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SharecloseShare pageCopy linkAbout sharingimage copyrightSumit KumarRajeshwari Devi, 58, died on Sunday after waiting for two days to get uninterrupted oxygen, an ambulance and a bed in a Covid-19 hospital.She kept waiting and gasping but it was too late by the time help arrived. She was taken to a hospital emergency room on 16 April after her oxygen saturation level dropped. Her CT scan showed that she had developed chronic pneumonia.But without her Covid report the hospital refused to admit her. She spent around 36 hours in the emergency room on oxygen support in the northern Indian district of Robertsganj. The staff there told her family they were running out of oxygen and she needed to be moved to a bigger hospital but there was no ambulance or any promise of a bed. The desperate family took her in their car to a hospital where a bed had become available after the intervention of a politician. She had no oxygen support in the car – she died minutes before she could be admitted to hospital. Ashish Agrahari, her son, says his mother “would have had a chance at survival if treatment was given in time”.Heartbreaking stories such as this are coming in from across India as a second Covid wave wreaks havoc. Data suggests that this wave is proving to be more infectious and deadlier in some states, although India’s death rate from the virus is still relatively low. But the county’s healthcare system is crumbling amid the surge in cases – doctors say it’s hard for them to “see the light at the end of the tunnel this time”. Sharp rise in casesThe rise in case numbers has been exponential in the second wave. On 18 June last year, India recorded 11,000 cases and in the next 60 days, it added 35,000 new cases on average every day. On 10 February, at the start of the second wave, India confirmed 11,000 cases – and in the next 50 days, the daily average was around 22,000 cases. But in the following 10 days, cases rose sharply with the daily average reaching 89,800.Experts say this rapid increase shows that the second wave is spreading much faster across the country. Dr A Fathahudeen, who is part of Kerala state’s Covid taskforce, said the rise was not entirely unexpected given that India let its guard down when daily infections in January fell to fewer than 20,000 from a peak of over 90,000 in September.Big religious gatherings, the reopening of most public places and crowded election rallies are being blamed for the uptick. Dr Fathahudeen said there were warning signs in February but “we did not get our act together”.”I said in February that Covid had not gone anywhere and a tsunami would hit us if urgent actions were not taken. Sadly, a tsunami has indeed hit us now,” he added.”A false sense of normalcy crept in and everybody, including people and officials, did not take measures to stop the second wave.”Shortage of bedsMany Indian cities are reporting a chronic shortage of hospital beds. It’s also evident in the desperate cries for help on social media platforms. Disturbing reports of people dying without getting timely treatment are coming from all over the country.Several state governments say they are creating new facilities but experts say it’s going to be hard to keep up with the pace of the rising number of infections.India has been consistently reporting more than 150,000 cases for days now. It reported 273,810 cases on Monday – the biggest daily spike since the pandemic began.Badly-affected cities like Delhi, Mumbai and Ahmedabad have almost run out of hospital beds. The situation is not very different in other cities, such as Lucknow, Bhopal, Kolkata, Allahabad and Surat. Public health expert Anant Bhan says officials did not use the lean period to boost facilities.”We didn’t learn any lesson from the first wave. We had reports of some cities running out of beds even in the first wave and that should have been a good enough reason to be prepared for the second wave,” he said.He adds that there appears to be a lack of co-ordination between states and the federal government over the supply of oxygen and essential drugs. “We need a consolidated response and resources should be shared between states.” The situation is much more dire when it comes to ICU beds. Several cities have just a few dozen ICU beds left and they are now frantically trying to build extra capacity in hotels and stadiums.But getting ICU beds up and running quickly is not easy. Dr Fathahudeen says adding beds alone is not enough. “We need to ensure that most of these beds have oxygen facility. We need more doctors and nurses to manage extra ICU beds,” he adds.He says it’s going to be a “daunting task” for the government to get such facilities up and running and ensure good quality of care in a short span of time.Unreported deathsThe number of daily deaths has risen sharply in the second wave. India reported 1,761 deaths on Monday, taking the toll to over 180,000 since the pandemic began.Crematoriums have been running day and night in several cities, and people have to wait for hours to get the deceased cremated or buried.Experts say this shows that the actual number of deaths could be much higher. Sanjeev Gupta, a photojournalist based in the central Indian city of Bhopal, reached one of the city’s crematoriums for what he thought was a usual assignment last week. Bhopal had reported only four Covid-related deaths on that day. But Mr Gupta was surprised to see dozens of funeral pyres burning. Additionally, several bodies were lined up to be cremated in the electric furnace. Mr Gupta says he was moved when a young man asked him to photograph the smoke coming out from the chimney of the electric crematorium. “He said the smoke represented his mother. It’s the most heartbreaking thing I have ever heard.”Another photojournalist in Lucknow, which is the capital of Uttar Pradesh state, told the BBC that he counted nearly 100 funeral pyres burning at one of the city’s crematoriums in the city on 14 April. The official death data for the whole state on that day was 85.”The sky had turned orange near the crematorium. I still get chills thinking about it. We are definitely not getting the right death data from the government,” he said.image copyrightEPAAnother photojournalist the BBC spoke to in Varanasi city in Uttar Pradesh state also talked about similar discrepancies in how deaths were being reported. Experts say there are several reasons for this. One of them is that many people are dying at home because they are not getting hospital beds or they are not being able to get tested for Covid. So, they don’t find a place as a Covid patient in the database managed by different states. Mr Bhan says testing facilities are still poor in smaller towns and even in some cities and “it’s possible we are missing many Covid-related deaths in these areas”.He adds that there seems to be an issue with recording Covid deaths in some states. There have been reports about administrative oversight as well but officials deny the allegation. “We need more transparency in numbers as it helps in managing the situation and also clearly tells you how severe the situation is,” Mr Bhan adds. Variants in playIndia on 25 March announced that a new “double mutant” variant of the coronavirus had been detected from samples collected from different states.Virologist Shahid Jameel explained that a “double mutation in key areas of the virus’s spike protein may make the virus more infectious and allow it to escape the immune system”.He says the change in the virus is the only “logical explanation” behind the surge. Health officials in the UK are now investigating whether a double mutant spreads more easily and evades vaccines.image copyrightSumit KumarDr Jameel adds that India started looking at mutations “fairly late”. “By December, India had done genome sequencing of only 5,000 samples. It wasn’t a concentrated effort.”In January, India put together a group of labs to speed up sequencing and these labs started functioning in February. “But unfortunately, the second wave started and the vision of sequencing roughly 5% of the total samples did not come through.”Sequencing becomes important in a pandemic as it allows scientists to monitor changes in the virus. “If you can catch a more infectious variant early on in a region, you can quickly put in public health measures to stop it from spreading wider in the community,” he explains.But it’s “never too late” to take measures. “We need to strengthen safety protocols and rapidly vaccinate people, and also keep an eye on mutations. If we do all this, we could reduce numbers significantly.”Read more stories by Vikas PandeyIndia’s Covid-19 patients turn to black market’Think about ICU workers before you party”I have cancer in my 30s, but can’t get a Covid jab’India in ‘delicate phase’ as Covid cases surgeThe vaccine pioneer the world forgot

For Altou, a 19-year-old model, having a ‘slim thick’ body is the key to getting more likes and more work.She’s one of thousands of women worldwide who have taken Apetamin, an appetite-stimulant promoted by social media influencers as a quick fix for the extreme hourglass figure popularised by celebrities like Kim Kardashian. It’s widely available online. But a new BBC Three documentary, Dangerous Curves: Get Thicc, Get Sick?, reveals that many don’t realise Apetamin is actually an unlicensed medicine – and its misuse is causing serious harm.The UK’s Medicines and Healthcare products Regulatory Agency (MHRA) told the BBC, ‘Apetamin is an unauthorised medicine which should not be sold, supplied or advertised without a licence. Taking unauthorised medicines can have serious health consequences’.The MHRA is investigating the sale of this product following the BBC’s enquiries.Dangerous Curves: Get Thicc, Get Sick? is on BBC iPlayer nowProduced by Jamie Ryan & Naomi PallasFilmed by Naomi PallasEdited by Owen KeanAssistant Producer: Jade ThompsonGraphics by Gerard GrovesExecutive Producer: Nisha Lilia Diu

The observation that most of the viruses that cause human disease come from other animals has led some researchers to attempt “zoonotic risk prediction” to second-guess the next virus to hit us. However, in an Essay publishing April 20th in the open access journal PLOS Biology, led by Dr Michelle Wille at the University of Sydney, Australia with co-authors Jemma Geoghegan and Edward Holmes, it is proposed that these zoonotic risk predictions are of limited value and will not tell us which virus will cause the next pandemic. Instead, we should target the human-animal interface for intensive viral surveillance.
So-called zoonotic viruses have caused epidemics and pandemics in humans for centuries. This is exactly what is occurring today with the COVID-19 pandemic: the novel coronavirus responsible for this disease — SARS-CoV-2 — emerged from an animal species, although exactly which species is uncertain.
Therefore, a key question is whether we can predict which animal or which virus group will most likely cause the next pandemic? This has led researchers to attempt “zoonotic risk prediction,” in which they attempt to determine which virus families and host groups are most likely to carry potential zoonotic and/or pandemic viruses.
Dr Wille and her colleagues identify several key problems with zoonotic risk prediction attempts.
First, they’re based on tiny data sets. Despite decades of work, we have probably identified less than 0.001% of all viruses, even from the mammalian species from which the next pandemic virus will likely emerge.
Second, these data are also highly biased towards those viruses that most infect humans or agricultural animals, or are already known to zoonotic. The reality is that most animals have not been surveyed for viruses, and that viruses evolve so quickly that any such surveys will soon be out of date and so of limited value.
The authors instead argue that a new approach is needed, involving the extensive sampling of animals and humans at the places where they interact — the animal-human interface. This will enable novel viruses to be detected as soon as they appear in humans and before they establish pandemics. Such enhanced surveillance may help us prevent something like COVID-19 ever happening again.
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Materials provided by PLOS. Note: Content may be edited for style and length.

A new mathematical model for the interaction of bacteria in the gut could help design new probiotics and specially tailored diets to prevent diseases. The research, from Chalmers University of Technology in Sweden, was recently published in the journal PNAS.
“Intestinal bacteria have an important role to play in health and the development of diseases, and our new mathematical model could be extremely helpful in these areas,” says Jens Nielsen, Professor of Systems Biology at Chalmers, who led the research.
The new paper describes how the mathematical model performed when making predictions relating to two earlier clinical studies, one involving Swedish infants, and the other adults in Finland with obesity.
The studies involved regular measurements of health indicators, which the researchers compared with the predictions made from their mathematical model — the model proved to be highly accurate in predicting multiple variables, including how a switch from liquid to solid food in the Swedish infants affected their intestinal bacterial composition.
They also measured how the obese adults’ intestinal bacteria changed after a move to a more restricted diet. Again, the model’s predictions proved to be reliably accurate.
“These are very encouraging results, which could enable computer-based design for a very complex system. Our model could therefore be used to for creating personalised healthy diets, with the possibility to predict how adding specific bacteria as novel probiotics could impact a patient’s health,” says Jens Nielsen.

When disease outbreaks happen, response time in developing and distributing treatments is crucial to saving lives. Unfortunately, developing custom drugs as countermeasures is often a slow and difficult process.
But researchers at the University of Colorado Boulder have created a platform that can develop effective and highly specific peptide nucleic acid therapies for use against any bacteria within just one week. The work is detailed in Nature Communications Biology and could change the way we respond to pandemics and how we approach increasing cases of antibiotic resistance globally.
The Facile Accelerated Specific Therapeutic (FAST) platform was created by Associate Professor Anushree Chatterjee and her team within the Department of Chemical and Biological Engineering. It can quickly produce new antibiotics for any system or disease — from highly adaptive microbial super bugs to radiation poisoning in astronauts — that are specifically designed to selectively target just the bacteria of interest. The paper demonstrates significant growth inhibition and other positive responses in resistant bacteria such as E. coli, which are adapting to current treatments much faster than new drugs can hit the market.
Traditional drug discovery methods usually take 10 or more years and are specific to one bug or another. That is because they are based on identifying molecules from one bacteria that can then be used against other bacteria to promote human health. Unfortunately, evolution over billions of years has resulted in bacteria strains today that are increasingly resistant to this kind of approach — aided in part by recent over prescription of antibiotics by doctors. FAST, on the other hand, can be used for any bug and enables speedy identification and testing of molecules that target new mechanisms in pathogens — getting ahead of that curve.
Kristen Eller, a PhD candidate in the Chatterjee Group, is the first author on the new paper. She said the FAST system utilizes bacteria’s genetic makeup to design specific and targeted antibiotics that stop their natural means of producing essential proteins, causing them to die. She added that the platform also provides a unique strategy to deliver these treatments to bacteria that are traditionally hard to target because they reside within our own host cells. To get around this, the platform essentially utilizes bacteria’s natural ability to invade our own cells and manipulates it instead to be a carrier of the therapeutic.
“The applications for the real world are immense in that we have created a platform — not just a single therapeutic,” she said. “It is adaptive, dynamic and can be altered to target any bacterial species that is a threat while also being modulated to develop antivirals as needed.”
Recently, another paper published in PNAS showed the use of the FAST platform to create novel antibiotics against a clinical isolate of carbapenem-resistant E. coli that was found to be resistant to pretty much all antibiotics.
Chatterjee said that last aspect is particularly important as particular strains evolve, change and become more resistant over time. The goal, she said, is to rapidly create tailored treatments specific to the region in question, the person seeking treatment or even the global health situation for example.
“The technology we use to treat these kinds of health issues has to be smart enough to keep up with evolving organisms and also quick enough to respond to real-time crisis,” she said. “Within this platform there are multiple steps where you can design and create new drug targets, which is really key.”
Chatterjee said the platform could eventually be modified to develop antivirals for treatment of common colds, the flu and most pressingly, COVID-19. For now, her team is working on collecting more data to develop potential COVID-19 treatments and beginning to work towards clinical trials.
“We need to think out of the box when it comes to keeping up with pathogens because they are always advancing and changing,” she said. “If we can establish these processes and techniques now, then we will be much better prepared next time there is a pandemic or outbreak.”
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Materials provided by University of Colorado at Boulder. Original written by Josh Rhoten. Note: Content may be edited for style and length.

Like a stern bodyguard for the central nervous sytem, the blood-brain barrier keeps out anything that could lead to disease and dangerous inflammation — at least when all is functioning normally.
That may not be the case in people with schizophrenia and other mental disorders, suggest new findings from a team led by researchers from the School of Veterinary Medicine, Perelman School of Medicine, and Children’s Hospital of Philadelphia (CHOP). In these individuals, a more permissive barrier appears to allow the immune system to get improperly involved in the central nervous system, the researchers showed. The inflammation that arises likely contributes to the clinical manifestations of neuropsychiatric conditions.
“Our hypothesis was that, if the immune function of the blood-brain barrier is compromised, the resulting inflammation will have an impact on the central nervous system,” says Jorge Iván Alvarez, an assistant professor at Penn Vet and senior author on the work, published in the journal Brain. “With that in mind, we think these findings could also be used to understand how the blood-brain barrier and neurological processes impact not only schizophrenia but mental disorders at large.”
The research team pursued the study focused on a rare condition called 22q11.2 deletion syndrome (22qDS), in which people are born missing a small portion of DNA from chromosome 22. Roughly a quarter of people with this syndrome go on to develop schizophrenia. Penn and CHOP have a community of researchers who study the condition, often as a way of probing deeper into the mysteries of schizophrenia.
This disorder had not been a focus for the Alvarez lab, however, until he gave a talk at CHOP on his area of expertise — the blood-brain barrier — and was approached by an attendee afterward.
“We started talking about the fact that, in this deletion syndrome, one of the missing genes is very important for blood-brain barrier function,” Alvarez says.

Researchers have found a causal link between caesarean section birth, low intestinal microbiota and peanut sensitivity in infants, and they report the effect is more pronounced in children of Asian descent than others, in a recently published paper in the journal of the American Gastroenterological Association.
“It’s important to know what predicts or increases risk of food sensitivities because they predict which infants will go on to develop asthma and other types of allergies,” said Anita Kozyrskyj, pediatrics professor in the University of Alberta’s Faculty of Medicine & Dentistry and adjunct professor in the School of Public Health.
The research team analysed the gut bacteria of 1,422 infants in the CHILD Cohort Study, by examining fecal samples collected at three or four months of age and again at one year. They identified four typical trajectories for bacterial development, including one in which the infants had persistently low levels of Bacteroides, a type of bacteria known to be critical to immune system development. This profile was most common in babies born by caesarean section.
The infants were given skin prick tests at one and three years of age to assess their reaction to a variety of allergens, including egg, milk and peanut. The babies with low Bacteroides levels were found to have a threefold increase in their risk of developing a peanut sensitivity by age three — and the risk was eight times higher for babies born to mothers of Asian descent.
The team did further statistical analysis to look for what are known as “mediation” or causal effects between the exposure and the outcome. “In this case we observed that there was an association between Asian ethnicity and peanut sensitivity, and then the mediation analysis provided additional evidence for the causal association with caesarean section,” explained Kozyrskyj, noting it is the first study to identify this link.
The researchers also observed that the infants with low Bacteroides also had lower levels of sphingolipids, proteins which are key to cell development and signalling in many parts of the body, including the immune system. Gut microbiota are the main source of these proteins. Children who have this deficiency in their immune cells may be more likely to develop food allergies, Kozyrskyj said.

A chemist from Purdue University has found a way to synthesize a compound to fight a previously “undruggable” cancer protein with benefits across a myriad of cancer types.
Inspired by a rare compound found in a shrub native to North America, Mingji Dai, professor of chemistry and a scientist at the Purdue University Center for Cancer Research, studied the compound and discovered a cost-effective and efficient way to synthesize it in the lab. The compound — curcusone D — has the potential to help combat a protein found in many cancers, including some forms of breast, brain, colorectal, prostate, lung and liver cancers, among others. The protein, dubbed BRAT1, had previously been deemed “undruggable” for its chemical properties. In collaboration with Alexander Adibekian’s group at the Scripps Research Institute, they linked curcusone D to BRAT1 and validated curcusone D as the first BRAT1 inhibitor.
Curcusones are compounds that come from a shrub named Jatropha curcas, also called the purging nut. Native to the Americas, it has spread to other continents, including Africa and Asia. The plant has long been used for medicinal properties — including the treatment of cancer — as well as being a proposed inexpensive source of biodiesel.
Dai was interested in this family of compounds — curcusone A, B, C and D.
“We were very interested by these compounds’ novel structure,” Dai said. “We were intrigued by their biological function; they showed quite potent anti-cancer activity and may lead to new mechanisms to combat cancer.”
Researchers tested the compounds on breast cancer cells and found curcusone D to be extremely effective at shutting down cancer cells. The protein they were targeting, BRAT1, regulates DNA damage response and DNA repair in cancer cells. Cancer cells grow very fast and make a lot of DNA. If scientists can damage cancer cells’ DNA and keep them from repairing it, they can stop cancer cells from growing.

Using a widely known field of mathematics designed mainly to study how digital and other forms of information are measured, stored and shared, scientists at Johns Hopkins Medicine and Johns Hopkins Kimmel Cancer Center say they have uncovered a likely key genetic culprit in the development of acute lymphoblastic leukemia (ALL).
ALL is the most common form of childhood leukemia, striking an estimated 3,000 children and teens each year in the United States alone.
Specifically, the Johns Hopkins team used “information theory,” applying an analysis that relies on strings of zeros and ones — the binary system of symbols common to computer languages and codes — to identify variables or outcomes of a particular process. In the case of human cancer biology, the scientists focused on a chemical process in cells called DNA methylation, in which certain chemical groups attach to areas of genes that guide genes’ on/off switches.
“This study demonstrates how a mathematical language of cancer can help us understand how cells are supposed to behave and how alterations in that behavior affect our health,” says Andrew Feinberg, M.D., M.P.H., Bloomberg Distinguished Professor at the Johns Hopkins University School of Medicine, Whiting School of Engineering and Bloomberg School of Public Health. A founder of the field of cancer epigenetics, Feinberg discovered altered DNA methylation in cancer in the 1980s.
Feinberg and his team say that using information theory to find cancer driver genes may be applicable to a wide variety of cancers and other diseases.
Methylation is now recognized as one way DNA can be altered without changing a cell’s genetic code. When methylation goes awry in such epigenetic phenomena, certain genes are abnormally turned on or off, triggering uncontrolled cell growth, or cancer.