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The General Election 2019: December 12: Against the Conservative Sociology of Squalor

The Political Philosophy, That Says That the Most Vital Part of the Public Affairs Management System, the System of Economics, That Shapes the Market and Directs the Course of Existence of the Entire Range of Business, Trade, Commerce and Financial Endeavours of a Nation and Ultimately Shapes the Human Condition of a Nation Should Not Be in the Ownership of the Entire Nation and Its People as Their State and Government Belong to Them and the Political Economics, That Says That the Survival of the Fittest or Richest Is the Ultimate Aim of Society, in Which the Vast Majority of the Population Must Exist and Perish Away in Serving a Live-in-Life Sentence of Suffering, Agony and Hardship and Must Accept All the High-Cruelties, High-Barbarities and High-Tortures, That Capitalism Creates, Distributes and Enforces are Nothing But a Brutal, Cruel, Ruthless and Inhuman Dictate of a Monstrous Social Jingoistic Jungle, Where Neither Civic Nor Community Can Exist Nor Can There Humanity Exist as Humanity Naturale as Individuals, as Families, as Communities, as Agencies and Organisations and as a Civic Society: And When Such a Monstrous Social Jingoistic Jungle is Established in a Country It Becomes Worse Than a Jungle and It Becomes Every Citizen's Civic and Moral Duty and an Existential Necessity of Humanity to Do All in Their Democratic Power to Eliminate Such Jingoistic Jungle and Replace It with a Civic Society Where Community, People, Families, Individuals and All Humanity are as Real, as Connected and as Active, as Engaged and as Creative as the Human Physiology Is in All Humans of a Given Society

''In simple terms, the sociology of squalor’s political economical basis was created from this fact that these two conservative-led governments have cut about £30 billion pounds from the working and non-working poor in the social security cuts, that’s 30x1000=£30,000 million pounds and, than, they added another £30 billions to that cut-away £30 billions and made a sum of £60 billions and gave that away to their rich masters as corporation tax cuts, that’s £60,000 million pounds! That meant that the working and non-working poor of this country had been made to pay for the financial crash while they had nothing to do with what caused the crash. That is the foundation on which they, they then, cut the size of the entire governments of all layers and all the central and local public, civic, community, family and youth services, national health service, the national social care, education, police, social services, higher education, judiciary, including, the legal aid and the cuts in number courts etc and much more have received cuts well beyond 50% and that’s a very conservative figure.''

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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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