The Arkive
 
|| Year Delta: London: Monday: September 24: 2018: We Keep On Walking On The Path of Humanics ||
First Published: September 24: 2015
VII London Poetry Festival 2018: Sunday-Monday: October 14-15: 19:30-22:00
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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Genetics

 

 

 

 

Genetics Arkive

 

 

 

 

 

 

 

 

 

 

 
Do Not Argue: Disrupt

 

 

 

|| September 16: 2018: University of Exeter News || ά. Research has shed new light on genetic processes, that, may, one day, lead to the development of therapies, that can slow or, even, reverse, how human cells age. A Study, led by the University of Exeter Medical School, has found that certain genes and pathways, that regulate splicing factors, a group of proteins in the human body, that tell the genes how to behave, play a key role in the ageing process. Significantly, the research team found that disrupting these genetic processes could reverse signs of ageing in cells.

The Study, published in the FASEB Journal, was conducted in human cells in laboratories. Aged or senescent, cells are thought to represent a driver of the ageing process and other groups have shown that, if, such cells are removed in animal models, many features of ageing can be corrected. This new work from this research found that stopping the activity of the pathways ERK and AKT, which communicate signals from outside the cell to the genes, reduced the number of senescent cells in in cultures grown in the laboratory. Furthermore, the researchers found the same effects from knocking out the activity of just two genes controlled by these pathways FOX01 and ETV6.

Professor Lorna Harries, of the University of Exeter Medical School, who led the research, said, ‘’We’re really excited by the discovery that disrupting targeted genetic processes can bring about, at leas,  a partial reversal of key elements of the ageing process in human cells. This suggests that they could be an important aspect in designing therapies, that could keep us healthier as we age. Our ultimate goal is to help people avoid some of the diseases partially caused by ageing cells, such as, Dementia and  ancer.”

The ERK and AKT pathways are repeatedly activated throughout life, through aspects of ageing including DNA damage and the chronic inflammation of ageing. The research suggests that this activation, may, hinder the activity of splicing factors, that tell genes how to behave. This, in turn, could lead to a build-up of senescent cells, those, which have deteriorated or stopped dividing as they age.

To stop the activity of the ERK and AKT pathways, the Study used inhibitors, which are, already, used as cancer drugs in clinics. When the pathways were disrupted, the researchers observed an increase in splicing factors, meaning better communication between protein and genes. 

They, also, noted a reduction in the number of senescent cells. Researchers saw a reversal of many of the features of senescent cells, that have been linked to the ageing process, leading to a rejuvenation of cells.

Dr Eva Latorre, of the University of Exeter Medical School, who carried out the research, said, “This study is part of a fast-evolving body of work into how we age. We used compounds, that are, already, widely available in clinics for cancer and are known to be relatively safe. It’s still early days and we need to understand far more about the complex relationships of how our cells and genetic processes influence ageing, yet, it’s an exciting contribution to how we may one day be able to influence healthier ageing.”

The Paper: ‘FOXO1 and ETV6 genes may represent novel regulator splicing factor expression in cellular senescence: Eva Latorre, Elizabeth L. Ostler, Richard G.A. Faragher and Lorna W. Harries: Published in the FASEB journal: .:::ω.

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Possible Genetic Link Has Been Discovered Between the Circadian Rhythms and Mood Disorders

 

 

|| September 03: 2018: University of Glasgow News || ά. Circadian rhythms are regular 24-hour variations in behaviour and activity, that control many aspects of human lives, from hormone levels to sleeping and eating habits. In the largest ever genetic study of circadian rest-activity cycles in humans, scientists at the University of Glasgow, have identified a possible genetic link between circadian disruption and mood disorders.

The new findings, published in EBioMedicine, follow research published earlier this year in The Lancet Psychiatry, which found that disrupted circadian rhythms were associated with increased risk of mood disorders, including, major depression and bipolar disorder. Circadian rhythms occur in plants, animals and throughout biology. They are fundamental for maintaining health in humans, particularly, mental health and wellbeing.

The findings of this new study identified two areas of the human genome, that, may, contain genetic variants, that increase risk of disruption to rest-activity cycles. The researchers found that one of these areas contained the gene Neurofascin, which binds to the protein product of a well-known candidate gene for bipolar disorder:Ankyrin G, suggesting a direct biological link between circadian disruption and severe mood disorder. Genetic loading for circadian disruption was, also, significantly, associated with mood instability.

For the study, the researchers used genetic information and activity data from 71,500 participants in the UK Biobank cohort to obtain an objective measure of daily rest-activity rhythms, called relative amplitude. This measure was used in comparing gene variants carried by individuals with and without low relative amplitude to identify potential genetic associations with several mood disorder features, including mood instability, neuroticism, depression and bipolar disorder.

Finding genes for low relative amplitude suggests that disrupted rest-activity cycles have a biological basis and are not simply the result of random or environmental circumstances. It, also, implies that the link between disrupted rest-activity cycles and mood disorders, may, originate in the action of such genes.

Professor Daniel Smith, of Psychiatry, who is a Senior Author, said, ‘’These new findings extend our understanding of the complex genetic architecture of rest-activity cycles and how these, might, relate to mood instability, neuroticism, depression and bipolar disorder. Ultimately, our goal is to use this genetic information to develop and efficiently target or stratify new and improved treatment options.”

The Paper: Genome-wide association study of circadian rhythmicity in 71,500 UK Biobank participants and polygenic association with mood instability: Published in EBioMedicine. The study was funded by the Medical Research Council. :::ω.

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New Research Finds Genes to Drive Ageing and Make Normal Processes Damaging

 

 

|| August 14: 2018: UCL News || ά. Ageing in worms, mainly, results from the direct action of genes and not from random wear and tear or loss of function and the same is likely to be true in humans, according to research by scientists at UCL, Lancaster University and Queen Mary University of London. The study, published in Current Biology and funded by Wellcome, shows that normal biological processes, which are useful early on in life, continue to ‘run-on’ pointlessly in later life, causing age-related diseases.

The deteriorative part of ageing, called, ‘senescence’, is the main cause of disease and death worldwide as it leads to dementia, cancer, cardiovascular disease and chronic obstructive pulmonary disease but scientists have struggled to identify what causes it. To address this, researchers have focused on discovering the basic principles of ageing by studying simple animals, such as, Caenorhabditis Elegans, a nematode worm, used in this study, which lives on fruit and dies of old age, after, only, two to three weeks. 

“Discovering the causes of ageing in these little creatures could provide the key to understanding human ageing and where late-life diseases come from.” said Professor David Gems, UCL Institute of Healthy Ageing, Corresponding Author, who led the research team. 

“I've been studying ageing in C. Elegans for 25 years and it's amazing to see its underlying mechanisms revealed. It is so important because, if, you want to treat a disease you really need to understand what causes it. And senescence has really become the mother of all diseases, so understanding it is good news for all of us.”

The study describes how biological processes, that make young worms better able to reproduce run-on pointlessly in older worms, causing disease. “Since genes we’ve found driving the destructive processes of ageing in worms are known to control lifespan in mammals, we think the findings are applicable to humans and mark a real paradigm shift in our understanding of ageing.” said Dr Marina Ezcurra, UCL and Queen Mary, First Author of the study.

Specifically, they focused on autophagy, where body cells consume their own biomass to recycle components and extract energy. They found that the worms’ intestine consumes itself, autophagy, to create the yolk needed for eggs and in elderly worms, this process causes severe deterioration of the intestine and obesity from a build-up of pooled fats. In turn, this further impacts on the health of the worm by promoting growth of tumours in the uterus and shortens lifespan.

“This really surprised us since autophagy is usually thought to protect against ageing rather than cause it.” said Dr Alex Benedetto, a Lead Author on the study, formerly at UCL but now at Lancaster University.

“It seems that worms crank-up autophagy, which is considered good, to maximise reproductive success, which is good, too, but they end up overdoing it, causing senescence.”

The finding suggests parallels with bone erosion in lactating mammals. In women, a process originally designed to leach calcium from bone to create milk for breastfeeding, may, have negative effects after menopause, when it, instead, contributes to osteoporosis, osteoarthritis and calcified blood vessels.

When useful biological programmes run-on in later life, they can become disease-causing ‘quasi-programmes’. Such programmes were recently proposed and the findings support that they are indeed a major underlying cause of ageing.

This does not mean that aging is programmed but instead, that it is a continuation of developmental growth driven by genetic pathways to the point where these becomes harmful. Other examples include an increase in blood pressure causing hypertension and an increase to the eyes’ near vision point causing long-sightedness and a need for reading glasses.

The results of this study are consistent with the results of another recent study from the same research team at UCL showing how the futile activation of genes in unfertilised eggs, which are programmed to generate embryos, cause tumours to form in ageing worms.

“For decades scientists studying ageing have thought of ageing bodies as wearing out much like cars do, from a build-up of damage. What's exciting about this new work is that it shows something completely different. It turns out that we are not like cars, what kills us when we're old is not random damage but our own genes. It seems that natural selection is short-sighted and ageing is the price we pay.” said Dr Benedetto. :::ω.

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New Research Identifies the Genetic Link for Prostate Cancer

 

 

|| July 15: 2018: Cardiff University News || ά. New research has uncovered insights into the mechanisms, that underlie prostate cancer, providing potential targets for new cancer therapies. Prostate cancer is the third most common cause of cancer-related deaths in the UK and researchers from Cardiff University have identified a genetic alteration, that is linked to poor prognosis for patients with the disease.

Advanced prostate cancer patients initially respond well to hormonal therapies but nearly all will, eventually, develop an aggressive form of the disease, called, castrate-resistant prostate cancer. Previously, genetic mutations in a tumour suppression gene, PTEN, have been shown to activate the cell signalling pathway, PI3K, which gives prostate cancer cells their ability to grow uncontrollably.

The new research has uncovered the role of another genetic mutation in prostate cancer, which influences the aggressive nature of the disease. Dr Helen Pearson, Cardiff University’s European Cancer Stem Cell Research Institute, said, “We’ve identified a new genetic mutation, that, may, drive the growth of prostate cancer cells. In our research, we found that when prostate cells were given a mutation in the PIK3CA gene, they rapidly formed tumours, that developed resistance to hormone therapy.

We, also, found that both PTEN and PIK3CA genetic alterations are present in prostate cancer and that they can work together via potentially independent mechanisms to accelerate the development of the tumour, as well as, causing the cancer to become resistant to hormone therapy.

Survival of patients with castrate-resistant prostate cancer is poor, so it is vital to develop novel and targeted treatments for this aggressive disease.”

Professor Wayne Phillips, from the Peter MacCallum Cancer Centre, Melbourne, Australia, said, “This research gives a new insight into the development of prostate cancer and provides a foundation for new targeted therapeutic approaches to tackle this disease.”

The research was the result of an international collaboration between Dr Helen Pearson from Cardiff University and Professor Wayne Phillips at the Peter MacCallum Cancer Centre, Melbourne, Australia. 

The Paper: Identification of Pik3ca mutation as a genetic driver of prostate cancer that cooperates with Pten loss to accelerate progression and castration-resistant growth: Published in Cancer Discovery:::ω.

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Molecular Brake on Human Cell Division Prevents Cancer

 

 

 

 

|| July 08: 2018: Karolinska Institutet News || ά. Researchers at Karolinska Institutet and the University of Sussex have discovered that the process of copying DNA generates a brake signal, that stalls cell division. This molecular brake ensures that the cell has two complete copies of DNA before it divides and, thus, prevents DNA damage and cancer development. The study is published in the scientific journal Molecular Cell.

One of biology’s great mysteries is how a single fertilised egg can generate millions of cells, that, together, make up a human body, while, simultaneously, restricting growth to prevent lethal diseases, such as, cancer. This process is strictly regulated by our DNA, the genetic book carried by each single cell in the body. Before a cell divides and generates two new daughter cells, it has to copy its DNA. How cells decide when to divide is a long-standing question in science.

Now, an international collaboration between Karolinska Institutet and the University of Sussex, led to the discovery of this built-in molecular brake on human cell division. “By creating cells, that can not copy their DNA and by following protein activities over time in single cells, we found that DNA replication blocks the enzymes, that trigger cell division.

Immediately after DNA replication is completed, the machinery, that starts cell division is activated. This fundamental mechanism contributes to determining when human cells will divide.” says Dr Arne Lindqvist, Senior Researcher at the Department of Cell and Molecular Biology at Karolinska Institutet, who led the study.

The researchers, also, show that the molecular brake ensures that the amount of DNA damage is minimised. When the brake is not functional, the cell divides before it is ready resulting in large amounts of DNA damage.

“Our study highlights the dangerous consequences of hasty cell division and provides important clues on how cells, might, gain DNA mutations, that, ultimately, give rise to cancer.” Says the Lead Author Dr Bennie Lemmens, Post Doctoral Researcher at the Department of Medical Biochemistry and Biophysics at Karolinska Institutet.

The research was supported by the Wenner-Gren Foundation, the Swedish Research Council and the Swedish Cancer Society, among others.

The Paper: DNA replication determines timing of mitosis by restricting CDK1 and PLK1 activation: Bennie Lemmens, Nadia Hegarat, Karen Akopyan, Joan Sala-Gaston, Jiri Bartek, Helfrid Hochegger, Arne Lindqvist: Molecular Cell: Online: June 28: 2018

Caption: The process of copying DNA works as a molecular brake on cell division: Image Illustration: Bennie Lemmens:::ω.

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New Research Identifies a Regulator Axis for the Cancer Relevant Matrix Metalloprotease MMP14

 

 

|| July 01: 2018: University of Helsinki News: Päivi Lehtinen Writing || ά. Membrane-associated metalloprotease, MMP14, plays a significant role in different cancer tissues, for instance, in breast cancer and melanoma patients high MMP14 levels increase the risk to develop metastasis. The study, conducted at the University of Helsinki, showed that Prox1 negatively regulates MMP14 protein levels by suppressing transcription of the MMP14 gene.

Cancer and development are two different processes, that, surprisingly, involve similar processes and regulatory circuits. With this premise, Dr Silvia Gramolelli, a post-doctoral researcher in Professor Päivi Ojala´s group, University of Helsinki, uncovered a new regulatory axis for MMP14, also, called MT1-MMP. When expressed on the surface of the cells, MMP14 eats up the extracellular matrix, thus, allowing the migration and invasion of the cells into the surrounding tissue.

MMP14 participates in tissue remodelling during development and in physiological processes, such as, wound healing but it, also, plays a significant role in different cancer tissues, for instance, in breast cancer and melanoma patients high MMP14 levels increase the risk to develop metastasis.

“The regulation of MMP14 levels is, thus, very important in both physiology and cancer and exploring how it is regulated is crucial for better understanding of these processes.” Dr Gramolelli says.

Dr Gramolelli investigated whether Prox1, a transcription factor, instrumental for lymphatic endothelial cell specification, development of several organs and in colorectal cancer stem cells, is suppressing MMP14.

“This hypothesis stemmed from the observation that in different cancers and healthy tissues with high MMP14 very low or no Prox1 was expressed.”, Professor Ojala says.

Indeed, the study, published on June 22 in Scientific Reports, showed that Prox1 negatively regulates MMP14 protein levels by suppressing transcription of the MMP14 gene. By manipulating Prox1 levels it was possible to modulate the amount of MMP14 in a plethora of systems and in a mouse model. 

“The most surprising result was that by reintroducing Prox1 in highly invasive and metastatic breast cancer cells the ability of these cells to invade, the first step in metastasis formation, was inhibited.” Dr. Gramolelli says.

“This research for the first time links Prox1 to MMP14 in a regulatory axis, that occurs and contributes to several physiological and pathological processes and could provide new leads to many aspects of biomedical research.”

For more information, contact: Dr Silvia Gramolelli, PhD: University of Helsinki: Faculty of Medicine:Translational Cancer Biology Research Programme: Tele: +358 29 412 5523: email: silvia.gramolelli at helsinki.fi

Professor Päivi Ojala, PhD: University of Helsinki: Faculty of Medicine:Translational Cancer Biology Research Programme: Tele: +358 29 415 9445: email: paivi.ojala at helsinki.fi

The Paper: PROX1 is a transcriptional regulator of MMP14: Silvia Gramolelli, Jianpin Cheng, Ines Martinez-Corral, Markus Vähä-Koskela, Endrit Elbasani, Elisa Kaivanto, Ville Rantanen, Krista Tuohinto, Sampsa Hautaniemi, Mark Bower, Caj Haglund, Kari Alitalo, Taija Mäkinen, Tatiana V. Petrova, Kaisa Lehti and Päivi M. Ojala: Scientific Reports: June 22: 2018

Caption: Confocal image of a Kaposi´s sarcoma tumor section stained with MMP14:reen: and Prox1:magenta: specific antibodies. Nuclei were counterstained with Hoechst 33342:blue: Image: Professor Ojala Lab:::ω.

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New Research Discovers Gene Responsible for Unique Appearance of the Dorsal Wings of Butterflies




|| June 24: 2018: National University of Singapore News || ά. Butterflies, often, display strikingly different colour or patterns on the dorsal, top and ventral, bottom sides of their wings. A study by researchers from the National University of Singapore has shown that the gene Apterous A is responsible for the appearance of the dorsal wings of butterflies. The diversity in the appearance of the dorsal and ventral wings of many butterflies has evolved due to the varying functions of each wing surface.

This interesting discovery was made when Associate Professor Antonia Monteiro and her PhD student, Ms Anupama Prakash, who are from the Department of Biological Sciences at the NUS Faculty of Science, studied the expression and functions of apterous A in the African Squinting Bush Brown Butterfly, Bicyclus Anynana, which has a well annotated genome, during its wing developmental stage. When the butterflies are resting with their wings closed, the ventral surfaces are exposed; the patterns on these surfaces, usually, enable camouflage and avoidance of predators.

In contrast, the dorsal surfaces, seen when the wings are opened, are, often, coloured and patterned, specifically, to attract potential mates. The mechanisms involved in how these distinct differences occur, however, were not clear. The gene Apterous A has been found to play a role in the wing development of some insect species, in functions, such as, the outgrowth of the wing and determination of the dorsal-ventral boundary. The research team, thus, hypothesised that it could be involved in differentiating the appearance of the two wing surfaces.

The biologists investigated the expression of Apterous A in the butterfly’s wings and, then, selectively removed it from the genome in a gene knockout process to verify its functions in wing development and patterning. The experiments showed that Apterous A was expressed solely on the dorsal wing surfaces of the butterflies and not on the ventral surfaces. Additionally, during the gene knockout process, the researchers discovered that mutating Apterous A in the butterflies’ genome caused defects in wing development.

However, the scientists, also, observed additional effects on the butterfly wings. “When this gene is mutated, the dorsal wing patterns of butterflies with the mutated genome develop the same patterns as their ventral wing surfaces. This means that Apterous A is involved in the determination of the appearance of the dorsal surface.” said Ms Prakash.

This gene is likely to interact with other genes found on the dorsal wing surfaces to direct the patterning of the dorsal wing surface. During their studies, the research team discovered that Apterous A, also, acts as an inhibitor of the formation of eyespot patterns, markings, that resemble an eye on the dorsal surfaces of the butterfly wings. When the gene was deleted, multiple additional eyespots developed on these dorsal wing surfaces, as many as, the number present on the ventral surfaces.

“In the evolution of butterfly wing patterns, eyespots appeared on the dorsal wing surfaces of butterflies long after their origin on the ventral surfaces but the reason for this was unclear.” said Associate Professor Monteiro.

“We discovered that in the small regions on the dorsal wing surfaces, where a few eyespot centres were observed, there was an absence of Apterous A gene expression. This implies that the local repression of Apterous A is likely to have caused eyespots to, finally, develop at these locations.”

The researchers, also, noticed that the presence of the Apterous A gene had an effect on sex-specific wing traits on the fore and hind wings on the dorsal surfaces. On males’ dorsal forewings, it acts as a repressor, inhibiting the male pheromone producing organs and silver scale development. On their dorsal hindwings, however, it acts as an activator, promoting the development of pheromone disseminating hairs and silver scales.

The researchers believe that the Apterous A gene likely interacts with other sex-specific and wing-specific factors to impact the development of these traits. “This study has identified a gene, that influences surface-specific wing patterns in butterflies. This can, potentially, be used as a biomarker to understand how specific cells produce the different colours and patterns, that we see on butterfly wings.” said Ms Prakash.

“Since Apterous A is expressed, only, in cells of the dorsal surface, we can now identify dorsal-specific cells based on this gene expression. This is very useful, if, for example, we want to study how a certain colour develops. In some butterfly species, such as, the Morphos, the ventral surface is, mostly, brown while the dorsal surface is blue. Isolating dorsal-specific cells by using Apterous A as a marker can help us study how these blue scales are developing.” she said.

The research team will continue studying the function of the Apterous A gene in butterflies. This will include determining, if, the gene performs similarly in other families of butterflies and in butterflies without surface-specific wing patterns, as well as, investigating the way it represses eyespot pattern development.

The findings were published in Proceedings of the Royal Society of London in early 2018.

Caption: Antonia Monteiro, Associate Professor and Anupama Prakash, PhD Student: Image: National University of Singapore:::ω.

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O Little Ant in the Valley of The Himalaya Mind as to What Little You Can and Do Know and the Infinity You Can Not and Do Not Know So That You Keep Perspective and Humility for Your Own Safety: Gene Scissors May Increase Cancer Risk




|| June 12: 2018: University of Helsinki News: Elisa Lautala Writing || ά. According to researchers from the University of Helsinki and Karolinska Institute, gene editing using CRISPR-Cas9, may, inadvertently increase cancer risk. Another research team at Novartis Research Institute in Boston, also, independently obtained similar results. CRISPR-Cas9 can be programmed to remove and replace gene defects in the DNA. It is a promising biological tool for medical treatments and the method is currently tested in clinical trials for cancer immunotherapy in the US and China.

New trials are expected to be launched soon to treat inherited blood disorders, such as, sickle cell anaemia. In two independent studies published in the journal Nature Medicine, scientists at the Karolinska Institute, the University of Helsinki and the Novartis Research Institute in Boston report that the use of CRISPR-Cas9, may, trigger a mechanism designed to protect cells from DNA damage. As the result, the cells, which lack this mechanism, linked to protein known as p53, edit much better than normal cells.

This can lead to a situation where genome edited cell populations have increased numbers of cells in which this important mechanism is missing.

“By picking cells, that have successfully repaired the damaged gene we intended to fix, we, might, inadvertently, also, pick cells without functional p53.’’ says Dr Emma Haapaniemi from Karolinska Institute, the First Author of the other study.

“If, transplanted into a patient, as in gene therapy for inherited diseases, such cells could give rise to cancer risk, raising concerns for the safety of CRISPR-based gene therapies.”

The researchers found that by decreasing activity of p53 in a cell, they could efficiently edit with CRISPR-Cas9. However, the safety of it is uncertain.

The research was led by Professor Jussi Taipale from the University of Helsinki and the University of Cambridge. According to him, there is a lot of potential in CRISPR-Cas9 but more research is needed on its possible side effects and how they could be prevented.

 

“We are not saying that CRISPR-Cas9 is bad or dangerous. Like with any medical treatment, there are always side effects and potential harm from treatment and this should be balanced against the benefits of the treatment.”

Contact information: Emma Haapaniemi: email: emma.haapaniemi at ki.se: Jussi Taipale: email: jussi.taipale at helsinki.fi: tel. +358 504486335

The Paper: CRISPR/Cas9-genome editing induces a p53-mediated DNA damage response: Haapaniemi, E et al: Nature Medicine: June 11: 2018:::ω.

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Cell Types Underlying Schizophrenia Identified




|| June 10: 2018: Karolinska Institutet News: || ά. Scientists at Karolinska Institutet in Sweden and University of North Carolina, USA, have identified the cell types underlying Schizophrenia in a new study published in Nature Genetics. The findings offer a roadmap for the development of new therapies to target the condition.

Schizophrenia is an often devastating disorder causing huge human suffering. Genetic studies have linked hundreds of genes to Schizophrenia, each contributing a small part to the risk of developing the disease. The great abundance of identified genes have made it difficult to design experiments. Scientists have been struggling to understand what is linking the genes together and whether these genes affect the entire brain diffusely or certain components more.

By combining new maps of all the genes used in different cell types in the brain with detailed lists of the genes associated with Schizophrenia, scientists in the current study could identify the types of cells, that underlie the disorder. The genetics point towards certain cell types being much more implicated than others.

One finding was that there appeared to be a few major cell types contributing to the disorder, each of which originates in distinct areas of the brain.

“This marks a transition in how we can use large genetic studies to understand the biology of disease. With the results from this study, we are giving the scientific community a chance to focus their efforts where it will give maximum effect.” says Dr Jens Hjerling-Leffler, Research Group Leader at the Department of Medical Biochemistry and Biophysics at Karolinska Institutet, one of the main authors. ‘’The findings offer a roadmap for the development of new therapies.’’

“One question now is whether these brain cell types are related to the clinical features of Schizophrenia. For example, greater dysfunction in one cell type could make treatment response less likely. Dysfunction in a different cell type could increase the chances of long-term cognitive effects. This would have important implications for development of new treatments, as separate drugs may be required for each cell type involved.” says another report author Professor Patrick Sullivan at the Department of Medical Epidemiology and Biostatistics at Karolinska Institutet and Yeargan Distinguished Professor in the Department of Genetics and Psychiatry at the University of North Carolina.

As a result of rapid progress in two separate fields of science; human genetics and single cell transcriptomics, it, only, recently, has become possible to study diseases in this way. In coming years the researchers suggest that the approach should lead to breakthroughs in the biological understanding of other complex disorders, such as, autism, major depression and eating disorders.

“Understanding which cell types are affected in a disease is of critical importance for developing new medicines to improve their treatment. If, we do not know what causes a disorder we can not study how to treat it.” says Dr Nathan Skene, Postdoctoral Researcher at the Department of Medical Biochemistry and Biophysics at Karolinska Institutet and UCL Institute of Neurology, UK, one of the Lead Authors.

The study was financed by the Swedish Research Council, Strat-Neuro, the Wellcome Trust, the Swedish Brain Foundation, the Swiss National Science Foundation, and the US National Institute of Mental Health.

Schizophrenia genetic results were generated with support from the Medical Research Council Centre, Programme and Project Grants and funding from the European Union’s Seventh Framework Programme for research, technological development and demonstration.

The authors report the following potentially competing financial interests. PF Sullivan: Lundbeck, advisory committee. J Hjerling-Leffler: Cartana, Scientific Adviser and Roche, grant recipient.

The Paper: Genetic identification of brain cell types underlying schizophrenia:Nathan G Skene, Julien Bryois, Trygve E Bakken, Gerome Breen, James J Crowley, Héléna A Gaspar, Paola Giusti-Rodriguez, Rebecca D Hodge, Jeremy A Miller, Ana B Muñoz-Manchado, Michael C O’Donovan, Michael J Owen, Antonio F Pardiñas, Jesper Ryge, James T R Walters, Sten Linnarsson, Ed S Lein, Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium, Patrick F Sullivan and Jens Hjerling-Leffler: Nature Genetics: Online: May 21: 2018 ::: ω.

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New Research Finds A New Gene for Canine Congenital Eye Disease

 

|| June 02: 2018: University of Helsinki News: Maria Kaukonena Writing Writing || ά. A new gene for canine congenital eye disease has been identified by a collaborative research, led by Professor Hannes Lohi’s research group at the University of Helsinki. Defective RBP4 leads to vitamin A deficiency and abnormal eye development during pregnancy. The study defines a novel recessive mode of maternal inheritance, which, may, underlie other types of birth defects.

This research done in collaboration between the University of Helsinki, UC Davis and the University of Jyväskylä describe a new genetic cause for canine congenital eye disease in Irish Soft-Coated Wheaten Terriers. The affected dogs suffer from bilateral microphthalmia, i.e, very small eyes and anatomical defects, resulting in incurable blindness. Similar findings are seen in the Microphthalmia-Anophthalmia-Coloboma:MAC spectrum of human congenital eye malformations, which are important causes of childhood blindness.

"This is the first dog model for MAC disorder and, may, help to understand the human disease." says DVM Ms Maria Kaukonen, First Author of the study and a PhD student at the University of Helsinki

The genetic and functional analyses showed a deletion mutation in the RBP4 gene. The encoded protein:RBP binds vitamin A and transfers it from liver to other tissues. Vitamin A transport is essential during pregnancy as the lack of this nutrient causes abnormal eye development.  During pregnancy, the foetus receives vitamin A through the placenta.

"The mutation changes RBP structure so that the protein is secreted abnormally from liver and does not function. This greatly reduces RBP and vitamin A levels in bloodstream." says Professor Tom Glaser from UC Davis, another author of the study. 

RPB4 has been implicated in human MAC disease. The study demonstrates, once again, the clinical and genetic similarity of human and canine eye disorders.

The study demonstrates a new recessive mode of genetic inheritance, which has not been described before. The researchers discovered that the dam’s genotype determines the puppy’s disease risk as both the dam and puppy must be homozygous for the mutation to manifest the disease.

"Interestingly, the disease is apparent only when both the puppy and mother are homozygous for the RBP4 mutation. Normally, recessive diseases in mammals depend only on the individual’s genetic make-up. Our findings highlight the delicate interaction between the mother and foetus during pregnancy. It is possible that there are similar birth defects with this type of genetic relationship." Says Professor Hannes Lohi, the Lead Author of the study.

As a part of the research, a DNA test has been developed for veterinary diagnosis and breeding purposes. DNA testing is important for breeders to avoid producing more blind dogs. The test can identify carriers and allow better breeding plans.

Veterinarians can, also, use the test for differential diagnosis and to confirm the genetic basis of a suspected condition. So far, the mutation has been found in Irish Soft-Coated Wheaten Terriers but according to Kaukonen it might be present in other breeds as well.

The study was supported by the Mary and Georg C. Ehnrooth Foundation, Evald and Hilda Nissi Foundation, the Academy of Finland, the Jane and Aatos Erkko Foundation, the Finnish Foundation of Veterinary Research, Genoscoper Oy, Wisdom Health and the US National Institutes of Health.

The Paper: Maternal Inheritance of a Recessive RBP4 Defect in canine congenital eye disease: Maria Kaukonen, Sean Woods, Saija Ahonen, Seppo Lemberg, Maarit Hellman, Marjo K. Hytönen, Perttu Permi, Tom Glaser, Hannes Lohi: Cell Reports: May 29: 2018: doi: 10.1016/j.celrep.2018.04.118. 

For further information coanct: Maria Kaukonen: email: maria.kaukonen at helsinki.fi

Hannes Lohi: email: hannes.lohi at helsinki.fi

Caption: Support Medical Detection Dogs::: ω. 

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A Gene in a Cold Climate




|| May 14: 2018: UCL News|| ά. A gene variant common in Europeans, may have, proliferated because it helped early humans adapt to cold weather, according to UCL research. For the study, published in PLOS Genetics, a team of researchers from UCL and the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, investigated the evolution of TRPM8, a gene coding for the only known receptor, that enables a person to detect and respond to cool and cold temperatures. This receptor is, also, activated by menthol and is responsible for the refreshing feeling of mint-containing products.

A genetic variant in TRPM8, that is upstream from the gene and, may, regulate its expression, was found to be at highest frequency in individuals of European descent in northern climates, likely because it played a role in early human populations adapting to cold temperatures. This TRPM8 variant has been previously associated with a slightly higher risk of migraines and, although, the percentage of the population, that suffers migraines varies, it tends to be higher in the populations with the highest frequency of the cold-adaptive variant of the TRPM8 gene.

The researchers found that the genetic variant became increasingly common in populations living in cold, northern climates during the last 25,000 years. Only 05% of people with Nigerian ancestry carry the variant, compared to 88% of people with Finnish ancestry. Within the last 50,000 years, some humans left the warm climate of Africa to colonise colder locales in Asia, Europe and other parts of the world.

“This colonisation could have been accompanied by genetic adaptations, that helped early humans respond to cold temperatures, for example, by helping people reduce cold sensation or feel pain from the cold.” said Dr Aida Andres, (UCL Genetics Institute, who supervised the study.

“The direct link between cold sensation and migraine is unknown; however, both are related to pain, which provides a possible but speculative, link.” said Llead Author of the study, Dr Felix Key of the Max Planck Institute for the Science of Human History in Leipzig, Germany.

“Most genetic variants have very similar frequencies across human populations, so it was surprising to see this one with very low frequency in some populations in warm climates and very high frequency in populations in northern Europe.” said Dr Andres.

Funding for UCL’s contribution to the work was kindly provided by the Max Planck Society:

The Paper: Human local adaptation of the TRPM8 cold receptor along a latitudinal cline: Felix M. Key, Muslihudeen A. Abdul-Aziz, Roger Mundry, Benjamin M. Peter, Aarthi Sekar, Mauro D’Amato, Megan Y. Dennis, Joshua M. Schmidt, Aida M. Andrés: PLOS Genetics: May 03: 2018::: ω.

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The Largest Ever Family Study of Migraine Provides New Insight Into the Illness




|| May 05: 2018: University of Helsinki News: Mari Kaunisto Writing|| ά. An international research consortium has shown that an accumulation of many independent genetic risk variants is the reason as to why migraine tends to run in families. The genetic burden was shown to be greater in patients, who experience aura symptoms during attacks or have an early age of onset of migraine. The results of the largest genetic family study on migraine, thus far, were published online in the journal Neuron on May 03. The study was based on medical history and genetic data of 1,589 Finnish migraine families with more than 8,300 individuals.

This family cohort is unique in its size and several neurologists from all over Finland have participated in recruiting the participants. The study was co-ordinated by researchers from the University of Helsinki, Helsinki University Hospital, Folkhälsan Research Centre and the Broad Institute of MIT and Harvard. Migraine is one of the most common brain disorders worldwide, affecting approximately 15-20% of the adults in developed countries. In many families there are much more migraine patients than would be expected by chance alone. The molecular mechanisms of migraine and the reasons for familial clustering remain poorly understood.

“Both rare, high-impact and common genetic variants with smaller impact could contribute to the familial aggregation of migraine. In this study, we wanted to find out which one is more important and whether the genetic load is higher in certain types of migraine.” said Dr. Maija Wessman from the Folkhälsan Research Centre.

By studying more than 59.000 migraine patients, the researchers behind this study have earlier identified over 40 significant genetic risk variants, that predispose individuals to migraine. In addition, this earlier study provided evidence of hundreds or even thousands of additional variants, that have a smaller impact on migraine risk.

In the present study, the team combined information from all these implicated risk variants and calculated a personal genetic risk score for each of the study participants. This genetic risk score was used to estimate and compare the genetic burden conferred by common variants in different migraine patient subgroups.

One third of migraine patients experience additional neurological symptoms during attacks, called, aura. The Finnish family migraine cohort contained 2,420 patients with a diagnosis of migraine with typical aura and 540 patients diagnosed with less common hemiplegic aura symptoms. The family cohort was, also, compared against another large Finnish sample, the FINRISK population cohort with close to 15,000 participants, including 1,100 with migraine.

The researchers observed an overall increased genetic risk score in familial migraine cases compared to general migraine cases from the population and clear differences of the common variant load across different migraine subtypes.

Of special interest was the contribution of common and rare genetic variation to hemiplegic migraine, a disease primarily thought to be caused by rare pathogenic variants in three genes. Even, for this migraine subgroup, the results showed that the combined effect of common risk variants was greater than the effect of rare mutations. In fact, of all the migraine subtypes analysed, the genetic load was highest in this group of patients.

“Our study supports the hypothesis that migraine subtypes are genetically heterogeneous diseases and that common polygenic variation significantly contributes to the aggregation of the disease in families, both for common and rare migraine subtypes.” says Professor Aarno Palotie from the Institute for Molecular Medicine Finland FIMM at the University of Helsinki.

Further analyses showed that the genetic risk score was, also, associated with the age of onset of migraine headaches. Genetic load was significantly higher in migraine cases where headache onset occurred before 20 years of age compared to individuals with later onset. “We were surprised by the impact of the common variants in these families. However, much of the genetic predisposition to migraine still remains unexplained. It is likely that further studies will reveal more common and rare migraine risk variants.” said Professor Palotie.

“Unique cohort provides unique results. It is evident that a targeted, personalised treatment approach based on individual properties of the patients will be safer, more efficient and more cost effective than selecting the medication based on trial and error approach. This study brings us one step closer to the goal.” said Dr. Mikko Kallela from the Department of Neurology, Helsinki University Central Hospital.

The study was conducted in collaboration with members of the International Headache Genetics Consortium, the 23andMe research team and Merck and Co Inc, Kenilworth, NJ, USA.

For further information, contact: Research Director Aarno Palotie: Institute for Molecular Medicine Finland:FIMM: HiLIFE, University of Helsinki: Broad Institute of MIT and Harvard: Tel. +358-40-567 0826: Sari Kivikko: email: aarno.palotie at helsinki.fi

The Paper: Common variant burden contributes to the familial aggregation of migraine in 1,589 families: Neuron::: ω.

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It is Time People Stop Using the Expression Junk Genome: Genomic Junk of Iron Storage Gene FTH1 is Critical for Suppressing Prostate Cancer Growth

 



|| April 30: 2018: National University of Singapore News || ά. An abnormally high level of iron in the body is associated with prostate cancer and researchers from the Cancer Science Institute of Singapore:CSI Singapore, at the National University of Singapore, may have, uncovered the mechanism to explain this link. They have found the role of the iron storage gene, FTH1 and its pseudo-genes in regulating iron levels in cells and slowing down prostate cancer growth. The new findings could pave the way for future developments in prostate cancer diagnostics and therapeutics.

Prostate cancer is the most common cancer and the second leading cause of cancer death in men worldwide. The survival rate for prostate cancer is high, if, diagnosed early but it falls significantly at advanced stages. Currently, there is no available drug to treat aggressive or late-stage prostate cancer and the accuracy of current screening techniques remain relatively low at 20 to 30%. With global prostate cancer incidence rising rapidly, accounting for 09.6% of all newly diagnosed cancer cases in 2017, there is a need to attain better understanding of the underlying biological mechanisms leading to the disease in order to build more robust diagnostic tools and efficacious therapies against it.

In the study published in the scientific journal, Nucleic Acids Research, earlier this year, researchers from CSI Singapore focused their investigation on the iron storage gene, FTH1, noting the link between iron level in cells and the development of prostate cancer. It was found that the function of FTH1 is highly influenced by its pseudo-genes, a set of genes originating from their parental gene, which were previously thought to be non-functional and were classified as ‘genomic junk’. FTH1 and its pseudo-genes are, often, suppressed in prostate cancer and expression of both FTH1 and its pseudo-genes are required to reduce iron levels in cells and slow down prostate cancer growth.

Further experiments showed that FTH1 and its pseudo-genes are linked by a shared pool of microRNAs, that are, often, highly expressed in prostate cancer and these microRNAs inhibit the regulation of iron levels by the genes. As such, isolating and manipulating the pool of microRNAs can, therefore, relieve the inhibition, restore the iron regulatory functions of FTH1 and its pseudo-genes and their tumour suppressive effects.

“Our study presents an interesting finding in the form of the multi-component, tumour suppressive FTH1 gene:pseudogene network, which can be harnessed for future diagnostic and drug development. The highly expressed microRNAs, that link FTH1 and the pseudo-genes are attractive biomarkers, as well as, therapeutic targets for prostate cancer.

Targeting or restoring proper iron storage could, also, be a potential avenue for therapeutic development.” said Assistant Professor Yvonne Tay, Principal Investigator at CSI Singapore, who led the study.

High iron levels in cells is, also, linked to various types of cancer apart from prostate cancer. As such, the research team will further explore and delineate this regulatory network, not only in prostate cancer but, also, other cancer types to uncover more potential biomarkers and druggable targets for more effective cancer treatment.

Caption: Assistant Professor Yvonne Tay, left, Principal Investigator at the Cancer Science Institute of Singapore at the National University of Singapore and Dr Chan Jia Jia, right, a Research Fellow in Assistant Professor Tay’s group uncovered new biomarkers and therapeutic targets for prostate cancer linked to the FTH1 iron storage gene: Image: National University of Singapore ::: ω.

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Early Life Experiences Influence DNA in the Adult Brain
 
 


|| April 14: 2018: Salk Institute News || ά. In the perennial question of nature versus nurture, a new study suggests an intriguing connection between the two. Salk Institute scientists report in the journal Science that the type of mothering a female mouse provides her pups, actually, changes their DNA. The work lends support to studies about how childhood environments affect brain development in humans and could provide insights into neuropsychiatric disorders, such as, depression and schizophrenia.

“We are taught that our DNA is something stable and unchanging, which makes us who we are but, in reality, it’s much more dynamic.” saysProfessor  Rusty Gage, at Salk’s Laboratory of Genetics. “It turns out, there are genes in your cells, that are capable of copying themselves and moving around, which means that, in some ways, your DNA does change.” For, at least, a decade, scientists have known that most cells in the mammalian brain undergo changes to their DNA, that make each neuron, for example, slightly different from its neighbour.

Some of these changes are caused by 'jumping' genes, officially, known as, long interspersed nuclear elements:LINEs, that move from one spot in the genome to another. In 2005, the Gage lab discovered that a jumping gene called L1, which was, already, known to copy and paste itself into new places in the genome, could jump in developing neuronal brain cells.

The team had hypothesised that such changes create, potentially, helpful diversity among brain cells, fine-tuning function but, might, also, contribute to neuropsychiatric conditions. “While we’ve known for a while that cells can acquire changes to their DNA, it’s been speculated that, maybe, it’s not a random process.” says Ms Tracy Bedrosian, a former Salk Research Associate and first Author of the study. “Maybe,  there are factors in the brain or in the environment, that cause changes to happen more or less frequently.”

To find out, Professor Gage, Ms Bedrosian and colleagues began by observing natural variations in maternal care between mice and their offspring. They, then, looked at DNA from the offspring’s hippocampus, which is involved in emotion, memory and some involuntary functions. The research team discovered a correlation between maternal care and L1 copy number: mice with attentive mothers had fewer copies of the jumping gene L1 and those with neglectful mothers had more L1 copies and, thus, more genetic diversity in their brains.

To make sure the difference wasn’t a coincidence, the researchers conducted a number of control experiments, including, checking the DNA of both parents of each litter to make sure the offspring didn’t just inherit their numbers of L1s from a parent, as well as, verifying that the extra DNA was, actually, genomic DNA and not stray genetic material from outside the cell nucleus.

Lastly, they cross-fostered offspring, so that mice born to neglectful mothers were raised by attentive ones and vice versa. Initial results of the correlation between L1 numbers and mothering style held: mice born to neglectful mothers but raised by attentive ones had fewer copies of L1 than mice born to attentive mothers but raised by neglectful ones.

The researchers hypothesised that offspring, whose mothers were neglectful were more stressed and that somehow this was causing genes to copy and move around more frequently. Interestingly, there was no similar correlation between maternal care and the numbers of other known jumping genes, which suggested a unique role for L1. So, next, the researchers looked at methylation, the pattern of chemical marks on DNA, that signals whether genes should or should not be copied and that can be influenced by environmental factors.

In this case, methylation of the other known jumping genes was consistent for all offspring. But it was a different story with L1: mice with neglectful mothers had noticeably fewer methylated L1 genes than those with attentive mothers, suggesting that methylation is the mechanism responsible for the mobility of the L1 gene.

“This finding agrees with studies of childhood neglect, that, also, show altered patterns of DNA methylation for other genes.” says Professor Gage, who holds the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Diseases. “That’s a hopeful thing, because once you understand a mechanism, you can begin to develop strategies for intervention”

The researchers emphasise that, at this point, it’s unclear whether there are functional consequences of increased L1 elements. Future work will examine whether the mice’s performance on cognitive tests, such as, remembering which path in a maze leads to a treat, can be correlated with the number of L1 genes.

The work was funded by the National Institutes of Health, the G. Harold and Leila Y. Mathers Charitable Foundation, the Leona M. and Harry B. Helmsley Charitable Trust, the Engman Foundation, the JPB Foundation, Annette C. Merle-Smith, and a NARSAD Young Investigator Award.

The Paper: Early life experience drives structural variation of neural genomes in mice: Tracy A. Bedrosian, Carolina Quayle, Nicole Novaresi and Fred H. Gage: Science: March 23: 2018::: ω.

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Genetic Link to IBS Identified in Women
 
 


|| April 08: 2018: Karolinska Institutet News || ά. New research, co-ordinated from Karolinska Institutet, links certain DNA variants to increased risk of irritable bowel syndrome:IBS in women. The findings, published in the scientific journal Gastroenterology, might, help explain why IBS is more common in women than in men. Irritable bowel syndrome is the most common gastrointestinal disorder. More than 10 per cent of the population, women more than men, suffer from recurrent symptoms, including, abdominal pain, gas, diarrhoea and constipation. What causes IBS is largely unknown, which hampers the development of effective treatment for many patients.

“Exploiting the large UK Biobank resource, as well as, several patient cohorts from European and US expert centres, we have been able to study genetic predisposition to IBS with increased statistical power, better than ever before.” says Corresponding Author Professor Mauro D’Amato, visiting professor at Karolinska Institutet’s Department of Medicine in Solna and Co-ordinator of the bellygenes initiative, that led to the discovery. The researchers used genotype data from more than 300,000 UK Biobank participants in a genome-wide association study:GWAS.

They found DNA variants, that associate with increased risk of a doctor’s diagnosis of IBS in women but not in men, specifically from, a region on chromosome nine, previously reported to, also, influence puberty timing in women, age at first menstruation.

By following up this result in 2,045 patients from IBS expert centres in Sweden, Belgium, the Netherlands, Italy and the US, the researchers observed further associations with constipation-predominant IBS, as well as, harder stools, again only in women.

“Although, we can not point to individual genes at this early stage, we believe, these results are exciting, as they converge with existing data on female preponderance and a role of sex-hormones in IBS.” says Professor Mauro D’Amato.

In addition to Karolinska Institutet, researchers and clinicians from several other institutions participated in the study, including, the Mayo Clinic and University of California Los Angeles in the US, IKMB in Kiel Germany, TARGID in Leuven Belgium, BioDonostia HRI in San Sebastian Spain, the Universities of Bologna in Italy, Groningen and Maastricht in the Netherlands, and others.

The research was supported by grants from the Swedish Research Council, the Health Department of the Basque Government, the Spanish Ministry of Economy and Competitiveness, the National Institutes of Health and the EU FP7 among others.

The Paper: Female-specific Association Between Variants on Chromosome 9 and Self-reported Diagnosis of Irritable Bowel Syndrome: Bonfiglio F, Zheng T, Garcia-Etxebarria K, Hadizadeh F, Bujanda L, Bresso F, Agreus L, Andreasson A, Dlugosz A, Lindberg G, Schmidt PT, Karling P, Ohlsson B, Simren M, Walter W, Nardone G, Cuomo R, Usai-Satta P, Galeazzi F, Neri M, Portincasa P, Bellini M, Barbara G, Latiano A, Hübenthal M, Thijs V, Netea MG, Jonkers D, Chang L, Mayer EA, Wouters MM, Boeckxstaens G, Camilleri M, Franke A, Zhernakova A, D’Amato M: Gastroenterology, online April 04: 2018

Caption: Mauro D’Amato. Image: Ferdinando Bonfiglio: Karolinska Institutet ::: 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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For Stories Published in Genetics in Year Gamma Arkive

 

 

 

 

 

 

 

 

  

 

 

Life's Laurel Is You In One-Line-Poetry A Heaven-Bound Propagated Ray Of Light Off The Eye Of The Book Of Life: Love For You Are Only Once

 

 

Life: You Are The Law The Flow The Glow: In Joys In Hurts You Are The Vine-Songs On The Light-Trellis

 

 

 

 

   
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

|| 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 ||
|| Regine Humanics Foundation Ltd: A Human Enterprise: Registered as a Not For Profit Social Enterprise in England and Wales: Company No: 11346648 ||