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  1. neurosciencestuff: (Image caption: diagram of the research findings (Taken from article’s Table of Contents Image) bFGF is produced in the injured zone of the cerebral cortex. Ror2 expression is induced in some population of the astrocytes that receive the bFGF signal, restarting their proliferation by accelerating the progression of their cell cycle) How brain tissue recovers after injury: the role of astrocytes A research team led by Associate Professor Mitsuharu ENDO and Professor Yasuhiro MINAMI (both from the Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University) has pinpointed the mechanism underlying astrocyte-mediated restoration of brain tissue after an injury. This could lead to new treatments that encourage regeneration by limiting damage to neurons incurred by reduced blood supply or trauma. The findings were published on October 11 in the online version of GLIA. When the brain is damaged by trauma or ischemia (restriction in blood supply), immune cells such as macrophages and lymphocytes dispose of the damaged neurons with an inflammatory response. However, an excessive inflammatory response can also harm healthy neurons. Astrocytes are a type of glial cell*, and the most numerous cell within the human cerebral cortex. In addition to their supportive role in providing nutrients to neurons, studies have shown that they have various other functions, including the direct or active regulation of neuronal activities. It has recently become clear that astrocytes also have an important function in the restoration of injured brain tissue. While astrocytes do not normally proliferate in healthy brains, they start to proliferate and increase their numbers around injured areas and minimize inflammation by surrounding the damaged neurons, other astrocytes, and inflammatory cells that have entered the damaged zone. Until now the mechanism that prompts astrocytes to proliferate in response to injury was unclear. The research team focused on the fact that the astrocytes which proliferate around injured areas acquire characteristics similar to neural stem cells. The receptor tyrosine kinase Ror2, a cell surface protein, is highly expressed in neural stem cells in the developing brain. Normally the Ror2 gene is “switched off” within adult brains, but these findings showed that when the brain was injured, Ror2 was expressed in a certain population of the astrocytes around the injured area. Ror2 is an important cell-surface protein that regulates the proliferation of neural stem cells, so the researchers proposed that Ror2 was regulating the proliferation of astrocytes around the injured areas. They tested this using model mice for which the Ror2 gene did not express in astrocytes. In these mice, the number of proliferating astrocytes after injury showed a remarkable decrease, and the density of astrocytes around the injury site was reduced. Using cultured astrocytes, the team analyzed the mechanism for activating the Ror2 gene, and ascertained that basic fibroblast growth factor (bFGF) can “switch on” Ror2 in some astrocytes. This research showed that in injured brains, the astrocytes that show (high) expression of Ror2 induced by bFGF signal are primarily responsible for starting proliferation. bFGF is produced by different cell types, including neurons and astrocytes in the injury zone that have escaped damage. Among the astrocytes that received these bFGF signals around the injury zone, some express Ror2 and some do not. The fact that proliferating astrocytes after brain injury are reduced during aging raises the possibility that the population of astrocytes that can express Ror2 might decrease during aging, which could cause an increase in senile dementia. Researchers are aiming to clarify the mechanism that creates these different cell populations of astrocytes. By artificially controlling the proliferation of astrocytes, in the future we can potentially minimize damage caused to neurons by brain injuries and establish a new treatment that encourages regeneration of damaged brain areas. *Glial cell: a catch-all term for non-neuronal cells that belong to the nervous system. They support neurons in various roles. Via
  2. bpod-mrc: Metal Detectors Cisplatin – a chemotherapy drug based on the metal platinum – has been used to treat cancers for many years; however, resistance to platinum has become an issue, prompting researchers to look for other metal compounds. Researchers tracked the activity of different compounds based on the metals zinc (top left), osmium (top right) and calcium (bottom) in ovarian cancer cells using x-ray fluorescence. Colours shown represent the compound’s concentration – white being strongest. The team could see that one, called organo-osmium FY26, made its way into and was concentrated in the cell’s energy-producing mitochondria (highlighted in red top right), killing the cell from the inside. Organo-osmium FY26 is fifty times more active and also more selective than cisplatin, making it a promising candidate for a new cancer treatment. Written by Katie Panteli Images from work by Dr. Carlos Sanchez-Cano and colleagues Department of Chemistry, University of Warwick, Coventry, UK Image copyright held by,, Research published in Chemistry – A European Journal, January 2017 You can also follow BPoD on Twitter and Facebook Via
  3. cardiacattack: descantforhope: mudphudkangaroo: writingbiologi: zooophagous: adamygdalam: probablyasocialecologist: dr-archeville: hectocotyli-everywhere: ohnofixit: the-exercist: fitblrholics: If you look at the ingredients list and it’s a bunch of words you don’t even know… neither does your body (x) Just like if you break apples and grapefruit down into their chemical components, I’m willing to bet that most people wouldn’t recognize the “ingredients” either. It’s a bunch of words you don’t even know: External image Don’t use these scare tactics - Chemicals aren’t inherently bad. Literally everything is made up chemicals. Trust me, your body knows what niacin is. It knows how to digest fructose and calcium sulfate. Even if you only consume the most basic and “real” foods that are pulled directly off the vine, you’re still ingesting a series of chemical compounds that you probably can’t pronounce. That’s okay. thanks to drhoz for submitting! “If you can’t pronounce it, it’s bad for you” is literally the worst pseudo-scientific scaremongering bullshit tactic. I hate it so much. I’m pretty sure you can pronounce “arsenic”, but that doesn’t change the fact that arsenic is highly toxic. On the other hand, you couldn’t pronounce “cycloadenosine monophosphate” or “nicotine-amide-dinucleotide-phosphate”, though both of them serve vital roles in human biochemistry and you would die if your body wouldn’t produce them. Cyanide: Easy to pronounce, very bad for you. Eicosapentaenoic acid: Difficult to pronounce, very good for you. It’s more important to know what the chemicals are and why they’re in there. Anti-intellectualism helps no one. – James Kennedy, ‘Chemophobia’ is irrational, harmful – and hard to break I’m gonna keep reblogging this until my knuckles fall off. This is especially hilarious because grapefruit is well known for being dangerous for some people because of how it can interact with certain medications. Do fruit loops do that? “Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy.” - Paracelsus Fava beans are like *known* to fuck up certain people with G6PD deficiency - which is insanely common. Ok look. This is nuts. Are fruit loops healthier than an actual piece of fruit? Pretty much no, never. Individual quirks of metabolism aside, I can’t think of a single reason I would ever tell someone to eat fruit loops over actual fruit. Every time I see this it’s like a smart off to say stupid shit. I guarantee I do more biochem on a regular basis than most (and you can ask other docs that know me, like @notacleverturnip, I do so much biochem all the time). I don’t give a fuck about pronunciation, I’m just trying to stop people from getting diabetes. The chemical scare tactic is not particularly useful but neither is telling someone that the ingredient list on fruit loops is like the same fucking thing as an apple. I swear to the gods of biochem and nutrition if this post (in all of its iterations, I don’t care for the scare tactics either) comes around again I’m going to throw a blog tantrum. Again. No one is saying fruit loops are healthy or the same as an apple. They’re saying you shouldn’t make eating decisions based on whether you can pronounce the ingredients or not. There’s obviously way more to nutrition than that, but fruit loops aren’t dangerous just because the ingredients are difficult to pronounce. That’s literally all this post is trying to say. It’s by no means a recommendation that fruit loops are super great and healthy. Via
  4. ucsdhealthsciences: Vision Guessed What do you see? The answer lies in the eye of the beholder. In this case, quite literally. The image, taken by Kim Baxter at Cambridge University Hospitals NHS Foundation Trust and a 2017 Wellcome Image Awards, depicts blood vessels feeding the retina of a human eye. They appear as white, spidery lines due to a fluorescent dye passing through. Via
  5. medresearch: New Assay May Lead to Better Treatment for Rheumatoid Arthritis Researchers at NYU Langone Medical Center have developed a test to measure the immunologic defect that triggers the inflammation present in rheumatoid arthritis. They believe that clinical trials for new rheumatoid arthritis drugs should shift from their sole focus on relieving inflammation to eliminating the B cells that produce the antibodies that cause this defect. “We have developed a test for measuring the underlying autoimmunity in rheumatoid arthritis patients that should be used to evaluate new treatment regimens,” says senior author Gregg Silverman, MD, professor in the departments of Medicine and Pathology at NYU Langone and co-director of its Musculoskeletal Center of Excellence. “We believe this provides a road to a cure for rheumatoid arthritis.” Read more Funding: This work was supported by the National Institutes of Health (NIH), an American Recovery and Reinvestment Act supplement, and a National Institute of Allergy and Infectious Diseases/NIH and NYU School of Medicine-Immunology and Inflammation Training grant. Raise your voice in support of expanding federal funding for life-saving medical research by joining the AAMC’s advocacy community. Via
  6. An Unexpected New Lung Function Has Been Found - They Make Blood: mindblowingscience: Researchers have discovered that the lungs play a far more complex role in mammalian bodies than we thought, with new evidence revealing that they don’t just facilitate respiration - they also play a key role in blood production. In experiments involving mice, the team found that they produce more than 10 million platelets (tiny blood cells) per hour, equating to the majority of platelets in the animals’ circulation. This goes against the decades-long assumption that bone marrow produces all of our blood components. Researchers from the University of California, San Francisco also discovered a previously unknown pool of blood stem cells that makes this happen inside the lung tissue - cells that were incorrectly assumed to mainly reside in bone marrow. “This finding definitely suggests a more sophisticated view of the lungs - that they’re not just for respiration, but also a key partner in formation of crucial aspects of the blood,” says one of the researchers, Mark R. Looney. “What we’ve observed here in mice strongly suggests the lung may play a key role in blood formation in humans as well.” While the lungs have been known to produce a limited amount of platelets - platelet-forming cells called megakaryocytes have been identified in the lungs before - scientists have long assumed that most of the cells responsible for blood production are kept inside the bone marrow. Here, a process called haematopoiesis was thought to churn out oxygen-laden red blood cells, infection-fighting white blood cells, and platelets - blood components required for the clotting that halts bleeding. But scientists have now watched megakaryocytes functioning from within the lung tissue to produce not a few, but most of the body’s platelets. Continue Reading. Via
  7. Neuroscientists Have Accidentally Discovered a Whole New Role for the Cerebellum: mindblowingscience: One of the best-known regions of the brain, the cerebellum accounts for just 10 percent of the organ’s total volume, but contains more than 50 percent of its neurons. Despite all that processing power, it’s been assumed that the cerebellum functions largely outside the realm of conscious awareness, instead coordinating physical activities like standing and breathing. But now neuroscientists have discovered that it plays an important role in the reward response - one of the main drives that motivate and shape human behaviour. Not only does this open up new research possibilities for the little region that has for centuries been primarily linked motor skills and sensory input, but it suggests that the neurons that make up much of the cerebellum - called granule cells - are functioning in ways we never anticipated. “Given what a large fraction of neurons reside in the cerebellum, there’s been relatively little progress made in integrating the cerebellum into the bigger picture of how the brain is solving tasks, and a large part of that disconnect has been this assumption that the cerebellum can only be involved in motor tasks,” says one of the team, Mark Wagner, from Stanford University. “I hope that this allows us to unify it with studies of more popular brain regions like the cerebral cortex, and we can put them together.” Continue Reading. Via
  8. neurosciencestuff: For the first time, Tübingen neuroscientists were able to differentiate between active and inactive cells in the brain morphologically, i.e. based on the cells’ structure. Investigating granule cells in the rat’s brain, they found a much larger proportion of inactive than active cells. Many things we think we know about the world have their origin in popular culture, not science. The most well-known false ‘fact’ about the brain is the misconception that we only use ten percent of the brain’s overall capacity. This so-called ’ten percent myth’, while accepted as such by neuroscientists, still regularly figures in advertisement, but also in books and short stories as well as films. As with any myth, however, there is a kernel of truth at the core of the matter: many neurons remain dormant for most if not all of our life, even while their direct neighbours show regular activity. A team of neuroscientists led by Dr. Andrea Burgalossi of the Werner Reichardt Centre for Integrative Neuroscience (CIN) at the University of Tübingen have now taken an important step towards understanding why some neurons are active and others are not: they can tell them apart morphologically. To be able to do so, the investigators employed so-called juxtacellular recordings in freely-moving rats. With this technique, electrodes are inserted right next to individual, functioning neurons in live organisms. This allows recording action potentials from these neurons while they work, and while simultaneously identifying the cells that the recordings are taken from for later analysis. During this analysis, morphological traits of the analysed cells are identified, most importantly their dendritic arbors, i.e. the filament structures which receive input signals from other neurons. The cells under investigation were granule cells (GCs) in the rat’s dentate gyrus (DG). Dentate GCs have been shown to be intimately connected to individual memories of places and individuals, and thus playing a central role in memory tasks. The researchers recorded from 190 GCs, only 27 of which they found to be active (ca. 14 percent). While this seems to give credibility to the ‘ten percent myth’, the team actually expected this outcome, as the DG is a brain structure where in any given task, only a very small percentage of neurons take part, while their neighbours remain dormant, waiting for their ‘cue’, as it were. Memory functions in the brain work according to a principle that neuroscientists call ‘sparse coding’, i.e. a comparatively small number of neurons encode complex information – possibly to make overlap between different memories more unlikely. Using a smaller subsample, the scientists looked for correlations between active and passive functionality and the respective cells’ morphology. Their results show that active GCs have much more complex dendritic arbors. They not only transfer and receive information from many more neurons than the inactive ones, they also have better cellular ‘infrastructure’ to do so. Despite their as of yet limited sampling, the scientists are positive that they can now tell apart active and inactive GCs, mostly by merely looking at them. “Explaining the causes of activity in some and inactivity in other neurons may still take a long time”, cautions Burgalossi, leader of the research group. “But finding a direct link between function and morphology is an important step forward. It will be even more challenging to find evidence of causality. But we are on the right track.” Via
  9. medresearch: Researchers Develop “MAGIC Algorithm” to Predict Whether Bone Marrow Transplant Patients May Die From Common Complication Researchers at Mount Sinai Health System have discovered a way to predict whether blood cancer patients who received a bone marrow transplant will develop graft-versus-host disease, a common and often lethal complication. The study, which involved 11 cancer centers internationally, used blood samples from almost 1,300 bone marrow transplant patients and found that two proteins (ST2 and REG3a) present in blood drawn a week after a transplant can predict whether a patient will develop a lethal version of graft-versus-host disease. Scientists at the Mount Sinai Acute GVHD International Consortium (MAGIC) created an algorithm, dubbed the “MAGIC algorithm,” that determines a patient’s risk of developing the disease by measuring concentrations of these proteins. The research was published in JCI (The Journal of Clinical Investigation) Insight. “The MAGIC algorithm gives doctors a roadmap to save many lives in the future. This simple blood test can determine which bone marrow transplant patients are at high risk for a lethal complication before it occurs,” says James L.M. Ferrara, MD, Professor of Pediatrics, Oncological Sciences and Medicine, Hematology and Medical Oncology at The Tisch Cancer Institute at the Icahn School of Medicine at Mount Sinai, and Co-director of MAGIC. “It will allow early intervention and potentially save many lives.” Read more Funding: The study was supported by grants P01 CA03942 and P30 CA106521 from the National Cancer Institute, an American Cancer Society Clinical Research Professorship (to Dr. Ferrara) and a Doris Duke Charitable Foundation Clinical Research Mentorship. Raise your voice in support of expanding federal funding for life-saving medical research by joining the AAMC’s advocacy community. Via
  10. neurosciencestuff: Neuroscientists call for deep collaboration to ‘crack’ the human brain The time is ripe, the communication technology is available, for teams from different labs and different countries to join efforts and apply new forms of grassroots collaborative research in brain science. This is the right way to gradually upscale the study of the brain so as to usher it into the era of Big Science, claim neuroscientists in Portugal, Switzerland and the United Kingdom. And they are already putting ideas into action. In a Comment in the journal Nature, an international trio of neuroscientists outlines a concrete proposal for jump-starting a new, bottom-up, collaborative “big science” approach to neuroscience research, which they consider crucial to tackle the still unsolved great mysteries of the brain. How does the brain function, from molecules to cells to circuits to brain systems to behavior? How are all these levels of complexity integrated to ultimately allow consciousness to emerge in the human brain? The plan now proposed by Zach Mainen, director of research at the Champalimaud Centre for the Unknown, in Lisbon, Portugal; Michael Häusser, professor of Neuroscience at University College London, United Kingdom; and Alexandre Pouget, professor of neuroscience at the University of Geneva, Switzerland, is inspired by the way particle physics teams nowadays mount their huge accelerator experiments to discover new subatomic particles and ultimately to understand the evolution of the Universe. “Some very large physics collaborations have precise goals and are self-organized”, says Zach Mainen. More specifically, his model is the ATLAS experiment at the European Laboratory of Particle Physics (CERN, near Geneva), which includes nearly 3,000 scientists from tens of countries and was able (together with its “sister” experiment, CMS) to announce the discovery of the long-sought Higgs boson in July 2012. Although the size of the teams involved in neuroscience may not be nearly comparable to the CERN teams, the collaborative principles should be very similar, according to Zach Mainen. “What we propose is very much in the physics style, a kind of ‘Grand Unified Theory’ of brain research, he says. “Can we do it? Clearly, it’s not going to happen within five years, but we do have theories that need to be tested, and the underlying principles of how to do it will be much the same as in physics.” To help push neuroscience research to take the leap into the future, the three neuroscientists propose some simple principles, at least in theory: “focus on a single brain function”; “combine experimentalists and theorists”; “standardize tools and methods”; “share data”; “assign credit in new ways”. And one of the fundamental premises to make this possible is to “engender a sphere of trust within which it is safe [to share] data, resources and plans”, they write. Needless to say, the harsh competitiveness of the field is not a fertile ground for this type of “deep” collaborative effort. But the authors themselves are already putting into practice the principles they advocate in their article. “We have a group of 20 researchers (10 theorists and 10 experimentalists), about half in the US and half in the UK, Switzerland and Portugal” says Zach Mainen. The group will focus on only one well-defined goal: the foraging behavior for food and water resources in the mouse, recording activity from as much of the brain as possible - at least several dozen brain areas. “By collaboration, we don’t mean business as usual; we really mean it”, concludes Zach Mainen. “We’ll have 10 labs doing the same experiments, with the same gear, the same computer programs. The data we will obtain will go into the cloud and be shared by the 20 labs. It’ll be almost as a global lab, except it will be distributed geographically.” Via
  11. neurosciencestuff: Food Knowledge is Resilient A SISSA research study published in a special issue of the journal Brain and Cognition, completely dedicated to the cognitive neuroscience of food, analyzes the lexical-semantic deficits of the food category in patients suffering from neurodegenerative diseases like Alzheimer’s. The study shows that knowledge about food is preserved more than other categories of stimuli, even in the case of severe syndromes. Further, perception of caloric intake affects a person’s ability to remember the name of a food; the higher the calories, the more knowledge is preserved. Professor Raffaella Rumiati of the International School for Advanced Studies (SISSA) in Trieste, first author and expert in semantic categorization of food, also served as editor of the special issue (along with Giuseppe Di Pellegrino, University of Bologna), and wrote the introduction to the issue. Perhaps it is because it is so crucial to our survival that lexical and semantic knowledge related to food is relatively well preserved even in diseases that lead to a general decline in memory and cognition, such as Alzheimer’s and Aphasia Primary Progressive. Raffaella Rumiati and her team at SISSA, in collaboration with Caterina Silveri of Catholic University “Agostino Gemelli” in Rome, observed the phenomenon while testing the cognitive performance of two groups of patients and a control group of healthy people in tasks concerning visual recognition of food and comprehension. “It should not be surprising that food resists even generalized cognitive decline,” says Rumiati. “It is not difficult to imagine how evolutionary pressure could lead to increased strength in cognitive processes related to fast recognition of what is probably the most important stimulus for survival.” Another fact revealed by the study supporting food supremacy was that in all three groups, patients and control, food information was processed better than “non–food.” Adds Rumiati, “We know from the literature that the names of the most caloric foods are acquired early in life.” Rumiati and colleagues discovered another interesting detail: the perception of caloric intake of each food is proportional to the strength with which we recognise their names. The more caloric the food seems, the better it is preserved. “This phenomenon may be closely related to what I said earlier: the more nutritious the food, the more important it is to recognize it.” Via
  12. Researcher Reveals Clues to Immunity as a Cause of High Blood Pressure A University of Arkansas for Medical Sciences (UAMS) researcher has shed light on the role of immune cells inside the kidneys in the development of salt-sensitive high blood pressure, publishing his findings in Nature Communications. “High blood pressure is very common, and this salt-sensitive version is present in about 40-50 percent of cases of hypertension initially and becomes worse as the disease progresses,” said Shengyu Mu, Ph.D., assistant professor in the Department of Pharmacology and Toxicology in the UAMS College of Medicine. “For many years, the recommendation for heart health has been to eat less salt. But studies have shown that while it does lower blood pressure; too little salt also increases the rate of cardiovascular events and mortality in patients, which is all the more reason for us to develop a better understanding of the causes of salt-sensitivity.” Specifically, Mu’s work uncovered the interaction of a particular type of white blood cell with kidney cells. Scientists suspected that these cells – T lymphocytes, or T cells –demonstrating that too many T cells in the kidneys might be the cause of salt sensitivity of high blood pressure. Read more Funding: This study was supported by American Heart Association Beginning Grant-in-Aid and financial support from Dr. Philip Palade and the University of Arkansas for Medical Sciences Foundation. The researchers are also funded in part by the National Institutes of Health and a VA Merit Award. Raise your voice in support of expanding federal funding for life-saving medical research by joining the AAMC’s advocacy community. Via
  13. currentsinbiology: Epstein-Barr virus and cancer: New tricks from an old dog After an infection with the Epstein-Barr virus (EBV), the virus persists in the body throughout a person’s lifetime, usually without causing any symptoms. About one third of infected teenagers and young adults nevertheless develop infectious mononucleosis, also known as glandular fever or kissing disease, which usually wears off after a few weeks. In rare cases, however, the virus causes cancer, particularly lymphomas and cancers of the stomach and of the nasopharynx. Scientists have been trying for a long time to elucidate how the viruses reprogram cells into becoming cancer cells. “The contribution of the viral infection to cancer development in patients with a weakened immune system is well understood” says Henri-Jacques Delecluse, a cancer researcher at the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) in Heidelberg. “But in the majority of cases, it remains unclear how an EBV infection leads to cancer development.” In their present publication, Delecluse, in collaboration with Ingrid Hoffmann, also from the DKFZ, and their respective groups present a new and surprising explanation for this phenomenon. The scientists have shown for the first time that a protein component of the virus itself promotes the development of cancer. When a dividing cell comes in contact with Epstein-Barr viruses, a viral protein present in the infectious particle called BNRF1 frequently leads to the formation of an excessive number of spindle poles (centrosomes). As a result, the chromosomes are no longer divided equally and accurately between the two daughter cells – a known and acknowledged cancer risk factor. By contrast, Epstein-Barr viruses that had been made deficient of BNRF1 did not interfere with chromosome distribution to the daughter cells. Anatoliy Shumilov, Ming-Han Tsai, Yvonne T. Schlosser, Anne-Sophie Kratz, Katharina Bernhardt, Susanne Fink, Tuba Mizani, Xiaochen Lin, Anna Jauch, Josef Mautner, Annette Kopp-Schneider, Regina Feederle, Ingrid Hoffmann, Henri-Jacques Delecluse. Epstein–Barr virus particles induce centrosome amplification and chromosomal instability. Nature Communications, 2017; 8: 14257 DOI: 10.1038/ncomms14257 After an infection with the Epstein-Barr virus (EBV), the virus persists in the body throughout a person’s lifetime. Credit: © Henri-Jacques Delecluse/DKFZ Via
  14. Bed Bugs: The Worst Bed Pest and How To Get Rid of Them Bed bugs have been and are still one of the worst nightmares of every homeowner. Can you imagine that creepy crawlies sleeping with you and squeaking every night? But fortunately, there are already proven effective methods to prevent and handle home pestilence from these viruses without spraying the entire house with harmful and toxic chemicals. Despite the usual effective sprays, repellents, and traps, these can sometimes be hazardous to you if not lethal when choked or even touched. Laying open to these preventive methods can cause eye, skin and respiratory irritation and even cause cancer when mishandled. But before we go ahead and discuss the steps on how to get rid of bed bugs, what are bed bugs, anyway? KNOWING YOUR REAL ENEMY BED BUGS What They Look Like – a brown or a reddish brown animal that has a flat, oval body and the same as the size of an apple seed. Headquarters – usually, they hang out around and in the bed itself. Their small and flat body makes it easy for them to hide around the corner of the bed frames, headboards, mattresses, behind your room wallpaper and even your clothes. Danger – this scourge does not transmit or pass through diseases. They only suck human and animal blood. Their bites cause itchiness and swelling. The person dealing with the pestilence can be both anxious and may experience insomnia. Good thing, we have some alternative ways on how to prevent and stop bed bugs. Methods that are milder, healthier and more environment-friendly. HOW CAN I KEEP BED BUGS OUT? The real horror of bugs in the bedroom can never be understood unless you experience it. Here are a few effective steps on how to KEEP THEM OUT: Clean up – Every virus loves a dirty environment. Clean up spills and crumbs right away every after bedroom meal. Stay dry – Wipe any cold water sweat from a glass on your bedside table. Heat up the textiles – all the linens (bed sheets, comforter, pillow cases, blankets, curtains and even towels) where bugs might hide should be washed with the highest temperature available for at least thirty minutes. Scrub the mattress – this ensures that the bed bugs in the mattress are also taken care off. It’s not enough to just wash the linens without touching the mattress. Make sure you use something like a stiff brush and a vacuum. Decide if the mattress can still be kept – there are times when the mattress will no longer be useful due to the huge amount of bed bugs on it. If that’s the case, unfortunately, you already need to replace your bed mattress. Be careful in throwing buggy materials. Properly wrap it and label it as a material with bugs. TAKEAWAY Most of the time, we think of our room as our own comfort zone. And it is very important that you’re comfortable in it. That’s why it is very important to clean our room every now and then. Never ignore that itchy feeling you get whenever you lay down in your bed. It might be those annoying blood-sucking bed bugs waiting to attack you. Via
  15. archaeologicalnews: One of the worst epidemics in human history, a sixteenth-century pestilence that devastated Mexico’s native population, may have been caused by a deadly form of salmonella from Europe, a pair of studies suggest. In one study, researchers say they have recovered DNA of the stomach bacterium from burials in Mexico linked to a 1540s epidemic that killed up to 80% of the country’s native inhabitants. The team reports its findings in a preprint posted on the bioRxiv server on 8 February. This is potentially the first genetic evidence of the pathogen that caused the massive decline in native populations after European colonization, says Hannes Schroeder, an ancient-DNA researcher at the Natural History Museum of Denmark in Copenhagen who was not involved in the work. “It’s a super-cool study.” In 1519, when forces led by Spanish conquistador Hernando Cortés arrived in Mexico, the native population was estimated at about 25 million. A century later, after a Spanish victory and a series of epidemics, numbers had plunged to around 1 million. Read more. Via