This is the first alliance of its kind bringing together scientists from Australia, China, Hong Kong, Singapore and the US.

The alliance, which is anchored by Professor Yuen Kwok Yung, a microbiologist from the University of Hong Kong (HKU) and Chairperson-designate of the alliance, and Columbia University AIDS pioneer Professor David Ho, aims to leverage the specific expertise of each institution to produce joint output.

The founding members institutions and representatives of PRA also include Doherty Institute – University of Melbourne, Australia, represented by Professor Sharon Lewin; Duke-National University of Singapore (NUS) Medical School, Singapore, by Professor Wang Linfa; Guangzhou National Laboratory, PRC, by Professor Zhong Nanshan; and Tsinghua University, PRC, by Professor Zhang Linqi.

Professor Chen Zhiwei from HKU will serve as PRA Secretary-designate.

“The PRA will involve research sharing and collaboration to bring together some of the leading minds internationally in virology and related disciplines to jointly seek solutions to pressing issues before the next pandemic hits,” said Professor Yuen.

The new alliance will focus on assessing the potential for animal viruses to jump to humans using artificially grown organoids, as well as faster tests to detect the first human case infected by a novel virus with pandemic potential, and to design drug treatment and vaccines pre-emptively before such outbreaks.

Members will share information on emerging infectious agents for early outbreak alerts, as well as research materials and reagents to provide a rapid research response.

Aims for the next pandemic include ensuring early alerts, responses and control through rapid molecular testing, minimising mortality with a broad spectrum of antiviral or neutralising antibodies and developing a universal vaccine platform to manufacture a specific vaccine in the shortest possible time frame. Through this research output, the alliance hopes that normal life could be maintained if there is another pandemic, with no city lockdowns or school closures.

“Given the history of pandemics, we expect more emerging infectious disease outbreaks, one of which may cause the next pandemic within another decade or so. By launching this alliance today, we are effectively gearing up to protect lives and avert future disruptions to our way of life,” said Professor Ho.

Having collaborated closely over the years, including when Hong Kong experienced an outbreak of severe acute respiratory syndrome (SARS) in 2003, Professor Ho and Professor Yuen spearheaded the idea to forge an alliance whose founding members are based in the Pacific Rim, where many infectious respiratory viruses have originated.

The founding members joined a signing ceremony at HKU, presided over by University President Professor Xiang Zhang, and HKU Dean of Medicine Professor Chak-sing Lau, who expressed their confidence in the alliance’s potential and commended its proactive approach to promoting worldwide readiness for pandemics. The members then chaired the PRA’s inaugural scientific symposium on pandemic virus research, convening experts from across the Pacific Rim and Asia.

The alliance plans to publish joint research and maximise the impact of its findings to help enhance pandemic preparedness around the globe.

One of the first global scientists to discover HIV and to shed light on the dynamics of AIDs in infected individuals, Columbia University Professor Ho founded the AIDS Institute at HKU. During the COVID[1]19 pandemic, HKU and Columbia research groups published eight collaborative articles on SARS-CoV-2 in leading scientific journals. The PRA will build upon this foundation of global collaboration.

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Neurodegenerative diseases such as Parkinson’s disease are caused by protein aggregations that disrupt the normal functioning of neurons in the brain. Researchers at Johns Hopkins Medicine and the University of Michigan have created a type of antibody that acts upon and unravels the protein clumps, known as Lewy bodies. The antibody’ success in targeting the problematic clumps lends hope to developing new treatments especially for neurodegenerative conditions.

In order to break apart the clumps, researchers had genetically modified nanobodies, which are smaller versions of antibody proteins, to squeeze through the membranes of brain cells, and bind to and break down the clumps of misshapen proteins, alpha-synuclein.

Normally, these nanobodies would break down inside the cells because of degrading chemical bonds within their structure. But, when the researchers engineered the nanobodies to lack these certain bonds, they found that the nanobodies remained stable without reducing their ability to bind to alpha-synuclein clumps.

After testing seven versions of the modified nanobodies, the researchers identified one, called PFFNB2, as the best candidate. In tests in live brain cells and tissue of mice, PFFNB2 was found to strongly bind and effectively break down alpha-synuclein clumps.

“We induced PFFNB2 expression in the cortex [where] it prevented alpha-synuclein clumps from spreading to the mouse brain’s cortex, the region responsible for cognition, movement, personality and other high-order processes,” said Ramhari Kumbhar, postdoctoral fellow at the Johns Hopkins University School of Medicine.

Additional tests in mice revealed that PFFNB2 only acted on existing alpha-synuclein clumps and was unable to prevent them from forming into clumps in the first place. Most importantly, PFFNB2 worked around the individual molecules that are vital to brain function.

“The success of PFFNB2 in binding harmful alpha-synuclein clumps in increasingly complex environments indicates that the nanobody could be key to helping scientists study these diseases and eventually develop new treatments” said Xiaobo Mao, Associate Professor of Medicine at Johns Hopkins University School of Medicine.

Researchers led by Columbia University have demonstrated that an experimental ultrasound treatment – delivered to nerves near the kidney – successfully produced clinically meaningful reductions in blood pressure. Called renal denervation, the brief pulses of ultrasound reportedly worked for people whose hypertension did not respond to a triple cocktail of medications.

In a 2019 clinical study following over 100 patients for six months pointed to promising positive results: the simple surgical procedure involves threading a catheter up to the renal arteries via an artery in the leg. Ultrasound energy is then used to, “thermally ablate and disrupt the renal sympathetic nerves while sparing the renal arterial wall.”

A newer study that recruited 136 patients with severe treatment-resistant hypertension showed that daytime ambulatory systolic blood pressure had dropped an average of eight points in patients receiving the renal denervation procedure, compared to a drop of just three points in the patients receiving a sham procedure – and this was observed just two months post-treatment.

“For patients with drug-resistant hypertension, a drop in blood pressure of eight points – if maintained over longer-term follow-up – is almost certainly going to help reduce the risk of heart attack, stroke, and other adverse cardiac events,” said cardiologist Dr. Ajay Kirtane, from Columbia University Vagelos College of Physicians and Surgeons.

“These results suggest that renal denervation has potential to become an important add-on to medication therapy – including for those who have difficulty managing several medications to control their hypertension. Additional studies will be needed to determine if this therapy may be effective for other groups, including older patients with hypertension and those with chronic kidney disease.”

The treatment has not yet been approved for clinical use by the FDA, but the researchers are hopeful.

Read: Isometric resistance training shown to safely reduce high blood pressure

Decades of overuse of antibiotics has rendered most of humanity’s best drugs useless against superbugs; researchers at the University of Hong Kong (HKU), however, have discovered new potential to diminish bacterial resistance by repurposing an existing rheumatoid arthritis (RA) drug, auranofin.

The team found that auranofin, an old drug used to treat RA since the 1980s, can restore the bacteria-killing function of two “last resort” antibiotics – carbapenems and colistins – which bacteria are becoming increasingly resistant towards. Colistin, in particular, is considered only for last-ditch use due to its severe side effects.

Auranofin apparently inhibits two key enzymes that bacteria use to resist antibiotics: the first is the metallo-β-lactamases (MBLs), which bacteria use to break down carbapenems; the second is the mobilised colistin resistance (MCR) enzyme, which breaks down colistin.

In later tests in mice with multidrug-resistant infections, the HKU researchers found that combining auranofin and colistin killed 10 times more of the bacteria in the animals’ livers and spleen than just the antibiotic alone; the combination could also effectively kill superbugs at much lower doses than usual. Most importantly, every single treated animal survived after a five-day treatment regime of auranofin and colistin.

Further tests will cement the possibility of reinforcing our defences against dangerous superbugs.

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A team of scientists from Singapore’s Nanyang Technological University (NTU) have developed a novel “Trojan horse” approach to killing evasive cancer cells by using a cancer-friendly peptide to cloak another cancer-fighting nanoparticle. The NTU scientists took advantage of cancer cells’ dependency on L-phenylalanine, which is an amino acid, to help their drug-free nanoparticle sneak into and destroy cancer cells.

The nanoparticle, called Nanoscopic-phenylalanine Porous Amino Acid Mimic (Nano-pPAAM), is 30,000 times smaller than the width of a human hair and is coated with L-phenylalanine peptides, which are essential to cancers’ growth. In laboratory experiments with mice, the NTU team found the “hidden” nanoparticles soon killed around 80% of breast, skin and gastric cancer cells, similar to what one would expect from standard chemotherapy drugs.

In short, Nano-pPAAM enters the cancer cells through an amino acid transporter cell and, once inside, stimulates the production of reactive oxygen species (ROS), which don’t harm healthy cells, but do cause the cancer cells to self-destruct. Better still, using the nanomaterial as a drug instead of as a drug-carrier allows it to bypass common issues that develop with cancer cells such as drug resistance.

Associate Professor Tan Ern Yu, a breast cancer specialist at Tan Tock Seng Hospital in Singapore, said that the “Trojan horse” approach could hold much promise for cancer cells that have failed to respond to conventional treatment like chemotherapy. “Such cancers could potentially still be susceptible to Nano-pPAAM since it works by a completely different mechanism – one that the cells will not have adapted to.”

An easy discharge of chemical waste believed to contain heavy metals into a river has escalated into a respiratory hazard for residents along the Straits of Johor, Malaysia.

There have been three consecutive waves of air pollution as the chemicals got washed along Sungai Kim Kim, where at least seven schools are located.

A local school headmaster, Mohd Asri Abdul Kadirof SK Tanjung Puteri Resort has said that many students suffered gas poisoning including dizziness, nausea and vomiting when strong winds blew hazardous fumes into the school. As more schoolchildren were affected, rescue personnel ordered the closure of the school by mid-morning and instructed the staff and students to go home.

Fishermen have claimed that thick sludge in the water is causing their boat engines to fail, costing their livelihood.

While the Johor Health Department has rubbished claims of fatalities tied to the incident, the National Disaster Management Agency has taken over the handling of the situation with three people arrested so far.

As of March 14, 2019 the total number of people affected by the chemical pollution is about 3,500 and all 111 schools in the area have been ordered to close.

More and more children live and play in the city, and the fast-paced lifestyle is a contributing factor to mental illness later in life – an increasing estimate by the World Health Organisation (WHO). However, a study from Aarhus University, Denmark,aims to counter the damage, for posterity.

For the study, researchers used satellite data to map the presence of green space around the childhood homes of almost one million Danes. Conclusive data has showed that children surrounded by high amounts of green space in childhood have up to a 55% lower risk of developing a known mental disorder – even after adjusting for other possible risk factors such as socio-economic status, urbanization, and family history of mental disorders.

The Danish researchers are aware that distinct factors of city life, such as noise, air pollution, infections and poor socio-economic conditions increase the risk of developing a mental disorder, but have noted a robust indication of a close relationship between green space, urban life, and mental health.

Lead researcher Kristine Engemann of the Department of Bioscience and the National Centre for Register-based Research at Aarhus University, has remarked on the uniqueness of the study data, which proves the need for a natural environment throughout childhood for developing mental stability.

Previous studies have already showed that more green space in the local area enhances a child’s cognitive development, creates greater social cohesion and increases physical activity levels.

Co-author Professor Jens-Christian Svenning of the Department of Bioscience at Aarhus University has added that the link between mental health and access to green space in any local area should be the chief consideration in urban planning to ensure greener and healthier cities and to improve the mental health of city-dwellers in the future.

Cameron Underwood, 26, had struggled for years with depression, and in 2016, he placed a shotgun under his chin and pulled the trigger.

Two years later, he made his first public appearance after undergoing a series of procedures to restore his face, teeth, and jaws.

“Thank you for not giving up on me,” he said Thursday during a press conference at New York University Langone Health.

Underwood needed five months of skin graft surgery in order for plastic surgeons to devise a plan to reconstruct his face.

The shotgun blast had left him missing most of his lower jaw, his palate and all but one tooth.

At New York Langone, a team of more than 100 medical professionals worked on redesigning Underwood’s countenance.

The face transplant, performed in January, took 25 hours.

His mother, Bev Bailey-Potter, told People magazine she contact NYU’s Langone center after reading an article about a face transplant performed by Dr. Eduardo Rodriguez.

A donor was found in January after 23-year-old Will Fisher, a New York City resident, died. He had listed himself as an organ donor.

“It hasn’t been easy,” Underwood said. “But it has been worth it.”

Researchers from Columbia University Medical Center found certain patterns of electrical signals emitted from the “smart” contact lenses correlate with a faster rate of glaucoma progression. The findings are being published online today in Ophthalmology, the journal of the American Academy of Ophthalmology.

Glaucoma remains a leading cause of blindness. One of the main indicators of the disease is high pressure in the eye, or intraocular pressure. Doctors often check eye pressure to gauge a patient’s eye health. However, these tests yield a single snapshot in time and are impractical to perform at night when eye pressure typically rises. With the advent of smart contact lenses that monitor patients continuously, scientists are hoping to solve that problem.

Researchers at Columbia tested the lenses on 40 patients between ages 40 and 89 undergoing treatment for open-angle glaucoma, the most common form of the disease. Over two years, scientists performed at least eight standard visual field tests on these patients. Half were classified as having slow disease progression while the other 20 had fast disease progression.

The patients then wore a smart contact lens for 24 hours, including overnight as they slept. The lens’ sensor detects changes in lens curvature. As eye pressure fluctuates, the curve changes, generating an electrical signal sent to a wireless device that records the signals. Similar to how an electrocardiogram shows a heartbeat, the profile of signals from the smart lens indirectly shows eye pressure changes over time.

Investigators found that patients with steeper spikes recorded overnight and a greater number of peaks in their signal profile overall tended to have faster glaucoma progression. This information provides more insight into glaucoma and also a blueprint for deciphering the signals from this new wearable technology. Using these findings, clinicians can better estimate the risk of progression by looking at a readout from the smart lens. The findings could also have implications when using the lenses to evaluate glaucoma treatments.

“What we see in these measurements is a signature that indicates which glaucoma patients will get worse and which are relatively stable, which you can’t do with a one-time eye pressure measurement,” said study author C. Gustavo De Moraes, M.D., MPH, an associate professor of ophthalmology at Columbia University Medical Center. “This could be very useful if you want to know whether a new medication is working for a patient. You can see how their eye is reacting to the therapy in a much more meaningful way.”

Dr Manolis Kallistratos, a cardiologist at Asklepieion Voula General Hospital in Athens, led the study.

The study gathered 200 men and 186 women, average age 61.4 years with arterial hypertension. The following measurements were performed in all patients: midday sleep time (in minutes), office BP, 24 hour ambulatory BP, pulse wave velocity, lifestyle habits, body mass index (BMI) and a complete echocardiographic evaluation including left atrial size. BP measurements were reported as diastolic and systolic BP.

Researchers found that people who took afternoon naps had 5% lower average 24 hour ambulatory systolic BP (6 mmHg) compared to non-nappers. Their average systolic BP readings were also 4% lower when they were awake (5 mmHg) and 6% lower while they slept at night (7 mmHg) compared to non-nappers.

Dr Kallistratos said: “Although the mean BP decrease seems low, it has to be mentioned that reductions as small as 2 mmHg in systolic blood pressure can reduce the risk of cardiovascular events by up to 10%.