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Sickle cell disease is the most prevalent inherited blood disorder in the world, affecting 70,000 to 100,000 Americans. However, it is considered an orphan disease, meaning it impacts less than 200,000 people nationally, and is therefore underrepresented in therapeutic research.
A team led by Abhishek Jain from the Department of Biomedical Engineering at Texas A&M University is working to address this disease.
“I’m trying to create these new types of disease models that can impact health care, with the long-term goal of emphasizing on applying these tools and technologies to lower health care costs,” said Jain, assistant professor in the department. “We strategically wanted to pick up those disease systems which fall under the radar in orphan disease category.”
Jain’s research is in organ-on-a-chip, where cells from humans can be grown on USB-sized devices to mimic the way the organ would work inside the body. This sort of system is ideal for testing new drug treatments, as drugs cannot be tested on humans, and animal models have not shown to be a good representation of how a patient and disease would interact with a treatment. For sickle cell disease patients, the organ-on-a-chip would also be beneficial because patients can present with mild to severe cases.
Jain works with Tanmay Mathur, a fourth-year doctoral student who trained as a chemical engineer in his undergraduate years. His research focused on microfabrication techniques and simulations, skills he said merged well into the organ-on-a-chip research he now performs in Jain’s lab. The team collaborates closely with the Texas Medical Center in Houston.
The work was recently published in the journal Bioengineering & Translational Medicine. Their paper builds off a 2019 publication in the journal Lab on Chip, where the team demonstrated that endothelial cells (cells that line the blood vessels) could be used to model the disease physiology of a patient without having to stimulate the model to perform differently than a healthy vessel.

New research from the University of Kent and Leeds Beckett University has found that feelings of shame and stigmatisation at the idea of contracting Covid-19 are linked to lower compliance of social distancing and the likelihood of reporting infection to authorities and potential contacts in Italy, South Korea and the USA.
In contrast, the study found that individuals who trust their Government’s response to the Covid-19 pandemic and feel a mutual solidarity are more likely to report Covid-19 contraction to authorities and acquaintances.
In Italy and South Korea, individuals are also more likely to follow social distancing regulations if they trust their Government’s response to the pandemic, while in the USA, trust does not lead to social distancing compliance. This could be explained by the behaviour of the former administration that emphasised values of deference to authority and an “American First” policy, while signalling contempt for scientific advice and social distancing.
Many governments around the world have responded to the Covid-19 pandemic by implementing lockdown measures of various degrees of intensity. To be effective, these measures must rely on citizens’ cooperation. These findings published by Frontiers in Psychology suggest that values of hierarchy and interdependence from governments shaming people into obedience may backfire and even make authorities less likely to trace and test new cases, while people may be less likely to comply with regulations. In turn this can negatively impact public health.
The research, led by Dr Giovanni Travaglino (Kent) and Dr Chanki Moon (Leeds Beckett), indicates the importance of cooperation and solidarity in explaining people’s compliance with the norms of social distancing.
Dr Travaglino said: “Our research highlights the importance of managing the stigma associated with Covid-19, which may undermine authorities’ efforts to control it. Governments and decision-makers may achieve better transparency and compliance by focusing on the importance of social cohesion and trustworthiness in their attempts to tackle the pandemic and manage public responses.”
Dr Moon said: “In our research, we identified that roles of trust in governments and self-conscious emotions (shame and guilt) were determinant factors for people’s compliance with social distancing and intentions of reporting infections to health authorities or acquaintances. When governments and decision-makers make policies and regulations in relation to Covid-19, they should be aware that stigmatising or blaming people for contracting the infection could potentially backfire. The governments’ efforts to boost trust are probably the key to overcoming the coronavirus crisis.”
Their research paper, ‘Compliance and Self-Reporting During the COVID-19 Pandemic: A Cross-Cultural Study of Trust and Self-Conscious Emotions in the United States, Italy, and South Korea’ is published by Frontiers in Psychology.
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Materials provided by University of Kent. Original written by Olivia Miller. Note: Content may be edited for style and length.

A new study from the University of Kent’s School of Anthropology and Conservation has found that Oldowan and Acheulean stone tool technologies are likely to be tens of thousands of years older than current evidence suggests.
They are currently the two oldest, well-documented stone tool technologies known to archaeologists.
These findings, published by the Journal of Human Evolution, provide a new chronological foundation from which to understand the production of stone tool technologies by our early ancestors. They also widen the time frame within which to discuss the evolution of human technological capabilities and associated dietary and behavioural shifts.
For the study, a team led by Kent’s Dr Alastair Key and Dr David Roberts, alongside Dr Ivan Jaric from the Biology Centre of the Czech Academy of Sciences, used statistical modelling techniques only recently introduced to archaeological science. The models estimated that Oldowan stone tools originated 2.617-2.644 million years ago, 36,000 to 63,000 years earlier than current evidence. The Acheulean’s origin was pushed back further by at least 55,000 years to 1.815-1.823 million years ago.
Early stone tool technologies, such as the Oldowan and Acheulean, allowed early human ancestors to access new food types, and increased the ease of producing wooden tools or processing animal carcasses.
Dr Key, a Palaeolithic Archaeologist and the lead author of the study, said: ‘Our research provides the best possible estimates for understanding when hominins first produced these stone tool types. This is important for multiple reasons, but for me at least, it is most exciting because it highlights that there are likely to be substantial portions of the artifact record waiting to be discovered.’
Dr Roberts, a conservation scientist and co-author of the study, said: ‘The optimal linear estimation (OLE) modelling technique was originally developed by myself and a colleague to date extinctions. It has proved to be a reliable method of inferring the timing of species extinction and is based on the timings of last sightings, and so to apply it to the first sightings of archaeological artifacts was another exciting breakthrough. It is our hope that the technique will be used more widely within archaeology.’
Although it is widely assumed that older stone tool sites do exist and are waiting to be discovered, this study provides the first quantitative data predicting just how old these yet-to-be-discovered sites may be.
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Materials provided by University of Kent. Original written by Olivia Miller. Note: Content may be edited for style and length.

Researchers at the Perelman School of Medicine at the University of Pennsylvania have produced a detailed molecular atlas of lung development, which is expected to be a fundamental reference in future studies of mammalian biology and of new treatments for diseases, such as COVID-19, that affect the lungs.
The researchers, who published their study in Science, generated a broad atlas of cell types in the developing and adult mouse lung by measuring the expression of genes in thousands of individual mouse lung cells across the lifespan, covering multiple cell types and stages of maturation, from early development in the womb to adulthood. Analyzing all this data, they predicted thousands of signaling interactions among different cell types in the developing lung, confirmed many of these with functional experiments, and identified several cells and molecular regulators that are critically important for normal lung development.
“This study provides foundational information to guide our understanding of how lung function develops, and how the early postnatal period of life is a time of rapid adjustment in the lungs to optimize gas exchange,” said study senior investigator Edward Morrisey, PhD, the Robinette Foundation Professor of Medicine, a professor of Cell and Developmental Biology, and director of the Penn-CHOP Lung Biology Institute at Penn Medicine.
The trove of new data is likely to be valuable in the development of future treatments for early-life lung problems, including insufficient lung development in premature babies. It may also speed the search for better therapies for pneumonia and chronic obstructive pulmonary disease (COPD), two of the leading causes of death worldwide.
The study focused largely on the developmental steps leading to the maturation of alveoli. These delicate sac-like structures in the lungs contain thin, capillary-rich membranes that orchestrate the exchange of carbon dioxide in the bloodstream for oxygen in inhaled air. There are hundreds of millions of alveoli in an average human lung, and the total surface area of their gas-exchange membranes has been estimated as approximately the same as a tennis court’s.
Many human diseases, from birth to old age, disrupt these vital structures. Yet the details of how cells emerge and signal to each other to bring about the formation of alveoli in early life have remained largely mysterious.
Morrisey’s team used two relatively new techniques called single-cell RNA sequencing and single cell ATAC sequencing to record the expression and accessibility of genes in thousands of individual cells at seven different time-points during lung development in mice. They then analyzed the gene activity in each cell type, at each time point, to predict which cells were making important signaling molecules and which were expressing the receptors that receive those signals. In this way they made a map of predicted interactions among all these cells, from which they could identify key factors in alveolar development. Lastly, they confirmed the activity of two of these pathways, the Wnt and Sonic Hedgehog (Shh) pathway, using genetic mouse models to inactivate their function in specific cell types identified in the single cell experiments.
A novel finding of the study was the identification of a cell type known as the alveolar type 1 epithelial cell (AT1), which was already known to help form alveolar gas exchange interface, as a crucial originator and hub of molecular signals that guide alveolar development. The researchers also determined that another cell type known as the secondary crest myofibroblast (SCMF) plays a key role in guiding the maturation of alveolar structures. Morrisey’s team moreover identified several transcription factor proteins — which regulate gene activity — as crucial for normal alveolar development. Some of these findings were also confirmed to occur in the human pediatric lung. The vast new dataset generated by the researchers should empower many future studies, including deeper studies of human lung development.
The molecular details of how alveoli develop will also inform future research aimed at treating disorders that affect these structures. Babies that are born very prematurely often suffer from respiratory distress because their alveoli are not yet fully developed. Pneumonias, which can be caused by bacteria or viruses — including SARS-CoV-2 — and can affect anyone from childhood to old age, usually feature a storm of alveoli-damaging immune molecules and immune cells, and the destruction of the alveolar gas-exchange interface. Similarly, COPD, which can result from long-term cigarette smoking, involves chronic inflammation and degeneration of alveolar structures.
“We are hopeful that our study will provide a framework for a better understanding of the molecular pathways that could be harnessed to promote lung regeneration after acute or chronic injury,” Morrisey said.

Neurodevelopmental disorders like autism and schizophrenia disproportionately affect males and are directly linked to early life adversity caused by maternal stress and other factors, which might be impacted by nutrition. But the underlying reasons for these male-specific impacts are not well understood. Researchers from the University of Missouri School of Medicine and the MU Thompson Center for Autism and Neurodevelopmental Disorders have uncovered possible reasons for male vulnerability in the womb, and they’ve learned a specific maternal dietary supplement called docosahexanoic acid (DHA) may guard against the impact of maternal stress on unborn males during early development.
“We believe differences in metabolic requirements for male and female embryos as early as the first trimester, combined with dynamic differences in the way the male and female placenta reacts to environmental factors, contributes to the increased risk for male neurodevelopmental disorders later in life,” said senior author David Beversdorf, MD, a professor of radiology, neurology and psychology at MU.
Beversdorf worked with principal investigator Eldin Jašarevic, PhD, an assistant professor of pharmacology at the University of Maryland School of Medicine and a team of researchers on the study which involved grouping 40 mice into four different cohorts. Group 1 mothers received a standard diet and were not exposed to any early prenatal stress (EPS). Group 2 got the standard diet while being exposed to (EPS), which consisted of restraint, light, noise and predator threat. Group 3 got a diet modified with supplemental DHA but was not exposed to EPS. Group 4 received DHA supplementation and EPS.
The team analyzed the embryos and placentas at 12.5 days of gestation and found exposure to prenatal distress decreased placenta and embryo weight in males but not females. In the DHA groups, they found the supplement reversed the impact of EPS on males.
“This study yielded two results regarding the interaction between maternal stress and dietary DHA enrichment in early stage embryos,” Beversdorf said. “First, stress on the mother during the first week of gestation appeared to influence gene expression pattern in the placenta, and the gender of the offspring determined the magnitude of disruption. Second, a maternal diet enriched with preformed DHA during periods of high stress showed partial rescue of stress-dependent dysregulation of gene expression in the placenta.”
Beversdorf said future studies will be needed to better understand the complex cellular and molecular mechanisms linking maternal diet consumption, chronic stress during pregnancy, placental gene expression and lasting health outcomes in offspring.
In addition to Beversdorf and Jašarevic, the study authors include University of Missouri colleagues Kevin Fritsche, PhD, professor of nutrition and exercise physiology; David Geary, PhD, professor of psychology; and Rocio Rivera, PhD, associate professor of animal science.
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Materials provided by University of Missouri-Columbia. Note: Content may be edited for style and length.

An international team of researchers has found that three commonly used antiviral and antimalarial drugs are effective in vitro at preventing replication of SARS-CoV-2, the virus that causes COVID-19. The work also underscores the necessity of testing compounds against multiple cell lines to rule out false negative results.
The team, which included researchers from North Carolina State University and Collaborations Pharmaceuticals, looked at three antiviral drugs that have proven effective against Ebola and the Marburg virus: tilorone, quinacrine and pyronaridine.
“We were looking for compounds that could block the entry of the virus into the cell,” says Ana Puhl, senior scientist at Collaborations Pharmaceuticals and co-corresponding author of the research. “We chose these compounds because we know that other antivirals which successfully act against Ebola are also effective inhibitors of SARS-CoV-2.”
The compounds were tested in vitro against SARS-CoV-2, as well as against a common cold virus (HCoV 229E) and murine hepatitis virus (MHV). Researchers utilized a variety of cell lines that represented potential targets for SARS-CoV-2 infection in the human body. They infected the cell lines with the different viruses and then looked at how well the compounds prevented viral replication in the cells.
The results were mixed, with the compounds’ effectiveness depending upon whether they were used in human-derived cell lines versus monkey-derived cell lines, known as Vero cell lines.
“In the human-derived cell lines, we found that all three compounds worked similarly to remdesivir, which is currently being used to treat COVID-19,” says Frank Scholle, associate professor of biology at NC State and co-author of the research. “However, they were not at all effective in the Vero cells.”
“Researchers saw similar results when these compounds were initially tested against Ebola,” says Sean Ekins, CEO of Collaborations Pharmaceuticals and co-corresponding author of the research. “They were effective in human-derived cell lines, but not in Vero cells. This is important because Vero cells are one of the standard models used in this type of testing. In other words, different cells lines may have differing responses to a compound. It points to the necessity of testing compounds in many different cell lines to rule out false negatives.”
Next steps for the research include testing the compounds’ effectiveness in a mouse model and further work on understanding how they inhibit viral replication.
“One of the more interesting findings here is that these compounds don’t just prevent the virus from potentially binding to the cells, but that they may also inhibit viral activity because these compounds are acting on the lysosomes,” Puhl says. “Lysosomes, which are important for normal cell function, are hijacked by the virus for entry and exit out of the cell. So, if that mechanism is disrupted, it cannot infect other cells.”
“It’s also interesting that these compounds are effective not just against SARS-CoV-2, but against related coronaviruses,” Scholle says. “It could give us a head start on therapies as new coronaviruses emerge.”
The work appears in ACS Omega and was supported in part by NC State’s Comparative Medicine Institute and the National Institutes of Health. NC State undergraduates James Levi and Nicole Johnson, as well as Ralph Baric, from the University of North Carolina at Chapel Hill, contributed to the work. Other collaborating institutions included: Instituto Oswaldo Cruz and University of Campinas, both in Brazil; Utah State University; the University of Maryland; and SRI International.
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Materials provided by North Carolina State University. Original written by Tracey Peake. Note: Content may be edited for style and length.

SMN or in full Survival Motor Neuron: Professor Utz Fischer has been analyzing this protein and the large molecular complex of the same name, of which SMN is one of the building blocks, for many years. He holds the Chair of the Department of Biochemistry at the Julius-Maximilian’s University of Würzburg (JMU), and he first discovered the molecule during his search for the root cause of spinal muscular atrophy. As scientists found out a few years ago, this disease is caused by a lack of the SNM complex.
The work group around Prof. Fischer has now succeeded in presenting a first three-dimensional model of the entire SNM complex. Once the structure of the complex is known, it is possible to understand the way how the complex works, and why the loss of its function leads to muscular atrophy. The scientists have published their findings in the current issue of the journal Nucleic Acids Research.
The new findings have been made possible by an integrative structural-biological approach that combines biochemical, genetic and biophysical technologies.
Resolution up to a millionth of a millimeter
“The structural analysis of large and complex molecules in atomic detail has been made possible by the ‘revolution-resolution’, which was primarily brought about by the developments in cryo-electron microscopy,” says Utz Fischer. The only snag about the technology, however, is the fact that it works best on structures that are more or less rigid and have few flexible sections.
Unfortunately, many molecular entities are not built like this, including the SMN complex. “This complex is of central importance for our cells because it supports the formation of molecular machines required for the expression of our genes,” says Prof. Fischer. However, in order to serve its function in the cell, it must be highly flexible and dynamic. As a result, a structural analysis by traditional strategies has been impossible so far.

Heavy elements known as the actinides are important materials for medicine, energy, and national defense. But even though the first actinides were discovered by scientists at Berkeley Lab more than 50 years ago, we still don’t know much about their chemical properties because only small amounts of these highly radioactive elements (or isotopes) are produced every year; they’re expensive; and their radioactivity makes them challenging to handle and store safely.
But those massive hurdles to actinide research may one day be a thing of the past. Scientists at the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) and UC Berkeley have demonstrated how a world-leading electron microscope can image actinide samples as small as a single nanogram (a billionth of a gram) — a quantity that is several orders of magnitude less than required by conventional approaches.
Their findings were recently reported in Nature Communications, and are especially significant for co-senior author Rebecca Abergel, whose work on chelators — metal-binding molecules — has resulted in new advances in cancer therapies, medical imaging, and medical countermeasures against nuclear threats, among others. Abergel is a faculty scientist who leads the Heavy Element Chemistry program in the Chemical Sciences Division at Berkeley Lab, and assistant professor in nuclear engineering at UC Berkeley.
“There are still so many unanswered questions with regards to chemical bonding in the actinide series. With such state-of-the art instrumentation, we are finally able to probe the electronic structure of actinide compounds, and this will allow us to refine molecular design principles for various systems with applications in medicine, energy, and security,” Abergel said.
“We demonstrated that you can work with less material — a nanogram — and get the same if not better data without having to invest in dedicated instruments for radioactive materials,” said co-senior author Andy Minor, facility director of the National Center for Electron Microscopy at Berkeley Lab’s Molecular Foundry, and professor of materials science and engineering at UC Berkeley.
Allowing researchers to work with just a nanogram of an actinide sample will significantly reduce the high costs of experiments conducted using previous methods. One gram of the actinide berkelium can cost a jaw-dropping $27 million, for example. An actinide sample that is only a nanogram also reduces radiation exposure and contamination risks, Minor added.

During the COVID-19 pandemic, people have grown accustomed to wearing facemasks, but many coverings are fragile and not easily disinfected. Metal foams are durable, and their small pores and large surface areas suggest they could effectively filter out microbes. Now, researchers reporting in ACS’ Nano Letters have transformed copper nanowires into metal foams that could be used in facemasks and air filtration systems. The foams filter efficiently, decontaminate easily for reuse and are recyclable.
When a person with a respiratory infection, such as SARS-CoV-2, coughs or sneezes, they release small droplets and aerosolized particles into the air. Particles smaller than 0.3 µm can stay airborne for hours, so materials that can trap these tiny particles are ideal for use in facemasks and air filters. But some existing filter materials have drawbacks. For example, fiberglass, carbon nanotubes and polypropylene fibers are not durable enough to undergo repeated decontamination procedures, while some further rely on electrostatics so they can’t be washed, leading to large amounts of waste. Recently, researchers have developed metallic foams with microscopic pores that are stronger and more resistant to deformation, solvents, and high temperatures and pressures. So, Kai Liu and colleagues wanted to develop and test copper foams to see if they could effectively remove submicron-sized aerosols while also being durable enough to be decontaminated and reused.
The researchers fabricated metal foams by harvesting electrodeposited copper nanowires and casting them into a free-standing 3D network, which was solidified with heat to form strong bonds. A second copper layer was added to further strengthen the material. In tests, the copper foam held its form when pressurized and at high air speeds, suggesting it’s durable for reusable facemasks or air filters and could be cleaned with washing or compressed air. The team found the metal foams had excellent filtration efficiency for particles within the 0.1-1.6 µm size range, which is relevant for filtering out SARS-CoV-2. Their most effective material was a 2.5 mm-thick version, with copper taking up 15% of the volume. This foam had a large surface area and trapped 97% of 0.1-0.4 µm aerosolized salt particles, which are commonly used in facemask tests. According to the team’s calculations, the breathability of their foams was generally comparable to that of commercially available polypropylene N95 facemasks. Because the new material is copper-based, the filters should be resistant to cleaning agents, allowing for many disinfection options, and its antimicrobial properties will help kill trapped bacteria and viruses, say the researchers. In addition, they are recyclable. The researchers estimate that the materials would cost around $2 per mask at present, and disinfection and reuse would extend their lifetime, making them economically competitive with current products.
The authors acknowledge funding from the Georgetown Environmental Initiative Impact Program Award, the McDevitt bequest to Georgetown University and Tom and Ginny Cahill’s Fund for Environmental Physics at University of California Davis.
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Materials provided by American Chemical Society. Note: Content may be edited for style and length.

SharecloseShare pageCopy linkAbout sharingA new “double mutant” variant of the coronavirus has been detected from samples collected in India.Officials are checking if the variant, where two mutations come together in the same virus, may be more infectious or less affected by vaccines.Some 10,787 samples from 18 Indian states also showed up 771 cases of known variants – 736 of the UK, 34 of the South African and one Brazilian.Officials say the variants are not linked to a spike in cases in India.India reported 47,262 cases and 275 deaths on Wednesday – the sharpest daily rise this year.The Indian SARS-CoV-2 Consortium on Genomics (INSACOG), a group of 10 national laboratories under India’s health ministry, carried out genomic sequencing on the latest samples. Genomic sequencing is a testing process to map the entire genetic code of an organism – in this case, the virus. The genetic code of the virus works like its instruction manual. Mutations in viruses are common but most of them are insignificant and do not cause any change in its ability to transmit or cause serious infection. But some mutations, like the ones in the UK or South Africa variant lineages, can make the virus more infectious and in some cases even deadlier.Virologist Shahid Jameel explained that a “double mutation in key areas of the virus’s spike protein may increase these risks and allow the virus to escape the immune system”.The spike protein is the part of the virus that it uses to penetrate human cells.Delhi orders Covid tests at airports as cases surgeSharp rise in India Covid cases ‘alarming’The government said that an analysis of the samples collected from India’s western Maharashtra state showed “an increase in the fraction of samples with the E484Q and L452R mutations” compared with December last year. “Such [double] mutations confer immune escape and increased infectivity,” the health ministry said in a statement. Dr Jameel added that “there may be a separate lineage developing in India with the L452R and E484Q mutations coming together”.Are double mutants a worry?Smitha Mundasad, BBC health reporterA “double mutant virus” – it’s a scary phrase. Breaking it down, the words suggests that Indian scientists have discovered two significant mutations – or changes – in different locations in a single variant of the virus. That is not so surprising. Viruses mutate all the time but the questions that need answering are: does the presence of this double mutation change how the virus behaves? Will this variant be more infectious now, or cause more severe disease? And importantly, will current vaccines still work well against it? Scientists will now be busy doing the detective work needed to find out the answers. Officials say because the proportion of tests that have come back with this double mutation is currently low, there is currently nothing to suggest this is behind the current surge in cases.What is clear is that this double mutation, as different as it sounds, requires the same public health response. Increased testing, tracking of close contacts, the prompt isolation of cases, as well as masks and social distancing will all help. Reducing the pressure on India’s over-burdened healthcare system is key. In terms of vaccines – so far, for many variants of concern around the world they have been shown to be effective, though sometimes less so when compared to the original viruses they were designed against. Scientists are confident that if needed, existing vaccines can be modified to target new mutations.The Indian government denies that the rise in cases is linked to the mutations. “Though VOCs [variants of concern] and a new double mutant variant have been found in India, these have not been detected in numbers sufficient to either establish a direct relationship or explain the rapid increase in cases in some states,” the health ministry said. The recent report comes after several experts had asked the government to step up genome sequencing efforts. “We need to constantly monitor and make sure none of the variants of concern are spreading in the population. The fact that it is not happening now doesn’t mean it will not happen in the future. And we have to make sure that we get the evidence early enough,” Dr Jameel told the BBC’s Soutik Biswas earlier this month.India became the fifth country in the world to sequence the genome of the novel coronavirus after isolating it from some of the first cases recorded in January last year. More than 11.7 million cases and 160,000 deaths later, efforts are continuing to identify mutations. The latest surge – which began this month – comes during what some experts have called a “delicate phase” for India – the healthcare system is already exhausted from a year-long battle against the coronavirus.States have already begun re-introducing restrictions, including curfews and intermittent lockdowns. Two major cities, Delhi and Mumbai, have also ordered randomised rapid tests at airports, railway stations and crowded areas such as shopping malls.