Wednesday, April 29, 2020

Oxford’s Coronavirus Vaccine might be ready before the end of this year

 COVID-19 vaccine may come out before the year ends, earlier than previous predictions that the production process might take a year or more. Researchers at Oxford University in England said their vaccine showed positive effects and million doses could be available by September.
The team at the university's Jenner Institute said the vaccine has already been proven harmless to humans in tests with other forms of coronavirus in the past year. That put them a few steps ahead of other ongoing experiments around the world. 
Most researchers need to start with small clinical trials. The Oxford team has been authorized to move to a combined Phase II and Phase III trial in May with more than 6,000 people to prove the effectiveness and safety of their potential coronavirus vaccine, the New York Times reported Monday.
Aside from the past year's study, a test in March at the National Institutes of Health's Rocky Mountain Laboratory in Montana provided new evidence that the Oxford vaccine works against COVID-19. Six rhesus macaque monkeys that received single doses were able to avoid infection even after exposure to heavy quantities of the virus. 
"The rhesus macaque is pretty much the closest thing we have to humans," Vincent Munster, one of the researchers who conducted the test, said. The team has yet to publish the findings in a peer-reviewed journal.
In the upcoming large-scale human trial, the Oxford researchers could consider the test as successful if a dozen participants in the placebo group become sick with COVID-19 compared to only one or two persons who receive the vaccine.
"It is a very, very fast clinical program," Emilio Emini, a director of the vaccine program at the Bill and Melinda Gates Foundation, said. "This big U.K. study is actually going to translate to learning a lot about some of the others as well."
If the Oxford trial fails, the study will still have a significant contribution to the global effort to find an effective vaccine for COVID-19. Other research teams could use data from the study to understand the nature of the coronavirus and how the immune system responds to infection and treatments. 

Trypophobia (fear or disgust of closely-packed holes) in details

Trypophobia is a fear or disgust of closely-packed holes. People who have it feel queasy when looking at surfaces that have small holes gathered close together. For example, the head of a lotus seed pod or the body of a strawberry could trigger discomfort in someone with this phobia.
Honey Bees on Honeycomb | High-Quality Animal Stock Photos ...
The phobia is not officially recognized. Studies on trypophobia are limited, and the research that is available is split on whether or not it should be considered an official condition.

Not much is known about trypophobia. But common triggers include things like:
  • lotus seed pods
  • honeycombs
  • strawberries
  • coral
  • aluminum metal foam
  • pomegranates
  • bubbles
  • condensation
  • cantaloupe
  • a cluster of eyes
Animals, including, insects, amphibians, mammals, and other creatures that have spotted skin or fur, can also trigger symptoms of trypophobia.

Symptoms are reportedly triggered when a person sees an object with small clusters of holes or shapes that resemble holes.
When seeing a cluster of holes, people with trypophobia react with disgust or fear. Some of the symptoms include:
  • goosebumps
  • feeling repulsed
  • feeling uncomfortable
  • visual discomfort such as eyestrain, distortions, or illusions
  • distress
  • feeling your skin crawl
  • panic attacks
  • sweating
  • nausea
  • body shakes

Researchers don’t agree on whether or not to classify trypophobia as a real phobia. One of the first studiesTrusted Source on trypophobia, published in 2013, suggested that the phobia may be an extension of a biological fear of harmful things. The researchers found that symptoms were triggered by high-contrast colors in a certain graphic arrangement. They argue that people affected by trypophobia were subconsciously associating harmless items, like lotus seed pods, with dangerous animals, such as the blue-ringed octopus.
studyTrusted Source published in April 2017 disputes these findings. Researchers surveyed preschoolers to confirm whether the fear upon seeing an image with small holes is based on a fear of dangerous animals or a response to visual traits. Their results suggest that people who experience trypophobia don’t have a nonconscious fear of venomous creatures. Instead, the fear is triggered by the creature’s appearance.

Related: Menstrually Related Mood Disorders
The American Psychiatric Association’s “Diagnostic and Statistical Manual,” (DSM-5) doesn’t recognize trypophobia as an official phobia. More research is needed to understand the full scope of trypophobia and the causes of the condition.


Not much is known about the risk factors linked to trypophobia. One studyTrusted Source from 2017 found a possible link between trypophobia and major depressive disorder and generalized anxiety disorder (GAD). According to the researchers, people with trypophobia were more likely to also experience major depressive disorder or GAD. Another study published in 2016 also noted a link between social anxiety and trypophobia.

To diagnosis a phobia, your doctor will ask you a series of questions about your symptoms. They’ll also take your medical, psychiatric, and social history. They may also refer to the DSM-5 to help in their diagnosis. Trypophobia is not a diagnosable condition because the phobia is not officially recognized by medical and mental health associations.

There are different ways a phobia can be treated. The most effective form of treatment is exposure therapy. Exposure therapy is a type of psychotherapy that focuses on changing your response to the object or situation causing your fear.
Another common treatment for a phobia is cognitive behavioral therapy (CBT). CBT combines exposure therapy with other techniques to help you manage your anxiety and keep your thoughts from becoming overwhelming.
Other treatment options that can help you manage your phobia include:
  • general talk therapy with a counselor or psychiatrist
  • medications such as beta-blockers and sedatives to help reduce anxiety and panic symptoms
  • relaxation techniques, such as deep breathing and yoga
  • physical activity and exercise to manage anxiety
  • mindful breathing, observation, listening, and other mindful strategies to help cope with stress
While medications have been tested with other types of anxiety disorders, little is known about their efficacy in trypophobia.
It may also be helpful to:
  • get enough rest
  • eat a healthy, balanced diet
  • avoid caffeine and other substances that can make anxiety worse
  • reach out to friends, family, or a support group to connect with other people managing the same issues
  • face fearful situations head on as often as possible

Trypophobia isn’t an officially recognized phobia. Some researchers have found evidence that it exists in some form and has real symptoms that can impact a person’s everyday life if they’re exposed to triggers.
Speak with your doctor or a counselor if you think you may have trypophobia. They can help you find the root of the fear and manage your symptoms.

credit: healthline

Research: Our bodies can detect sugar without tasting it

Sugar is everywhere in today’s food system and one of the most common ingredients in processed foods. It is often described as addictive.
The Senses: receptors / rod and cone cells some of the cells can detect sugar

Since refined sugar became widely available in the United States, the average consumption per person in the country increased by 10 times, to more than 45 kilograms per year.

The Centers for Disease Control and Prevention (CDC) estimate that people in the U.S. now derive around 14% of their daily calories from added sugar.

Such high consumption rates are concerning, given sugar’s association with type 2 diabetes and obesity, both of which are on the rise in the Western world.

Now, researchers from Columbia University, in New York, have identified some of the brain mechanisms behind sugar consumption, which may explain why sugar causes cravings that artificial sweeteners just can’t meet.
Related: Plant-based diet could help lower your risk of type 2 diabetes.

The findings are available in the journal Nature.

It all starts with taste receptors

Sugar is an important energy source for all animals, including humans. As a result, we have evolved specialized neural circuits to recognize and seek out sugar, and these start in the mouth.

The tongue has specific taste receptors to detect sweetness. These are activated by sugar, and they send signals to the brain.

Interestingly, though, animals can develop strong cravings for sugar, even if they lack the taste receptors for it, as the authors of the present study point out.

What’s more, they report, if animals without sweet taste receptors are given two drinks, one sweetened with sugar and the other with artificial sweetener, they still choose the sugary drink — despite being unable to taste either.

This suggests that the body may recognize sugar in another area, perhaps further down the digestive pathway.

To investigate, the researchers, from Columbia’s Zuckerman Institute, set out to look for these additional receptors in mice.
The gut-brain axis
The team began by administering sugar directly to the gut, bypassing the taste receptors entirely.

This is because there is a well-known connection between the gut and the brain, called the gut-brain axis. Seeing and smelling food, for example, causes the gut to secrete digestive fluids.

It seems that a similar connection exists for sugar. When the researchers gave the mice sugar directly to their guts, a region of their brains lit up with activity.

This region, called the caudal nucleus of the solitary tract, is part of the brain stem, one of the brain’s most primitive parts, which regulates fundamental processes such as breathing and heart rate.

“Something was transmitting a signal, indicating the presence of sugar, from the gut to the brain,” explains Alexander Sisti, Ph.D., a joint first author of the paper.

Related: How long can brain survive after the heart stops? (BRAIN DEATH)


Sugar-sensing neurons

Next, they wanted to find the receptor in the gut and shifted their attention to the vagus nerve. This is one of the longest nerves in the body, running from the brain stem to the colon, and it is a major method of communication between the gut and the brain.

The researchers watched the activity of cells in the vagus nerve when sugar was delivered to the gut, finding — for the first time — a group of sugar-sensing neurons in the pathway from the gut to the brain.

“By recording brain-cell activity in the vagus nerve, we pinpointed a cluster of cells in the vagus nerve that respond to sugar,” Sisti explains.

These receptors in the gut were activated by sugar — but not artificial sweeteners, which may explain why sweeteners have not significantly reduced sugar consumption since they were widely introduced 40 years ago.

Tricking the tongue, as well as the brain

Going forward, these findings could lead to the design of sweeteners that do a better job of tricking our neural circuitry.

“When we drink diet soda or use sweetener in coffee, it may taste similar, but our brains can tell the difference,” says joint first author and Ph.D. candidate Hwei-Ee Tan.

“The discovery of this specialized gut-brain circuit that responds to sugar, and sugar alone, could pave the way for sweeteners that don’t just trick our tongue but also our brain,” Tan explains.

It seems that this circuit recognizes the sugar molecule but does not depend on its caloric content, which is promising news for manufacturers interesting in developing healthier substitutes that activate the circuitry but contain fewer calories.

“These findings could spur the development of more effective strategies to meaningfully curtail our unquenchable drive for sugar, from modulating various components of this circuit to potentially [designing] sugar substitutes that more closely mimic the way sugar acts on the brain,” Tan adds.
Related article: Dental disease and missing teeth associated with increased risk in diabetes

Tuesday, April 28, 2020

This is how nanotechnology can help to fight COVID-19

Doctors have few tools to help tame this hyperinflammatory condition, but early research is suggesting that nanotechnology might safely deliver drugs to affected tissues, quieting the storm.
Nanotechnology – can help in fight against COVID-19
It's so far only been tested in mice, but researchers in Brazil and France said the approach could be "a new tool in the fight against the complex and multi-factorial phenomenon of uncontrolled inflammation." They reported their findings online April 27 in the journal Science Advances.
It's not clear why some young, robust patients experience life-threatening illness from COVID-19, while others have either mild or no symptoms.
But when severe illness does strike, it's often in the form of an out-of-control immune system response.
Inflammatory processes harm cells at multiple sites throughout the body and, if unchecked, this can lead to organ failure and death, noted a team led by Dr. Patrick Couvreur at the Institute Galien Paris-Sud, in France.
Key to the cytokine storm are connections "between inflammation and oxidative stress, both processes contributing to fuel one another, thereby establishing a vicious cycle," Couvreur's group explained.
Right now, there's no therapy that's able to interrupt this dangerous "crosstalk," they said. For example, anti-inflammatory drugs such as corticosteroids have not worked, because of their negative effects on tissue repair.
But the new findings may point the way to a successful treatment.
In their work, Couvreur's group focused on an extremely tiny "nanoparticle" formulation of adenosine, an anti-inflammatory compound already produced naturally by the body.
It's a powerful anti-inflammatory compound—maybe too powerful. If simply injected into the body, adenosine can trigger serious side effects, the research team said.
But the new nanotechnology approach appears to get around that, they added.
Couvreur's team created "multi-drug nanoparticles" by adding adenosine to squalene, a type of fat also found naturally in the body. Then they "encapsulated" both in the powerful antioxidant alpha-tocopherol, a type of vitamin E.
Using this nanotechnology approach, the researchers then delivered the compounds to the tissues of mice who were in hyperinflammatory states such as sepsis (blood infection) or an immunological state resembling the typical "cytokine storm" of COVID-19.
The result: A notable decrease in tissues of a key pro-inflammatory cytokine called tumor necrosis factor alpha, along with a concurrent rise in levels of an anti-inflammatory cytokine called interleukin-10, the researchers reported.
These changes were observed in important organs such as the lungs and kidneys just four hours after treatment, Couvreur's group said.
The team added that the combo treatment—adenosine plus tocopherol—appeared more effective than the use of either drug alone.
Of course, this study was conducted in mice, and many therapies that appear promising in animals don't pan out in humans. But Dr. Matthew Heinz, an expert in the fight against infectious diseases, said the findings do "make sense."
"I'm surprised this was something they were able to do so quickly," said Heinz, an internist and hospitalist at Tucson Medical Center in Arizona. "It's pretty encouraging to have evidence that something like this might help some of our more critically ill COVID-19 patients survive the hyperimmune response known as a cytokine storm."
Heinz previously worked in the Obama administration's response to the Ebola crisis, and was the former director of provider outreach in the Office of Intergovernmental and External Affairs, at the U.S. Department of Health and Human Services.
Reading over the new findings, he said that "because the research is COVID-related, it's quite possible this could be moved into human trials a lot quicker than during normal times."
Heinz added that "this is still a relatively early stage—we have a little ways to go here—but it's good to see this kind of research already coming out with some very encouraging results on how to approach this tremendously heartbreaking situation that's killing tens of thousands of people in the United States."
More information: Flavio Dormont et al. Squalene-based multidrug nanoparticles for improved mitigation of uncontrolled inflammation, Science Advances (2020). DOI: 10.1126/sciadv.aaz5466
Journal information: Science Advances 

Monday, April 27, 2020

How New Zealand achieved her victory against virus transmission

Prime Minister Jacinda Ardern on Monday claimed New Zealand had scored a significant victory against the spread of the coronavirus, as the country began a phased exit from lockdown.
Way Too Early" To Predict the End of Coronavirus Outbreak: WHO ...
"There is no widespread, undetected community transmission in New Zealand," Ardern declared. "We have won that battle."
After nearly five weeks at the maximum Level Four restrictions—with only essential services operating—the country will move to Level Three late on Monday.
That will allow some businesses, takeaway food outlets and schools to reopen.
But Ardern warned there was no certainty about when all transmission can be eliminated, allowing a return to normal life.
Everyone wants to "bring back the social contact that we all miss", she said, "but to do it confidently we need to move slowly and we need to move cautiously."
"I will not risk the gains we've made in the health of New Zealanders. So if we need to remain at Level Three, we will."
The easing of restrictions came as New Zealand, a nation of five million people, reported only one new case of COVID-19 in the past 24 hours, taking the total to 1,122 with 19 deaths

The increase in indoor carbon dioxide during this Corona virus stay home could reduce the thinking ability

See the source image
To combat the alarming global Corona virus pandemic governments have put measures to the population to stay in theirs homes in order to contain  the virus. during this stay home 90% of the people spend their time in indoors, in rooms with poor air quality and ventilation, Hence it is more important than before to make sure that the indoor air quality is healthy and CO2 levels are maintained at no more than 600ppm. Studies have shown that there are several times in a day when the CO2 in a room spikes to 1000ppm and more. This is indeed an unhealthy level of carbon dioxide and a cause for concern.
The elevated levels of carbon dioxide or CO2  impairs our cognitive ability.  It known that carbon monoxide and other VOCs (Volatile Organic Compounds) caused problems like asthma. CO2 was ignored and was not considered a gas that could be harmful. Yet many types of research conclude otherwise.

In studies done ,they found modest changes in the indoor air quality to have a major impact on a person’s decision making ability.

How does it affect our thinking ability?

According to medical research increased level of CO2 in the blood decreases the cerebral metabolism of oxygen. In simple words, the brain becomes oxygen deprived and has an impact on our thinking abilities. It is a well documented fact of what high levels of carbon dioxide can do to the brain. Space travel, scuba diving, fire fighting, airplanes and submarines are examples where high carbon dioxide levels have lead to fatalities.


Carbon dioxide dissolves in our blood and reacts with the water in our blood to create carbonic acid. This, in turn, dissolves into ions of hydrogen and bicarbonate. If there is an increase in the concentration of hydrogen ions in our blood the blood acidity level increases and creates electrolyte imbalance, causing increased discomfort and decline in intellectual performance. If you feel tired after just a couple of hours indoor (when you have had a restful night), feel sleepy, it could mean that the indoor air quality needs to be inspected for CO2.
People can argue that they spend at least an hour outdoors every day but, does that help? With our current lifestyle, most of us spend 90% of our time awake indoors in addition to the time we sleep. Whether it’s your home  the quality of the air circulating within could be poor with concentrated amounts of carbon dioxide. So, irrespective of the number of hours you spend outdoors, if the air quality indoors isn’t healthy you end up feeling sick.


 How can the indoor air quality be improved?


Improving the indoor air quality is important and here are a few easy and effective ways to improve your indoor air quality and reduce the concentration of carbon dioxide.


·        Make sure your home  has a periodic supply of fresh air. Opening windows for a few minutes two or three times a day can improve the air quality to a large extent


·        Keeping a few indoor plants that release oxygen especially at night helps improve the air quality by absorbing carbon dioxide, even after the sun goes down. Aloe Vera, Peepal, Tulsi (Indian Basil), and Gerbera are a few examples

·        Make sure that nobody smokes indoors. Indoor air quality turns poor with secondary smoke and is an important contributor to indoor air pollution

·        Installation of exhaust fans especially in kitchens helps reduce carbon dioxide released during cooking. Making sure that the smoke released during cooking does not circulate indoors. The absence of exhausts will increase the levels of carbon dioxide. This is especially important for smaller restaurants and houses

·        Regular maintenance of your HVAC (heating, ventilating and air conditioning) will ensure that there is no accumulation of CO2 indoors






Wednesday, April 22, 2020

US: Stem cell clinical trial for COVID-19 patients gets emergency federal approval

seem cellA team of doctors at the University of Miami (UM) Miller School of Medicine received emergency approval from the U.S. Food and Drug Administration (FDA) to conduct a clinical trial to treat patients with severe lung inflammation as a result of COVID-19.
The doctors will use stem cells obtained from umbilical cord blood and will deliver them via intravenous (IV) infusion to 12 patients. IV infusions of stem cells are known to travel directly to the lungs, the location where damage is being caused in severe cases of COVID-19. When a patient contracts the virus, their body produces cytokines, proteins that play an important role in the immune response. Unfortunately, having too many cytokines, known as a "cytokine storm", leads to a severe immune reaction which causes damage to the lungs.
Umbilical cord stem cells are known to contain anti-inflammatory properties and the UM team hopes that the treatment can alleviate the "cytokine storm" and lung inflammation. The rationale for this approach is based off of a small study in China where seven patients received this treatment and showed improvement in lung function and symptoms. Despite these positive results, it is important to note that this trial is in very early testing and will need to demonstrate significant improvement in larger patient groups.
In an article from the Miami Herald, Dr. Camillo Ricordi, principal investigator of the trial, discusses how the results of the therapy will be observed very quickly if successful.
"This is not a study you have to follow up with in six months, because the results are immediate. In one week, you know: Is it working or not?"
In the same article from the Miami Herald, Dr. Ricordi discusses how the team of UM researchers and doctors are preparing to expand the trial to more patients if it is successful.
"We are already doing cell production anticipating this. We are planning for success, but of course we have to see how it does with our patients."

A new malaria vaccine candidate

malaria
Researchers have discovered a promising new strategy for combating malaria, a mosquito-borne parasite that claims nearly a half-million lives each year.
For a study reported in the journal Nature, researchers screened blood samples from children who had natural immune resistance to severe malaria infection. The study identified an antibody to a particular malaria protein, called PfGARP, that appears to protect resistant children from severe disease. Lab tests showed that antibodies to PfGARP seem to activate a malarial self-destruct mechanism, causing parasite cells living inside human red blood cells to undergo a form of programmed cell death.
The team is hopeful that vaccinating individuals with PfGARP to generate anti-PfGARP antibodies, or directly infusing anti-PfGARP antibodies, would protect them against severe malaria. The team developed preliminary versions of those vaccines, and testing in nonhuman primates has shown promise, the researchers report.
"We demonstrated in two independent studies in nonhuman primates that vaccination with PfGARP protects against a lethal malaria parasite," said study senior author Dr. Jonathan Kurtis, a professor at the Warren Alpert Medical School of Brown University and laboratory director of the Center for International Health Research at Rhode Island Hospital. "What's exciting is that this is a vaccination strategy that attacks malaria in a way that it has never been attacked before—one in which the parasite becomes complicit in its own demise. We are hopeful that this vaccine, perhaps combined with other malarial antigens, will translate into a strategy that can help prevent severe malaria in people."
Testing of a human vaccine is likely years away, the researchers say, and there's no way to be certain it will work. But the team is hopeful that the approach taken in this study, which looks for the factors that contribute to naturally occurring disease resistance, will prove effective where other approaches have not.
Searching for antibodies
The results described in this new paper were nearly 20 years in the making, beginning with epidemiological research led by Michal Fried and Patrick Duffy of the National Institutes of Health. Starting around 2001, they began recruiting cohorts of children in Tanzania. The kids were enrolled at birth and followed for years to see who among them developed an acquired immune response to malaria.
"There was a ton of hard epidemiological work that went into simply identifying which kids were resistant and which weren't," Kurtis said. "Only after we knew their resistance levels could we use this information to identify the parasite targets that were recognized by antibodies made only by the resistant kids but not by the susceptible kids."
For this latest research, the team selected 12 resistant and 14 susceptible children from the Tanzanian cohort. The researchers looked at blood samples taken from the children around age two, when naturally acquired immunity seems to develop. Using a sophisticated method to introduce malaria proteins to each blood sample one by one, the researchers could look for any antibodies to a particular protein that were present in the resistant samples and not in the susceptible samples. That work identified PfGARP as a potential factor in conferring resistance.
Having identified PfGARP, the researchers then examined whether antibody responses to PfGARP were associated with resistance in a larger sample of 246 children. They found that children without anti-PfGARP antibodies were at 2.5 times higher risk of severe malaria compared to those who had the antibody.
"Kill switch"
The next step was trying to understand how anti-PfGARP antibodies affect the parasite. A series of laboratory experiments showed that the PfGARP protein is produced by malarial trophozoite cells, which live and feed off of nutrients inside red blood cells. The protein is then transported to the outer membrane of the red blood cell, where it makes the parasite cell vulnerable to the antibody.
"It's a kill switch," Kurtis said. "When the antibody binds to the protein, it sends a signal that tells the trophozoite to shrivel up and die. When we introduce the antibody to samples in petri dishes, we end up with 98% or 99% dead parasites."
The activity of the protein begs the question of why an organism would evolve such a self-destruct mechanism. Kurtis thinks it might have evolved as a means of sensing when the parasite's host is in distress.
"It's not necessarily in a parasite's best interest to kill its host," Kurtis said. "Keeping the host infected but alive means more chances for the parasite to reproduce. So what this might be is a means of sensing a host in distress and then reducing parasite load accordingly."
The anti-PfGARP antibody hijacks that evolved system and turns it against the parasite.
Having shown that PfGARP antibodies kill the parasite, the researchers developed two types of PfGARP vaccines. Both of those were shown to be protective in nonhuman primates exposed to a human form of malaria.
A new strategy
Previous efforts to develop vaccines against malaria have met with limited success. But the researchers involved in this latest work say there's reason to believe this new strategy may succeed where others have failed. That's because it attacks the parasite at a different point in the infection cycle from other vaccines.
When an infected mosquito bites someone, it injects thread-like cells called sporozoites, which travel through the bloodstream to the liver. There, the parasite morphs into a different type of cell called merozoites that exit the liver in large quantities to infect red blood cells. Once they've invaded red blood cells, the parasites morph again into trophozoites, which feed off of the nutrients inside the cell before they burst out to start the cycle again.
An existing vaccine that targets the first stage—aiming to prevent infection of the liver—has had limited success. That's partly, Kurtis says, because the time window to intervene is so small.
"It takes five minutes for the parasite to go from the mosquito to the liver," he said. "Because it's so quick, the amount of antibody needed to stop it is huge. And if just one sporozoite gets in, you've got malaria."
This new vaccine targets the trophozoite stage, which lasts up to a day, Kurtis says. The researchers are hopeful that the longer window for intervention will reduce the amount of antibody needed to kill the parasite, and thereby make for a more effective vaccine.
"This gives us 24 hours as opposed to 5 minutes to intervene," Kurtis said. "During that time, the parasite expresses PfGARP—a kill switch. We have designed a vaccine that activates it."
The researchers plan to continue testing different versions of the vaccine in animal models and ultimately to begin human trials in the coming years.
"This was an incredible team effort involving infectious disease experts, pathologists, epidemiologists, geneticists and molecular biologists," Kurtis said. "It really took all of these people to make this possible, and we're hopeful that the end result will be a vaccine that can save lives."
More information: Anti-PfGARP activates programmed cell death of parasites and reduces severe malaria, Nature (2020). DOI: 10.1038/s41586-020-2220-1 , https://www.nature.com/articles/s41586-020-2220-1
Journal information: Nature
Provided by Brown University

Tuesday, April 21, 2020

Study: Coronavirus Can Survive Higher Temperatures

 The new study reveals the coronavirus may be strong enough to withstand higher temperatures and won't die from it. 
Coronavirus Can Survive Higher Temperatures
Previously, experts hoped that the coming warmer months of summer can help eliminate SARS-CoV-2, which is the novel coronavirus strain behind the current pandemic. Based on previous similar pandemics and the typical cycle of the yearly flu season, their hopes made sense since these viruses usually start infecting people during the latter half of winter and start fading away when the summer comes.
As such, experts were hoping that even if summer does not outright kill the new coronavirus strain, they were hoping that summer would slow it down, at least until we develop a definitive vaccine for it.
This is the conclusion that researchers at the University of Aix-Marseille in France arrived to after the research that involved placing infected African green monkey kidney cells in a 140-degree Fahrenheit room was made. However, it's also important to know that the study hasn't been peer-reviewed yet.
Per the researchers, this new study had been tested in both "dirty" environments and "clean" laboratory conditions. In both scenarios, researchers said that both of these settings saw the virus replicate even while exposed for an hour at a temperature of 140 degrees. In fact, it took 15 minutes of exposure to 197.6-degree temperature to kill the virus.
To that end, the team behind the research also said that most of these patients had significantly lower viral loads, suggesting that lower heat levels may be effective in killing the virus after all. Then there's the preliminary results from a study conducted by the government, which supports the theory that warmer weather can slow down COVID-19.
"Sunlight destroys the virus quickly," the document said, suggesting that the virus can't survive in humidity, warmer temperatures and sunlight.
However, the Department of Homeland Security declined to confirm these supposed coronavirus findings, saying that "as policy, the department does not comment on allegedly leaked documents ."

Monday, April 20, 2020

Salt pregnancy test positive and negative


Are you wondering if you are pregnant or not? Or Are you suspecting to be pregnant due to an unprotected sex you had lately?

Here is a simple way to check by yourself if you are pregnant or not. It requires only salt. You do not have to visit a doctor or any health personnel. It is as simple and easy as ABC.
Salt is considered to be a very clean chemical compound since it is crystalline in nature. This characteristic nature of salt makes it a very good and popular chemical compound for testing if an individual is pregnant or not. Also, its chemical content is highly effective in detecting a hormone known as human chorionic gonadotropin (hCG) which is normally found in the urine of pregnant ladies or women.
This hCG (human chorionic gonadotropin) I am talking about is often released during pregnancy by the placenta.


Things you would need for the salt pregnancy test:

1. A transparent glass bowl (you can use any other bowl but most people prefer transparent glass bowl in order to notice clearly and quickly if there is a change in colour or not after the test).

2. Salt.

3. Urine.

3. Stirrer (it can be a spoon, spatula or anything that can be used to stir).


Follow the procedure below to test for pregnancy:

1. When you wake up early in the morning, the first thing to do is to go straight for the bowl and urinate into it.
Note: only morning urine should be used in order to acquire better results.

2. Now add a considerable amount of salt to the urine in the bowl.

3. Stir the solution with your stirrer for a few seconds.

4. Leave the solution for about ten (10) minutes.

5. Now, carefully check and observe if there is a change or not.


Conclusion.


If there is no change to the salt and urine, then you are probably not pregnant (negative).
Image result for salt pregnancy test positive and negative



But if the salt in the urine slightly or greatly changes or clumps and becomes like a milk cheese, then my dear, you are hundred percent (100%) pregnant (positive).

Saturday, April 18, 2020

Corona virus: use of hand sanitisers could boost antimicrobial resistance

Since the start of the coronavirus pandemic, scientists and governments have been advising people about the best hygiene practices to protect themselves. This advice has caused a significant surge in the sale and use of cleaning products and hand sanitisers. Unfortunately, these instructions rarely come with advice about using them responsibly or of the consequences of misuse.
But as with the misuse of antibiotics, the excessive use of cleaning products and hand sanitisers can lead to antimicrobial resistance in bacteria. There’s concern that the sudden overuse in cleaning products and hand sanitisers during the pandemic could lead to an increase in the number of antimicrobial-resistant bacterial species we encounter. This would put a greater strain on our already struggling healthcare systems, potentially leading to more deaths. What’s more, the problem could continue long after the current pandemic is over.
Antimicrobials (including antibiotic, antiprotozoal, antiviral and antifungal medicines) are important to our health. They help us fight against infections – particularly if your immune system is weak or compromised. However, some organisms (like bacteria) can change or mutate after being exposed to an antimicrobial. This makes them able to withstand the medicines designed to kill them. As the use and misuse of antimicrobials become more widespread, the number of resistant strains increases. Infections that were once easily treated are now becoming life threatening.
The processes that lead to antimicrobial resistance are many and varied. One route is through mutation. Some mutations occur after the bacteria’s DNA has been damaged. This can happen naturally during cell replication, or after exposure to genotoxic chemicals, which damage the cell’s DNA. Another route is if bacteria acquires resistant genes from another bacteria.
We usually (and correctly) associate antimicrobial resistance with the misuse of medications, such as antibiotics. Misuse could include failing to complete a course of antibiotics, or ignoring daily dose intervals. Both of these can increase the chance of the most resistant strains of bacteria in a population surviving and multiplying.
But bacteria can also acquire resistance after the inappropriate or excessive use of certain chemicals, including cleaning agents. Diluting sanitising agents, or using them intermittently and inefficiently, can provide a survival advantage to the most resistant strains. This ultimately leads to greater overall resistance.
Making matters worse are internet and social media “experts” offering advice about making homemade hand sanitisers they claim can kill the virus. For most of these products, there’s no evidence they’re effective. There’s also no consideration about any possible adverse effects from using them. What we do know is that many of these homemade products contain ingredients, such as alcohol, that have antibacterial properties in the right quantities. Anything that’s antibacterial has the potential to increase antimicrobial resistance.

Two novel viruses identified in Brazilian patients with suspected dengue

virus outbreakTwo new species of viruses have been identified in blood samples taken from patients in Brazil's northern region who had similar symptoms to those of dengue or Zika, such as high fever, severe headache, rash and red skin spots. One belongs to the genus Ambidensovirus and was found in a sample collected in the state of Amapá. The other belongs to the genus Chapparvovirus and was found in blood from the state of Tocantins. The study was supported by São Paulo Research Foundation - FAPESP. The results are published in the journal PLOS ONE.
"What surprised us most was finding an Ambidensovirus in a human sample. Viral species in this genus have been described only in insects, shellfish and other invertebrates. Never in mammals," said Antonio Charlys da Costa, a postdoctoral fellow at the University of São Paulo's Medical School (FM-USP) and one of the authors of the study.
According to Costa, different species of Chapparvovirus have been described in other mammals but, again, never in humans. "However, we don't yet know whether these viruses were active in the patients, let alone whether they caused the symptoms," he told.
For Eric Delwart, a senior investigator at the Vitalant Research Institute in the United States and supervisor of the project, scientists can use these findings to investigate whether novel viruses are present in other people in the region or in other populations and whether there is a risk of dissemination.
"So far no evidence has been found that these viruses have spread or that they're pathogenic," Delwart said. "However, it's scientifically interesting that Ambidensovirus has been detected in human hosts. The discovery shows how little we know about the ability of certain viruses to infect different kinds of cells."
Delwart also stressed the importance of reanalyzing existing clinical samples in  of potential emerging viruses. In the study discussed here, the samples analyzed were originally collected by central public health laboratories (LACENs) in several states across Brazil as part of their routine surveillance activities.
Viral diversity
The identification of the new species was possible thanks to a technique known as metagenomics, which entails the concomitant sequencing of all the genetic material in an entire blood, urine, saliva or fecal sample, including each of the microbes that exist within it. The technique can also be used, for example, to study all the bacteria and fungi in the soil of a region or to map the different species in a person's gut microbiota. Once all the  in a sample have been extracted and sequenced, bioinformatics tools are used to compare the results with known genome sequences described in databases.
Costa learned the methodology during his Ph.D. research, while he was on an internship at Delwart's laboratory. The supervisor in Brazil was Ester Sabino, a professor at FM-USP who headed the university's Institute of Tropical Medicine (IMT-USP) between 2015 and 2019.
The PLOS ONE article reports the results of analyses of 781 samples collected between 2013 and 2016. Anelloviruses were found in 80% of patients, while 19% contained type 1 human pegiviruses (HPgV-1). Neither genus is thought to cause significant pathologies. In 17%, the researchers detected parvovirus B19, which causes erythema infectiosum (slapped cheek syndrome or fifth disease), a common childhood ailment characterized by a mild fever and rashes on the face, arms, legs and trunk.
The viral species that had never been described, both belonging to the family Parvoviridae, were found in only two of the samples. The plasma samples were provided by the LACENs for Amapá, Tocantins, Paraíba, Maranhão, Mato Grosso do Sul, Piauí and Maranhão states.
"The study continues, and altogether we've received 20,000 samples for analysis. They send us samples that test negative for dengue, Zika and chikungunya. In our lab at IMT-USP, we perform molecular tests to detect other known flaviviruses [which cause yellow fever or West Nile fever, for example], alphaviruses [including Mayaro virus and several species that cause encephalitis] and enteroviruses [which can cause respiratory diseases and hand-foot-and-mouth syndrome, among others]. If we find none, we move on to the metagenomic analysis," Costa said.
The aim of the project, he added, is to describe the viral diversity found in Brazil and identify species that may be causing diseases in humans unnoticed amid outbreaks of disease caused by arboviruses.
A study published in the journal Clinical Infectious Diseases in 2019, for example, reported on a hidden outbreak of parvovirus B19 during a dengue epidemic in 2013-14. The principal investigator was the virologist Paolo Zanotto, a professor at the University of São Paulo. The study was supported by FAPESP.
"This is a significant case from a public health standpoint. If it infects pregnant women, parvovirus B19 can cause severe problems in their fetuses," Costa said.
Next steps
Further detailed studies will be required to determine whether the two novel viruses described are a human health hazard.
"We tried and failed to infect cell cultures in the lab, either because these viruses don't infect the type of cell used in the experiment or because the viral particles contained in the samples we analyzed were no longer viable. We don't know," Costa said.
However, the group obtained a second sample of the virus identified in the patient from Tocantins (a chapparvovirus) and is now developing a serological test. "The idea is to see whether this patient and their family have antibodies against this microorganism, in which case they were infected in the past and produced a response against the virus," Costa said.

Friday, April 17, 2020

COVID-19: How long is this likely to last?

Covid-19 | New ScientistLiving in self-isolation has profound socio-political implications, in addition to the effects that it has on a person’s mental health and well-being.

Although more and more studies are showing that quarantine and isolation methods are indeed effective and that we should all continue to keep our physical distance, it is hard not to grow impatient and wonder how long this is likely to last.
Medical News Today have spoken to several experts in infectious diseases, and in this Special Feature, we round up their opinions on the matter.
We also look at some of the predictions that other researchers have made on the availability of a vaccine and the impact it will have on the outcome of the pandemic.

The role of vaccines in a pandemic

The importance of vaccines in ending the pandemic is undeniable. But when will such vaccines become available? And should we wait?
Some experts have warned against relying on vaccines as a strategy for ending the current crisis.
Most vaccines are still likely to be 12–18 months away from being available to the entire population, and this period is long enough to cause lasting social and economic damage if the lockdown persists.
Speaking to the BBC about whether governments should rely on the advent of vaccines to end the pandemic, Mark Woolhouse, a professor of infectious disease epidemiology at the University of Edinburgh, United Kingdom, says, “Waiting for a vaccine should not be honored with the name ‘strategy;’ that is not a strategy.”
However, some researchers are optimistic that a vaccine will be available much sooner than the often quoted 12–18 months mark.

Vaccines: Between optimism and caution

For instance, Sarah Gilbert, a professor of vaccinology at Oxford University in the U.K., and her team have been working on a SARS-CoV-2 vaccine, which she believes will be available for the general population by the fall.
She explains that normally, it may take years of trials before a vaccine reaches the population, but during the pandemic, scientists can fast-track this process by doing as many of the necessary steps as possible in parallel.
“First, there is the need to manufacture the vaccine for clinical studies under tightly controlled conditions, certified and qualified — we need ethical approval and regulatory approval. Then, the clinical trial can start with 500 people in phase I.”
The vaccine could get approval “under emergency use legislation,” meaning that “in an emergency situation, if the regulators agree, it’s possible to use a vaccine earlier than in normal circumstances,” explains Prof. Gilbert.
Still, experts have cautioned that such estimates are overly optimistic. Their comments shed light on the difficulties of making vaccines available in general, not just Prof. Gilbert’s.
For instance, Prof. David Salisbury, associate fellow of the Centre on Global Health Security at the Royal Institute for International Affairs at Chatham House in London, U.K., warns, “[I]t is not just the availability of the first dose that we need to focus on.”
“We need to know by when there will be sufficient doses to protect all of the at-risk population, probably with two doses; and that means industrial scale manufacturing that governments do not have. It is also worth remembering that, too often, the bottlenecks for vaccine production are at the last stages — batch testing, freeze drying, filling and finishing: again, capacities that governments do not have.”
Prof. Ian Jones, a professor of virology at the University of Reading, U.K., stresses the importance of “good fortune” in vaccine research. Even if scientists produce a vaccine “sooner rather than later,” he says, “[t]his doesn’t necessarily mean that there will be enough doses for everyone to be vaccinated immediately, but with luck and commitment, this may be possible earlier than the often quoted 18-month-plus timetable.”

Martin Bachmann is another researcher who is optimistic that his lab will help make a vaccine available in 6–8 months.
A professor of vaccinology at the Jenner Institute at the University of Oxford in the U.K. and Head of the Department of Immunology at the University of Bern in Switzerland, Bachmann also spoke to MNT about where a vaccine fits into the puzzle that controlling the pandemic has become.
When MNT asked how long he thinks the pandemic will last, he replied:

“The real question is, can you keep it down long enough to have a vaccine? Without a vaccine, we are maybe looking at something like a year. But this would mean that 60–70% of the population would have had exposure to the virus.”
– Prof. Martin Bachmann

From pandemic to endemic

Other experts have also raised the possibility that this pandemic will lead to SARS-CoV-2 becoming endemic — meaning that the virus will stay with us forever.
In an interview for MNT, WHO advisor Prof. David Heymann — who is an infectious disease specialist with the London School of Hygiene & Tropical Medicine, U.K. — drew an analogy with HIV.
Regarding whether he thinks there is an end in sight, Prof. Heymann said, “with all new and emerging infections, what’s unknown is what the outcome will finally be — the final destiny of the infection. HIV emerged in the early 20th century and then became endemic throughout the world.”
“Seasonal influenza has emerged from the animal kingdom, and there are currently three endemic seasonal influenza viruses carried by humans,” he continued, adding, “there are many other diseases that are endemic, like tuberculosis, that are also thought to have come from the animal kingdom.”

“The question is: Will this new coronavirus become endemic like those infections, or will it be more like Ebola, which can be contained when an outbreak occurs, only to reappear at some future time? No one can predict with certainty the destiny of this virus.”
– Prof. David Heymann
The WHO advisor also stressed the importance of what happens after governments lift measures of physical distancing. “Certain severe measures in China have been very effective in curtailing outbreaks in China. But now, the question is: What happens when they release those severe measures? Will there be a second wave of infection? Nobody is able to predict this with certainty.”
Prof. Paul Kellam, an infectious disease specialist and professor of virus genomics at Imperial College London, U.K., also weighed in. When MNT asked how long he foresees the pandemic lasting, he said: “Well, that’s really hard to say.”
“Certainly, for the next 2 to 3 months, all of the countries that have a growing epidemic locally will be working hard to get it under control. And then we have to work out how we get people back to the life that they were used to, and how to get the economies running properly.”
“At the moment, that is something that we’ve got to think about and work quickly toward, but it looks like we’re going to be in this for the long haul.”
“Of course, there are already four human coronaviruses that are endemic in the human population,” Prof. Kellam continued. “These cause seasonal colds and respiratory illnesses, some of which can be quite serious in people with underlying health conditions. How they first came into the human population, and how fast they became an endemic infection is not known.”

“I think what we’re looking at now with SARS-CoV-2 is that process of becoming a new seasonal human pathogen. And so, in that sense, humans will be with this virus forever.”
– Prof. Paul Kellam
credit: medicalnewstoday