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Molecular Biology


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


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 helsinki.fi
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

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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.

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Scientists Figure Out How the Timer for Cell Division Works: And for Cancer That Might Mean When the Timer is Left to Run on It Will Kill It


|| November 12: 2017: University of Leuven News: Ilse Frederickx: Original: Katrien Bollen: English|| ά. Human cells use a timer to divide: each cell gets at least 30 minutes to divide its genetic material between the nuclei of two daughter cells. Researchers at KU Leuven have unravelled how this timer is switched on and off. Their findings open up perspectives for the treatment of cancer, as keeping the timer going would stop cancer cells from dividing. Our body is constantly building new tissue and replacing dead or damaged cells through cell division.

Skin cells, for instance, only last about a month before they are replaced by newly divided cells. Scientists, already, knew that cells have a built-in timer ensuring that their division takes at least half an hour. But the underlying mechanism of this timer was still a mystery. ''In cell division, it’s all about evenly distributing the chromosomes between the daughter cells.''  says Senior Suthor Mr Mathieu Bollen from the KU Leuven Department of Cellular and Molecular Medicine. “First, the chromosomes of a cell are duplicated. Two spindles with so-called microtubules then attach to these chromosomes, allowing the two copies of each chromosome to be separated and pulled into opposite directions.

This is how the chromosomes are evenly divided between two new cell nuclei. Then the actual division takes place, creating two daughter cells that are genetically identical to the parent cell.” If everything has gone well, that is. And that’s not usually the case right away. “Temporary issues with attachment of microtubules to the replicated chromosomes are common.

Sometimes there’s a missing link so that a chromosome does not end up in a daughter cell. In other cases, the microtubules pull both copies towards the same daughter cell. The result is a daughter cell with one chromosome too few or too many. These little errors usually cause the cell to die. But they, may, also, speed up the cell division process, as is sometimes the case in cancer cells.”

Dr Junbin Qian, the First Author of the paper, found that the timer gives cells the time to fix attachment-related problems. “At the start of the cell division process, the biochemical clock starts ticking, when a phosphate group is attached to a key protein. About half an hour later, this phosphate group is removed again. All the while, the distribution of the chromosomes is on hold, allowing the cell to add missing links and fix wrong ones.”

''The timer has potential for cancer therapy. You want to prevent cancer cells from dividing and spreading. Some of the current cancer therapies target the microtubules in the cell. One example is the drug Taxol, which is produced from yew clippings. Unfortunately, such drugs are toxic and have many unwanted side-effects.

Cancer cells are, also, building resistance to these substances. Now that we know how the cell division timer works, we can start looking for drugs, that keep the timer switched on: this brings cell division to a standstill, eventually, causing the cancer cells to die. Together with existing treatment methods, this could form an effective combination therapy, because you’d be attacking the cancer cells on several fronts.'' Mr Bollen said. ω.

Image: Two stages of cancer cell division. The cell contains two spindles with microtubules, in green. In the top image, these microtubules have attached themselves to contact points, in yellow, of the replicated chromosomes, in purple and are pulling the copies away from each other in opposite directions. In the bottom image, this process has been completed and the chromosomes are evenly distributed between what will become the nuclei of the new daughter cells. Image: KU Leuven:Junbin Qian

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For Stories Published in Molecular Biology in Year Gamma Arkive


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|| All copyrights @ The Humanion: London: England: United Kingdom || Contact: The Humanion: editor at thehumanion.com || Regine Humanics Foundation Ltd: reginehumanics at reginehumanicsfoundation.com || Editor: Munayem Mayenin || First Published: September 24: 2015 ||
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