author on the study, said, “Although, molecular analysis is, routinely, carried out in research laboratories from large surgically removed tumours, in current clinical practice the tissue available for clinical decision-making, may be, only, be the initial small tumour biopsy tissue. This study highlights how a precise understanding of the genetic changes, that occur within this biopsy material is crucial to both understanding and treating the disease.”

Professor Mark Lawler, Chair in Translational Cancer Genomics at Queen’s, said, “Molecular studies have indicated that a ‘one size fits all’ treatment approach for bowel cancer isn’t a viable option, if, we are to effectively tackle this disease. We have demonstrated the ability of molecular classification systems to stratify patients based on their molecular make-up in a series of colorectal biopsy samples obtained during a phase II clinical trial.

The ultimate aim of this work is to allow patients to receive a more tailored disease management plan based on the specific biology of their tumour. Thus, we can tailor treatment to the individual patient, maximising its effectiveness while minimising potential side effects.” This research study is part of the Stratification in Colorectal Cancer consortium, led by Professor Tim Maughan, from the University of Oxford and funded by a grant from the Medical Research Council:MRC and Cancer Research UK as part of the MRC’s stratified medicine initiative.

Professor Tim Maughan, of Clinical Oncology at the University of Oxford and Principal Lead of the S:CORT Consortium, said, “This work highlights the benefit of a UK wide approach, bringing together the collective expertise within our consortium to drive new approaches to improve bowel cancer outcomes. Our S:CORT Consortium is gaining new insights into the key factors, that influence bowel cancer development and its treatment and using this knowledge to maximise best treatment and quality of life for bowel cancer patients.”

S:CORT involves key partnerships with patients and patient advocacy groups. Mr Ed Goodall, a survivor of bowel cancer and a member of S:CORT, says, “As patients, we are delighted to be involved in this work at a meaningful level, giving our opinions in relation to the scientific approaches that are undertaken within the consortium. As a citizen of Northern Ireland it is, also, extremely, exciting to see the excellent work, that is being done by researchers at Queen’s University.”

Ms Deborah Alsina MBE, Chief Executive of Bowel Cancer UK and Beating Bowel Cancer, the UK’s leading bowel cancer charity and a partner in S:CORT, said, “We are delighted to be associated with this research. Our recent Critical Research Gaps in Colorectal Cancer Initiative highlighted the need for better research collaboration. This is an excellent example of the best UK science and clinical care in bowel cancer working together to develop innovative approaches to save more lives.''

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New Stem Cell Study Finds Strong Evidence for Likely Therapeutics for Stronger Muscles in Old Age


|| March 11: 2017: Karolinska Intitutet News || ά. As we grow older, our muscular function declines. A new study by researchers at Karolinska Institutet shows how an unexpectedly high number of mutations in the stem cells of muscles impair cell regeneration. This discovery, may, result in new medication to build stronger muscles, even, in old age. The study is published in Nature Communications. It has, already, been established that natural ageing impairs the function of our skeletal muscles. We know that the number and the activity of the muscles’ stem cells decline with age. However, the reasons for this has not been fully understood. In this new study, researchers have investigated the number of mutations, that accumulate in the muscle's stem cells or satellite cells.

“What is most surprising is the high number of mutations. We have seen how a healthy 70-year-old has accumulated more than 1,000 mutations in each stem cell in the muscle and that these mutations are not random but there are certain regions, that are better protected.” says Professor Maria Eriksson, at the Department of Biosciences and Nutrition at Karolinska Institutet. The mutations occur during natural cell division and the regions, that are protected are those, that are important for the function or survival of the cells. Nonetheless, the researchers were able to identify that this protection declines with age. “We can demonstrate that this protection diminishes the older you become, indicating an impairment in the cell's capacity to repair their DNA.

And this is something we should be able to influence with new drugs.” says Professoor Eriksson. The researchers have benefited from new methods to complete the study. The study was performed using single stem cells cultivated to provide sufficient DNA for whole genome sequencing.

“We achieved this in the skeletal muscle tissue, which is absolutely unique. We have, also, found that there is very little overlap of mutations, despite the cells being located close to each other, representing an extremely complex mutational burden.” explains one of the study's author, Dr Irene Franco, Post doctoral Researcher in Professor Maria Eriksson’s research group.

The researchers will now continue their work to investigate whether physical exercise can affect the number of accumulated mutations. Is it true that physical exercise from a young age clears out cells with many mutations or does it result in the generation of a higher number of such cells?

“We aim to discover whether it is possible to individually influence the burden of mutations. Our results, may be, beneficial for the development of exercise programmes, particularly, those designed for an ageing population.” says Professor Eriksson.

The researchers gained access to the muscle tissue used in the study via a close collaboration with clinical researchers, including, Ms Helene Fischer at the Unit for Clinical Physiology at Karolinska University Hospital. The study has been a co-operative project between researchers at Karolinska Institutet, Science for Life Laboratory:SciLifeLab, Uppsala University, Linköping University and Stockholm University, in addition to several affiliated institutes in Italy.

The research is financed by the Swedish Research Council, Centre for Innovative Medicine:CIMED, the David and Astrid Hagelén Foundation, the Swedish Society of Medicine, the Gun and Bertil Stohnes Foundation, the Osterman Foundation, the Marianne and Marcus Wallenberg Foundation, Wallenberg Advanced Bioinformatics Infrastructure and the EU Commission funding programme, Marie Skłodowska-Curie.

The Paper: Somatic mutagenesis in satellite cells associates with human skeletal muscle aging: Irene Franco, Anna Johansson, Karl Olsson, Peter Vrtačnik, Pär Lundin, Hafdis T. Helgadottir, Malin Larsson, Gwladys Revêchon, Carla Bosia, Andrea Pagnani, Paolo Provero, Thomas Gustafsson, Helene Fischer, Maria Eriksson: Nature Communications Online: February 23: 2018

Caption: 01: Professor Maria Eriksson: 02: Irene Franco: Images: Ulf Sirborn: ω.

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Molecular Link Discovered Detween Vitamin A and Intestinal Health


|| February 26: 2017: Monash University News || ά. New research from Monash University has found a signalling molecule, that helps maintain intestinal health in mice. Published in PLoS Pathogens, these findings could provide new ways to fight disease. Monash Biomedicine Discovery Institute’s Professor Colby Zaph and an international research team have shown the active form of vitamin A regulates immune system responses in the mouse intestine. It does so by controlling activity of a protein in innate lymphoid cells, called, ‘Hypermethylated in cancer 1’:HIC1.

With further research, these findings could open up new strategies to protect against infection and intestinal imbalance, which can lead to conditions, such as, food allergy and irritable bowel syndrome. “Vitamin A has long been known to play a central role in the balance between intestinal immune health and disease but the precise molecular mechanisms of how it affected immune cells was unknown.” Professor Zaph said. “Identifying HIC1 provides a potential target to modulate intestinal inflammation.” The intestinal immune system must strike a balance between fighting infection and maintaining tolerance to harmless or beneficial microbes and food particles.

Previous research has shown that the active form of Vitamin A, produced from dietary vitamin A by some intestinal cells and all-trans-retinoic acid:atRA helps maintain this balance in mice by regulating the activity of innate lymphoid cells. However, the molecular details of this process have been unclear.

The new study focused on the protein HIC1, which was first identified in cancer cells but, which also, helps regulate gene expression in normal cells. The research team had previously shown that atRA influences HIC1 activity and that HIC1 helps maintain intestinal health in mice. Now, they have investigated the molecular details of HIC1’s role.

The researchers deleted the HIC1 gene in certain innate lymphoid cells in the mouse intestine and found that this increased the susceptibility of the mice to infection with the bacterium Citrobacter rodentium, which is similar to pathogenic E. coli species, that infects humans. Further investigation showed that the increased susceptibility was due to a reduction in production by the innate lymphoid cells of IL-22, a protein, that plays a key role in the intestinal immune response.

About the Monash Biomedicine Discovery Institute: Committed to making the discoveries, that will relieve the future burden of disease, the newly established Monash Biomedicine Discovery Institute at Monash University brings together more than 120 internationally-renowned research teams. Our researchers are supported by world-class technology and infrastructure and partner with industry, clinicians and researchers internationally to enhance lives through discovery.

The Paper: HIC1 links retinoic acid signalling to group 3 innate lymphoid cell-dependent regulation of intestinal immunity and homeostasis: Kyle Burrows, Frann Antignano, Alistair Chenery, Michael Bramhall, Vladimir Korinek, T. Michael Underhill, Colby Zaph: PLOS Pathogens

Caption: Professor Colby Zaph: Image: Monash University: ω.

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New Cell Model Could Lead to Treatments for Neurological Diseases


|| February 19: 2017: Karolinska Institutet News || ά. Researchers from Karolinska Institutet and KTH Royal Institute of Technology have developed a new cell model for human brain helper cells, known as, astrocytes. The model could, potentially, be used in large scale drug screening in the search for treatments for neurological diseases, such as, Alzheimer’s. The research is published in the scientific journal Stem Cell Reports. Astrocytes are star shaped cells, that are found in the brain and spine and were long thought to be the 'glue', that binds nerve cells.

However, recent advances show that they are, in fact, responsible for complex regulation of a variety of critical brain functions. They have, also, been proven to be central to neurological disease,  such as, Alzheimer’s. But for research, these cells prove problematic. “Human astrocytes are, significantly, more complex than those found in mice, for example, mice do not develop the same brain diseases as humans. We, therefore, need better ways to study this cell type.” says Ms Anna Falk, Associate Professor at Karolinska Institutet’s Department of Neuroscience. Together with Ms Anna Herland at KTH and researchers at AstraZeneca, Ms Anna Falk developed a new cell model for human astrocytes.

Drawing on Nobel Prize-winning technology, the researchers reprogrammed human skin cells to create induced pluripotent stem cells or iPS cells, which were, then, guided with growth factors to become astrocytes.

Beginning with stem cells, researchers can produce an infinite number of astrocytes, which is important for the large-scale use within the pharmaceutical industry. “The historically high statistics of clinical failures in developing drugs against neurological diseases have now made drug companies increasingly interested in improved cell models in which human cells are used.” says Ms Anna Herland, Assistant Senior Lecturer at the Department of Micro and Nano-systems at KTH. “Our work has been focused on development of a cell model, that follows human embryonic development of astrocytes.”

Compared with cell models used in the pharmaceutical industry today, Ms Falk and Ms Herland’s model shows wider functionality. A pilot drug screening with a few substances showed that the model has the potential to identify new candidates, which can go into drug development for neurological diseases.

"Our model of human astrocytes is an important step forward in order to understand and attack human neurological diseases, where astrocytes have an important role.” says Ms Anna Herland. “With this model, we can begin to study how astrocytes develop and receive their functional diversity during embryonic development”.

The research was supported by the Swedish Research Council, the Swedish Foundation for Strategic Research, Vinnova, the European Commission, the Wallenberg Foundations and the Swedish Knowledge Foundation.

The Paper: Human iPS-derived astroglia from a stable neural precursor state show improved functionality compared to conventional astrocytic models: Lundin Anders, Delsing Louise, Clausen Maryam, Ricchiuto Piero, Sanchez José, Sabirsh Alan, Mei Ding, Synnergren Jane, Zetterberg Henrik, Brolén Gabriella, Hicks Ryan, Herland Anna, Falk Anna: Stem Cell Reports, online 15 February 15: 2018

Caption: Anna Falk: Associate Professor: Neuroscience: Karolinska Institutet: Image: Stefan Zimmerman: ω.

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Tissue Mechanics is Essential for Cell Movement

|| February 15: 2017: UCL News || ά. Cells, that form facial features, need surrounding embryonic tissues to stiffen so they can move and develop, according to new UCL-led research. The discovery has important implications for understanding the causes of facial defects, which account for a third of all birth defects globally, 03.2 million each year and are the primary cause of infant mortality. It is the first time that the mechanical properties of the environment surrounding embryonic cells has been shown to be crucial in cell movement and development, rather than genes or molecules.

The researchers say that it is likely that a similar mechanism is used by other cells involved in spreading cancer and wound healing. For the study, published today in Nature, researchers from UCL and the University of Cambridge investigated the importance of mechanical cues in the collective migration of neural crest cells in frog embryos. Frogs were chosen as a model organism as their neural crest cells behave in a similar way to those of humans and their movement is often used to study the spread of cancer. In addition, the embryo development of frogs can be studied without inflicting harm, which isn’t true for other animal models.

“We’ve known that cell movement is essential for many processes in the body, including, the formation of embryos and cancer spread, but until now, most effort has been put into understanding the molecular cues, that drive movement, rather than the role the mechanical environment plays.” explained study Lead Author, Professor Roberto Mayor, UCL Cell and Developmental Biology.

“We were surprised to see how important tissue hardness is for movement; it’s the difference between walking on a hard pavement relative to soft sand. The cells sense the increasing hardness of their environment before moving to form the features of the face and skull. Knowing this will, hopefully, inform the development of preventative treatments for facial defects.”

The research team tested the hardness of the embryonic tissue at various stages of development using a probe, that touches the surface and measures its deformation under a known pressure. They found that during development, the tissue holding the NC cells stiffened and became denser with cells, which triggered the cells’ orchestrated movement.

They modified the stiffness of the embryo tissues using actin and myosin, the same molecules used for muscle contraction and found the hardness at which NC cells migrated. This was replicated using synthetic surfaces of the same stiffness in the laboratory.

“We’ve found a new link between two previously unconnected processes: the thickening and hardening of tissues and the movement of cells. This is a really exciting discovery as it shows the importance of tissue mechanics and molecules in co-ordinating embryo development. We hope, it inspires others working in oncology and tissue engineering to explore the role of tissue mechanics in other important fields.” said study First Author Dr Elias H Barriga, UCL Cell and Developmental Biology and the UCL London Centre for Nanotechnology.

The work was funded by the Medical Research Council, Biotechnology and Biological Sciences Research Council, Wellcome, National Institutes of Health and European Research Council. 

The Paper: Tissue stiffening coordinates morphogenesis by triggering collective cell migration in vivo: Nature: Elias H. Barriga, Kristian Franze, Guillaume Charras and Roberto Mayor

Caption: Neural crest cells: Image: UCL

Whatever Your Field of Work and Wherever in the World You are, Please, Make a Choice to Do All You Can to Seek and Demand the End of Death Penalty For It is Your Business What is Done in Your Name. The Law That Makes Humans Take Part in Taking Human Lives and That Permits and Kills Human Lives is No Law. It is the Rule of the Jungle Where Law Does Not Exist. The Humanion

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Immune Response Mechanism: New Research Finding Raises Hope for Allergy Treatment

|| November 16: 2017: University of Edinburgh News || ά. Scientists have made a fundamental discovery about how our body’s immune system clears harmful infections. Edinburgh researchers have identified a previously unknown mechanism by which the responses of key cells of the immune system are regulated. Researchers say that the finding could inform research into improved treatments for allergies or chronic inflammatory diseases, such as, lung and liver fibrosis.

The research team made the discovery by studying how the immune system in mice fights off parasitic worms. These parasites provoke a strong immune response, enabling researchers to carry out in-depth studies of the defence mechanisms involved. They found that chemical signals from infecting organisms activate cells, called Th2 cells, causing them to multiply and express a key protein, known as, EGFR. The cells then migrate from the lymph nodes, where they are stored, to the site of infection, where they release defence proteins to expel the parasites.

Researchers found that Th2 cells release defence molecules, when they detect the damage caused by invading parasites, but can only perform this task if they express EGFR.

According to the researchers, this safety mechanism, unknown until now, blocks the release of defence molecules in the absence of parasites and, thereby, prevents tissue damage.

The study, published in the journal Immunity, was funded by the Medical Research Council, European Union and Austrian Science Fund. It was carried out in collaboration with other scientists from the UK, Germany, Ireland, Austria and The Netherlands.

''We found an entirely new mechanism by which immune responses against parasites are regulated. These findings give us fresh insight into the functioning of local immune responses and should allow us to develop better vaccines against parasite infections.'' said Dr Dietmar Zaiss, School of Biological Sciences.