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Genetic Factors Tied to Obesity May Protect Against Diabetes

 

 

 

|| November 05: 2018: University of Exeter News || ά. New research finds that some genetic variations associated with obesity actually protect against Type Two Diabetes, heart attack and stroke. Experts believe that, where on the body people store surplus fat, whether round their middle or round the liver, may be, genetically determined. Exactly where extra fat is stored matters more than the amount when it comes to insulin resistance and risk of diabetes and other conditions.

Now 14 new genetic variants, that dictate where the body stores surplus fat have been pinpointed by scientists from across Europe, including, from Brunel University London and the University of Exeter. And surprisingly, some genetic factors, that increase obesity work to lower metabolic risk. “Where fat is stored is more important in terms of diabetes risk or other consequences than the actual amount of fat.” said Brunel Geneticist Professor Alex Blakemore.

“There are some genetic factors, that increase obesity but, paradoxically, reduce metabolic risk. It is to do with where on the body the fat is stored. Directly under the skin is better than around the organs or especially, within the liver.

The research team looked at data from the UK bio bank from more than 500,000 people aged between 37 and 73. They used magnetic resonance imaging:MRI scans of these people’s waists to match where they stored extra fat with whether they showed signs of Type 2 diabetes, heart attack and risk of stroke.

They found 14 genetic variations or changes in DNA molecule linked with higher body mass index:BMI but lower risk of diabetes, lower blood pressure and lower risk of heart disease. The study, published in the journal Diabetes, showed that, as they gain weight, people, who carry these genetic factors store it safely under the skin and so have less fat in their major organs, such as, the liver, pancreas and kidneys.

“There are many overweight or obese individuals, who do not carry the expected metabolic disease risks associated with higher BMI.” said Dr Hanieh Yaghootkar at the University of Exeter Medical School. “Meanwhile, some lean or normal weight individuals develop diseases like Type Two Diabetes.

Since a large proportion of many populations are overweight or obese, our findings will help understand the mechanisms, that delay or protect overweight or obese individuals from developing adverse metabolic outcomes, including, Type Two Diabetes, heart disease and hypertension.”

The Paper: Genome-wide and abdominal MRI-imaging data provides evidence that a genetically determined favourable adiposity phenotype is characterized by lower ectopic liver fat and lower risk of Type Two Diabetes, heart disease and hypertension: Published in Diabetes:::ω.

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Diabetes: Unconventional Mesencephalic Astrocyte-Derived Neurotrophic Factor May Regenerate Insulin Producing Cells in the Pancreas

 

 

|| November 01: 2018: University of Helsinki News || ά. Diabetes Mellitus is characterised by high blood glucose levels. These high levels are caused by the inability of the insulin-producing β-cells in the pancreas to maintain sufficient levels of circulating insulin. Current medications alleviate diabetic symptoms but they can not reconstitute physiological insulin secretion. This increases the risk of vascular complications, which, might, lead to conditions, such as, heart disease, stroke and kidney disease. 

Typical for Type One and the later stages of Type Two Diabetes is the β-cell loss preceded by sustained cell stress. The stress is caused by problems in dealing with aggregated proteins, that lead to the self-destruction of β-cells. One of the main goals in improving current diabetes therapy is to find ways to protect β-cells from stress and activate their regeneration. Ms Maria Lindahl and her team at the University of Helsinki have found that the removal of mesencephalic astrocyte–derived neurotrophic factor:MANF, specifically, from β-cells, in adult mice results in the loss of β-cells in diabetes.

"This indicates that MANF expression is needed for the survival, maintenance and function of pancreatic β-cells in mice. MANF was, also, found to protect stressed β-cells from death and to induce the proliferation of β-cells from old mice." Ms Maria Lindahl says.

“This discovery further suggests that MANF has therapeutic potential for the treatment of Type One and Type Two Diabetes, where β-cell protecting and regenerating therapies are not available.” says Ms Tatiana Danilova from Ms Maria Lindahl's team.

In previous collaborative studies at the University of Helsinki by the groups directed by Professor Mart Saarma and Professor Timo Otonkoski, found MANF deficiency in mice led to Diabetes due to the progressive loss of insulin-producing pancreatic β-cells. MANF was found to be important for the survival and proliferation of both human and mouse β-cells in culture.

The Paper: Danilova T, Belevich I, Li H, Palm E, Jokitalo E, Otonkoski T, Lindahl M. MANF is required for the postnatal expansion and maintenance of the pancreatic β-cell mass in mice: Diabetes: October 2018 http://diabetes.diabetesjournals.org/content/early/2018/10/03/db17-1149

Caption: Islets of Langerhans containing MANF-expressing β-cells, in red, contain more insulin-containing β-cells, in green, A: than those, that lack MANF-expressing β-cells, B: Image: Maria Lindahl:::ω.

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The First Successful UK Surgery Conducted in the Womb for Babies with Spina Bifida
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

|| October 24: 2018: UCL News || ά. A team from UCL, University College London Hospitals:UCLH and Great Ormond Street Hospital:GOSH has operated on the abnormally developed spinal cords of two babies in the womb, in a medical first for the UK. The team repaired the defect in the spine of two babies with open Spina Bifida, in separate operations this summer. The mothers and babies are recovering well. The operations brought together researchers from UCL working with NHS clinicians from UCLH and GOSH in partnership with University Hospitals Leuven in Belgium to carry out the operations in the UK for the first time.

Until now, mothers could choose to have the foetal surgery abroad or have post-natal surgery after the baby is born, which is the current practice in the UK. This specialist foetal surgery will give the baby a significantly better chance in life, as compared to post-natal surgery, as babies with Spina Bifida are, very often, incapable of walking, and, may, require a series of operations to drain fluid from the brain, shunt placement, later in life. “In Spina Bifida, the spinal canal does not close completely in the womb, leaving the spinal cord exposed from an early stage in pregnancy. This results in changes to the brain, as well as, severe permanent damage to the nerves on the lower half of the body.” said the Lead Neuro-surgeon Dr Dominic Thompson of GOSH.

“Operating in the womb involves opening the uterus, exposing the Spina Bifida without delivering the baby, closing the defect and, then, repairing the uterus to leave the baby safely inside.” said the Lead foetal Surgeon Dr Jan Deprest of UCLH and Leuven.

“Closure of Spina Bifida in the womb using this method is an alternative to post-natal surgery and has been shown to improve short and medium-term outcomes. While neither intervention is fully curative, in foetal surgery, the defect is closed earlier, which prevents damage to the spinal cord in the last third of pregnancy. We are, also, researching the minimal access, foetoscopic, technique through the GIFT-Surg Project framework and, if, we can show it to have equal benefit, we will be offering this option to patients.”

The UCLH and GOSH team has been training with Professor Deprest and his team in Belgium, where more than 40 operations, some on English patients from UCLH, have been conducted since 2012. They have, also, benefited from close links with the Children’s Hospital of Philadelphia, where the team led by N Scott Adzick pioneered this operation and has conducted more than 320 similar operations since 2011.

The 30-strong team involved in the first two operations was co-ordinated by Foetal Medicine Consultant Dr Anna David, UCL Institute for Women’s Health and UCLH. Professor David, who is, also, supported by the National Institute for Health Research :NIHR UCLH Biomedical Research Centre, said, “We have been working for three years to bring this service to UK patients through the creation of a Centre for Pre-natal Therapy at UCL, UCLH and GOSH.

“Our resolve to offer this service was based on the findings of a large, multi-centre, randomised control trial in the US, which compared pre-natal closure to post-natal closure and the observation that foetal surgery could be safely reproduced in Europe by proper training.

“The US trial authors found that pre-natal closure was associated with a 50% reduction in the need for surgical shunt placement in the new-born baby and a significant improvement in motor function at 30 months of age.

“The reduction in need for shunts is, particularly, important.” said Professor Paolo De Coppi, UCL Great Ormond Street Institute of Child Health. “As long-term follow-up of children, that have undergone pre-natal closure in the womb suggests that brain function, mobility and total independence were higher in non-shunted than shunted children aged five.” Professor De Coppi is supported by the NIHR GOSH Biomedical Research Centre.

The Centre for Pre-natal Therapy programme at UCLH and GOSH has been made possible due to generous charitable funding totalling £450,000 from GOSH Children’s Charity and UCLH Charity. Professor Donald Peebles, UCLH Clinical Director for Women’s Health, said, “These vital funds have provided training for the surgical team and will fund surgery for the first 10 patients. While we currently only perform an open foetal surgery approach, we are developing the foetoscopic approach in pre-clinical models and hope this could further minimise maternal complications.”

The GIFT-Surg project aims to develop new foetoscopic tools and imaging techniques to support pre-natal therapy and is funded by the Wellcome Trust and the Engineering and Physical Sciences Research Council:EPSRC.:::ω.

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New Discovery Restores Insulin Cell Function in Type Two Diabetes
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

|| October 21: 2018: Lund University News || ά. By blocking a protein, VDAC1, in the insulin-producing beta cells, it is possible to restore their normal function in case of Type Two Diabetes. In pre-clinical experiments, the researchers behind a new study have, also, shown that it is possible to prevent the development of the disease. The findings are published in the scientific journal Cell Metabolism. The researchers at Lund University in Sweden believe that the active substance, which inhibits the protein VDAC1, could play a part in future drug development for the treatment of Type Two Diabetes.

Pre-diabetics, may, experience elevated blood glucose levels for many years before developing Type Two Diabetes. High glucose levels initiate a series of negative processes. Among other things, they increase the production of VDAC1, a so-called channel protein within the cells, that, with the help of a substance, ATP, releases energy from the cell’s power plants, the mitochondria, to other parts of the cell, to be used for insulin secretion. At constant high levels of glucose, however, the levels of the VDAC1 protein increase, causing VDAC1 to attach to the cell surface.

The energy, ATP, then, leaks out of the cell and causes cell death due to a lack of energy. This, in turn, leads to impaired blood glucose control, that, eventually, causes organ complications, such as, cardiovascular disease, kidney disease, blindness and stroke.

“The goal is to be able to administer the substance to newly diagnosed Type Two Diabetics to allow the insulin-producing beta cells to retain their function. Or, even, better, to give it to pre-diabetics to prevent the onset of Type Two Diabetes.”, says Associate Professor and Research Ream Leader Albert Salehi, who conducted the study together with Professor Claes Wollheim.

“It is a small study, based on cell donations from six deceased people with Type Two  Diabetes, as well as, a limited number of experiments in animal models. Further studies are needed to demonstrate how blocking VDAC1 affects kidney, heart, muscle and fat tissue, for example. However, the results, thus far, have been so promising that we have patented the use of the active substance within the diabetes field. We are very happy about that and this initial study would not have been possible without the financial support from the Forget Foundation.” says Mr Albert Salehi.

When the researchers blocked VDAC1 in beta cells from organ donors with Type Two Diabetes, the energy supply was restored and the insulin secretion was normalised. The experiments were, subsequently, repeated on mice, which are known to develop genetically conditioned diabetes. As a result, the disease did not develop and the insulin production was maintained for five weeks, at which point, the treatment was discontinued and the glucose levels increased.

In addition to specific VDAC1 antibodies and VDAC1 inhibitors obtained in collaboration with Israeli researchers, the researchers in Lund used the diabetes drug, Metformin and achieved the same effect.

“We have shown a whole new mechanism for how Metformin works on beta cells. The fact that Metformin not only works outside the pancreas but, also, protects the beta cells and improves insulin secretion in people with Type Two Diabetes was recently demonstrated by a Canadian research team. The effect is, probably, achieved through an impact on VDAC1.”, says Mr Albert Salehi.

There are connections between Type Two Diabetes, Dementia and Alzheimer’s Disease. The authors of the study point out that there is, also, a link between VDAC1 and Alzheimer’s Disease, as high levels of VDAC1 can be found in brain cells in the parts of the brain, that are affected at an early stage of the disease.

“We believe that the substance, may, have a good effect, also, on these patients by preventing the brain cells from dying and, thereby, improving the patients’ cognitive abilities.”, says Mr Albert Salehi.

Diabetes is one of the major widespread diseases, affecting more than 400 million people worldwide. Approximately, 200 million people have diabetes without knowing it. The disease is caused by genetics and lifestyle. An improved diet and more exercise can be sufficient treatment for some, while others need drugs. Like other forms of Diabetes, Type Two Diabetes can lead to cardiovascular disease, damage to the eyes, kidneys and nerves.

In most studied tissues and cells, VDAC1 is more prevalent than VDAC2. Both VDAC1 and VDAC2 function as ion channels, that allow ATP to penetrate. In beta cells, however, VDAC2 is more prevalent, which indicates that it plays an important role in the beta cells. However, islets with beta cells donated from deceased persons with Type Two Diabetes have more VDAC1 and less VDAC2, compared to islets from healthy donors.

The proteins act as each other’s opposites: when VDAC1 increases, VDAC2 decreases and vice versa. This discovery was, also, made by the research team. Using confocal microscopes, the researchers were able to locate VDAC1 but not VDAC2 to the surface of the beta cells in Type Two Diabetics. In healthy cells and the cells from people, who were treated with Metformin, the protein was rather located inside the cells on the mitochondria. This was confirmed by immunofluorescence staining of the pancreas of non-diabetics and Type Two Diabetics.

The study was funded by the Forget Diabetes campaign, a new foundation for fundraising from private individuals, businesses and other foundations, the Mats Paulsson Foundation and the Bo and Kerstin Hjelt Diabetes Foundation.

The Paper: Publication: Preserving Insulin Secretion in Diabetes by Inhibiting VDAC1 Overexpression and Surface Translocation in β Cells:::ω.

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A Major Clinical Study Reports: Three-D Mammography Detects 34% More Breast Cancers in Screening Than Traditional Mammography

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

|| October 18: 2018: Lund University News || ά. After screening 15,000 women over a period of five years, a major clinical study in Sweden, has shown that three-D mammography or breast tomosynthesis, detects over 30% more cancers compared to traditional mammography, with a majority of the detected tumours proving to be invasive cancers. The extensive screening study was conducted by Lund University and Skåne University Hospital in Sweden and the results are now published in the journal Lancet Oncology.

In traditional mammography screening, all breast tissue is captured in a single image. Breast tomosynthesis, on the other hand, is three-dimensional and works according to the same principle as, what is known as, tomography. This means that several low-dose x-ray images are taken of the breast from different angles, which are reconstructed by a computer to show thin layers of the breast. With more and improved image information and less overlapping tissue structures, the chance of detecting tumours increases. Further, the radiation dose, may be, lowered in certain circumstances.

“With breast tomosynthesis, 34 per cent more cancer tumours were detected compared to the current standard mammography screening. At the same time, we were able to reduce the compression of the breast during examination, something, that, may, encourage more women to participate in screening.” says Ms Sophia Zackrisson, Associate Professor at Lund University and a Radiologist at Skåne University Hospital:SUS.

“We did, however, need to call back a few more women for additional examinations compared to traditional mammography. We needed to confirm that these women did not have cancer, as this method finds more structures in the breast in general. So, there was an increased call-back rate.

There is a need to improve screening for many women and breast tomosynthesis is clearly the most appropriate method to transition to in breast cancer screening. Breast tomosynthesis will be introduced, it’s just a question of when and to what extent

Breast tomosynthesis is already used at Skåne University Hospital, among other places, to investigate suspected breast cancer. Prior to a possible large-scale introduction in the general breast cancer screening programme, the research team is now conducting a cost-benefit study.

All types of screening involve a risk of overdiagnosis, which, in turn, may, lead to unjustified treatments. Therefore, the research team, in collaboration with their European colleagues, will conduct a meta-study, in which, they will aggregate and analyse their collective research results.

The lack of radiologists, who can review the increased image material generated by three-D methods presents a further challenge before large-scale introduction. However, the method used at Skåne University Hospital, may be, more efficient than those previously examined in international studies. In Skåne, only, the three-D method has been used, whereas other studies have combined three-D with traditional mammography screening. This leads to more image material and a higher radiation dose.

“We have shown that we can achieve the same result with a simpler and, perhaps, even, better method.”says Ms Sophia Zackrisson. In the future, parts of the image review in connection with breast tomosynthesis, may be, automated with the help of computers but it will take time. There is currently a lack of appropriate ready to use and tested software. Studies are underway, including, in Ms Sophia Zackrisson’s research team.

About the study: Close to 15,000 women participated in the screening study, conducted at Skåne University Hospital in Malmö in 2010–2015. The study’s midway results were published three years ago. The new results published in the journal Lancet Oncology confirm that breast tomosynthesis is superior to today’s mammography screening in the detection of cancer tumours.

The Paper: One-view breast tomosynthesis versus two-view mammography in the Malmö Breast Tomosynthesis Screening Trial:MBTST: a prospective, population-based, diagnostic accuracy study:::ω.

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The World’s First Trans-Atlantic Clinical Trial at the University of Southampton Offers New Hope for the Children Going Through Neuroblastoma

 

 

 

|| October 14: 2018: University of Southampton News || ά. Children with an aggressive form of cancer are being given new hope in a world-first trans-Atlantic clinical trial, that will test a new three-part treatment. The study, involving doctors and cancer scientists in Southampton, America and Germany, will boost the body’s immune system to kill off Neuroblastoma, one of the most common childhood cancers. The Phase One trial is funded by UK charities Solving Kids’ Cancer Europe, JACK and US charities Solving Kids’ Cancer and Band of Parents.

It will be one of many to be conducted at the University of Southampton’s Centre for Cancer Immunology, which is the UK’s first and only centre, dedicated to cancer immunology research. The centre recently opened at University Hospital Southampton, due to the University’s successful £25m fundraising campaign. Neuroblastoma affects around 100 children, mostly, under the age of five, in the UK every year and develops from immature nerve cells. It, usually, starts as a tumour in the abdomen or chest, however, in many children, it spreads to other places in the body such as, the bones and bone marrow.

In those cases, less than half of patients are cured despite intensive treatment, which includes surgery, chemotherapy, radiotherapy and stem cell transplants. More recently, a form of immunotherapy known as anti-GD2, which uses antibodies to lock onto cancer cells so the immune system can find, fight and destroy them, has shown the potential to improve survival rates.

This new Study, led by Dr Juliet Gray, Associate Professor of Paediatric Oncology at the University of Southampton, involves combining mIBG, a special form of targeted radiotherapy, which delivers radioactive iodine directly to neuroblastoma cells, with two different antibody therapies for the first time.

One of these therapies, Nivolumab, has shown exciting results in adult cancers. It blocks a harmful protein, called, PD-1 and gives patients’ own immune cells a boost so that they can be set free to kill tumour cells. The researchers will give Nivolumab alongside the currently-used anti-GD2 to target specific cancer cells while protecting normal healthy cells.

The trial will be run from four centres, the University of Southampton’s Centre for Cancer Immunology, UCH, Madison Children’s Hospital, Wisconsin and the University of Greifswald, Germany. It is, also, the first trial to be sponsored by University Hospital Southampton NHS Trust.

“Immunotherapy with anti-GD2 has been shown to increase the number of children with Neuroblastoma, who stay in remission and has become a standard component of treatment but, sadly, a large number of children still relapse and die from their disease.” said University of Southampton’s Dr Gray, who is, also, a Consultant Paediatric Oncologist at Southampton Children’s Hospital.

“Work in the laboratory has shown that combining these types of antibodies with radiotherapy is, potentially, a very powerful way of eradicating Neuroblastoma tumours and these three different therapies appear to work together to generate strong, protective immunity to the tumour. This Trans-atlantic trial will be the first time they have been tested together and we are hopeful the combination of treatments will, substantially, improve the cure rate of children with this form of cancer.”

Mr Stephen Richards, CEO of Solving Kids’ Cancer Europe, said, “Cutting-edge clinical trials offer real hope for children with high-risk neuroblastoma and their families. The numbers of children affected are small, so funding collaborative international research is the only way we will improve survival rates and find a cure for this devastating disease.”

The researchers plan to give an initial course of mIBG-targeted radiotherapy followed by Nivolumab and anti-GD2 over a period of six months. Although, the initial stages of the treatment process will require children to be in hospital, it is hoped that the therapy will be well tolerated and will, eventually, be delivered largely on an outpatient basis.

The trial’s objective is to ensure the combination is safe to deliver to children with Neuroblastoma in order to develop further studies to compare it with current treatments.:::ω.

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Precision Medicine: Targeted Drugs for Advanced Cancer Move From Specialist Units to Community Setting: It Is Hurting All: Give Them All a Painkiller Is Old Medicine: Where Does It Hurt: How Does the Hurt Occur and How the Bio-chemical Genetic Molecular and Neural Pathways of the Mechanism of the Hurt Being Caused: Answer These Questions and Deliver the Therapies Precisely to Each Hurt That Is Specific and Individual: Saving Resources Wastes Suffering and Loss of Lives: Invest in Precision Medicine IS the Call From the Future of Medicine

 

 

 

 

 

 

 

 

 

 

 

|| October 10: 2018 || ά. Nearly one in four patients with advanced cancer, treated at Comprehensive Cancer Care Network:NCCN centres in the US, are receiving innovative drugs matched to DNA mutations in their tumours. This achievement, to be reported at the ESMO 2018 Congress in Munich, shows that advanced precision medicine is spreading from highly specialist cancer units to other healthcare facilities so more patients can benefit, wherever they are treated. “We have shown that we can perform large-scale tumour profiling and use the results to match patients to targeted treatment in the type of community setting, where most patients are treated in the United States.” said Dr Ricardo H Alvarez, Medical Oncologist, Cancer Treatment Centres of America, Atlanta, USA.

“At our hospitals, we can identify patients with advanced cancer, refractory to previous treatment and take tissue or liquid biopsies, which, we send to a central laboratory for analysis and get results within three weeks. If, these show alterations in tumour DNA, which can be matched to a targeted medicine, we initiate treatment, usually, with a drug, that has been approved for use against a different tumour type or through enrolment in a gene-directed clinical trial.” In the new Study, tumour DNA data were analysed from 6,177 patients with advanced cancer treated by over 50 oncologists at five hospitals of Cancer Treatment Centres of America, from 2013-2017.

DNA alterations were identified in 94%, 5839:6496, of tumour samples, of which 47% were considered clinically relevant. Analysis of a large subset of patients showed that 23%, 1169:4490, received treatment matched to DNA alterations in their tumours. This compares with 11% of patients being enrolled in clinical trials of targeted treatment on the basis of tumour DNA alterations in previously reported studies at academic centres. “In the next few years, we hope that as many as 50% of our patients will receive matched treatment through clinical trials or off-label treatment with approved medicines.” said Dr Alvarez.

“It is so encouraging to see how precision medicine is changing the way we treat our patients in the community and our next step is to analyse the effects of targeted treatment on survival and quality of life.” The tumours, most commonly, treated by the community oncologists were breast, 18%, colorectal, 15%, lung, 14% and gynaecological, 11%. The most frequent clinically relevant tumour DNA changes were in the KRAS, 23% and PIK3CA, 15%, genes, with the most common alterations being gene amplification, 32%.

Of patients whose DNA alterations were matched to targeted drugs, 57%, 662:1169, received therapies already approved by the US Food and Drug Administration for a different type of tumour, and 15%, 178:1169, received treatments in clinical trials.

Dr Joaquin Mateo, the Lead Author of the recently published paper on ESCAT, ESMO Scale for Clinical Actionability of molecular Targets, aimed at simplifying and standardising choices for targeted cancer treatment, welcomed the findings of the US oncologists, “This is an important study because of the large number of patients and what it tells us about the impact of genomic research on patient care and clinical decisions in the community, where the majority of patients are treated. Studies like this are building the evidence we need to implement precision medicine within the oncology community and offer it more widely to our patients.” said Dr Mateo, who is the Principal Investigator of the Prostate Cancer Translational Research Group from the Vall d’Hebrón Institute of Oncology, Barcelona, Spain.

He looks forward to more detailed information about how tumour profiling determined treatment decisions and the cost of analysing DNA samples from such large numbers of patients. “The affordability of precision medicine is an important issue and we will need to address the challenge of ensuring efficient use of funds, if, we can only apply the results of tumour DNA testing to the treatment of a quarter of patients.”

Dr Mateo suggested that some variability in matching targeted treatment to tumour DNA alterations between studies, may be, due to a lack of standard criteria for determining what is a match and to differences in availability of targeted treatments.

“We need to be confident that matches and the reporting of genomics data and their interpretation are robust across all treatment centres, whether they are in hospital or the community. This will make targeted treatments based on these DNA alterations more likely to benefit our patients.”

For this reason, he hopes for full implementation of the ESCAT, which grades classes of alterations in tumour DNA according to their relevance as markers for selecting patients for targeted treatment, based on the strength of clinical evidence supporting them. “We hope that the ESCAT will provide a common language for determining relevant mutations and identifying patients most likely to benefit from targeted treatment.”

The Paper: Abstract 1891O_PR ’Mutational Landscape of Metastatic Cancers Discovered from Prospective Clinical Sequencing at Community Practice Cancer Programme’ will be presented by Dr Ricardo Alvarez during Proffered Paper Session on Saturday, October 20, 2018, 11:00 to 12:30, CEST, in Room 21, Hall B3. Annals of Oncology, Volume 29 Supplement  October 08, 2018

About the European Society for Medical Oncology:ESMO: ESMO is the leading professional organisation for medical oncology. With 18,000 members representing oncology professionals from over 150 countries worldwide, ESMO is the society of reference for oncology education and information. ESMO is committed to offer the best care to people with cancer, through fostering integrated cancer care, supporting oncologists in their professional development, and advocating for sustainable cancer care worldwide.:::ω.

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Often-Overlooked Natural Killer Cells May Hold the Key to Cancer Immunotherapy
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

|| October 01: 2018: University of Ottawa News || ά. Immune checkpoint inhibitors are revolutionising the treatment of cancer but new research challenges the central dogma of how these drugs work. This research, published in the Journal of Clinical Investigation, shows, for the first time, that often-overlooked immune cells, called, Natural Killer:NK cells play a crucial role in responding to checkpoint inhibitors. T cells and NK cells can both recognise and kill cancer cells but they do so in very different ways. NK cells recognise patterns of changes on cancer cells and are the immune system’s first line of defense.

A T cell, on the other hand, recognises a single abnormal molecule on a cancer cell and initiates a more focused attack. “Checkpoint inhibitors work by waking up the body’s own immune system and unleashing an immune attack on cancer cells.” said Dr Michele Ardolino, a Scientist at the Ottawa Hospital and an Assistant Professor at the University of Ottawa. “For many years, everyone assumed that checkpoint inhibitors targeted immune cells, called, T cells. But our research shows that they, also, target Natural Killer cells and these cells play a key role in the how this treatment works.

‘’In the cancer immunotherapy field there has been a singular focus on mobilising anti-tumour T cells.’’  said Dr Raulet. “We believe that NK cells have an important place at the table. Checkpoint therapy combined with other NK-directed immunotherapies, may, enable us to target many types of tumours, that are currently non-responsive to available therapies.”

In the current study, Dr Ardolino and Dr Raulet and their colleagues investigated the effect of checkpoint inhibitors in various mouse models of cancer. They found that checkpoint inhibitors could shrink tumours, even, in mice with no anti-cancer T cells, meaning that some other kind of cell must be responding to the checkpoint inhibitors.

When the mice were depleted of NK cells, it greatly reduced or eliminated the anti-cancer effect of the checkpoint inhibitors. They, also, showed that NK cells produce the same checkpoint receptor molecules, that T cells do, meaning they can respond directly to checkpoint inhibitors.

“This research helps solve a mystery, that’s been seen in the clinic, where certain cancers are very susceptible to checkpoint inhibitors, even, though, their T cells don’t seem to be activated.” said Co-lead Author Mr Jonathan Hodgins, a PhD student at the Ottawa Hospital and the University of Ottawa. “If, we’re right, NK cells are, probably, being activated in these patients.”

The researchers are now investigating approaches to further enhance the cancer-killing ability of NK cells. “My dream is that when people come to the hospital with cancer, we’ll be able to take a biopsy and determine not only the mutations in their cancer but, also, profile how their immune system is interacting with their cancer.” said Dr Ardolino. “Then, we would give the patient the immunotherapy treatments, that is most likely to work for them.”

Dr. Ardolino, a native of Italy, worked in Dr Raulet’s lab in California before he was recruited to the Ottawa Hospital and the University of Ottawa in 2016. Ottawa is a leader in the field of cancer immunotherapy, particularly, in the emerging field of NK cell research. For example, Dr Rebecca Auer discovered that surgery suppresses NK cells and can, therefore, help cancer spread.

She’s leading several clinical trials to test novel approaches to reverse this. Dr Ardolino, Dr Auer, Dr John Bell and others are, also, investigating the use of viruses to enhance cancer-killing by NK cells. The research team is, also, interested in creating genetically engineered NK cells to attack cancer cells, similar to CAR-T cells.

“NK cells are the new T cells.” said Dr Auer, a Surgical Oncologist and the Director of Cancer Research at the Ottawa Hospital and an Associate Professor at the University of Ottawa. “This field is exploding, and we’re poised to be at the forefront.”:::ω.

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New Drug Candidate Makes Cancer Cells More Sensitive to Radiotherapy
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

|| September 27: 2018: Karolinska Institutet News || ά. Researchers from Karolinska Institutet and Kancera AB have developed a molecule, that makes cancer cells sensitive to radiotherapy. In a study published in Nature Communications, the researchers describe a new way to block cancer cells' ability to repair their DNA and, thus, stop the survival of cancer cells. Radiotherapy is one of the most common cancer treatments. It damages the DNA, causing cancer cells to stop growing and die, if, the damage is left unrepaired.

Unfortunately, some cancers are resistant to radiotherapy and the treatment, also, damages the DNA in healthy cells, thus, limiting the amount of radiation, that can be used with respect to normal tissue damage. In collaboration with the Swedish company Kancera AB, researchers at Karolinska Institutet have discovered this new mechanism, that cancer cells use to repair DNA damage. In the current study, the researchers discovered that cancer cells use a protein, called, PFKFB3, to repair the DNA damage, that occurs in radiation therapy.

They found that the protein locates to sites of DNA damage in the cell nucleus, where the protein regulates the cancer cell's ability to repair its DNA and, thus, survive. The research groups at Kancera AB and Karolinska Institutet have now developed a new drug candidate, which blocks the protein and its ability to repair DNA damage. They demonstrated that cancer cells treated with the drug do not survive upon radiotherapy in laboratory experiments.

“It is known that the levels of PFKFB3 is much higher in cancer cells than in healthy cells. However, the discovery that PFKFB3 regulates DNA repair upon radiotherapy is new and very exciting.” says Ms Nina Gustafsson, Assistant Professor and Team Leader in Translational Medicine at the Department of Oncology-Pathology, Karolinska Institutet, who led the study together with Professor Thomas Helleday at the same department.

Since normal, healthy cells are not dependent on PFKFB3 for proper DNA repair, the researchers hope that combination therapy with radiation or chemotherapy will be well tolerated. The goal is now to further develop the drug and lay the foundation for a new cancer treatment with less side effects than the treatments currently available.

The study was led by researchers at Karolinska Institutet, operating at SciLifeLab and Kancera AB and conducted in collaboration with researchers from Stockholm University, University of Sheffield, Sprint Bioscience, Roma Tre University, Emory University School of Medicine and some other institutions.

The research has been funded by the Swedish Society for Medical Research, the European Union's Horizon 2020 research and innovation programme, together with Torsten Söderberg and Ragnar Söderberg Foundation and more.

The Paper: Targeting PFKFB3 radiosensitises cancer cells and suppresses homologous recombination: Nina M.S. Gustafsson, Katarina Färnegårdh, Nadilly Bonagas, Anna Huguet Ninou, Petra Groth, Elisee Wiita, Mattias Jönsson, Kenth Hallberg, Jemina Lehto, Rosa Pennisi, Jessica Martinsson, Carina Norström, Jessica Hollers, Johan Schultz, Martin Andersson, Natalia Markova, Petra Marttila, Baek Kim, Martin Norin, Thomas Olin, Thomas Helleday: Nature Communications Online: September 24: 2018:::ω. 

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Simple Factors That Can Avoid Harmful Side Effects in Type Two Diabetes

 

 

 

|| August 12: 2018: University of Exeter News || ά. Clinicians can match people with Type Two Diabetes to the right drug for them to improve control of blood sugar and help avoid damaging side-effects, simply by factoring in simple characteristics such as sex and BMI into prescribing decisions, new research has shown. The study, by the University of Exeter Medical School, could dramatically improve benefits of drugs and reduce the risk of potentially harmful side-effects, such as, weight gain and hypoglycaemia, at no additional cost to the NHS.

Metformin is the first line of drug treatment in Type Two Diabetes but many patients will, eventually, need additional drugs on top of Metformin to lower their blood sugar levels. Currently, clinicians have to make prescribing decisions on these additional drug options based on limited available guidance. Recent research involving the Exeter team has showed there is great regional variation across the UK in the prescribing of these additional drugs. The new study, funded by the Medical Research Council and published in the journal Diabetes Care, provides a starting point for a more evidence-based approach to the prescribing of drugs after Metformin.

Based on a patients’ gender and BMI, the authors found important differences in the likely success of the commonly-prescribed drugs Sulfonylureas and Thiazolidinediones in lowering blood sugar levels and in the risk of common side effects.  For example, obese females were far more likely to have good blood glucose control on Thiazolidinediones than Sulfonylureas, whilst non-obese males had the opposite result; they were far more likely to have good blood glucose control on Sulfonylureas than Thiazolidinediones.

The researchers used anonymous data from more than 29,000 patients, who had either taken part in trials or were treated in UK GP practices. By combining these datasets, the researchers were able to show their findings were robust and, potentially, applicable to many of the 03.5 million-plus people currently diagnosed with Type Two Diabetes in the UK.

Mr John Dennis, of the University of Exeter Medical School, was the Lead Author on the study. He said, “Our findings are important as they provide the first evidence that personalised or ‘precision’ medicine approaches in diabetes can be based on simple patient characteristics available to any doctor, rather than expensive genetics or other technology.

This simple personalised approach could be implemented immediately within the NHS without any additional cost. The study is, also, a powerful demonstration of how the sharing of patient data can meaningfully benefit patients, in this case, helping to make sure individual patients get the best drug for them.”

Professor Andrew Hattersley, a Consultant in Diabetes at the Royal Devon and Exeter Hospital and Research Professor at the University of Exeter Medical School, said, “At the moment, clinicians are in the difficult position of making decisions that impact on health in Type Two Diabetes based on very little evidence. Now, we can create clear guidelines to enable much more informed conversations about what these treatments will mean for people, in order to get better health outcomes and avoid harmful side effects.”

Dr Richard Evans, the Programme Manager for Stratified Medicine and Molecular Pathology at the MRC, said, “This research used shared clinical trial data from a large number of patients to show that simple patient characteristics can help inform the choice of therapy in diabetes; the results are likely to show real impact, and significant benefits to patients when they are implemented in patient care.

Diabetes afflicts one in 17 people in the UK, research into precision or stratified approaches to this condition is crucial to getting patients the most appropriate treatment in the most efficient way, underpinned by solid evidence.”

The Paper: Sex and BMI alter the benefits and risks of sulfonylureas and thiazolidinediones in type 2 diabetes: A framework for evaluating stratification using routine clinical and individual trial data: Published in Diabetes Care:::ω.

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New Research Finds a New Potential Target for the Treatment of Diabetes

 

 

|| July 29: 2018: Karolinska Institutet News || ά. Researchers at Karolinska Institutet have discovered that one of the building blocks in the calcium channels in the pancreatic beta cells play an important role in regulating our blood glucose values. Treatments aimed at this building block, may be, a new way to combat, primarily, Type Two Diabetes. The research has been published in the scientific journal Cell Reports. Beta cells in the pancreas produce the hormone insulin, which regulates the blood glucose level in our bodies.

In Diabetes, the beta cells have lost part or all of their function. Calcium ions, Ca2+, act as an important signal for the release of insulin. When blood glucose increases, this causes the levels of Ca2+ in the beta cells to increase, triggering the release of insulin. Under normal conditions the Ca2+ signal displays a specific regular pattern when the cells are stimulated by glucose. When, on the other hand, the beta cells are not able to release normal amounts of insulin, as in Diabetes, this pattern changes.

The level of Ca2+ increases in the beta cell when a specific calcium channel, made up of several different building blocks, opens in the beta cell’s wall. Professor Per-Olof Berggren’s research group at Karolinska Institutet has previously shown that one of the building blocks in the channel, the so-called β3 sub-unit, plays an important regulatory role.

“In our new study, we are able to show that beta cells, from Diabetic mice, have an increased amount of the β3 sub-unit and that this causes an altered Ca2+ pattern, a reduced release of insulin and, thereby, impaired blood glucose regulation.” says Professor Per-Olof Berggren at the Rolf Luft Research Centre for Diabetes and Endocrinology at the Department of Molecular Medicine and Surgery at Karolinska Institutet, who led the study.

When the researchers reduced the amount of the β3 sub-unit in the beta cells in the Diabetic mice, the Ca2+ signal normalised and, thereby, the release of insulin, resulting in better regulation of the blood glucose levels. They, also, saw that the mice, that totally lacked the β3 sub-unit demonstrated a better beta cell function and blood glucose regulation when they were given a diabetogenic diet. When the researchers tried transplanting beta cells without the β3 sub-unit into mice with Diabetes, the blood glucose regulation of the mice improved.

Experiments with human beta cells showed that the release of insulin deteriorates with increased amounts of the β3 sub-unit. “Our findings indicate that just this building block in the calcium channel can be a new target for treating Type Two Diabetes. However, even in Type One Diabetes manipulation of the beta three sub-unit, may be, beneficial in order to establish better functioning insulin secreting beta cells for transplantation.” says Professor Per-Olof Berggren.

The research was financed by the National Research Foundation of Korea:NRF, the Korea-Sweden Research Co-operation Programme, the Swedish Foundation for Strategic Research, the Swedish Diabetes Association, Karolinska Institutet’s Foundations and Funds, the Swedish Research Council, the Novo Nordisk Foundation, the Erling-Persson Family Foundation, the Strategic Research Programme in Diabetes at Karolinska Institutet, the European Research Council:ERC, 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 Managing Director of the bioetech company Biocrine AB and Co-authors Martin Köhler and Shao-Nian Yang are consultants at the company. No other corporate interests have been reported.

The Paper: Blocking Ca2+-channel β3 subunit reverses diabetes: Kayoung Lee, Jaeyoon Kim, Martin Köhler, Jia Yu, Yue Shi, Shao-Nian Yang, Sung Ho Ryu, and Per-Olof Berggren: Cell Reports: Online: July 24: 2018:::ω.

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Commonly Prescribed Medications Found to Be Linked to the Rise in Harmful Side Effects in Dementia Patients

 

 

 

|| July 25: 2018: University of Exeter News || ά Medications, which are commonly prescribed to people with dementia, have been linked to an increase in harmful side-effects, research involving the University of Exeter has concluded. The research, presented at the Alzheimer’s Association International Conference examined the impact of opioid-based painkillers or a class of sleep medication, known as, Z drugs, Zolpidem, zopiclone and Zaleplon.

These are prescribed to an estimated 200,000 with dementia living in care homes across the UK in total. In the opioid painkiller research, a team of researchers from the University of Exeter, King’s College London and the University of Bergen highlight a tripling in harmful side effects related to the use Buprenorphine in people with dementia, compared to those on a placebo. Researchers, also, identified a mechanism, that, may be, causing the problem.

In a randomised controlled trial of 162 Norwegian care home residents, the researchers found a significant rise in side effect, such as, personality changes, confusion and sedation, which can seriously impact people’s lives in dementia. The trial team, led by the University of Bergen, studied 162 people from 47 Norwegian care homes, who had advanced dementia and significant depression.

In those, who were assigned Buprenorphine as part of their treatment pathway, harmful side-effects more than tripled. The researchers, also, found that those taking Buprenorphine were significantly less active during the day.

In the Z-drugs research, the researchers compared data for 2,952 people with dementia, who were newly prescribed the medication with data for 1,651 who were not, in order to evaluate the benefits and harms of the medicines. They found that people, who take Z-drugs are more likely to fracture a bone than those, who do not. Bone fractures are related in turn to an increased risk of death in people with dementia.

Researchers are now calling for studies to examine alternative non-drug approaches to treating pain and insomnia and appropriate dosing of painkillers, such as, Buprenorphine for people with dementia. Professor Clive Ballard, of Age-Related Diseases at the University of Exeter Medical School, said, “Research into anti-psychotics highlighted that they increased harmful side effects and death rates in people with dementia.

This compelling evidence base helped persuade everyone involved in the field to take action, from policy makers to clinicians, reducing prescribing by 50 per cent. We now urgently need a similar concerted approach to opioid-based painkillers and Z-drugs, to protect frail elderly people with dementia from fractures and increased risk of death.”

Importantly, research led by Professor Ballard’s team and presented at the conference gives insight into the mechanism of why people with dementia are more susceptible to opioid-based painkillers, suggesting they over-produce the body’s natural opioids.

The study treating arthritis in Alzheimer’s mice found increased sensitivity to the opioid-based painkiller morphine in mice with Alzheimer’s disease compared to those without. Those with Alzheimer’s disease responded to a much lower dose to ease pain and experienced more adverse effects when the dose was increased to a normal level.

Looking into this further the study found that the Alzheimer’s mice produced more of the body’s natural endogenous opioids, such as, endorphins. The study, presented as a poster at AAIC, also, concludes that dosing of opioid-based painkillers urgently needs to be reviewed in people with dementia to enable safe and effective treatment of pain and prevent unnecessary harm and deaths. :::ω.

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Blood in Stools May Indicate a Range of Chronic Diseases

 

 

 

|| July 22: 2018: University of Dundee News|| ά. Faecal bleeding, may be, a marker of a range of chronic disease, including, several cancers, previously thought to be unrelated, according to new research from the University of Dundee. The presence of blood in stools has long been associated with colorectal cancer. The new study, led by Professor Bob Steele of Dundee’s School of Medicine, has shown that patients, who recorded a positive faecal occult blood test:FOBT were much more likely to die not only from colorectal cancer but, also, a range of other diseases.

Professor Steele and his team looked at data for 134,000 patients, who have participated in FOBT screening in Scotland since 2,000 and linked their test results with mortality data from the National Records of Scotland over the same period. Not only were those, who had a positive result more likely to die of colorectal cancer, their risk of dying from all other causes was, also, higher. Furthermore, faecal bleeding was significantly associated with increased risk of dying from circulatory disease, respiratory disease, digestive diseases, neuro-psychological disease, blood and endocrine disease and non-colorectal cancer.

While further research into the links between faecal bleeding and these diseases is required, Professor Steele hopes that it could, one day, be used to reduce the risk of premature mortality and to explore the underlying reasons for different patterns of mortality across the world.

“This is the first observational study to demonstrate a link between faecal bleeding and increased risk of death from a range of diseases other than colorectal cancer.” he said. “Over the past 18 years, we have operated a bowel screening programme, that looks for traces of blood in faeces and this has been very successful in detecting the disease in its earliest stages and increasing survival rates.

Anyone with a positive FOBT result, then, receives a colonoscopy to look for tumours or polyps, that could explain the bleeding but there are quite a number of patients for whom blood in their stool turns out to be a false positive and who do not have colorectal cancer.

We were always curious as to why this should be so we went back to the early cohorts to examine outcomes for those with positive compared to negative FOBT results. What we found is that, if, you had a positive test you were more likely to die from colorectal cancer, which is what we expected but we, also, found that all-cause mortality was higher.

We then linked this data with specific causes of death and found that the risk of dying from a series of other diseases, such as, heart attacks, circulation disorders, respiratory disease and many other cancers was, also, higher.

The reason for this is not clear as yet but we think that it, might be, related to levels of inflammation throughout the body as this is a marker of general ill-health and chronic inflammation is a driving factor behind whole series of whole host of other diseases. In any event, if, someone is found to have unexplained blood in their faeces, it, may, mean that they are at risk of developing chronic disease and, may, benefit from attention to their lifestyle.”

Faecal bleeding is associated with the male sex, age and deprivation. After adjusting for these factors, the risk of dying from colorectal cancer remained higher among those with a positive FOBT result, as did all-cause mortality and many specific diseases. Professor Steele was, also, able to link the data with a unique database of prescribing information, that exists in Tayside to prove that these results were not caused by medicines, that can cause bleeding.

“At present, if, somebody with blood in their stool, who goes on to have a colonoscopy, that doesn’t show any tumour or polyps in the bowel we don’t investigate further. It is only recently that we’ve become interested in other causes of death, that are unlikely to directly cause blood in stool but are somehow linked.’’ said the Professor.

‘’The next stage is to carry out prospective studies to see, if, there is a link between lifestyle diseases and faecal bleeding and whether it is reversible. Perhaps in future we should be saying in these instances that we need to look at risk factors for other diseases, such as, smoking or obesity, to see, if, interventions can be implemented at this stage to help prevent premature death.”

Professor Steele holds a Chair in Surgery at the University is one of the UK’s leading authorities on cancer screening. He is Director of the Scottish Colorectal Cancer Screening Programme, having acted as Clinical Lead for the UK demonstration pilot, that was used to inform the decision to introduce national screening programmes throughout the UK.

He is a Fellow of The Royal Society of Edinburgh and was elected a Fellow of Academy of Medical Sciences earlier this year. :::ω.

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Researchers Use Cryo-Electron Microscopy for the First Time to See the Molecular Machinery of the Herpes Virus As to How It Infects Humans: Paving the Way for Potential Drug Development Opportunities

 

 

  

|| July 19: 2018: University of Glasgow News || ά. For the first time, researchers have been able to use a Nobel Prize winning technology, cryo-electron microscopy, to show  the detailed structure of the common Herpes Virus. Researchers at the University of Glasgow used the advanced technique to gain high resolution images of the biological mechanisms this virus uses to infect people. The findings were published in PLOS Biology on July 05.

The researchers now hope that these findings could lead to the development of new drugs to treat the illness this virus causes. The herpes family include the viruses, that cause both cold-sores and chicken pox. Members of this family of viruses can, also, cause cancers and severe illnesses in the unborn child. However, at only 1:10,000th of a millimetre in diameter, the capsid or shell, the Herpes Virus uses to store its DNA and infect its host, has until now been difficult for scientists to anaylse.

Herpes Viruses cause infection by introducing their DNA into our cells. To do this, they package their DNA inside a protective coat, called, a capsid. The capsid is spherical in shape and highly symmetrical.

The researchers used cryo-electron microscopy to show the structure of a motor-like assembly, called, a portal. Herpes Viruses pump their DNA into pre-assembled capsids through the portal. When a Herpes Virus infects our cells, the DNA is ejected from the capsid by the same portal machinery.

Dr David Bhella, the Lead Author of the study from the MRC-University of Glasgow Centre for Virus Research, said, “Cryo-electron microscopy, combined with new computational image processing methods allowed us to reveal the detailed structure of the unique machinery by which the virus packs DNA into the capsid. The DNA is packed very tightly, reaching a pressure similar to that inside a bottle of Champagne. 

We hope that this study will, eventually, lead to the development of new medicines to treat acute herpes virus infections, through the design of drugs, that will block the action of the portal motor.”

As well as showing the shape of the portal machinery, this study, also, established how the virus packs its DNA inside the capsid. Individual strands of DNA were seen to be wound up in a spool, rather like a ball of wool. The development of cryo-EM as a technique for resolving detailed atomic structures was developed at the MRC Laboratory of Molecular Biology.

Dr Jonathan Pearce, Head of Infections and Immunity at the MRC, said, “Dr Bhella and his team have now used this technique to elucidate the structure of the Herpes Virus, revealing a ‘molecular machine’, that is involved in virus replication. The findings provide scientists with a better understanding of the virus and its anatomy and, in turn, an insight into potential new therapeutic targets.

These elegant experiments exemplify the potential of the Scottish Centre for Macromolecular Imaging due to be launched later this year at the CVR, led by Dr Bhella, which will support vital research into diseases posing the greatest threat to human health.”

The study, ‘Structure of the herpes-simplex virus portal-vertex’ is published in PLOS Biology. The work was funded by the Medical Research Council:MRC.:::ω.

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All That Can Be Done and Always There’s So Much More That Can Be Done: All About Congenial Hyper-Insulinism

 

 

|| July 19: 2018: University of Exeter News || ά. A charitable organisation is providing vital funding for people with a rare condition across the world to have genetic screening at the University of Exeter. The US-based non-profit organisation Congenital Hyperinsulinism International will fund genetic testing for babies around the world from families, who could not, otherwise, afford the testing. Getting the right diagnosis and treatment can help avoid brain damage and other severe complications. Dear Reader, wherever you are in this world, whether in Exeter or East London in South Africa or New Hampshire in the USA or in Alexandria in Egypt or in Boston, no, not in the USA but in good old United Kingdom, do tell people about this work, about this condition so that parents get to hear where and how to seek help but, more importantly, that they should gather forces.

The world is a tiny little place. Believe us not: count eight hundred billion plus stars in the little Milky Way Galaxy and among which our little nano-dot sun is literally a ‘dwarfed’ out thing and now find your earth there! It does not look that big, does it? And, yet, in this tiny little earth there are so many so called geo-political pretend-giants stomping and fretting and yelling the world how big and mighty they are with their puddle-views and by their puddlesque blindness, seeking to take the world down towards insanity. But, leaving all that aside, we can make this tiny little place even more tiny by our infinite reach! And by getting together, gathering forces and joining hands  we only enhance our abilities and reach, that allow us access to a reservoir of human strength and spirit from the fellow travellers.

A few parents from far flung corners of the earth came together to bring this agency into existence and they are now able to offer this to so many others, who, otherwise, can not have it. Tell the world that the world is not just going and being run down by insanity but that there are far better ‘insane’ people, ‘insane’ humanity out there all-where, determined to carry on with the good work. They open not their mouths with diarrhoea but they believe, act and work with goodness in their hearts and souls and in their vision a determined resolve to keep on being and doing good and tirelessly they keep on going: seeking to do: to change, to make better.

Congenital Hyperinsulinism is a condition in which babies are born secreting too much insulin. Made in the pancreas, insulin is the hormone, that regulates blood sugar levels. Having too much means babies can be born very large and suffer from problems associated with low blood sugar. If, the condition is not treated appropriately, the brain can be starved of vital fuels, which can cause learning difficulties, blindness or, even, death.

The world-leading Hyper-Insulinism research team at the University of Exeter Medical School, who work closely with the NHS genetics laboratory at the Royal Devon and Exeter Hospital, has received samples from 86 countries and provided genetic testing for more than 3,000 families affected by this condition, who could not afford to pay for the test.

Dr Sarah Flanagan, of the University of Exeter Medical School, who leads the research programme, said, “This genetic testing is absolutely vital for families. For many children with this condition the only way to prevent brain damage is to undertake pancreatic surgery.

The genetic result can help determine whether all or just part of the organ should be removed, which can mean better outcomes for the children. I’m delighted that Congenital Hyperinsulinism International is providing funding for this crucial work for people worldwide, who could no,  otherwise, afford this test.” 

Congenital Hyperinsulinism International was set up by eight parents of children with Congenital Hyper-Insulinism from Australia, the US, Canada and Ireland, and one nurse caring for a child with Hyper-Insulinism. It held its first conference in 2006 and is now a leading global organisation in raising awareness, providing information and bringing together families from across the world, who are affected by the condition. 

The non-profit organisation has so far pledged nearly £17,700 to cover six months’ of testing. It intends to contribute a further £35,000 to cover 18 months in total.

Ms Julie Raskin, Executive Director of Congenital Hyperinsulinism International, co-founded the charitable organisation. Her son, Ben, was born with Ccongenital Hyper-Insulinism and is now 22 years old.

Ms Raskin said, “We are on a mission to end preventable brain damage and death from Congenital Hyper-Insulinism and to ensure those living with it get the best possible care. Partnering with the University of Exeter Medical School to ensure that cost and geography are not barriers to genetic testing is an enormous step forward for the global Congenital Hyper-Insulinism community.” :::ω.

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New Research Finds Potential for Developing the First Lassa Virus Vaccine

 

 

 

|| July 15: 2018: University of Southampton News || ά. A study, led by the University of Southampton, has discovered new hope, which could support the creation of the first vaccine for the deadly Lassa Virus. This highly infectious agent is amongst a panel of viruses, which includes Ebola, that cause severe haemorrhagic fever in humans. As there is currently no effective vaccine or treatment available to combat this virus, the findings, published in Proceedings of the National Academy of Sciences of the United States of America, will support efforts to generate a vaccine to tackle the subsequent outspread of the disease.

The Lassa Virus is commonly found in West Africa and is transmitted to humans, mainly, through handling rats, food or household items contaminated by rats’ urine and faeces. The virus can spread between people through direct contact with the body fluids of a person infected with Lassa Fever, as well as, contaminated bedding and clothing. According to figures released by the Nigeria Centre for Disease Control:NCDC, the current Lassa Virus outbreak in Nigeria has resulted in a total of 444 confirmed cases, including, 111 recorded deaths to date. This is the largest outbreak of the Lassa Virus ever reported in Nigeria.

Any successful vaccine to combat the Lassa Virus would likely include the viral spike, that functions on the virion surface and is responsible for helping the virus enter a target cell. It is hoped that by including mimics of the viral spike the body’s immune system will make antibodies against the spike, that are capable of neutralising the virus.

Making a vaccine against Lassa Virus is difficult and one characteristic of the virus, which enables it to avoid detection by the immune system, is a dense coat of sugars, that are attached onto the surface of the spike, otherwise known as, glycans.

Professor Max Crispin, Principal Investigator of the study from the University of Southampton, said, “We hope that by understanding the glycan shield of Lassa Virus we will be able to help in the efforts to generate an effective vaccine.

Given the impact of Nigeria’s largest-ever Lassa Fever outbreak this year, it is critical that we begin to identify the idiosyncrasies, which could help to create a vaccine to combat this highly infectious agent and ensure it is contained.” 

As part of the study, titled, ‘Structure of the Lassa virus glycan shield provides a model for immunological resistance’, the research team has created a detailed map of the glycan shield, which has shed light on why the virus is so immunologically resistant.

The findings provide a potential blueprint for understanding how glycans render the glycoprotein spikes of Lassa Virus and how the infection could be combated. Professor Thomas Bowden, Co-author of the study from the University of Oxford, said, "The development of a vaccine for a virus, such as, this is a long and complex process.

These findings have important implications for researchers developing vaccines against Lassa Virus, providing a benchmark to assess future vaccine candidates.”:::ω.

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Post-Ebola Syndrome: New Study Finds Ebola Survivors Suffer From Severe Neurological Problems

 

 

|| July 14: 2018: University of Liverpool News || ά. Researchers have shed new light on the psychiatric and neurological problems, that Ebola survivors can suffer from and call for more specialist support for the most severely affected patients. A new report, published in Emerging Infectious Diseases, details a broad range of disorders among Ebola survivors in Sierra Leone, including, stroke and debilitating migraine-type headaches. Some survivors are left unable to care for themselves.

The observational study was led by researchers at the University of Liverpool and King’s Sierra Leone Partnership of King’s College London, based in Connaught Hospital, Freetown and in collaboration with the Ebola Survivors Clinic at Military Hospital 34, Freetown, Sierra Leone, as part of an ongoing effort to better understand Post-Ebola Syndrome:PES and improve on-going patient care following the 2014-2016 outbreak in West Africa.

To better understand the neurological and psychiatric effects of PES, adult patients with pre-determined, significant symptoms, such as, confusion, depression and psychosis, were identified from the patient notes of over 300 Ebola survivors. 34 selected patients were invited to attend a joint neuro-psychiatric clinic in 2016, where they underwent a full neurological examination, psychiatric screening and specialist investigations, including, brain scan imaging.

The most frequent neurological diagnosis was migranous headache, followed by stroke, peripheral sensory neuropathy and focal peripheral nerve lesions. Most survivors had co-existent mental health needs, with the most frequent psychiatric diagnoses being major depressive disorder and generalised anxiety disorder.

Dr Janet Scott, who lead the Post-Ebola Syndrome Project at the University of Liverpool, said, “We knew that a disease as severe as Ebola would leave survivors with major problems, however, it took me aback to see young and previously active people, who had survived but were now unable to move half their bodies or talk or pick up their children.

These cases are on the severe end of the spectrum but thanks to support from the Wellcome Trust, we’ve been able to further investigate these cases and learn more about Ebola Virus Disease in the process. Our findings support the need for larger, case-controlled studies. Post-Ebola Syndrome is not going away and those with the condition deserve better treatment.” 

Dr Patrick Howlett, from King’s College London, carried out this study. He said, “We found a broad set of neurological and psychiatric symptoms, from minor to extremely severe and disabling, are present in Ebola survivors well over a year after discharge from hospital. In our selected group intermittent headaches were the most frequent neurological feature, with a variety of associated symptoms. Connaught Hospital continues to provide specialist neurological care for these patients, however, there is an urgent need to support training for specialist medical professionals, who can meet the needs of this survivor population.

This was a broad collaboration co-ordinated from the University of Liverpool. The ‘Survivors Clinic’ was based at Military Hospital 34, in Freetown and got specialist input in Neurology and Psychiatry was provided by a Connaught Hospital, Freetown, with support from King’s Sierra Leone Partnership. We called on the particular skills of Radiology and Ophthalmology Departments at the Royal Liverpool Hospital to interpret the CT Brain Scans and retinal images. It highlights the need for a team effort in considering these complex clinical cases.”

Psychiatrist Dr Stephen Sevalie, 34 Military Hospital, said, “Psychiatric features of insomnia, depression and anxiety are common and our findings suggest that there is, also, a need for better understanding of the psychiatric and psychological consequences of Ebola Virus Disease. Although, our Ebola Survivors Clinic includes an onsite councillor, there are many more, who won’t have access to the specialist care they need so we will continue to research and provide hands on support to ensure this happens.”

The study and investigators were supported by the Wellcome Trust  Enhancing Research Activity in Epidemic Situations:ERAES programme and grants from the National Institute for Health Research:NIHR Health Protection Research Unit in Emerging and Zoonotic Infections at the University of Liverpool. Additional support was received from Advancing Partners and Communities, a programme funded by the United States Agency for International Development through JSI Research and Training Institute.

Professor Mike Turner, Wellcome’s Head of Infection and Immunobiology, said, “It has become clear that many people, who survived Ebola infection in West Africa in 2014 have had long term effects on their health. This new study shows the damaging neurological and psychological effects of the virus, with survivors experiencing chronic migraines and strokes, as well as, depression and anxiety. These findings demonstrate the devastating long-term impact Ebola has had on survivors’ quality of life and their ability to participate in family life and with their community.” 

The Paper: Case Series of Severe Neurologic Sequelae of Ebola Virus Disease during Epidemic, Sierra Leone:::ω.

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New Research Finds That Stopping Antibiotics Before the Resistance Reaches the Tipping Point Is the Way to Beat Anti-Microbial Resistance

 

 

|| July 12: 2018: University of Exeter News || ά. Treatments using antibiotics should stop as soon as possible to prevent patients passing the ‘tipping point’ of becoming resistant to their effects, new research has shown. A team of researchers, led by Professor Ivana Gudelj from the University of Exeter and featuring Professor Robert Beardmore and Professor Emily Cook, has uncovered new evidence that suggests reducing the length of the antibiotic course reduces the risk of resistance.

For the study, the researchers examined how microbial communities, groups of micro-organisms, that share a common living space in the body, reacted to different antibiotic cycling patterns, which sees the medication restricted or increased, under laboratory conditions. They found that changes both in the duration and dose of antibiotics used and in sugar levels, which mimics the variable sugar levels in human patients, could push these microbial communities beyond a ‘tipping point’, creating an irreversible shift to becoming drug resistant.

The researchers insist that this new study demonstrates that resistant species can increase within the body, even, after an antibiotic is withdrawn, if, a tipping point was unwittingly passed during treatment. The study is published in the journal Nature Ecology and Evolution on Monday, July 09.

Professor Beardmore, a mathematical biosciences expert from the University of Exeter, said, “It’s a sensible idea that, when you take an antibiotic away, resistance goes away, too, but we wondered what kinds of antibiotic treatments don’t behave like that. After all, in some clinical studies, resistance didn’t disappear when the antibiotic did.”

Antibiotic resistance occurs when microbes develop the ability to defeat the drugs designed to kill them and so they multiply unhindered. Antibiotics are the most effective treatment for a wide-range of microbial infections, including, strep throat and pneumonia.

For decades, patients have been instructed to complete courses of antibiotics because the perceived wisdom had been that taking too few tablets would allow bacteria to mutate and become resistant. However, more recently it has been suggested that the longer microbes are exposed to antibiotics, the more likely it is that resistance will develop. 

Little research has been conducted to show how the length of a course of antibiotics impacts resistance, which, despite differences in patients, for example, in their blood sugar levels, are recommended to be the same for all.

In the new study, the researchers examined how microbial communities containing Candida Albicans and Candida Glabrata reacted to different doses of an antimicrobial when fed with sugar. Both species are commonly found together in healthy people but are, also, opportunistic pathogens, which can cause infection.

The study showed that as the antimicrobial was introduced, the communities were reduced, while the removal of the treatment allowed them to flourish again. The researchers showed that, if, sugar levels dropped in the community, it could reach a ‘tipping point’ whereby resistance would persist, even, after the antimicrobial had stopped being used.

The new research opens up the possibilities for further studies to better understand when the best time would be to stop antibiotic treatment, to prevent resistance occurring.

Co-author Professor Ivana Gudelj said, ‘’Our body is a mother ship for microbial communities but we’ve still expected to understand drug resistance by studying microbial species one at a time, in the lab.

We show this can be misleading because microbes have intricate relationships, that the drugs make, even, more complicated and, yet, our theories of antibiotic resistance have ignored this, until now. So that’s the first surprise: even, sugars can affect antibiotic resistance.”

The Paper: Drug-mediated metabolic tipping between antibiotic resistant states in a mixed-species community: Published in Nature Ecology and Evolution online:  Monday, July 09: 2018:::ω.

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New Research Finds New Means to Inhibit Capillary Leakage in Sepsis

 

 

|| July 01: 2018: University of Helsinki News || ά. Leakage from the blood capillaries is a key mechanism, leading to septic shock and multi-organ failure, which affect millions of patients annually worldwide. However, there is no effective way to inhibit the vessel leakiness. A new study by scientists at the University of Helsinki and Wihuri Research Institute demonstrates that vascular leakage can be inhibited by targeting vascular integrins. Increased capillary permeability and, subsequent leakage from the capillaries, is associated with numerous difficult to cure diseases, including, Qcute Respiratory Distress Syndrome:ARDS, severe Dengue Fever and Malaria and Sepsis.

Currently, there is no effective therapy to inhibit capillary leakage and to maintain vessel stability in these diseases. The latest research published in the Proceedings of the National Academy of Sciences of USA indicates that a monoclonal antibody targeted against β1-integrin inhibits vascular leakage in a mouse model of Sepsis. Integrins are heterodimeric cell surface receptors, that mediate interactions between cells and the surrounding extracellular matrix. β1-integrin is a key molecule in endothelial cells, which form the inner layer of the blood vessel wall. Previously, β1-integrin has been known to regulate blood vessel formation and vessel stability.

 

Scientists have now identified a new function for β1-integrin in vascular leakage associated with severe inflammation and Sepsis. Principal Investigator, Dr Pipsa Saharinen, at the University of Helsinki and Wihuri Research Institute, said, ‘’We made a remarkable discovery: a molecule, that was previously known to mediate vessel stability, behaved in an opposite manner in inflammation, by inducing vessel destabilisation and leakage.

We found that inflammatory agents induced cell contractility, that was mediated via β1-integrin, leading to gap formation between endothelial cells and increased permeability.’

The scientists used a mouse model of gram-negative Sepsis, also, termed Endotoxemia, which was induced in mice by a bacterial component, LPS. The scientists found that the antibody against β1-integrin bound to the vascular endothelium, improved the junctions between endothelial cells and decreased vascular leakage in sepsis. In addition, the antibody protected the mice from sepsis-induced heart failure.   

The antibody against β1-integrin was effective as a prophylactic treatment but, also, as an intervention therapy, i.e, when the antibody was administered after the onset of the disease. 

‘’This is important since it mimics more the situation in real life. Sepsis, may, develop unexpectedly and proceed fast. When the patients arrive at the hospital, the disease, may have, already, progressed. It would be important to have the means to inhibit vessel leakiness and the development of a more severe disease. In our study, the antibody against β1-integrin was effective in inhibiting vascular leak in mice, even, when it was administered after the onset of the leakage.’’ Dr. Saharinen said.

In Sepsis the body’s own inflammatory reaction becomes overwhelming. Due to the increased level of numerous inflammatory agents, it has been so far difficult to develop a targeted therapy for sepsis.

‘’Using endothelial cells in culture, we found that β1-integrin is a key mediator of not only one but several inflammatory agents, that are upregulated in Sepsis. Furthermore, we found that a vascular growth factor Angiopoietin-2, which is known to play a role in the pathogenesis of Sepsis, regulated β1-integrin signalling in endothelial cells.

Although, there is still a lot of work to do to, these exciting results could, ultimately, help us develop an effective treatment to block capillary leak in Sepsis.’’ Dr Saharinen said.

For further information contact: Associate Professor, Dr Pipsa Saharinen: Tele: +358-50 448 6361: email: pipsa.saharinen at helsinki.fi

The research was carried out at Wihuri Research Institute, University of Helsinki, University of Turku and University of Oulu.

The study was funded by the Academy of Finland, Cancer Society of Finland, European Research Council, Helsinki Institute of Life Science:HILIFE, Sigrid Juselius Foundation and Jenny and Antti Wihuri Foundation.

Caption: Image One: Leakage of the vascular tracer: red: from dermal blood vessels: green: in systemic inflammation: Image Two: Dr Elina Kiss: Left and M.Sc  Laura Hakanpää: Right in Associate Professor Pipsa Saharien’ Lab at HILIFE: Image One Credit: Laura Hakanpää:Saharinen Lab: Image Two Credit: Joel Noutere: Saharinen Lab :::ω.

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Year Gamma Arkive 2017-18

Year Beta Arkive 2016-17

Year Alpha Arkive 2015-16

 
|| 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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The Door of Learning and Seeking Must Always Remain as Open as the Universe and as Resolutely Active as the Ray of Light

 

 

 

 

 

 

 

 

 

 

 

Reading this page, we hope and imagine, that practitioners of Medicine and the countless numbers of professionals who work within the field of Medicine as well as the students of the discipline, would feel encouraged and inspired to join us and write about their subject discipline for and in The Humanion. Please, get involved and create and shape debates on the future of Medicine. We would particularly, be interested in issues impacting on profound questions that Medicine faces such as the death penalty and the stance of the profession of Medicine and euthanasia, human drug trials, drugs and poverty and practical and day to day issues that Medicine faces. Please, get in touch and do get involved. We are not looking for work for the 'professionals' but for the thinking mind, which means that writing should not be too technical and too much punctuated by too much professional jargons. We would very much be interested about writing from Medicine professionals working with national and international charity organisations.

Only in the transparent pool of knowledge, chiselled out by the sharp incision of wisdom, is seen the true face of what truth is: That what  beauty paints, that what music sings, that what love makes into a magic. And it is life: a momentary magnificence, a-bloom like a bubble's miniscule exposition, against the spread of this awe-inspiring composition of the the Universe. Only through the path of seeking, learning, asking and developing, only through the vehicles and vesicles of knowledge, only through listening to the endless springs flowing beneath, outside, around and beyond our reach, of wisdom, we find the infinite ocean of love which is boundless, eternal, and being infinite, it makes us, shapes us and frees us onto the miracle of infinite liberty: without border, limitation or end. There is nothing better, larger or deeper that humanity can ever be than to simply be and do love. The Humanion

Create and Pave: Intelligence and Learning




|| December 09: 2017 || ά. Learning is a Bio-Intuitional Cognition Process Set by Nature in All Living Organisms on a Scale of the Lowest Level and Degree of Sheer Biological Awareness to the Highest Level and Degree of Consciousness That is Capable of Forming Itself Both as Individual Person and as a Member of the Unity of Many Persons or Community or Society and That is Capable to Congnise, Combining Both Bio and Intuitional in an Alignment of All Components of the Faculty of Rationality by Which It Thinks Through and Comes to Cognition and That is Learning and This Learning is Deposited in a 'Bank', Called, Memory: From a Single Cell Living Organism with Just Biological Awareness on Biological Cognition to a Human Brain:Mind:Will:Soul with Bio-Intuitional Cognition Learning Can and Does Take Place. There is None and Can Not Be Any Intelligence or Learning Outside Living Organisms, Where We Find Things, Matters, Energies, Time, Space and Void Existing Under Absolute, Incorporated, Inherent and Ingrained Eternal Natural Laws Without Exceptions at All Times, That Not a Single Variable Existing in It Can Alter or Not Obey, Signifying There is No 'Will' There, Which Does and Can Only Arise Out of Intelligence Through Learning and All, That is Outside the Living-Life, Form Part of What We Call The Mechanoprincipium, Which Only the Highest Possible Bio-Intuitional Intelligence, i.e, Humanity is Capable of Perceiving.

Therefore, the Very Absurd Ideas, That the Misguided, Manipulative and Profiteering Market Mechanism is Seeking to Portray, Establish, Impose and Dictate to Humanity as Artificial Intelligence and Machine Learning are Nothing But Means to Expand the Scope, Prowess and Reach of Dehumanisation and Must Be Rejected, Resisted, Fought and Defeated Outright. We Have, Almost, More Than Half of All Humanity and the Great Majority of Women, Forced and Sentenced to Live and Die in No Education, in Desperate Hunger, Desperate Poverty and Abject Poverty and Malnutrition and Without Medical Care, in Homelessness and Unemployment and Much More Besides and, Yet, These Forces are Wasting All Precious Human and Other Priceless Resources Into Such Absolute and Utter Audacity of Imposing Their Machinations on Humanity as If to Suggest That for an Injured Soul Dying in Absolute Agony of Bleeding, Hurts and Pains the Necessity is Not to Take Her:Him to the Nearest Accident and Emergency Unit of a Hospital But Get a Plastic Toy-Robot-Doctor to Sit Next to Him Speaking Utter Imbecility! This Can Not, Should Not and Must Not Be Let to Succeed. The Most Vital and Most Scarce Human Resources Must Not Be Let to Be Squandered in This Absurd and Utterly Misguided Pursuit of Dehumanisation. Our High-Most Priority is to Ensure That the Entire Humankind, in All Nations on Earth, is Afforded the Right to Get an Education and Get Universal Human Rights and Not a Single Soul Die of Hunger or for the Lack of Medicare.

This is What is Called Intelligence and This Why It is Called Learning: Because are Humans and We Ask and Question and We Empathise and We Sympathise and We Love and We Hope and We Imagine and We Learn and We Dream and We Want to Ensure Our Brothers and Sisters and All Our Children are as Valued, as Safe, as Protected, as Respected and as Nurtured as Everyone Else. This is Called Humanity and This Arises Out of This Intelligence, That is an Inalienable and Inseparable Part of the Biological Mechanism and Architecture of Life and Which Can Not and Does Not Exist Outside This Living-Life and That Mother Nature Has Endowed Each One of Us With, When We Arrive at Our Existence. Therefore, O Humanity Rise to Reject, Fight and Defeat This Attack of Ruthless Dehumanisation by These Concocted, Brewed and Miss-constructed Ideas Being Sought to Be Implanted in Our Heads and Minds. The Humanion uses Machine Processed Programming:MPP for Machine or Artificial Intelligence and Programmed Algorithmic Machination:PAM for Machine Learning, refusing the very concepts that machines can have intelligence and that they are, therefore, capable to learn. Likewise, The Humanion does not use the terms, self-driven or self-driving or autonomous vehicles for machines are not and can not be deemed to be having 'self', that absolutely applies to humans and autonomy applies to humans as individuals and as groups, societies, peoples, nations etc and can not be applied to machines. Therefore, Auto-driven is the term we use for Self-driven or Self-driving or autonomous vehicles etc. This relates to profound, vital and fundamental issues and we must be careful as to how we use terminology, that, albeit, inadvertently, dehumanises humanity.

At the General Medical Council GMC Conference 2016

 

 

 

 

 

 

 

 

 

Image: GMC

 

 

 

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 ||