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The Entire Spectrum of Colours and All the Forms, Manners and Expressions of Light are Made Invisible in This White: Or, Rather, Mix All the Colours and You Have This White: Or, Arrange All the Colours and Find an Infinite Rainbow: Or Take the Colours and Light Away and There Resides the Darkness But As Such That in Its Invisible Sphere There Still Remains Another Infinite Rainbow at Various States, That We Can Not See With Our Eyes: Take That All Away and You Have the Utter, Absolute and Primeval Duantum Darkness Within Which Our Matter Universe is Constructed and Does Function: Unless, We Remember This Every Nano-Second of Our Existence We Loose Our Sense and Joy of Eternal Wonder, Awe and Astonishment of This Magnificent Universe, Which is Outside, True, But Which is Nano-Seismically Constructed in the Human Physiology and Psychology: The Study of Medicine Will Always Remain and Fall Short Until It Sees and Learns That It is Dealing with the Universe, When It Goes About Learning and Healing This Human Physiology and Psychology: Alphansum Sovereign Necessarius: Munayem Mayenin


New Immune Pathway Involved in Resistance to Parasite Worms Found in Undercooked Pork




|| Monday: April 29: 2019: Lancaster University News || ά. Scientists from Lancaster University have discovered that immune responses, originally found to prevent fungal infections, are, also, important in eliminating Trichinella Spiralis, a round worm and the causative agent of Trichinosis. People acquire Trichinellosis by consuming raw or undercooked meat, infected with the Trichinella parasite, particularly, wild game meat or pork.

Consumption of contaminated meat contains ‘nurse cells’ of the parasite. Once in the stomach these ‘nurse cells’ hatch, releasing infective larvae, which, then, bury themselves within the lining of the small intestine. Previously, immune responses to expel the parasite have been shown to rely on white blood cells, called, T-helper two cells, specialised for eliminating gastro-intestinal parasites. However, scientists at Lancaster discovered that following this T-helper two response, a second T-helper 17 response, previously, shown to be specialised for eliminating fungal infections and certain bacterial infections occurred.

In collaboration with Professors Mark Travis and Richard Grencis from the University of Manchester, they were able to identify how these T-helper 17 cells arose and that they were key in maintaining the intestinal muscle contractions needed to flush out the worms.

The findings have been published in the journal PLOS Pathogens and show that mice, lacking the ability to activate a key signalling molecule, important in producing T-helper 17 cells have a reduced ability to expel the parasite. Interestingly, they saw a delayed transit time in the small intestine hinting at alterations in muscle contraction.

In isolating the small intestine they demonstrated that a key molecule, produced from T-helper 17 cells, termed IL-17, could increase intestinal contraction and restoring levels of this IL-17 in their mice rescued their ability to expel the parasite.

“We were quite surprised by what we found during this study. Normally, these immune responses are thought of as acting quite distinctly, depending on what type of infection you, may, have. It’s well established that the T-helper two response is beneficial during gastro-intestinal worm infections, so, traditionally, any other response would be thought of as hindering worm expulsion. So, it was quite surprising to see that this late acting T-helper 17 response was actually beneficial to the mouse’s ability to resolve an infection and get rid of the worm.’’ said Dr John Worthington from the Department of Biomedical and Life Science in the Faculty of Health and Medicine led the research.

“Our study provides novel insights into how the immune system interacts with muscle contraction during intestinal inflammation. Although, the occurrence of this infection is very rare in the developed world, we hope, it will help us to design new treatments for the many millions of people, who suffer from intestinal parasitic infections worldwide and, may, even, inform other intestinal diseases, involving altered muscle function.”::::ω.

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Antibody Therapy Training Phagocytes to Destroy Tumours Now Tested on Patients















|| February 25: 2019: University of Turku News || ά. Developed by researchers at the University of Turku, an immune-therapeutic antibody therapy re-educates macrophages to activate passivated cytotoxic T-cells to kill cancer. The antibody therapy prevented the growth of tumours in several mouse models. The development of the therapy has now progressed to patient testing in a phase I:II clinical trial. One reason behind many unsuccessful cancer treatments is the cancers’ ability to hijack the immune system to support its own growth.

This is assisted by the so-called tumour-associated macrophages, that can be educated by cancer cells to dampen anti-tumour immune responses. Macrophages are phagocytes, that form the first line of defence towards invading pathogens and they have a crucial role in maintaining tissue homeostasis. Macrophages have a large repertoire of functions in immune activation and resolving inflammation. In collaboration with Professor Sirpa Jalkanen, of Immunology, Dr Maija Hollmén’s research group investigated the possibility to utilise tumour-associated macrophages to increase the immunological detection and killing of cancer cells.

Professor Jalkanen has studied the function of Clever-1 for a long time. Previously, her group has observed that Clever-1 controls leukocyte trafficking between tissues. Published in the journal Clinical Cancer Research, the Study found that blocking Clever-1 function on macrophages activated the immune system and was highly effective in inhibiting cancer progression.

By inhibiting Clever-1 functions, tumour-associated macrophages, that, normally, impair adaptive immune cell activation, such as, cancer cell killing by cytotoxic T-cells, were managed to be re-educated so that they had increased ability to present antigen and secrete pro-inflammatory cytokines, leading to increased activation of killer T-cells.

‘’These results are highly promising and present a completely new way to activate anti-cancer immunity.’’ says Doctoral Candidate Miro Viitala, who is the main Author of the Paper.

‘’Macrophages are an ideal drug development target as they express several molecules, that can be activated or impaired to transfer the macrophages into cells, that destroy cancer. In itself, this would increase beneficial inflammation in the tumour micro-environment, which would improve the efficiency of immune checkpoint inhibitors in those patients, whose response is weak due to lack of tumour-specific T-cell activation.’’

The antibody therapy, targeting Clever-1 worked in the studied tumour mouse models as efficiently as the PD-1 antibody therapy, that is in clinical use. The PD-1 antibody maintains the functionality of the killer T-cells. It is notable that the Clever-1 antibody therapy, targeting macrophages, also, increased the activity of the killer T-cells efficiently.

In certain mouse models of cancer, a combination of anti-Clever-1 and anti-PD-1 therapies prevented tumour growth and formation of metastases more effectively than either treatment alone.

‘’Every cancer is different. Therefore, it is important to explore the types of cancer where Clever-1 antibody therapy most effectively works on and to find biomarkers, that can be used to identify beforehand the patients, that will benefit the most from this kind of therapy.’’ Viitala says.

The Paper: Immunotherapeutic Blockade of Macrophage Clever-1 Reactivates the CD8+ T Cell Response Against Immunosuppressive Tumors: Miro Viitala, Reetta Virtakoivu, Sina Tadayon, Jenna Rannikko, Sirpa Jalkanen, Maija Hollmén: Published in the journal Clinical Cancer Research:  February 12: 2019

More information: Maija Hollmén:::ω.

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New Clinical Trial for Osteo-Arthritis Drug Gets Funding




|| February 22: 2019: University of Liverpool News || ά. An innovative treatment for Osteo-arthritis, being trialled at the University of Liverpool, has been awarded a grant from Innovate UK, the leading government innovation agency. Osteoarthritis is the most common type of Arthritis in the UK, affecting more than eight million people and is the leading cause of joint pain and stiffness in older people. The University’s Clinical Trials Unit, in partnership with AKL Research and Development Ltd and the NHS, is leading a clinical trial to test a potential new drug treatment for Osteo-arthritis.

As part of their research and development programme, AKLRD identifies promising phytochemicals, found in natural products, which can be synthesised. Trials have identified two molecules, which act synergistically and have been brought together to create the ‘APPA’, a patented drug, which is an investigational medicine and not yet approved for use. In a variety of pre-clinical animal testing trials, APPA clearly demonstrated significant pain relief from Osteo-athritis, improved functionality and the slowing of cartilage destruction. These results led to the clinical trial being launched.

Innovate UK is part of UK Research and Innovation with a remit to drive the science and technology innovations, that will grow the UK economy. It has recognised APPA’s potential as a powerful treatment despite it only being at the Phase One trial stage, awarding AKLRD £675,000. This will contribute to the development of APPA in its Phase Two trial, which is expected to commence later this year, based on anticipated favourable results in the Phase One trial.

The trial, which is a partnership between the University of Liverpool, the pharmaceutical Industry and the NHS, is being led by Rheumatologist Professor Robert Moots from the University’s Institute of Ageing and Chronic Disease and is occurring in the Phase I unit at the Royal Liverpool University Hospital.

Professor Moots, said, “Millions of osteo-arthritis patients are suffering every day with severe pain because the current prescription drugs available are, often, not effective or can not be used long-term. “APPA has the potential to be an effective treatment for OA, that could not only tackle the pain it causes but, do so with excellent tolerability and, also, we hope, stop the disease from causing further joint damage. It’s incredibly exciting that Innovate UK has clearly recognised the potential of this new drug, which could transform the lives of OA patients.”

Mr David Miles, the Chief Executive Officer of AKLRD, said, “For APPA to be recognised as a disruptive innovation is incredibly exciting. The award from Innovate UK will allow us to secure the future development of what we believe could be an important medicine for OA patients, who currently have limited treatment options. We believe APPA not only tackles pain but will, also, put the brakes on the inflammatory cascade, that we know is responsible for the devastating consequences of OA.”

Mr Chris Sawyer, Innovation Lead, at Innovate UK, said, “This is an exciting area of research in a disease with high incidence and major debilitation in many sufferers. Supporting AKLRD to pursue the development of this important medicine is aligned perfectly with Innovate UK’s objective to support UK business growth in the health and life sciences sector.

AKLRD underwent a highly competitive process to be awarded the grant, with five independent expert assessors evaluating its submission. The assessors praised the ‘strong’ and ‘exciting proposal with large potential’ and described AKLRD’s work as an ‘exciting area of research in a disease with high incidence and major debilitation in many sufferers.”

Innovate UK is part of UK Research and Innovation with a remit to drive the science and technology innovations that will grow the UK economy. Since 2007 Innovate UK has committed more than £01.8 billion to innovation, helping 8,000 organisations with projects, estimated to add more than £16 billion to the UK economy and nearly 70,000 jobs. Innovate UK competitions provide grants between £25,000 and £10 million.

The forthcoming Phase II trial will be recruiting nationally in collaboration with Aintree University Hospital NHS Foundation Trust.:::ω.

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New Rapid Test for Sepsis Could Save Thousands of Lives




|| February 21: 2019: University of Strathclyde News || ά. Researchers at the University of Strathclyde have developed an innovative, low cost test for earlier diagnosis of Sepsis, which could save thousands of lives. The simple system for sensitive real-time measurement of the life threatening condition is much quicker than existing hospital tests, which can take up to 72 hours to process. Using a micro-electrode, a bio-sensor, this device is used to detect, if, one of the protein biomarkers of Sepsis, interleukin-6, is present in the bloodstream.

IL-6 is a molecule, secreted by the immune system and the levels of it in the blood increase in many of those, who have the condition. The results of the research project show that increased levels of the molecule can be detected by the test as quickly as two and a half minutes. The small size of the devices, micro-electrodes on a needle shaped substrates, makes them ideal for initial testing and, also, continuous monitoring for Sepsis, which is notoriously difficult to diagnose. Dr Damion Corrigan, from the department of Biomedical Engineering at Strathclyde, said, “The research shows that the tools we’ve developed could underpin a rapid test for Sepsis.

We’ve developed a needle shaped sensor with different electrodes and have shown we can detect one sepsis biomarker in almost real time, at the clinically relevant levels. When levels go up, as they do in Sepsis, we can detect that, too. Sepsis is quite complex and difficult to diagnose but IL-6 is one of the best markers.

Our research so far shows you can measure a single Sepsis marker but, there are, actually, eight sensors on the needle, each about the same diameter as a human hair and the idea is that in the future we can get multiple markers on the one microchip for a more comprehensive test.”

The device takes a pin prick of blood, which is, then, put on the chip for the result to be read. Its needle shape means it can, also, be implanted and used on patients in intensive care. The UK Sepsis Trust estimates that around 52,000 people in the UK die every year and six million globally from the condition, yet, with early diagnosis and the correct treatment, most people make a full recovery.

Sepsis develops, when the chemicals the immune system releases into the bloodstream to fight an infection instead cause inflammation throughout the entire body. Without quick treatment, it can lead to multiple organ failure and death. A delay of just one hour for giving the correct antibiotic can mean an increase in the likelihood of death.

It is, usually, diagnosed, based on simple measurements, such as, body temperature, heart rate and breathing rate, with patients, often, giving a blood test. There is a reliance on clinical judgement and hospital laboratory techniques to diagnose the condition, that can take up to 72 hours to provide a result. Researchers at the University of Leeds, Dr Chris Russell and Dr Paul Steenson, made the sensing element, using micro-fabrication, while the Strathclyde team did all the measurements and developed the test using the sensor.

Dr Corrigan said, “At the moment the 72-hour blood test is a very labour intensive process because the doctor orders the test on a computer with samples going to a central laboratory for processing and return of the result. The type of test we envisage could, for example, be at the bedside and involve doctors or nurses being able to monitor levels of Sepsis biomarkers for themselves. If, GP surgeries had access they could, also, do quick tests, which could, potentially, save lives. It could, also, be available in AandE departments so that anyone coming in with a question mark could be quickly ruled in or out.

With sepsis, the timing is key. For every hour that you delay the antibiotic treatment, the likelihood of death increases. I would hope the test could improve survival rates by ensuring people get treatment more quickly. It’s not just saving lives, a lot of people, who survive Sepsis, suffer life changing effects, including, limb loss, kidney failure and post-traumatic stress disorder. The test could stop a lot of suffering.”

The project’s Clinical Advisor and Co-author of the Paper, Consultant Anaesthetist Dr David Alcorn, who is based at Paisley’s Royal Alexandra Hospital, said that he believed the ‘extraordinary’ technology could have global implications. He said, “Dr Corrigan and his team have produced a tiny electrode capable of detecting Sepsis and, at the same time, diagnosing the type of infection and the recommended antibiotic, all in the space of minutes. “The implications for this are massive and the ability to give the right antibiotic at the right time to the right patient is extraordinary.

Finding the correct drug not only targets care for that patient but, will cut down on needless antibiotics and the reduced chance of antibiotic resistance. I can, definitely, see this having a clear use in hospitals, not only in this country but, all round the world.”

Dr Ron Daniels BEM, the CEO of the UK Sepsis Trust said that the earlier diagnosis and treatment across the UK would save at least 14,000 lives a year. He said, "Any kind of test, that enables us to identify Sepsis earlier, before symptoms, even, present themselves, could help save, even, more lives and bring us closer to our goal of ending preventable deaths from Sepsis.

Systems like this are so important as, with every hour before the right antibiotics is administered, risk of death increases. No test is perfect in the identification of Sepsis, so it’s crucial we continue to educate clinicians to think sepsis in order to prompt them to use such tests."

The project was funded by Tenovus Scotland and the Dowager Countess Eleanor Peel Trust. A Spokesman for the Trust said, “We are very encouraged by the success of the project and look forward to future developments arising from the work.” Professor Alan Foulis, the Chair of Tenovus Scotland Strathclyde, said, "Tenovus Scotland aims to support pilot scientific studies with real clinical potential, so this is an excellent example of the kind of research we like to fund.”

One family, who the test could have made a difference to was the Sutherlands. After Mr Sutherland developed a persistent sore throat in 2015 he visited his GP but, was sent home without treatment after it was ruled he was simply suffering from a virus. Just hours after a second visit that same week to an emergency doctor, father of two from Fishcross in Clackmannanshire, who has two young daughters Lacey, eight, and Isla, four, collapsed at home.

His wife Ms Melanie Sutherland called an ambulance and on arrival at hospital suffered two cardiac arrests. Mr Sutherland had Sepsis and as his body went into shock and his organs started to shut down, doctors warned his wife that he might not survive the night. After eight days in a coma, he woke up and went on to make an almost complete recovery. But the couple believe that had their GP had access to the simple test developed by Strathclyde researchers that Mr Sutherland might have been diagnosed long before his condition became life threatening.

Mr Sutherland said, “I started to feel unwell over the weekend with a sore throat. That Tuesday I went to the doctors, when it got worse but, they told me, it was a vital infection and sent me away. As the week went on, it got worse and by the Thursday it was really bad. My wife took me to the out of hours doctor that night and by this point I was really unwell and could barely move. But I was given an anti-sickness injection and, then, I was sent home.

No one mentioned Sepsis, although, looking back, I had all the symptoms. It’s hard to diagnose, so, if, this test had been around, it could have made all the difference to what happened with me.” Nursery Learning Assistant Ms Melanie Sutherland, 29, said, “I phoned an ambulance and when I told one of the paramedics that Ryan had had a sore throat, he mentioned Sepsis for the first time. I didn’t, even, know what it was. “Ryan was so unwell they had to stabilise him before they could move him. By the time I arrived at Forth Valley Royal Hospital twenty minutes behind the ambulance he was already in intensive care after suffering two cardiac arrests.

He had gone into Septic shock and his throat was so closed over they struggled to get the tube for him to breathe down it. His body was starting to shut down. It was terrifying. They told me he may not last the night.”

Mr Sutherland’s life hung in the balance but, after eight days he woke up. He had lost three stones in weight and was so weak he had to walk with a zimmer frame at first.

The Paper: Published: Science Direct

Caption: Image: University of Strathclyde:::ω.

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Diabetes: Human Cells Can Also Change Functions: New Research May Pave the Way for New Diabetes Treatment












|| February 18: 2019: University of Geneva News || ά. Researchers at the University of Geneva demonstrate the ease, in which, some human pancreatic cells can make insulin. In diabetes, this type of cell conversion could compensate for the loss or dysfunction of cells, that, naturally, produce this hormone. This would be a world first. Biology textbooks teach us that adult cell types remain fixed in the identity they have acquired upon differentiation. By inducing non-insulin-producing human pancreatic cells to modify their function to produce insulin in a sustainable way, researchers at the University of Geneva, show, for the first time, that the adaptive capacity of our cells is much greater than previously thought.

Moreover, this plasticity would not be exclusive to human pancreatic cells. The research has been published in the journal Nature. The human pancreas harbours several types of endocrine cells, i,e, α, β, δ, ε and ϒ, that produce different hormones, responsible for regulating blood sugar levels. These cells are bundled into small clusters, called, pancreatic islets or islets of Langerhans. Diabetes occurs when, in the absence of functional β cells, blood sugar levels are no longer controlled. At the the University’s Faculty of Medicine, Professor Pedro Herrera and his team had, already, demonstrated, in mice, that the pancreas has the ability to regenerate new insulin cells through a spontaneous mechanism of identity change of other pancreatic cells.

But what about the human being? Moreover, is it possible to artificially promote this conversion? To explore whether human cells have this ability to adapt, Geneva scientists used islets of Langerhans from both Diabetic and non-diabetic donors. They first sorted the different cell types to study two of them in particular: α cells, glucagon producers and ϒ cells, pancreatic polypeptide cells.

“We divided our cells into two groups: one, where we introduced only a fluorescent cell tracer and the other, where, in addition, we added genes, that produce insulin transcription factors specific to β cells.” says Professor Pedro Herrera. The researchers, then, reconstructed ‘pseudo-islets’, with only one cell type at a time to, accurately, study their behaviour.

“First observation: the simple fact of aggregating cells, even, into monotypic pseudo-islets, stimulates the expression of certain genes, linked to insulin production, as, if, the ‘non-β’ cells, naturally, detected the absence of their ‘sisters’. However, in order for the cells to start producing insulin, we had to, artificially, stimulate the expression of one or two key β cell genes.” says Mr Kenichiro Furuyama, a Researcher in the Department of Genetic Medicine at the Faculty of Medicine of the University and the First Author of this work.

One week after the experiment began, 30% of the α cells were producing and secreting insulin in response to glucose. ϒ-Cells, under the same treatment, were, even, more effective and numerous in converting and secreting insulin in response to glucose.

In the second step, the researchers transplanted these monotypic pseudo-islets of modified human α cells into Diabetic mice. “Human cells proved to be very effective. The mice recovered!” says Professor Pedro Herrera. “And as expected, when these human cell transplants were removed the mice became Diabetic again.

We obtained the same results with cells from both Diabetic and non-diabetic donors, showing that this plasticity is not damaged by the disease. In addition, this works in the long term: six months after transplantation, the modified pseudo-islets continued to secrete human insulin in response to high glucose.”

A detailed analysis of these human glucagon cells, that have become insulin producers shows that they retain a cell identity close to that of α cells. Auto-immune Diabetes or Type One Diabetes, is characterised by the destruction of β cells by the immune system of patients.

The researchers, then, wondered whether these modified α cells would, also, be targeted by auto-immunity, since, they remain different from β-cells. To test their resistance, they co-cultured them with T cells from patients with Type One Diabetes. “We found that modified α cells triggered a weaker immune response and, therefore, might be, less likely to be destroyed than native β cells.”

Today, pancreas transplantation is performed in cases of extremely severe Diabetes, by transplanting either the entire pancreas or, preferably, only, pancreatic islets, a much less invasive approach. This technique is very effective but, has its limits: like any transplant, it goes hand in hand with immune-suppressive treatment.

Despite this, the transplanted cells disappear after a few years. “The idea of using the intrinsic regenerative capacities of the human body makes sense here.” Professor Pedro Herrera emphasises. However, many hurdles remain before a treatment resulting from our discovery can be proposed. We, must, indeed, find a way, pharmacological or by gene therapy, to stimulate this change of identity in the cells concerned within the patient’s own pancreas but, without causing adverse effects on other cell types.”

This work was funded by the National Institute of Diabetes and Digestive and Kidney Diseases, part of the US National Institutes of Health, a bonus of excellence of the Swiss National Science Foundation and the Fondation privée des HUG among others.

Caption: Pseudo-islet made up of human alpha cells. These cells produce glucagon:blue but can ‘learn’ to make insulin:red. The GFP protein:green allows tracing the origin of the cells, thus, certifying their change of identity: Image: Pedro Herrera: University of Geneva.:::ω.

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Autism Spectrum Disorder: New Study Shows How Exposure to Air Pollution Early in Life May Lead to Autism



|| February 17: 2019: University of Washington News || ά. Exposure to air pollution, particularly, traffic-related air pollution, has, previously, been linked to Autism Spectrum Disorder in epidemiological studies. And, now, a new animal Study from the University of Washington School of Public Health describes a possible mechanism, by which, this relationship, might, occur. The Study was published in the journal Brain, Behaviour and Immunity.

In an earlier Study, researchers from the School found that mice exposed to very unhealthy levels of diesel exhaust or particulate matter, during pregnancy and early in development, displayed behavioural alterations, typical of Autism Spectrum Disorder. That is, an increase in repetitive behaviour, disrupted communication and deficits in social interactions. Similar hazardous air quality levels have, recently, been experienced in Seattle during the summer months as wildfires raged through the region.

Ms Yu-Chi Rachel Chang, an alumna of the School’s Department of Environmental and Occupational Health Sciences, conducted this Study as part of her doctoral dissertation in toxicology. The current Paper describes experiments on mice, that show developmental exposure to diesel exhaust could cause subtle changes in the structure of the cerebral cortex, the outer layer of neural tissue of the cerebrum of the brain, as seen in the brains of autistic patients. Researchers, also, propose a series of bio-chemical and molecular changes, that, may, underlie such cortical alterations.

“These studies provide an animal model, that will allow further investigations on the biological plausibility for an association between air pollution and Autism Spectrum Disorder.” said Professor Lucio Costa, a Senior Author of the new Study and of Environmental and Occupational Health Sciences at the UW School of Public Health.

“From a public health point of view, it adds to the concerns of air pollution as a possible etiological factor for developmental and neuro-degenerative disorders.” The proposed mechanism begins with increased neuro-inflammation and leads to decreased expression of the protein reelin, which activates a signalling pathway required for proper positioning of neurons in the brain, both events are common with Autism.

The mechanism, also, includes activation of the JAK2:STAT3 pathway, which plays a role in foetal brain development. Future studies are needed to better understand how gene-environment interaction impacts Autism Spectrum Disorder and to improve protection for vulnerable populations, according to Study Authors.

The Senior Author of the Paper is Mr Toby Cole is a Research Scientist in the Department of Environmental and Occupational Health Sciences at the UW School of Public Health and Manager of the Rodent Behavioural Laboratory in the UW Centre on Human Development and Disabilities. Co-authors of the Paper are Mr Ray Daza, former Lab Manager for the Centre for Integrative Brain Research at Seattle Children’s Research Institute and Professor Robert Hevner, of Neurological Surgery at the UW School of Medicine. Both are now at the University of California, San Diego.:::ω. 

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Medical Oncology: The Targeted Anti-cancer Therapies International Congress 2019 in Paris: February 25-27



|| February 17: 2019 || ά. The European Society for Medical Oncology:ESMO, the leading professional organisation for Medical Oncology, is holding its Targeted Anti-cancer Therapies International Congress 2019, the premier forum for discussion of early phase drug development and translational research. The Congress, to be held on February 25-27 in Paris, will bring together around 400 attendees from all over the world.

The Congress is aimed at all basic scientists, physicians and translational researchers from academic settings, industry and regulatory agencies for the common aim of speeding up the development of new anti-cancer treatment for the benefit of cancer patients. The Congress programme, designed by a faculty of international renown experts, will provide a glimpse into the future of cancer care, major updates and innovation in the field of cancer treatment, using new targeted agents and immune-therapy will be presented along with new points to consider, including, the role of liquid biopsies as alternative to conventional tissue biopsies.

The issue of combination in the use of immune-therapeutic medicines will be largely discussed, as well as, new immuno-oncology methodological approaches, the inclusion of children and adolescents in early phase trials and the dynamic change in the distribution of cancer types in those trials.

In addition to the usual congress sessions, dedicated workshops and meet the expert sessions are planned to allow interactivity among participants.

During the opening session, Dr Geoffrey Shapiro will be presented the Congress 2019 Honorary Award for his leadership in developmental therapeutics, particularly, in solid tumours. Dr Shapiro will deliver a keynote lecture, ‘Development of Cyclin-Dependent Kinase Inhibitors: A brief history and future directions’.

About the International Congress on Targeted Anticancer Therapies: The Congress is a peculiar ESMO event, focusing on early phase drug development and translational research. The Congress series has been at the forefront of revolutionary transformation in early drug development and has succeeded in broadening the conversation on phase I trials to include a wide circle of stakeholders.

About the European Society for Medical Oncology:ESMO: ESMO is the leading professional organisation for medical oncology. With more than 20,000 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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