Monthly Archives: June 2020

After nearly 150 years, we may finally understand how general anesthesia makes us drift into unconsciousness although some of the specifics remain murky.

These drugs dislodge molecules held in the fatty membrane that surrounds brain cells. Once the drugs reach this fatty shell, the freed molecules bounce around like billiard balls within the membrane and alter the function of proteins embedded in its surface, according to a new study in cultured cells and fruit flies.

The new findings could help resolve a mystery that has lingered for decades.

Related: From dino brains to thought control 10 fascinating brain findings

"People have been seriously hammering on this for at least 100 years," said study author Scott Hansen, an associate professor in the departments of molecular medicine and neuroscience at The Scripps Research Institute in La Jolla, California.

But not everyone thinks the new study can reveal why anesthetics put humans "to sleep."

"Let's just say there's a large difference between the fruit fly brain and the human brain," said Dr. Emery Brown, a professor of Medical Engineering and Computational Neuroscience at the Massachusetts Institute of Technology and a professor of Anaesthesia at Harvard Medical School, who was not involved in the study.

Since dental surgeon Dr. William Morton first used the chemical ether as an anesthetic in the 1840s, scientists have sought to understand how the drug and other anesthetics interact with the brain. Nineteenth-century scientists suspected that anesthetics somehow disrupted the fatty membrane surrounding cells, including brain cells, as the drugs repel water while readily mixing with oils and fats, he said. Later research, conducted in the 1980s, suggested that anesthetics bind directly to proteins lodged inside the fatty membrane and directly interfere with the activity of said proteins, driving down the overall activity of brain cells, The Scientist reported. But Hansen and his colleagues suspected this wasn't the whole story.

In experiments in cultured cells and fruit flies, the authors found that anesthetics disrupt specific pockets of fat within the cellular membrane; those disruptions then free molecules and trigger chain reactions elsewhere on the cell surface. The authors posit that these molecular changes, among other mechanisms, caused fruit flies to lose consciousness, as evidenced by the insects becoming immobile for several minutes.

However, experts told Live Science that these animal experiments can only tell us so much about how the drugs work in humans.

While the study reconfirms that anesthetics are "dirty drugs," meaning they target multiple cellular systems at once, it cannot say exactly how disruptions to the fatty membrane alter consciousness, or even how those changes alter activity throughout the brain, Brown told Live Science.

The drugs disrupt the membrane, "okay, but now finish the story," he said. "How does that then drive [activity in] certain parts of the brain?" Understanding how anesthetics work could help doctors use the drugs more precisely in the clinic, Brown said.

This understanding might also hint at how the brain naturally shifts in and out of consciousness, as it does during sleep, Hansen added.

"Back in the day," when anesthetics first entered widespread use, scientists theorized that many of the physiological effects of drugs stemmed from changes to the fatty membrane of cells, a gateway that determines when molecules may enter or exit, said Francisco Flores, a research scientist and instructor in the Anesthesia Department at Massachusetts General Hospital who was not involved in the study. As technology progressed, scientists discovered that many drugs interact with specific proteins anchored in the fatty membrane, and subsequently, research efforts focused more on these membrane-bound proteins than the fats surrounding them, known as lipids, he said.

"However, for anesthetics, the lipid hypothesis survived for longer," Flores said. Anesthetics can cross the blood-brain barrier, a border of cells that separates circulating blood from brain tissue and allows only certain molecules to pass through. All anesthetics, as well as other drugs that pass the blood-brain barrier, repel water and readily interact with lipids, "so there's still a chance that they can do something in the membrane," he said.

But nineteenth-century scientists could not observe how anesthetics warped the lipid membrane; the task required superresolution microscopes that had not been invented at the time, Hansen said. Hansen and his co-authors used such a microscope, called dSTORM, to observe how cells reacted when bathed in the anesthetics chloroform and isoflurane.

Related: 10 facts every parent should know about their teen's brain

They found that different types of fats within the cell membrane reacted differently to the drugs.

One pocket of fats, known as GM1, contains high concentrations of cholesterol molecules, tightly packed together and dotted with specific sugar molecules. Upon exposure to anesthetic, the fats within these GM1 clusters spread out, and in doing so, release various proteins that were enmeshed with them. One such protein, called PLD2, escapes to a different bundle of fats and initiates a series of chemical reactions.

Specifically, the reaction opens a tunnel through the cell called a TREK1 ion channel, which allows positively charged particles to exit the cell. In a brain cell, this mass exodus of positive particles makes the cell more negatively charged and could suppress that cell's electrical and chemical activity. That, theoretically, could push the brain into an unconscious state, Hansen said.

But it may not be that straightforward, Brown noted.

To see if their cell experiments carried over to animals, the authors dissected the brains of fruit flies and found that, after exposure to chloroform, fats within the lipid membranes of the flies' brain cells spread out just as had been observed in cell culture. In addition, mutant fruit flies without the ability to make PLD2 became resistant to the chloroform treatment and required a larger dose to become sedated, researchers reported in the study, which was published May 28 in the journal Proceedings of the National Academy of Sciences.

Because the mutant flies were not completely immune to chloroform, the authors concluded that multiple mechanisms likely allow the drug's anesthetic effect to take hold. Disruptions to cells' lipid membrane may contribute to this overall effect, but at this point, their relative influence remains unclear, Brown noted. "Dirty" anesthetics trigger a number of reactions in the brain through different chemical and metabolic pathways, and scientists don't yet know how membrane disruptions affect the overall activity within that circuitry, he said.

These interactions will be difficult to untangle in the somewhat-simple fly brain, and even more challenging to understand in the human brain, Brown said.

That said, Hansen and his co-authors hypothesize that membrane disruptions may play a broader, unsung role in the effects of anesthetics on humans. Theoretically, anesthetics may indirectly affect many proteins by first disrupting the lipid membrane, Hansen said. Many proteins lodged in the lipid membrane have fatty acids stuck to their structures, for instance, and some of these proteins interact with brain chemicals and help drive activity of brain cells. One hypothesis is that if anesthetics target the fatty acids attached to these proteins, the drugs could conceivably alter their function and sedate the brain, Hansen said.

"Again, this is speculative," and would need to be confirmed with future studies, he added. Similar studies should be done with other drugs that cross the blood-brain barrier, not just anesthetics, to determine whether the effect appears unique or common to many classes of drug, Flores said. Hansen said he wants to see whether chemicals with similar effects already exist in the brain, and perhaps help put us to sleep.

While the new study opens many interesting avenues for future research, for now, the results remain fairly preliminary, Brown said.

"Do I do something different in the operating room now that I've read that paper? No," Brown said.

Originally published on Live Science.

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Anesthesia may work by targeting the fat in our brains - Live Science

Lab tests and clinical pilot study

In test tubes and 3D-human miniature livers, the researchers showed that the drug inhibited signaling of cytokines, immune system-proteins known to overreact and drive inflammation in severe cases of COVID-19 infection. It also helped reduce the viral load of SARS-CoV-2, the virus that causes COVID-19, and the level of the signal molecule interleukin-6 (IL-6), a predictor of mortality from acute respiratory distress syndrome associated with COVID-19.

In addition to the lab tests, a small pilot study of three men and one woman with bilateral COVID-19 pneumonia was conducted in Milan, Italy. After 10-12 days of treatment with baricitinib, all four patients showed improvements in signs and symptoms such as cough, fever and reductions in viral load and plasma IL-6 levels.

Collectively, these data suggest that baricitinib may lower inflammation and viral load in COVID-19, says Ali Mirazimi, adjunct professor in the Department of Laboratory Medicine, Karolinska Institutet, who led the functional virus studies.

Additional trials of baricitinib are currently underway in 85 hospitalized COVID-19 patients across three hospitals in Northern and Central Italy, with encouraging initial results in patient outcomes, according to the researchers.

We are integrating and carefully analyzing these trial data and providing functional and mechanistic follow-up studies to scrutinize baricitinibs mode of action, says Volker Lauschke, associate professor of personalized medicine and drug development at the Department of Physiology and Pharmacology, Karolinska Institutet, who led the functional testing of baricitinib.

The study was funded by Eli Lilly and Company and the Sacco Baricitinib Study Group. Several of the authors reported potential conflicts of interests, including employment and shareholdings in Eli Lilly and Company, which owns the trademark for the baricitinib drug Olumiant. For a full list of disclosures, please see the full article.

Reference:Stebbing, et al. (2020) Mechanism of Baricitinib Supports Artificial Intelligence-Predicted Testing in COVID-19 Patients. EMBO Molecular MedicineDOI:10.15252/emmm.202012697

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

Original post:
Rheumatoid Arthritis Drug Could Be Repurposed To Treat COVID-19 Patients - Technology Networks

TSAILE, Ariz. A research paper authored by two Din College science professors about the coronavirus (COVID-19) pandemic and its impact upon Native Americans provides clarification of the transmission and virulence of the virus, the professors say.

The paper, The Medical Basis for Increased Susceptibility of COVID-19 among the Navajo and other Indigenous Tribes: A Survey, was written by Dr. Joseph DeSoto and Dr. Shazia Tabassum Hakim.

The paper concludes, in part, that ethnic and anatomic expression patterns of angiotensin converting enzyme 2 (ACE2) and associated pathophysiology suggests that Native Americans and Asians may be particularly susceptible to this disease (Covid-19).

It was submitted April 30 and accepted for publication May 29 in the Journal of Biomedical Research and Reviews. DeSoto and Hakim said the document represents the first comprehensive world-wide scientific understanding of the high rate of infectivity among the Navajo and Indigenous tribes of the SAR-CoV-2 from a molecular medical perspective on Covid-19.

Angiotensin Converting Enzyme 2 (ACE2) is a type of protein found on the surface of a number of cells in the respiratory, digestive, nervous and reproductive systems. The protein, in general, serves as a door where the virus enters the cells, the team explained.

And the key that the virus has is to open the door is a spike with the protein S, Hakim stated. When this right key S is inserted into the door lock (ACE-2), the magic happens and the virus enters the host cell, hijacks the host cells DNA machinery and starts producing its own proteins, multiplies, increases in number and infects more cells of the host body.

There are four things that aggravate COVID-19 as it pertains to the Navajo Nation, De Soto said. Medically, its the high rate of diabetes, hypertension, genetics and poor protein diets among the Navajo; poor health care infrastructure and technology; poverty, with the associated lack of water access; and dense multi-generational living arrangements.

The two professors work in the Science, Technology, Engineering and Math (STEM) division of the Din College. They said in December they had started talking amongst themselves about the causes of COVID-19, and then started reviewing the literature.

Late in December 2019, we read every single thing that was published out there in the scientific community, DeSoto said. We discussed it and evaluated it long before the virus came over here. Then based on the best medical evidence, we realized that this might soon be a problem. So, we started discussing, evaluating and analyzing and then we wrote and completed the paper.

Two more papers are being published within weeks in major peer reviewed Medical and Scientific Journals by De Soto and Hakim, The Medical Treatment for COVID-19, and with Dr. Fred Boyd, of Din College, a well-known molecular physiologist, The Pathophysiology of COVID-19, both of which have already received international attention via preprints.

The Navajo Nation has the highest COVID-19 rate in the United States which is 450% higher than the national average.

DeSoto, who was senior author and is a medical school graduate of Howard University. His specialty is molecular medicine and pharmacogenetics. Hakim has a background in microbiology and infectious diseases. She is a graduate of the University of Karachi in Pakistan.

Hakim said she and DeSoto are working on another manuscript related to the eating habits, food scarcity and the unavailability of the varieties of fruits and vegetables in Navajo communities.

The Journal of Biomedical Research and Review is an international, peer reviewed, open access, scientific and scholarly journal which publishes research papers, review papers, mini reviews, case reports, case studies, short communications, letters, editorials, books, theses and dissertations from various aspects of medicine, engineering, science and technology to improve and support health care.

Information provided by Din College

More:
Din College researchers believe more reasons behind high Covid-19 Cases on Navajo - Navajo-Hopi Observer

NEW YORK While some potential vaccines have emerged in the global race to find a way to stop the spread of COVID-19, many scientists and researchers believe antibody based therapies hold great promise for treating people already infected with the disease.

HOW DO ANTIBODY THERAPIES WORK?

These therapies use antibodies generated by infected humans or animals to fight off the disease in patients. They date back to the late 19th century, when researchers used a serum derived from the blood of infected animals to treat diphtheria.

For COVID-19 treatment, researchers are studying the use of convalescent plasma and other treatments made with blood from recently recovered patients.

More recently, scientists have developed treatments called monoclonal antibodies -- antibodies that can be isolated and manufactured in large quantities to treat diseases like Ebola or cancer. Companies, like Eli Lilly and Co and Regeneron Pharmaceuticals in the United States, are trying to use this approach to develop their treatments.

Unlike convalescent plasma, manufacturers do not need a steady supply of antibody-rich blood to produce monoclonal antibodies, so this approach could be easier to scale up.

HOW ARE THEY DIFFERENT FROM VACCINES?

In general, the goal of a vaccine is to generate an immune response that can prevent someone from getting ill with a disease, whereas antibody-derived products are generally designed to treat disease.

And while some drugmakers have suggested antibody treatments can be used prophylactically - Regeneron's Chief Scientific Officer George Yancopoulos has said their treatment could be a bridge to a vaccine - it could be expensive.

"You might go into nursing homes or the military and use it because antibodies have a pretty long half life," said Dr. Betty Diamond, Director of Molecular Medicine at the Feinstein Institutes for Medical Research.

"You might decide that you are going to use this as a prevention in this very high risk group, but you wouldn't do that for the whole country."

The amount of protein in antibody drugs makes the treatment more expensive than vaccines in general, Feng Hui, chief operating officer at Shanghai Junshi Biosciences, said.

Designing antibody drugs to treat or protect high risk people, including those with weak immune systems, could require hundreds, or even over a thousand times more protein than found in a vaccine shot, according to Junshi.

WHO IS DEVELOPING ANTIBODY THERAPIES FOR COVID-19?

Eli Lilly is collaborating with Junshi and Canadian biotech firm AbCellera Biologics to develop different antibody treatments, both of which have started early stage testing in humans.

Regeneron plans to start clinical studies later this month to test its antibody cocktail treatment, which was derived from antibodies from genetically-modified mice. It aims to have hundreds of thousands of preventative doses available "by the end of the summer or the fall."

The CoVIg-19 Plasma Alliance, which includes Japan's Takeda Pharmaceuticals and CSL Behring, is working on hyperimmune globulin therapy derived from convalescent plasma, which could offer a standardized dose of antibodies and doesn't need to be limited to patients with matching blood types.

The Antibody Therapy Against Coronavirus (ATAC) project, funded by the European Commission and led by Sweden's Karolinska research institute, is looking at a similar approach as well as monoclonal antibodies. Under the project, monoclonal antibodies extracted from convalescent plasma are now being tested on human volunteers in Germany and on animals in Switzerland.

Britain's GlaxoSmithKline is working with Vir Biotechnology Inc to develop potential antibody treatments which select the best antibodies out of the plasma.

AbbVie has also announced a collaboration to develop antibody therapies.

Singapore's state research body A*Star is working with Japan's Chugai Pharmabody Research on an antibody for clinical use.

(Reporting by Michael Erman; Additional reporting by Francesco Guarascio in Brussels, Roxanne Liu in Beijing and John Geddie in Singapore; Editing by Miyoung Kim & Simon Cameron-Moore)

See original here:
Explainer: What Are Antibody Therapies and Who Is Developing Them for COVID-19? - The New York Times

The paper also suggests the likeliness of the gut microbiota being disrupted in severe COVID-19 patients, which may affect disease outcomes, including predisposition to secondary bacterial infections of the lung.

Jose Bengoechea, Professor of Molecular Microbiology and Director of Wellcome Wolfson Institute for Experimental Medicine at Queen's University, explains: "The lack of therapies to treat severe COVID-19 patients led clinicians to use a number of treatments to modify the activity of their immune system.

"However, it is important to note that these interventions may also increase the risk of potentially fatal secondary bacterial respiratory infections.

"Therefore, careful consideration should be given whether any potential new therapy may affect the patients' defences against bacterial infections. We believe that there is an urgent need to develop new therapeutics to treat COVID-19 targeting the virus/bacteria co-infection scenario."

The research also raises concerns about the impact of COVID-19 on antimicrobial resistance (AMR) globally.

See more here:
COVID-19: Researchers warn of sharp rise in antimicrobial resistance - National Herald

Estonian scientists are developing a DNA-based method of analysis that enables them to identify food components and specify the origin of a foodstuff.

Bioinformatics specialists at the University of Tartu, in cooperation with the Competence Centre on Health Technologies, have published a research paper in the journal Frontiers in Plant Science in which they indicated the possibility to identify components in thermally processed food using DNA analysis even if the quantities were very small. The scientists analysed thermally processed cookies that contained a small amount of lupin flour. The DNA analysis provided reliable identification of lupin even when the lupin flour content in the dough was just 0.02%.

Food always contains the DNA traces of the plants, animals and microorganisms that have been used or that the food or its raw materials have come into contact with in the production process. DNA analysis can provide valuable information on the content, origin, safety and health benefits of food and will make the identification of counterfeit foods and non-compliances in the ingredients specified on the packaging more reliable in the future. For example, certain cases gained attention last year in which the origin of honey and the authenticity of Estonian honey needed verification. The novel DNA analysis would make it possible to solve such issues.

According to Kairi Raime, the lead author of the article, Research Fellow of Bioinformatics at the Institute of Molecular and Cell Biology and a doctoral student at the University of Tartu, their method is a major step forward in the development of DNA-based methods for food analysis. Our method helps to identify the actual biological contents and origins of food via DNA information and thus ensures the safety and authenticity of the food, she explained. Raime is planning to defend her PhD dissertation on the topic.

The DNA may be significantly degraded in processed food. Scientists extracted DNA from the cookies and analysed it using DNA sequencing technology. For the analysis of a single biscuit, approximately 20 million DNA sequences were obtained. Based on these, and by using bioinformatic analysis, it was possible to specify the DNA of the species found in the sample analysed. The main issue was the preparation of the DNA for sequencing, as the DNA is often degraded in food and even minute amounts of DNA molecules must be identified.

Kaarel Krjutkov, Head of the Precision Medicine Laboratory of the Competence Centre on Health Technologies and Senior Research Fellow of Molecular Medicine at the University of Tartu, whose laboratory was used to prepare the sequencing of the DNA extracted from the biscuits, noted that faking the DNA fingerprint of a food is complicated and expensive, and it is therefore cheaper to offer authentic food. People can see that in medicine, precise DNA analysis is already a reality, but in food industry and in the field of food safety, the golden age of DNA-based analysis is yet to come, Krjutkov remarked.

The research used a method based on short, unique DNA sequences (k-mers) for analysing genomic DNA data, which enables the scientists to quickly identify plant or bacterial DNA present in a food or an environmental sample. The Chair of Bioinformatics at the Institute of Molecular and Cell Biology at the University of Tartu has been developing competence in the bioinformatics of k-mers and DNA analysis over the last five years. The software developed in the Chair of Bioinformatics has been used both in medicine and for providing food safety.

The article authors earlier cooperation resulted in the NIPTIFY foetal chromosomal disorder test, which helps to detect, with almost 100% accuracy, the DNA sequences causing foetal Down syndrome in the mothers blood sample as early as the tenth week of pregnancy. The genome analysis method developed in the Chair of Bioinformatics is used to identify pathogenic bacteria, specify their disease-causing capabilities and predict antibiotic resistance. This enabled Maido Remm, Professor of Bioinformatics at the University of Tartu, and his working group to advise the management board of a production company contaminated with a dangerous strain and to help determine the spread of type ST1247 in the company during the listeria outbreak in autumn 2019.

According to Remm, the research article proves that DNA sequencing can also be used for identifying allergenic ingredients in processed food. DNA sequencing is a promising diagnostic method which makes it possible to quickly obtain precise information about food and the microbes around us, he said. The use of sequencing and k-mers makes it possible in a very short time to implement a diverse range of diagnostic tests that meet the needs of researchers and companies.

Read this article:
Novel DNA analysis will help to identify food origin and counterfeit food in the future - Baltic Times

Arsenicum album 30C (Aa30C) is a homeopathic drug that Indias Ministry of AYUSH prescribed through an advisory on March 6, in the context of the COVID-19 pandemic. In section i. Preventive and prophylactic and sub-section Homoeopathy, the ministry advised the recommended dose thus: Arsenicum album 30, daily once in empty stomach for three days.

To make the drug, a mother tincture of the medicine is first made by dissolving by arsenic trioxide in a mixture of glycerine, alcohol and water or sometimes by heating arsenic with water. One millilitre of this tincture is diluted with 99 ml of water plus ethyl alcohol, and given a few machine-operated, moderate, equal and successive jerks, called succussions. This leads to a 100-fold dilution. The process is repeated 30-times to produce the final product, of 30C potency. A few drops of this, loaded on sugar pills, is administered to an individual. Apparently, each dilution plus succussion step makes the formulation more potent, and the process is called potentisation.

Starting with a mother tincture that has 200 grams of arsenic trioxide in 1 litre of liquid, the 30C potency medicine has one molecule of the active material present in a volume equivalent to that of 1 million Suns. In terms of the active material, an individual is consuming zero molecules.

However, this should not surprise us. Homeopathy was first proposed in Germany by Samuel Hahnemann (1755-1843) as an alternate medicinal strategy, more than 200 years ago. This was a time when the chemistry to show the above effect was not known (now it is in school textbooks). This was also an era where orthodox medicine was crude, often involving blood-letting. Compared to this, homeopathy seemed safe and humane. But today, when science has since made numerous strides, it is problematic that homeopathic principles still evade the rigours of scientific questioning.

From nothingness to water memory

Homeopathy takes recourse in the notion that water, when it comes in contact with the active material, develops molecular memory. In the absence of this active material in the final formulation, it is this memory-laden water that triggers an immune response in the human body. Note that the active material arsenic, in this case is chosen based on the homeopathic law of similars, i.e. a substance that induces the symptoms of a disease.

Unfortunately, there is no evidence of water having any kind of memory. Even the journal Nature was touched by this controversy. It should also strike us that if water remembered what it touched, it would have lots of memories of anything it touched.

Any scientific response to such lack of evidence should be rigorous experimentation to demonstrate effects, or the lack of it. However, the actual response to any critique of homeopathy has often been that science does not know everything yet.

The quest to explain how homeopathy works has also led to hypotheses that suggest the active material somehow survives in even the most dilute homeopathic medicines. Here, the original active material finds its way into the final drug via interaction of the drug and bubbles formed during succussions. However, the methods used in the study are not standard for potentisation. The physics of bubbles catching the active material is unclear, and control experiments like checking for contaminants were not performed.

More importantly, even if traces of active material are present, how do they trigger physiology to act against an external agent (like the novel coronavirus)? We dont know. For a chemical to be accepted as a drug, it takes years of experimentation, involving laboratory experiments, animal trials and human trials over multiple phases. But proponents of homeopathy have claimed that it cannot be subjected to such trials because it provides highly individualised doses. However, the mass distribution of Aa30C is anything but individualised.

Most popular narratives on homeopathy consist of anecdotes and scientific-sounding terms like vital force or biphasic actions. Hahnemann himself explained that homeopathy worked through a dematerialised spiritual force.

We also hear things like a thousand people were given this medicine and then 95% did not get the disease, so it works. This is not what a trial is and these experiments are worthless unless compared with 1,000 people who are given placebos (i.e. blank doses).

The fact that homeopathy thrives is not proof of its efficacy just like the existence of tarot readers and astrologers does not prove that these practices have any scientific basis.

Homeopathy puts on an aura of respectability thanks to scientific journals from major publishers that cater to it.

Many reputed institutions have looked at the available literature and their conclusions are unequivocal. The US National Institutes of Health say, Theres little evidence to support homeopathy as an effective treatment for any specific health condition. The UKs National Health Services (NHS) state, Theres been extensive investigation of the effectiveness of homeopathy. Theres no good-quality evidence that homeopathy is effective as a treatment for any health condition.

A report prepared by a committee appointed by the UK parliament in 2010 called the British governments position on homeopathy confused and recommended that the government stop funding homeopathy on the NHS. The report argued that homeopathy undermines the relationship between NHS doctors and their patients, reduces real patient choice and puts patients health at risk. Since 2017, the NHS has severely restricted access to homeopathy.

After an extensive literature survey, Australias National Health and Medical Research Council concluded in 2015 that there was no reliable evidence from research in humans that homeopathy was effective for treating the range of health conditions considered: no good-quality, well-designed studies with enough participants for a meaningful result reported either that homeopathy caused greater health improvements than placebo, or caused health improvements equal to those of another treatment.

Also read: Will COVID-19 Change AYUSH Research in India for the Better?

A false shield

A much-quoted statement by the WHO sometimes distorted during the Ebola outbreak in 2014 said, In the particular context of the current Ebola outbreak in West Africa, it is ethically acceptable to offer unproven interventions that have shown promising results in the laboratory and in animal models but have not yet been evaluated for safety and efficacy in humans as potential treatment or prevention (emphasis added). However, the words in bold are often omitted in public statements, such as in the AYUSH ministry advisory.

All the hype and publicity surrounding Aa30C have set the stage for people to desperately chase what they think is a wonder drug. Clarifications of the type issued by the AYUSH ministry, stating that their recommendation is only in the general context or that it is only for add-on preventive care, is like water off a ducks back. Panic-buying of Aa30C has already been reported. News of random, untracked distributions by various agencies and buyers flocking to pharmacies to buy the concoction at inflated prices continue to pour in.

The problem is significant because people are likely to believe that by imbibing this medicine, they have just acquired a shield against the COVID-19. A corporator in Mumbai mentioned that some people, when questioned about their being out during a lockdown, said that they had taken Arsenicum album. They believed that they would now be immune to the disease.

Anurag Mehra, Supreet Saini and Mahesh Tirumkudulu teach in IIT Bombay.

Read more:
A Homeopathic Defence Against COVID-19 Is No Defence at All - The Wire

Computational analysis of large datasets is becoming increasingly important in many areas of scientific research. This is particularly true in molecular biology, where we study the molecular underpinnings of life. Here, research is broadly classified as wet-lab or dry-lab depending on its nature.

A wet-lab is a traditional experimental laboratory in which scientific research is carried out using chemicals and biological samples (including patient material). These substances or materials require special handling by trained professionals, using sensitive equipment. Such experiments allow us to study some phenomenon, to try and understand or explain what we observe.

A dry-lab is a laboratory where real-world phenomena are studied and analysed using computational, statistical and mathematical techniques. Scientists here build computer models to simulate the occurrence under investigation. The data used to construct these models is usually sourced from wet-lab experiments.

Researchers in wet and dry-labs work in unison to further scientific discovery. For example, computational scientists in a dry-lab identify a handful of promising drugs from a database of millions of molecules. These selected molecules are then physically tested in a wet-lab and the computational results are confirmed or refuted. Molecules which are confirmed with a wet-lab experiment are used to refine further computational searches. More targeted lists of potential drugs for experimental verification are generated in an iterative, cyclic process.

Despite the recent drive to push experiments from in vivo (in living organisms), to in vitro (in a test tube), to in silico (in a silicon chip or computer) to reduce time and cost, it is not possible to conduct proper scientific research without integrating wet and dry approaches.

Researchers in wet-labs and dry-labs have different backgrounds and training. Dry-lab scientists generally have a background in mathematics and computer programming. Wet-lab researchers typically have backgrounds in more traditional sciences and laboratory techniques.

Nowadays, the interdisciplinary nature of modern research requires a researcher to have skills in both areas. Students are particularly encouraged to train in both wet- and dry-lab techniques to gain a feeling and understanding of what interests them most.

Jean Paul Ebejer is a computational scientist who specialises in bioinformatics and computer-aided drug design. Byron Baron is a wet-lab scientist who specialises in protein science. They are both lecturers in dry and wet-lab techniques at the Centre for Molecular Medicine and Biobanking at the University of Malta.

Tiny insects called aphids are essentially born pregnant, says Ed Spevak, curator of invertebrates at the St Louis Zoo. Aphids reproduce asexually, producing miniature replicas of themselves, Spevak adds. When that happens, a newly-hatched female has eggs already growing inside of her. Aphids will also use sexual reproduction when their environment say, the weather becomes unpredictable. This ensures offspring are more genetically diverse, and thus healthier and more resilient.

A team of scientists studying the origin of SARS-CoV-2, the virus that has caused the COVID-19 pandemic, found that it was especially well-suited to jump from animals to humans by shapeshifting as it gained the ability to infect human cells. Conducting a genetic analysis, researchers from Duke University, Los Alamos National Laboratory, the University of Texas at El Paso and New York University confirmed that the closest relative of the virus was a coronavirus that infects bats. But that viruss ability to infect humans was gained through exchanging a critical gene fragment from a coronavirus that infects a scaly mammal called a pangolin, which made it possible for the virus to infect humans.

https://www.sciencedaily.com/releases/2020/05/200529161221.htm

For more soundbites, listen to Radio Mocha every Saturday at 7.30pm on Radju Malta and the following Monday at 9pm on Radju Malta 2 https://www.fb.com/RadioMochaMalta/

According to Guinness, Guinness is not black but dark red.

The scientific name for the Plains bison is Bison bison bison.

The WHO estimates that one million healthy life years are lost in Western Europe every year due to noise pollution.

Europes highest railway station is underground (it is found in the Swiss Alps).

Nihonium, number 113 in the periodic table, was created in the lab by firing atoms into each other. The team were successful just three times in over four trillion attempts.

For more trivia, visit http://www.um.edu.mt/think

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Dry- and wet-lab research: two sides of the same coin - Times of Malta