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Scientists Develop Blood Test That Spots Tumor-Derived DNA in People With Early-Stage Cancers 

Scientists Develop Blood Test That Spots Tumor-Derived DNA in People With Early-Stage Cancers  | Amazing Science | Scoop.it

In a bid to detect cancers early and in a noninvasive way, scientists at the Johns Hopkins Kimmel Cancer Center report they have developed a test that spots tiny amounts of cancer-specific DNA in blood and have used it to accurately identify more than half of 138 people with relatively early-stage colorectal, breast, lung and ovarian cancers. The test, the scientists say, is novel in that it can distinguish between DNA shed from tumors and other altered DNA that can be mistaken for cancer biomarkers.


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A Speedier Way to Catalog Human Cells (All 37 Trillion of Them)

A Speedier Way to Catalog Human Cells (All 37 Trillion of Them) | Amazing Science | Scoop.it

Many types of cells remain unknown, but researchers have discovered a faster way to group cells by function, paving the way for a complete census.

 

There are some questions in biology that you’d think were settled long ago. For instance: How many types of cells are there in the human body? “If you just Google this, the number everyone uses is 200,” said Jay Shendure, a geneticist at the University of Washington. “But to me that seems absurdly low.” A number of scientists like him want to build a more complete catalog.

 

Yet there are an estimated 37 trillion cells in the human body. The traditional ways to identify cell types — such as carefully tracing the shape of individual cells under a microscope — are too slow and crude for the job.

 

Dr. Shendure and his colleagues recently published a report describing a speedy new method for taking such a cell census. Instead of inspecting one cell at a time, they measured the activity of genes inside 42,035 cells at once. Although still at an experimental stage, the method may become an essential tool for cataloging every cell type in the human body, experts said.


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Scientists reveal source of human heartbeat in 3D

Scientists reveal source of human heartbeat in 3D | Amazing Science | Scoop.it

A pioneering new study is set to help surgeons repair hearts without damaging precious tissue.

 

A team of scientists from Liverpool John Moores University (LJMU), The University of Manchester, Aarhus University and Newcastle University, have developed a way of producing 3D data to show the cardiac conduction system -- the special cells that enable our hearts to beat -- in unprecedented detail. The findings were published in Scientific Reports.

 

The new data in this study gives them a much more accurate framework than previously available for computer models of the heartbeat and should improve our ability to make sense of troublesome heart rhythms like atrial fibrillation that affects 1.4 million people in the UK. The data reveals exactly where the cardiac conduction system is in a normal heart. For example, it shows just how close it runs to the aortic valve.

 

Professor Jonathan Jarvis who is based at the LJMU School of Sport and Exercise Sciences explained: "The 3D data makes it much easier to understand the complex relationships between the cardiac conduction system and the rest of the heart. We also use the data to make 3D printed models that are really useful in our discussions with heart doctors, other researchers and patients with heart problems.

 

"New strategies to repair or replace the aortic valve must therefore make sure that they do not damage or compress this precious tissue. In future work we will be able to see where the cardiac conduction system runs in hearts that have not formed properly. This will help the surgeons who repair such hearts to design operations that have the least risk of damaging the cardiac conduction system."

 

Co-author Dr Halina Dobrzynski, who is based in The University of Manchester's Cardiovascular Division, has been working on the anatomy of the cardiac conduction system for 20 years. She says: "This is just the beginning. The British Heart Foundation is supporting my group to visualize this system in 3D from aged and failing hearts. With my research assistant Andrew Atkinson and working with Professor Jonathan Jarvis, Robert Stephenson and others, we will produce families of data from aged and failing hearts in 3D."

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Untreatable gonorrhoea on the rise worldwide

Untreatable gonorrhoea on the rise worldwide | Amazing Science | Scoop.it

Gonorrhoea is becoming as incurable as it was in the 1920s, before the first drugs to treat it were discovered. More than 60% of countries surveyed around the world have reported cases that resist last-resort antibiotics, according to an announcement by the World Health Organization (WHO) on 6 July, 2017. The announcement included information about a new gonorrhoea drug in development.

 

Since the 1930s, several classes of antibiotics have been used to kill the bacterium that causes gonorrhoea, Neisseria gonorrhoeae. Widespread use — and misuse — of these drugs, however, has led to a rise of antibiotic-resistant strains of the bacteria. “The best time to have had gonorrhoea was the eighties, since there were many drugs to treat it with,” says Ramanan Laxminarayan, director of the Center for Disease Dynamics, Economics and Policy in Washington DC. Increasingly, that's no longer the case, he says.

 

Health agencies in the United States, Europe and Canada have in recent years flagged drug-resistant gonorrhoea as an emerging threat. If left untreated, gonorrhoea can increase a woman’s risk of developing HIV infection, infertility or ectopic pregnancy — among other effects. When the WHO partnered with the Drugs for Neglected Diseases initiative (DNDi), a non-governmental organization in Geneva, Switzerland, in May 2016 to confront antimicrobial resistance, gonorrhoea was at the top of the list.

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Researchers Identify Liver Fibrosis-Causing Protein

Researchers Identify Liver Fibrosis-Causing Protein | Amazing Science | Scoop.it

An international team of scientists has identified a long-sought protein that causes liver fibrosis (scarring), paving the way for new treatments. The research was published in the journal Nature Genetics.

 

The team led by Professor Jacob George and Dr. Mohammed Eslam of the Westmead Institute for Medical Research in Sydney, Australia, has unequivocally shown that variations in the interferon lambda 3 (INLF3) protein are responsible for tissue damage in the liver.

 

The researchers had previously identified that the common genetic variations associated with liver fibrosis were located on chromosome 19 between the IFNL3 and IFNL4 genes.

 

In the new study, they analyzed liver samples from 2,000 patients with hepatitis C, using state-of-the art genetic and functional analysis, to determine the specific IFNL protein responsible for liver fibrosis. They demonstrated that following injury there is increased migration of inflammatory cells from blood to the liver, increasing IFNL3 secretion and liver damage.

 

Notably, this response is determined to a great extent by an individual’s inherited genetic makeup. “This was a significant outcome that will help to predict risk of liver disease for individuals, enabling early intervention and lifestyle changes,” said Prof. George, who is the corresponding author of the study.

 

“We have designed a diagnostic tool based on our discoveries, which is freely available for all doctors to use, to aid in predicting liver fibrosis risk. This test will help to determine whether an individual is at high risk of developing liver fibrosis, or whether a patient’s liver disease will progress rapidly or slowly, based on their genetic makeup. This important discovery will play a vital role in reducing the burden of liver disease into the future,” he said. “This discovery holds great promise for the development of effective therapeutic treatments for liver disease,” added co-lead author Dr. Eslam.

 

“There is an urgent need for a safe pharmacologic therapy that can prevent of regress the progression of liver damage. There are currently no treatments available for patients with advanced fibrosis, and liver transplantation is the only treatment for liver failure,” he said. “Now that we’ve identified IFNL3 as the cause of liver scarring, we can work towards developing novel treatments specifically targeting this gene. This could be medicine targeting IFNL3 that is tailored to an individual’s genetic makeup, but could also include modifying usual treatment depending on whether a patient has IFNL3 risk genes.”

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Mice Provide Insight Into Genetics of Autism Spectrum Disorders

Mice Provide Insight Into Genetics of Autism Spectrum Disorders | Amazing Science | Scoop.it

While the definitive causes remain unclear, several genetic and environmental factors increase the likelihood of autism spectrum disorder, or ASD, a group of conditions covering a “spectrum” of symptoms, skills and levels of disability.

 

Taking advantage of advances in genetic technologies, researchers led by Alex Nord, assistant professor of neurobiology, physiology and behavior with the Center for Neuroscience at the University of California, Davis, are gaining a better understanding of the role played by a specific gene involved in autism. The collaborative work appears June 26 in the journalNature Neuroscience.

 

“For years, the targets of drug discovery and treatment have been based on an unknown black box of what’s happening in the brain,” said Nord. “Now, using genetic approaches to study the impact of specific mutations found in cases, we’re trying to build a cohesive model that links genetic control of brain development with behavior and brain function.”

 

The Nord laboratory studies how the genome encodes brain development and function, with a particular interest in understanding the genetic basis of neurological disorders.

 

There is no known specific genetic cause for most cases of autism, but many different genes have been linked to the disorder. In rare, specific cases of people with ASD, one copy of a gene called CHD8 is mutated and loses function. The CHD8 gene encodes a protein responsible for packaging DNA in cells throughout the body. Packaging of DNA controls how genes are turned on and off in cells during development. 

 

Because mice and humans share on average 85 percent of similarly coded genes, mice can be used as a model to study how genetic mutations impact brain development. Changes in mouse DNA mimic changes in human DNA and vice-versa. In addition, mice exhibit behaviors that can be used as models for exploring human behavior.


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Thousands of mouse genes could help decipher human disease providing important disease models

Thousands of mouse genes could help decipher human disease providing important disease models | Amazing Science | Scoop.it

Thousands of mouse genes (around 15% of the mouse genome) are now available from the IMPC - an important milestone for genotype-to-phenotype research.

 

Researchers at the European Bioinformatics Institute (EMBL-EBI) and their collaborators in the International Mouse Phenotyping Consortium (IMPC) have fully characterised thousands of mouse genes for the first time. Published in Nature Genetics, the results offer hundreds of new disease models and reveal previously unknown gene functions. The 3328 genes described in this publication by the IMPC represent approximately 15% of the mouse genome.


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The Top 10 Trends Shaping the Future of Pharma

The Top 10 Trends Shaping the Future of Pharma | Amazing Science | Scoop.it

The medical community gradually acknowledges the importance of digital health, but they don’t yet embrace it enough or cannot get behind it with such a speed as it would require. For doing so, the first step is always getting to know what’s coming. So, here are the trends changing the pharmaceutical industry in the near future.


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Scientists identify single-gene mutations (CARD11) that lead to atopic dermatitis

Scientists identify single-gene mutations (CARD11) that lead to atopic dermatitis | Amazing Science | Scoop.it

Researchers have identified mutations in a gene called CARD11 that lead toatopic dermatitis, or eczema, an allergic skin disease. Scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and other institutions discovered the mutations in four unrelated families with severe atopic dermatitis and studied the resulting cell-signaling defects that contribute to allergic disease. Their findings, reported in Nature Genetics, also suggest that some of these defects potentially could be corrected by supplementation with the amino acid glutamine.

 

The scientists analyzed the genetic sequences of patients with severe atopic dermatitis and identified eight individuals from four families with mutations in the CARD11 gene, which provides instructions for production of a cell-signaling protein of the same name. While some people with these mutations had other health issues, such as infections, others did not, implying that mutations in CARD11 could cause atopic dermatitis without leading to other medical issues often found in severe immune system syndromes.

The scientists next set out to understand how the newly discovered CARD11 mutations contribute to atopic dermatitis.

 

Each of the four families had a distinct mutation that affected a different region of the CARD11 protein, but all the mutations had similar effects on T-cell signaling. With cell culture and other laboratory experiments, the researchers determined that the mutations led to defective activation of two cell-signaling pathways, one of which typically is activated in part by glutamine.  

 

Growing cultured T cells from patients with CARD11 mutations with excess glutamine boosted mTORC1 activation, a key part of one of the affected pathways, suggesting the potential to partially correct the cell-signaling defects that may contribute to atopic dermatitis. The scientists now are planning a study to assess the effect of supplemental glutamine and leucine, another amino acid that activates mTORC1, in people with atopic dermatitis with and without CARD11 mutations.

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How DNA-encoded libraries are revolutionizing drug discovery

How DNA-encoded libraries are revolutionizing drug discovery | Amazing Science | Scoop.it

With the bar-coding technology, drugmakers leverage the chemistry of large numbers.  Forty trillion is the kind of number that gives one pause. Consider it written out with its 13 zeros: 40,000,000,000,000.

 

Assembling and maintaining a collection of 40 trillion of anything seems like a mind-bogglingly massive task. But in February the Danish biopharmaceutical company Nuevolution announced that it had created a library of 40 trillion unique molecules—quite possibly the largest collection of synthetic compounds in the world.

 

You might think it would require every building in Copenhagen to store batches of 40 trillion different compounds. Not so, says Alex Haahr Gouliaev, Nuevolution’s chief executive officer. “All of that fits into an Eppendorf tube and is handled by one person for screening,” he says.

 

The substance that makes it possible to maintain this multitudinous mixture of molecules is the same substance that contains the code of life—DNA.

 

Nuevolution covalently attaches a short, unique strand of DNA to each of its 40 trillion compounds. Instead of holding the directions for life, though, these DNA strands encode the recipe used to synthesize each linked molecule. This trick enables the firm to store all the compounds as a mixture in a small volume and later sequence, or read, them out. As the cost for DNA sequencing plummets and the repertoire of DNA-compatible chemical reactions grows, these so-called DNA-encoded libraries are becoming a go-to resource for finding new drug candidates and research tools for large pharmaceutical companies, small biotech companies, and academics alike.


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Pharmacological characterisation of the highly NaV1.7 selective spider venom peptide Pn3a

Pharmacological characterisation of the highly NaV1.7 selective spider venom peptide Pn3a | Amazing Science | Scoop.it
Human genetic studies have implicated the voltage-gated sodium channel NaV1.7 as a therapeutic target for the treatment of pain.

 

As the Nav1.7 channel appears to be a highly important component in nociception, with null activity conferring total analgesia,[14] there has been immense interest in developing selective Nav1.7 channel blockers as potential novel analgesics.[27] Nav1.7 is a sodium ion channel that in humans is encoded by the SCN9A gene.[3][4][5] Since Nav1.7 is not present in heart tissue or the central nervous system, selective blockers of Nav1.7, unlike non-selective blockers such as local anesthetics, could be safely used systemically for pain relief. Moreover, selective Nav1.7 blockers may prove to be far more effective analgesics, and with fewer undesirable effects, relative to current pharmacotherapies.[27][28][29]

 

A number of selective Nav1.7 (and/or Nav1.8) blockers are in clinical development, including funapide (formerly TV-45070, XEN402), raxatrigine (formerly CNV1014802, GSK-1014802), PF-05089771, PF-04531083, DSP-2230, AZD-3161, NKTR-171, GDC-0276, and RG7893(formerly GDC-0287).[30][31][32] Ralfinamide (formerly NW-1029, FCE-26742A, PNU-0154339E) is a multimodal, non-selective Nav channel blocker which is under development for the treatment of pain.[33]

 

Spiders are the most successful venomous animals with an estimated 100,000 extant species [1]. The vast majority of spiders employ a lethal cocktail to rapidly subdue their prey, which are often many times their own size. However, despite their fearsome reputation, less than a handful of these insect assassins are harmful to humans [2,3]. Nevertheless, it is this small group of medically important species that first prompted scientists more than half a century ago to begin exploring the remarkable pharmacological diversity of spider venoms.

 

Amongst the ranks of animals that employ venom for their survival, spiders are the most successful, the most geographically widespread, and arguably consume the most diverse range of prey. Although the predominant items on a spider’s dinner menu are other arthropods, larger species will readily kill and feed on small fish, reptiles, amphibians, birds, and mammals. Thus, spider venoms contain a wealth of toxins that target a diverse range of receptors, channels, and enzymes in a wide range of vertebrate and invertebrate species.

 

Spider venoms are complex cocktails composed of a variety of compounds, including salts, small organic molecules, peptides, and proteins [4,5,6,7,8,9]. However, peptides are the primary components of spider venoms, and some species produce venom containing >1000 unique peptides of mass 2–8 kDa [10]. Based on the number of described spider species and a relatively conservative estimate of the complexity of their venom it has been estimated that the potential number of unique spider venom peptides could be upwards of 12 million [11]. In recent years there has been an exponential increase in the number of spider-toxin sequences being reported [12] due to the application of high-throughput proteomic [13,14] and transcriptomic [15,16,17] approaches, or a combination of these methods [10,18,19]. In the last 18 months alone the number of toxins in the ArachnoServer spider-toxin database [20,21] has more than doubled, and is now excess of 900 (see http://www.arachnoserver.org/). Nevertheless, our knowledge of the diversity of spider-venom peptides is still rudimentary, with less than 0.01% of potential peptides having been isolated and studied.

 

Although only a small number of spider venom peptides have been pharmacologically characterized, the array of known biological activities is impressive [9]. In addition to the well known neurotoxic effects of spider venoms, they contain peptides with antiarrhythmic, antimicrobial, analgesic, antiparasitic, cytolytic, haemolytic, and enzyme inhibitory activity. Furthermore, the crude venom of Macrothele raveni has antitumor activity, for which the responsible component has not yet been identified [22,23]. Finally, larger toxins such as the latrotoxins from the infamous black widow spider (Latrodectus mactans) and related species induce neurotransmitter release and they have played an important role in dissecting the process of synaptic vesicle exocytosis [24].

 

Since spiders employ their venom primarily to paralyse prey, it is no surprise that these venoms contain an abundance of peptides that modulate the activity of neuronal ion channels and receptors. Indeed, the majority of characterized spider-venom peptides target voltage-gated potassium (KV) [25], calcium (CaV) [26,27], or sodium (NaV) [26,28] channels. More recently, novel spider-venom peptides have been found that interact with ligand-gated channels (e.g., purinergic receptors [29]) and recently discovered families of channels such as acid sensing ion channels [30], mechanosensitive channels [31], and transient receptor potential channels [32]. Not only do most of these peptides have selectivity for a given class of ion channel, they can have anything from mild preference to exquisite selectivity for a given channel subtype. This potential for high target affinity and selectivity makes spider-venom peptides an ideal natural source for the discovery of novel therapeutic leads [33].

 

Despite the advent of automation and the rise of high-throughput and high-content screening in the pharmaceutical industry there has been a sharp decline in the rate of discovery and development of novel chemical entities [34,35]. A group of scientists reviewed the emerging role that venom-derived components can play in addressing this decline with an emphasis on technical advances that can aid the discovery process [36]. It is worth noting that two of the 20 FDA-approved peptide pharmaceuticals were derived from animal venoms (i.e., ziconitide and exendin-4) [37].

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Diabetes breakthrough increases insulin producing cells and could lead to a cure

Diabetes breakthrough increases insulin producing cells and could lead to a cure | Amazing Science | Scoop.it

A potential cure for Type 1 diabetes looms on the horizon in San Antonio, and the novel approach would also allow Type 2 diabetics to stop insulin shots.

 

The discovery, made at UT Health San Antonio, increases the types of pancreatic cells that secrete insulin. UT Health San Antonio researchers have a goal to reach human clinical trials in three years, but to do so they must first test the strategy in large-animal studies, which will cost an estimated $5 million.

 

Those studies will precede application to the U.S. Food and Drug Administration for Investigational New Drug (IND) approval, Bruno Doiron, Ph.D., a co-inventor, said. The scientists received a U.S. patent in January, and UT Health San Antonio is spinning out a company to begin commercialization. The strategy has cured diabetes in mice.

 

“It worked perfectly,” Dr. Doiron, assistant professor of medicine at UT Health, said. “We cured mice for one year without any side effects. That’s never been seen. But it’s a mouse model, so caution is needed. We want to bring this to large animals that are closer to humans in physiology of the endocrine system.”

 

Ralph DeFronzo, M.D., professor of medicine and chief of the Division of Diabetes at UT Health, is co-inventor on the patent. He described the therapy: “The pancreas has many other cell types besides beta cells, and our approach is to alter these cells so that they start to secrete insulin, but only in response to glucose [sugar],” he said. “This is basically just like beta cells.”

 

Insulin, which lowers blood sugar, is only made by beta cells. In Type 1 diabetes, beta cells are destroyed by the immune system and the person has no insulin. In Type 2 diabetes, beta cells fail and insulin decreases. At the same time in Type 2, the body doesn’t use insulin efficiently. The therapy is accomplished by a technique called gene transfer. A virus is used as a vector, or carrier, to introduce selected genes into the pancreas. These genes become incorporated and cause digestive enzymes and other cell types to make insulin.

 

Gene transfer using a viral vector has been approved nearly 50 times by the U.S. Food & Drug Administration to treat various diseases, Dr. DeFronzo said. It is proven in treating rare childhood diseases, and Good Manufacturing Processes ensure safety. Unlike beta cells, which the body rejects in Type 1 diabetes, the other cell populations of the pancreas co-exist with the body’s immune defenses. “If a Type 1 diabetic has been living with these cells for 30, 40 or 50 years, and all we’re getting them to do is secrete insulin, we expect there to be no adverse immune response,” Dr. DeFronzo said.

 

The therapy precisely regulates blood sugar in mice. This could be a major advance over traditional insulin therapy and some diabetes medications that drop blood sugar too low if not closely monitored. “A major problem we have in the field of Type 1 diabetes is hypoglycemia (low blood sugar),” Dr. Doiron said. “The gene transfer we propose is remarkable because the altered cells match the characteristics of beta cells. Insulin is only released in response to glucose.”

 

People don’t have symptoms of diabetes until they have lost at least 80 percent of their beta cells, Dr. Doiron said. “We don’t need to replicate all of the insulin-making function of beta cells,” he said. “Only 20 percent restoration of this capacity is sufficient for a cure of Type 1.”

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Aspirin May Prevent Cancer from Spreading, New Research Shows

Aspirin May Prevent Cancer from Spreading, New Research Shows | Amazing Science | Scoop.it

If ever there was a wonder drug, aspirin might be it. Originally derived from the leaves of the willow tree, this mainstay of the family medicine cabinet has been used successfully for generations to treat conditions ranging from arthritis to fever, as well as to prevent strokes, heart attacks and even some types of cancer, among other ills. Indeed, the drug is so popular that annual consumption worldwide totals about 120 billion tablets.


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A new “atlas” of cancer genes could help personalize therapies for patients

A new “atlas” of cancer genes could help personalize therapies for patients | Amazing Science | Scoop.it

Researchers use a big-data approach to find links between different genes and patient survival.

 

Understanding the genetic changes in tumors that distinguish the most lethal cancers from more benign ones could help doctors better treat patients. Recently, Swedish researchers launched a new open-access catalog that maps many of those genetic changes. This “atlas” links thousands of specific genes involved in numerous cancers to patient survival and also reveals potential new drug targets.

 

The new atlas is one of several ongoing efforts to make sense of data that’s been collected by public databases—like the National Cancer Institute’s Cancer Genome Atlas—that act as repositories for tumor samples. The goal is to glean practical information, like markers of disease, that can be used to develop cancer drugs and diagnostics.

 

To generate the atlas, researchers led by Mathias Uhlén, a professor of microbiology at the Royal Institute of Technology in Sweden, used a supercomputer to analyze 17 major types of human cancers from nearly 8,000 tumor samples. Uhlén says his team was looking for “holistic changes across the genome caused by these mutations.”

 

They then mapped all the genes found in those cancer cells to find out how proteins made by these genes affect patient survival. Genes carry instructions for making proteins, and the level of gene expression increases or decreases the amount of protein that genes make. These resulting proteins can dramatically influence biological processes like cancer.


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Mummy Has Oldest Case of Prostate Cancer in Ancient Egypt

Mummy Has Oldest Case of Prostate Cancer in Ancient Egypt | Amazing Science | Scoop.it

Study suggests disease was more prevalent than previously believed.

 

 Some 2,250 years ago in Egypt, a man known today only as M1 struggled with a long, painful, progressive illness. A dull pain throbbed in his lower back, then spread to other parts of his body, making most movements a misery. When M1 finally succumbed to the mysterious ailment between the ages of 51 and 60, his family paid for him to be mummified so that he could be reborn and relish the pleasures of the afterworld.

 

A few years ago, an international research team has diagnozed what ailed M1: The oldest known case of prostate cancer in ancient Egypt and the second oldest case in the world. The earliest diagnosis of prostate cancer came from the 2700-year-old skeleton of a Scythian king in Russia. Moreover, this study published in the International Journal of Paleopathology, suggests that earlier investigators may have underestimated the prevalence of cancer in ancient populations because high-resolution computerized tomography (CT) scanners capable of finding tumors measuring just 1 to 2 millimeters in diameter only became available in 2005. "I think earlier researchers probably missed a lot without this technology," says team leader Carlos Prates, a radiologist in private practice at Imagens Médicas Integradas in Lisbon.

 

Prostate cancer begins in the walnut-sized prostate gland, an integral part of the male reproductive system. The gland produces a milky fluid that is part of semen and it sits underneath a man's bladder. In aggressive cases of the disease, prostate cancer cells can metastasize, or spread, entering the bloodstream and invading the bones. After performing high-resolution scans on three Egyptian mummies in the collection of the National Archaeological Museum in Lisbon, Prates and colleagues detected many small, round, dense tumors in M1's pelvis and lumbar spine, as well as in his upper arm and leg bones. These are the areas most commonly affected by metastatic prostate cancer. "We could not find any evidence to challenge this diagnosis," Prates says.

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Seeing more with PET scans: New chemistry for medical imaging

Seeing more with PET scans: New chemistry for medical imaging | Amazing Science | Scoop.it
Researchers have found a surprisingly versatile workaround to create chemical compounds that could prove useful for medical imaging and drug development.

 

The chemical mechanism, discovered by scientists at the Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab) and UC Berkeley, could also broaden our understanding of basic chemical reaction processes involving common helpers, called catalysts, like copper and gold.

 

While studying chemical reactions of a gold-containing molecule, the research team happened upon a chemical mechanism that can be used to form trifluoromethyl (CF3) compounds and attach them to other chemical compounds. Their discovery could aid in the synthesis of new "radiotracers" - chemical compounds that contain a radioactive form, or isotope, of an element - for use with a noninvasive, high-resolution 3-D medical imaging technology known as PET (positron emission tomography) scanning.

 

Drug companies have shown an increasing interest in incorporating CF3 compounds - which contain carbon and fluorine - in a range of pharmaceuticals. These compounds can make drugs more selective, effective, or potent. The antidepressant Prozac, HIV drug Sustiva, and anti-inflammatory Celebrex are among the examples of drugs containing CF3 compounds.

 

So in testing the biological uptake of drugs that incorporate CF3 compounds, it's useful to incorporate fluorine-18 (18F), a radioactive isotope of fluorine in the CF3 compound as a sort of label or "tracer" that can be detected by PET scanners.


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New microscope can scan tumors during surgery and examine cancer biopsies in 3-D

New microscope can scan tumors during surgery and examine cancer biopsies in 3-D | Amazing Science | Scoop.it

When women undergo lumpectomies to remove breast cancer, doctors try to remove all the cancerous tissue while conserving as much of the healthy breast tissue as possible. But currently there’s no reliable way to determine during surgery whether the excised tissue is completely cancer-free at its margins — the proof that doctors need to be confident that they removed all of the tumor. It can take several days for pathologists using conventional methods to process and analyze the tissue.

 

That’s why between 20 and 40 percent of women have to undergo second, third or even fourth breast-conserving surgeries to remove cancerous cells that were missed during the initial procedure, according a recent study. 

 

The new light-sheet microscope — which is described in a new paper published June 26, 2017 in Nature Biomedical Engineering — offers other advantages over existing processes and microscope technologies. It conserves valuable tissue for genetic testing and diagnosis, quickly and accurately images the irregular surfaces of large clinical specimens, and allows pathologists to zoom in and “see” biopsy samples in three dimensions.

 

“The tools we use in pathology have changed little over the past century,” said co-author Nicholas Reder, chief resident and clinical research fellow in UW Medicine’s Department of Pathology. “This light-sheet microscope represents a major advance for pathology and cancer patients, allowing us to examine tissue in minutes rather than days and to view it in three dimensions instead of two — which will ultimately lead to improved clinical care.”

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Need to Fix a Heart Attack? Try Photosynthesis Provided by Cyanobacteria

Need to Fix a Heart Attack? Try Photosynthesis Provided by Cyanobacteria | Amazing Science | Scoop.it

Injecting plant-like creatures like cyanobacteria into a rat's heart can jumpstart the recovery process, study finds.

 

Coronary artery disease is one of the most common causes of death and disability, afflicting more than 15 million Americans. Although pharmacological advances and revascularization techniques have decreased mortality, many survivors will eventually succumb to heart failure secondary to the residual microvascular perfusion deficit that remains after revascularization. A group of scientists now present a novel system that rescues the myocardium from acute ischemia, using photosynthesis through intramyocardial delivery of the cyanobacterium Synechococcus elongatus.

 

By using light rather than blood flow as a source of energy, photosynthetic therapy increases tissue oxygenation, maintains myocardial metabolism, and yields durable improvements in cardiac function during and after induction of ischemia. By circumventing blood flow entirely to provide tissue with oxygen and nutrients, this system has the potential to create a paradigm shift in the way ischemic heart disease is treated.


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One in five 'healthy' adults seems to carry disease-related genetic mutations

One in five 'healthy' adults seems to carry disease-related genetic mutations | Amazing Science | Scoop.it

Some doctors dream of diagnosing diseases—or at least predicting disease risk—with a simple DNA scan. But others have said the practice, which could soon be the foundation of preventative medicine, isn’t worth the economic or emotional cost. Now, a new pair of studies puts numbers to the debate, and one is the first ever randomized clinical trial evaluating whole genome sequencing in healthy people. Together, they suggest that sequencing the genomes of otherwise healthy adults can for about one in five people turn up risk markers for rare diseases or genetic mutations associated with cancers.

 

What that means for those people and any health care system considering genome screening remains uncertain, but some watching for these studies welcomed the results nonetheless. “It's terrific that we are studying implementation of this new technology rather than ringing our hands and fretting about it without evidence,” says Barbara Biesecker, a social and behavioral researcher at the National Human Genome Research Institute in Bethesda, Maryland.

 

The first genome screening study looked at 100 healthy adults who initially reported their family history to their own primary care physician. Then half were randomly assigned to undergo an additional full genomic workup, which cost about $5000 each and examined some 5 million subtle DNA sequence changes, known as single-nucleotide variants, across 4600 genes—such genome screening goes far beyond that currently recommended by the American College of Medical Genetics and Genomics (ACMG), which suggests informing people of results for just 59 genes known or strongly expected to cause disease.


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Cancer Immunotherapy - Where Are We Today?

Cancer Immunotherapy - Where Are We Today? | Amazing Science | Scoop.it

The immune system is naturally equipped to protect us against cancer. Cytotoxic T lymphocytes—otherwise known as killer T cells—are especially effective at targeting tumors. However, cancers sometimes figure out how to outsmart the immune system and protect themselves. Immunotherapy aims to reverse that situation.

 

This review is highlighting a wide scope of immune-based approaches that are already improving outcomes for patients. Many of these treatments work by either directly or indirectly enhancing the activity of T cells.

 

Much of what we know about the immune system and its relationship to cancer was discovered by scientists affiliated with the Cancer Research Institute (CRI), which since 1953 has served as the world’s leading (and for several decades only) nonprofit organization dedicated exclusively to transforming cancer patient care by advancing immunotherapy and the science behind it.

 

It’s clear now that immunotherapy can provide long-term benefits to sizable subsets of patients with diverse types of cancer, and new clinical breakthroughs are happening all the time. Thus far in 2017 there have been eight immunotherapy approvals, with two immunotherapies (durvalumab and avelumab) gaining approval for the first time. These clinical breakthroughs were made possible in part by decades of discoveries made by Cancer Research Institute (CRI) scientists.

 

One of the most important figures who helped advance immunotherapy (and the science that supports it) to this point was Dr. Lloyd J. Old, who actually worked with Dr. William B. Coley’s daughter, Helen, at CRI. Now known as the “Father of Modern Tumor Immunology,” Dr. Old directed CRI’s scientific and medical efforts for 40 years (1971-2011), during which time he made major discoveries about the immune system and cancer, and helped establish the scientific foundation upon which today’s immunotherapies were developed.

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Cancer cells seem to streamline their genomes in order to get a growth advantage

Cancer cells seem to streamline their genomes in order to get a growth advantage | Amazing Science | Scoop.it

Research from the Stowers Institute provides evidence suggesting that cancer cells might streamline their genomes in order to proliferate more easily. The study, conducted in both human and mouse cells, shows that cancer genomes lose copies of repetitive sequences known as ribosomal DNA. While downsizing might enable these cells to replicate faster, it also seems to render them less able to withstand DNA damage.

 

The findings, published in PLoS Genetics, suggest that ribosomal DNA copy number could be used to predict which cancers will be sensitive to DNA-damaging chemotherapeutics.

 

“Drugs that damage DNA are often used to treat cancer, but it’s not clear why they would selectively kill cancer cells,” says Jennifer L. Gerton, Ph.D., an investigator at the Stowers Institute who led the study. “Our results suggest that off-loading copies of ribosomal DNA could create instability in the genome that makes cells particularly susceptible to chemotherapy with DNA-damaging drugs.”

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Eye-opening picture of the fetal immune system finally emerges

Eye-opening picture of the fetal immune system finally emerges | Amazing Science | Scoop.it

A human fetus in its second trimester is extraordinarily busy. It is developing skin and bones, the ability to hear and swallow, and working on its first bowel movement. Now, a study published on 14 June in Nature finds that fetuses are also acquiring a functioning immune system — one that can recognize foreign proteins, but is less inclined than a mature immune system to go on the attack (N. McGovern et al. Naturehttp://dx.doi.org/10.1038/nature22795; 2017).

 

The results add to a growing body of literature showing that the fetal immune system is more active than previously appreciated. “In general textbooks, you see this concept of a non-responsive fetus is still prevailing,” says immunologist Jakob Michaelsson at the Karolinska Institute in Stockholm. But the fetal immune system is unique, he says. “It’s not just immature, it’s special.”

 

A developing fetus is constantly exposed to foreign proteins and cells, which are transferred from the mother through the placenta. In humans, this exposure is more extensive than in many other mammals, says immunologist Mike McCune at the University of California, San Francisco. As a result, laboratory mice have proved a poor model for studying the developing human fetal immune system.

 

But fully understanding that development could reveal the reasons for some miscarriages, as well as explain conditions such as pre-eclampsia, which is associated with abnormal immune responses to pregnancy and causes up to 40% of premature births. And organ-transplant surgeons have long been interested in how a developing fetus and its mother tolerate one another without either of them launching an immune attack — the hope is to find ways to suppress the immune system’s response to transplanted organs. 

 

For Jerry Chan, an obstetrician and gynaecologist at the KK Women’s and Children’s Hospital in Singapore, understanding the fetal immune system was important for his goal of developing stem-cell treatments and gene therapies for genetic disorders in developing fetuses. Chan and his colleagues wanted to know whether there was a developmental stage at which such treatments could be given without the risk of the therapies themselves being attacked by the immune system. 

 

To do this, Chan teamed up with immunologist Florent Ginhoux at the Agency for Science, Technology and Research in Singapore to study dendritic cells, immune cells that break down foreign material and present fragments of it to other immune cells called T cells. Some T cells are then activated to target the foreign material for destruction. The team found that human fetuses have functional dendritic cells by 13 weeks of gestation. But although the cells behave much like the adult versions, their response to foreign human proteins differs: rather than mark the foreign material for annihilation, fetal dendritic cells are more likely to activate a special category of T cell called regulatory T cells, which suppress immune responses.

 

This could reflect a need to avoid a catastrophic immune response against a mother’s cells. “You don’t want too much immune response in a developing fetus,” says Ginhoux. “It is very dangerous — this is a critical point in development.” Previous studies had found specialized immune cells — including T cells and natural killer cells — in fetuses as young as nine weeks, says Ginhoux. But the dendritic-cell findings are particularly important because these cells orchestrate immune responses, says Michaelsson. Without them, he says, the body can’t target specific foreign material for destruction.

 

The results highlight the fact that the fetal immune system is not merely an immature, less-active version of its adult counterpart, but one that has its own distinct function, says transplant immunologist William Burlingham at the University of Wisconsin in Madison.

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Huntington's disease trial test is 'major advance' due to neurofilament light chain

Huntington's disease trial test is 'major advance' due to neurofilament light chain | Amazing Science | Scoop.it

Experts describe the early research as a "major advance" in this field. The study, in the Lancet Neurology, suggests the prototype test could help in the hunt for new treatments. Huntington's disease is an inherited and incurable brain disorder that is currently fatal. Around 10,00 people in the UK have the condition and around 25,000 are at risk. It is passed on through genes, and children who inherit a faulty gene from parents have a 50% chance of getting the disease in later life. People can develop a range of problems including involuntary movements, personality changes and altered behavior and may be fully dependent on carers towards the end of their lives.

 

In this study, an international team - including researchers from University College London - looked at 200 people with genes for Huntington's disease - some of whom already had signs of the disease, and others at earlier stages. They compared them to some 100 people who were not at risk of getting the condition. Volunteers had several tests over three years, including brain scans and clinical check-ups to see how Huntington's disease affected people's thinking skills and movement as the condition became more severe. At the same time scientists looked for clues in blood samples - measuring a substance called neurofilament light chain (NFL) - released from damaged brain cells. They found levels of the brain protein were high in people with Huntington's disease and were even elevated in people who carried the gene for Huntington's disease but were many years away from showing any symptoms. And researchers found NFL levels rose as the condition worsened and as people's brains shrank over time.

 

Dr Edward Wild, at UCL, said: "Neurofilament light chain has the potential to serve as a speedometer in Huntington's disease, since a single blood test reflects how quickly the brain is changing. "We have been trying to identify blood biomarkers to help track the progression of Huntington's disease for well over a decade and this is the best candidate we have seen so far."

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Poison for cancer cells: New method identifies active agents in mixtures of hundreds of substances

Poison for cancer cells: New method identifies active agents in mixtures of hundreds of substances | Amazing Science | Scoop.it
The pharmaceutical industry is always on the lookout for precisely such substances to deploy them against threads like cancer. In the case of cancer, for example, when the proteasome is blocked, rapidly growing cancer cells choke on their own waste. The first medication of this kind is already generating annual revenues of over one billion US dollars. The scientists are now looking for further substances with lesser side effects.

Following preliminary studies, one such candidate was a toxic substance produced by the bacterium Photorhabdus luminescens. This is the poison that kills the larvae of the garden chafer. Using his new methodology, the scientists discovered that the bacterium lives inactively in the intestines of the threadworm. When it lays its eggs, the worm infects the larvae. The sudden change in environment causes the bacterium to emit toxins. After the larva dies, the bacterium ceases to produce toxins. Once the threadworms hatch from the protective egg membrane, they ingest the inactive bacterium into their intestines, and the cycle can start again.

Since the newly developed method also works in intensively colored solutions and in the presence of hundreds of other substances, the workgroup at the Chair of Biochemistry succeeded in isolating the unknown poison directly from the bacterial brew: It turned out to be two structurally very similar compounds, cepafungin I and glidobactin A. The latter was previously considered the strongest proteasome blocker. In spite of the resemblance, cepafungin I had never been tested as a proteasome blocking agent. The tests of the research group showed that Cepafungin I is indeed a strong Proteasomhemmer. In effect, it even surpasses the previous record holder.

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Scientists Create Artificial Womb That Could Help Prematurely Born Babies

Scientists Create Artificial Womb That Could Help Prematurely Born Babies | Amazing Science | Scoop.it

Scientists have created an "artificial womb" in the hopes of someday using the device to save babies born extremely prematurely. So far the device has only been tested on fetal lambs. A study published Tuesday involving eight animals found the device appears effective at enabling very premature fetuses to develop normally for about a month.

 

"We've been extremely successful in replacing the conditions in the womb in our lamb model," says Alan Flake, a fetal surgeon at Children's Hospital of Philadelphia who led the study published in the journal Nature Communications.

 

"They've had normal growth. They've had normal lung maturation. They've had normal brain maturation. They've had normal development in every way that we can measure it," Flake says. Flake says the group hopes to test the device on very premature human babies within three to five years. "What we tried to do is develop a system that mimics the environment of the womb as closely as possible," Flake says. "It's basically an artificial womb."

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