Back in March, Michigan’s Covid-19 cases exploded — leaping from zero to 3,657 in just two weeks. Detroit’s three big automakers closed factories temporarily, and the state’s largest health care system warned it was reaching capacity.

Click Here:

In the midst of this crisis, Joseph Roche, an associate professor in the physical therapy program at Wayne State University, had an idea.

From his research into muscular dystrophies, Roche understood that inflammation can do significant damage to the body. When he read that in severe Covid-19 cases, runaway inflammation was causing damage to tissues and organ failure, he dove into the data as well as older research on SARS.

Initially, it appeared that the virus might cause immune cells to overproduce molecules called cytokines, causing a severe inflammatory response known as a cytokine storm. But what Roche suspected as he sifted through early case studies was that it wasn’t the immune system’s cytokines causing so much of the damage but an entirely different pathway in the circulatory system knocked off balance by the virus: bradykinin signaling.

He believed that an accumulation of two peptides, des-Arg(9)-bradykinin, abbreviated to DABK, and bradykinin — both part of a system that regulates blood pressure and other functions — were starting a feedback loop of inflammation and tissue injury. By stopping this reaction, he argued in an open letter to the scientific community in April and in a May paper published in the Journal of the Federation of American Societies of Experimental Biology, doctors could prevent some of Covid-19’s worst effects.

Several months later and 500 miles away, a group of researchers unaware of Roche’s work started feeding the world’s second-fastest computer data from about 17,000 genetic samples from 1,300 Covid-19 patients. The team, based at the Oak Ridge National Laboratory in Tennessee, asked the $200 million computer to look for patterns in how Covid-19 was changing genes and impacting different systems in the body.

After almost a week of data crunching, the supercomputer landed on something they found surprising: bradykinins. “I was literally at home on a Sunday afternoon looking at different visualizations, and it just jumped out at me,” Daniel Jacobson, a computational systems biologist at Oak Ridge, says.

He calls these haywire reactions a “bradykinin storm,” and like Roche, believes they may help researchers treat severely ill Covid-19 patients, possibly staving off damage to organ systems or even preventing deaths. Outside researchers agree: Elements of the supercomputer’s analysis have been corroborated since it was published in July, and researchers say it could help lead the way to more effective treatments.

Here’s a deep dive into what has been published on bradykinin signaling since the pandemic began, and what we know about how this compound might be instigating some of the worst Covid-19 damage.

Why bradykinin signaling might be making Covid-19 so much worse

How Covid-19 can prompt an inflammatory cascade gets complicated, but Roche and other experts now think bradykinin might be the key to the vascular changes, lung damage, and even neurological symptoms the disease can cause.

The virus usually enters the body through the airways and lands on cells, where a protein called ACE2 functions as a doorway. As the virus replicates in the body, it finds other cells that have ACE2 receptors, such as those in the lungs, hearts, intestines, kidneys, and brain.

“The virus not only uses ACE2 as an entryway into cells but also tells that cell’s nucleus to start reducing ACE2 expression,” Roche says. This causes an accumulation of an enzyme called DABK, which creates conditions for inflammation.

This is where bradykinin might come in. When the virus binds with ACE2 receptors, DABK piles up, and bradykinin levels increase—causing an inflammatory cascade. “It creates a vicious feedback loop,” Roche says, amplifying inflammatory processes, including producing more cytokines.

Scientists initially thought that Covid-19 caused the immune system to release an overwhelming flood of cytokines — as often happens in response to a viral infection. In fact, promising treatments like remdesivir lower cytokine production. But recent evidence suggests that Covid-19 patients may not have particularly elevated levels of cytokines compared to people critically ill with other respiratory conditions, and other interventions attempting to lower cytokine production failed to reduce mortality — suggesting something else is going on.

That something, says Jacobson, might be a bradykinin storm instead. This hypothesis fits with a surprising number of Covid-19’s bizarre symptoms.

Researchers have observed many vascular symptoms, but previously blamed cytokine storms’ inflammation or direct damage from the virus. But bradykinin can impact how your blood coagulates — possibly explaining the strange clotting problems reported in Covid-19 patients and the high percentage of Covid-19 deaths from heart attacks, strokes, and deep vein thrombosis. As the virus causes bradykinin to accumulate in the cells it has hijacked, it makes your blood vessels permeable, letting your blood leak out. This could also explain the “Covid toes,” that have been linked to blood circulation.

In the lungs, increasing gaps in the cells of blood vessels can spell further damage. Lungs are covered in capillaries, so these gaps start leaking blood and immune cells into the interior surface of the lungs, potentially providing the reason for Covid-19 patients’ respiratory distress.

To make things worse, according to the supercomputer analysis, the virus might also increase the natural production of hyaluronic acid—a biopolymer familiar to skincare aficionados, as it can absorb more than 1,000 times its weight in water. As bradykinin causes blood vessels to leak water into your lungs, it hits the hyaluronic acid in your lungs and forms a hydrogel. “It’s like trying to breathe through Jell-O,” Jacobson says. “At that point, unfortunately no matter how much oxygen you’re pumping through a ventilator, you can’t get a gas exchange through the hydrogel.”

Bradykinin dysregulation may also be behind the thyroid problems some Covid-19 patients are reporting. Previous research has found that, in addition to influencing the circulatory system, bradykinin is an important regulator of thyroid hormones.

Ilaria Muller, an endocrinologist at the Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico in Milan, and colleagues recently found that many patients who were hospitalized had abnormally low levels of thyroid-stimulating hormones, suggesting thyrotoxicosis and at least temporary thyroid damage. She says this damage could come from direct damage from the virus through the thyroid’s ACE2 receptors or from systemic inflammation.

More surprisingly, bradykinin storms also help offer an explanation for some of Covid-19’s neurological symptoms — from headaches to long-term nerve damage — which in one study afflicted 57 percent of Covid-19 patients. High levels of bradykinin in particular can cause the blood-brain barrier to break down, potentially allowing the virus into the brain and causing inflammation and damage.

Finally, as Elemental reports, the theory may even explain why men seem to be more likely to have worse cases of Covid-19. Some aspects of the RAS systems have receptors on the X chromosome, meaning that women have twice the levels of these stop-gap proteins, possibly giving them extra protection against the virus.

The supercomputer model also found different gene expression patterns in the lavage fluid from the lungs of COVID-19 patients. This is rare data, in part because getting that fluid can be dangerous to healthcare professionals, who may get infected while taking the samples, so this procedure is no longer carried out. A clinical trial measuring actual bradykinin levels in samples from Covid-19 patients’ lungs would provide a lot of valuable information but is unlikely to happen because of the transmission risk.

When something like a virus tweaks part of the body’s intertwined systems, you often end up with rippling consequences—in this case, a dire trend toward inflammation, possibly through both bradykinin pathways and cytokine production. Essentially, the bradykinin pathway gets off the track—and then it’s like a runaway train, potentially causing damage in many locations around your body.

What do bradykinin storms mean for possible Covid-19 treatments?

After finding the potential role of bradykinins in severe Covid-19 in March, Roche went looking for a way to halt this inflammatory cascade. “It’s like a set of gear wheels—inflammation, injury, inflammation—and you’re trying to jam up the wheels,” he says. Along with his wife, Renuka Roche, an assistant professor in occupational therapy at Eastern Michigan University, he started to explore potential treatments that were ready to use.

As clinicians trained to pay a lot of attention to recovery through rehabilitation, he says, “We know that health care does not end with just saving a person’s life.” Roche says life quality is important too, meaning any intervention that could minimize damage would be a true advancement in the fight against Covid-19’s ravages.

Treatment targeting bradykinin signaling wouldn’t have to be perfect to improve lung damage and long-term outcomes. “If you’re able to even dampen the cycle by 50 percent, that means that much tissue may be spared,” Roche says.

In the medical literature, the Roches found a medication called icatibant that is both known to be safe and inhibits bradykinin signaling. It was already approved by the FDA, with the added benefit of an expired patent, meaning generic versions could be made much more affordably. They reached out to the Canadian and Indian governments about starting rapid research on icatibant in late March, wrote an open letter to the scientific community in April, and published a paper on their hypothesis in May.

At the same time, Frank van de Veerdonk, an infectious disease specialist at Radboud University Medical Center in the Netherlands, was reaching similar conclusions. He knew that ACE2 is an important part of the RAS, and in April, hypothesized that a dysregulated bradykinin system was causing blood vessels to leak into Covid-19 patients’ lungs.

More recently, “We published data in patients with icatibant targeting bradykinin in Covid-19 as a treatment,” van de Veerdonk wrote Vox in an email. While not a controlled clinical trial, van de Veerdonk published a study where nine hospitalized patients were treated with icatibant and matched to similar Covid-19 patients who were not; the patients who’d received icatibant needed less supplemental oxygen and experienced no adverse effects from the drug.

In the US, Quantum Leap Healthcare Collaborative has started a clinical trial of five potential treatments, including icatibant. (They are still currently enrolling patients.) “The safety of the drug is well understood, and it’s fast-acting,” says Paul Henderson, director of collaboration at Quantum Leap.

In general, he says bradykinin receptors are interesting because they are upstream of most of the inflammatory response, including cytokines. If proven effective, he says, these treatments will probably also be useful for influenza and other diseases that cause acute respiratory distress.

Henderson doesn’t discount cytokines’ inflammatory impact altogether but suggests that interventions targeting cytokines may have been “taking out too little of all the processes going on to have much impact.” Imagine how much easier it is to dam a river at its headwater than closer to its mouth—similarly, interventions further “upstream” in biological pathways could have a larger impact.

In some ways, this work could be as important as finding a vaccine. “Reducing the burden on the health care system and preventing the very sickest from dying is really important,” Henderson says.

But he also cautions that, like with cancer, there is unlikely to be one “magic bullet drug.” Instead, it’s more likely a combination therapy, including anti-inflammatory medications and antivirals, will be necessary. “You’ll likely need different interventions in different stages of infection,” he says. “It is extremely complicated.”

Nevertheless, since Jacobson’s paper came out, his hypotheses have been supported by other research. For example, vitamin D is known to regulate RAS, and vitamin D deficiencies have been associated with severe cases of Covid-19.

This fits with a part of the supercomputer analysis that suggested the virus activates genes that break down more vitamin D. Lo and behold, at the end of August, a clinical trial in Spain on vitamin D found that it significantly reduced the need for ICU treatment in Covid-19 patients.

Similarly, another analysis, run by the World Health Organization, which incorporates seven different clinical trials, found that corticosteroids, which inhibit a protein activated by the bradykinin receptor, reduced the risk of Covid-19 death — fitting the computer model’s prediction neatly.

Bradykinin storms may also have implications for long-haul Covid-19 patients. Jacobson is now collaborating with Covid patient groups to gather data. “We’re looking at the top 100 symptoms and trying to map them to this mechanism,” he says, adding that several of his fellow researchers are long-haulers.

He says one of the next questions they hope to address is whether bradykinin dysfunction continues even after the virus has cleared, if the virus itself is persisting in different organ systems or some combination of both.

When new information raises more questions

The notion of bradykinin storms are appealing because they offer a tantalizingly unified theory that would explain so many of Covid-19’s inscrutable impacts. Joshua Zimmerberg, a biophysical virologist at the Eunice Kennedy Shriver National Institute of Child Health and Human Development at the National Institutes of Health, who was not involved in any of the bradykinin research, says the evidence is now compelling. “When you have independent confirmation, when people come to the same conclusion for different reasons—that’s very good evidence.”

But he warns against raising hopes for immediate treatments. “We all crave simple pathways and simple ideas, but inflammation is really complicated. There are still a lot of inflammatory diseases without good treatments.” Dampening bradykinin production too much, or at the wrong time—for example, early in the infection, when the natural inflammation cycle is needed to fight the virus—might actually be harmful.

Roche says the next steps are for large-scale randomized placebo-controlled clinical trials on potential drugs that inhibit bradykinin. “The hypothesis, [Jacobson’s] gene expression data, [van de Veerdonk’s] small-scale case series—these won’t move the needle,” he says. Data is needed to add drugs to doctors’ arsenal against the pandemic. But he’s gracious about more widespread attention only being directed toward bradykinin now, after he’s spent months trying to raise its profile.

“The pandemic has exposed key weaknesses in health care itself,” he says. “We need to empower ourselves with as much knowledge as we can, so we can serve our patients and protect ourselves.”

Lois Parshley is a freelance investigative journalist. Follow her Covid-19 reporting on Twitter @loisparshley.

America is now in the middle of a big experiment: reopening schools and colleges during the Covid-19 pandemic. And so far, how things are going depends on which type of school is involved.

At the K-12 level, while there have been some outbreaks, reopenings haven’t led to the explosion of cases that some feared. Still, this comes with a big caveat: Many schools haven’t fully opened up yet, partly or entirely limiting teaching to virtual sessions. And for schools that have opened, we still don’t have very good data on K-12 schools’ reopenings, and there’s still a lot we simply don’t know about how kids transmit the coronavirus.

According to the Covid Monitor, there have been more than 52,000 cases in K-12 schools as of October 15. That’s significant, but a small portion of the 3 million coronavirus cases in the US since August. At the very least, K-12 schools don’t seem to be a primary driver of Covid-19 in the US right now.

“It hasn’t been as chaotic as I had anticipated,” Tara Smith, an epidemiologist at Kent State University, told me. “I expected things would be worse by now, but it’s been going all right so far in general.”

But at colleges and universities, reopening appears to be going much worse, with multiple big outbreaks over the past few months. The problem so far doesn’t seem to be transmission within classrooms so much as transmission outside of them — in dorms, fraternities, sororities, bars, restaurants, and other indoor spaces used to congregate, party, eat, and drink.

The outbreaks spawned almost immediately as colleges and universities reopened. In September, a USA Today analysis found college towns comprised 19 of the 25 biggest coronavirus outbreaks in the US. Outbreaks have forced some colleges and universities to change plans and permanently or temporarily move classes online across the country, from California to Michigan to North Carolina.

The college outbreaks have resulted in deaths. In September, 19-year-old Appalachian State University student Chad Dorrill died, despite friends and family describing him as a “super healthy” athlete with a lack of known preexisting conditions. Dorrill seemingly contracted the coronavirus while living off-campus — leading to neurological complications, potentially caused by undetected Guillain-Barré syndrome, that ultimately killed him.

“It’s not a hoax, that this virus really does exist,” Emma Crider, a student at Appalachian State, told the New York Times. “Before this, the overall mentality was ‘out of sight, out of mind.’”

Some colleges and universities are trying to prevent and counter these outbreaks with extremely aggressive testing regimes, testing each student on campus up to twice a week. The hope is that this will catch any new coronavirus cases before they lead to massive outbreaks — mirroring the kind of strategy employed in Germany, New Zealand, and South Korea to control their respective epidemics. But it’s too early to say how this will work in a higher education setting, especially in communities that have big Covid-19 epidemics outside their schools.

How this all plays out could help decide whether America sees a much-feared coronavirus surge this fall and winter. Coupled with the holidays bringing people together and changing weather pushing some parts of the country indoors, experts worry that school reopenings could lead to a big spike in Covid-19 in the coming months. While the holidays and weather remain in play, mitigating the spread from schools could stop at least one point of concern.

There are consequences beyond Covid-19, too. There’s already solid evidence that remote learning isn’t good enough to make up for the benefits of in-person teaching, meaning kids fall further and further behind as long as schools don’t fully reopen. And when kids aren’t sent off to school, it’s tremendously disruptive to entire families — forcing parents to stay home, often having to supervise their kids to make sure they’re actually logging on to their classes.

“We’re really not acknowledging how much work and strain it is on families when you have a kindergartner doing virtual learning,” Saskia Popescu, an infectious disease epidemiologist, told me.

A failure to get Covid-19 under control and reopen schools, then, doesn’t just mean more coronavirus cases and deaths — on top of the more than 210,000 deaths the US has already seen — but impacts that will cascade over the short and long term across American society.

K-12 reopenings seem to be going fine overall, but there’s a lot we don’t know

It’s still unclear how many K-12 schools, exactly, have fully reopened. Given the country’s sprawling network of school districts, each under varying levels of state and local control, we simply don’t have a good way to track what every school is doing at a national level.

According to Education Week, four states have ordered schools to reopen. Seven, along with Washington, DC, and Puerto Rico, have mandated partial or full closures. The remaining 39 states have by and large left it up to individual school districts or local governments to decide.

Schools can try to fully restart in-person learning, go remote only, or follow a hybrid model. Among those allowing in-person teaching, some require masks for teachers and students. Some are putting students into cohorts or pods — meaning they have to stick to the same group of peers while in school. Some have spread out desks or limited capacity in classes, and have shifted schedules to reduce how many people are in the building at any moment. A few have taken more aggressive measures, like improving ventilation systems in schools, holding at least some classes outside, or instituted aggressive testing programs.

So far, there doesn’t seem to have been a massive surge of Covid-19 due to K-12 schools reopening for in-person instruction. Confirmed cases in K-12 schools make up less than 2 percent of all cases reported in the US since August.

One caveat: A lot of states and districts still aren’t reporting Covid-19 cases in K-12 schools. The Covid Monitor, as an independent group, collects public and media reports on top of the official data to try to fill in the gaps. But it’s certainly missing a lot of cases, meaning its number is a minimum estimate.

Still, it certainly seems like the massive epidemics many feared haven’t happened (at least yet). A USA Today analysis of Florida’s school reopenings, for example, concluded, “Among the counties seeing surges in overall cases, it’s college-age adults — not schoolchildren — driving the trend.” In California, officials similarly reported that they so far had found no link between K-12 schools reopening and increased coronavirus transmission.

“There are some reasons to be hopeful,” Katherine Auger, a health policy researcher at Cincinnati Children’s Hospital, told me. “We aren’t hearing of huge outbreak stories in the news.”

Experts cautioned, however, that the results are early. And they shouldn’t be used as an excuse to open recklessly or without proper safety measures like social distancing, masking, testing, and contact tracing.

Part of the problem is there’s still a lot we don’t know about K-12 schools’ ability to spread Covid-19. For one, we still don’t know for certain how much children, especially younger kids, spread the coronavirus.

What we do know with more certainty is that there seem to be differences in how sick kids get from Covid-19, depending on age. A recent study from the Centers for Disease Control and Prevention found that adolescents ages 12 to 17 were roughly twice as likely as children ages 5 to 11 years old to have a confirmed coronavirus infection. Whether that means younger children are less likely to get and transmit the coronavirus, or merely less likely to develop significant symptoms and get tested, is still an open question.

The testing component is particularly important. As the New York Times reported, it can be very difficult to get a coronavirus test for younger children. If kids can’t get tested, then new infections simply aren’t going to get caught and recorded. Some schools are taking steps to test their staff and students, but many are not — blinding them to potential outbreaks.

Still, some experts have cited data like this to argue that at least K-3, K-5, or K-8 schools could open safely, with few, if any, serious outbreaks. “Those are the kids who need the in-person learning, need the social interaction,” Auger said. “It makes sense developmentally that college students and high school students would be able to learn more readily in a remote setting.”

One concern is that, even if the coronavirus doesn’t seem to transmit among children or hurt them as much, the same isn’t necessarily true for teachers. That fear has led a lot of teachers, backed by powerful unions, to resist full or even partial reopenings.

Colleges and universities seem to be going worse — with some exceptions

Colleges and universities have taken a variety of approaches in reopening. Some are trying to fully reopen, many are sticking to online only, and others are doing a hybrid model. Some allow students to live on campus, although typically at a reduced capacity. Many of the schools are taking a fairly hands-off approach to what students do — merely recommending social distancing and masking — although some have adopted very aggressive testing and masking regimes.

So far, the experience has ranged from mostly fine to outright disasters, with major outbreaks forcing some universities and colleges across the country to move classes back online temporarily or permanently, sometimes after just weeks of reopening.

The outbreaks don’t appear to originate in classrooms, but rather in places where students tend to work, socialize, and party. A recent CDC study backed this up, concluding that Covid-19 clusters in an unnamed North Carolina university were likely fueled by “student gatherings and congregate living settings, both on and off campus.”

To put it another way, the outbreaks seem to be coming from dorms, fraternities, sororities, bars, and restaurants. It’s in these kinds of indoor spaces, where college students work, party, eat, and drink, that Covid-19 has spread. Experts have described large parties, indoor dining, and bars as especially risky: People are close together for long periods of time; they can’t wear masks as they eat or drink; the air can’t dilute the virus like it can outdoors; and alcohol could lead people to drop their guards further.

This was predictable: As Smith said, “This is what you would expect from college students.”

For young people, a big consideration is that Covid-19 is simply less threatening to them than to older adults. That may make them feel like they can party and socialize without major consequences.

But young people can still get sick and die from Covid-19 — and some have. Young people also eventually socialize with their parents, grandparents, teachers, and other older peers. Another CDC study found this to be a consistent trend over the summer: Outbreaks would start among the young, eventually spreading to older populations — leading to many more cases and deaths as a result. That could be particularly bad for colleges and universities if students carry the virus around the country when they go back home for holidays or breaks, potentially triggering epidemics not just locally at or near their campuses but nationwide.

To avoid such outbreaks, some colleges and universities have embraced very aggressive testing regimes — testing all students as they get on campus, then testing each of them two times a week after. By constantly testing, these schools hope to stop a few cases from turning into a big outbreak.

On top of testing and tracing, colleges and universities have taken various steps to get their students to follow other basic Covid-19 precautions, such as social distancing and masking. Some universities have outright prohibited their students, with the threat of suspension or expulsion, from going to parties or other gatherings, or even interacting with anyone outside of their dorm and classes.

Whether all of that works remains to be seen. For testing and tracing, the early results seem promising, with several of the most aggressive schools reporting few, if any, Covid-19 cases. And it follows the kind of model that’s helped other places, including whole nations, control their epidemics.

Some experts are worried that the aggressive testing regimes could lead to a false sense of security. They pointed to the White House, where very aggressive testing has been used to justify relaxing on social distancing and masking. That seemed to contribute to the ongoing outbreak at the White House, spanning from President Donald Trump to a presidential valet.

Aggressive testing “is not a replacement for all the other measures,” Lauren Ancel Meyers, a mathematical biologist at the University of Texas Austin, told me. “It’s just a needed addition to armament of intervention strategies that we have.”

A recent New York Times story showed that false sense of security in action, reporting that “students like Logan Morrione can wander on and off the Waterville, Maine, [Colby College] campus, attend most classes in person and even do without masks in some social situations.”

Truly reopening schools requires getting Covid-19 under control

Setting aside whatever is happening within classrooms, the biggest problem for schools is that America still has a lot of coronavirus cases. In the past week, the US reported more than double the cases per person a day as Canada and at least 100 times the cases per person a day as South Korea, Australia, and New Zealand.

With so many cases across the US, and especially in educational settings where students are coming in from around the country, there are simply more chances that the virus will end up on campus. Meyers emphasized this is the No. 1 factor any school should consider before reopening.

This is why many experts spent much of the summer calling for America to suppress the coronavirus: If cases were driven to a low enough level, that could allow schools, from K-12 to colleges and universities, to open much more safely.

But despite experts’ warnings, many states reopened bars and indoor dining — fueling large outbreaks. Some places were slow to mandate masks, with 17 states still not requiring them. The US, in effect, prioritized a false sense of normalcy and the reopening of bars and indoor dining over the reopening of schools. Universities are seeing this directly as bars and indoor dining lead to a surge of coronavirus cases on campus.

“It’s something we really should have seen coming,” Popescu said.

The bad outcomes within some schools could set up the US for a broader vicious cycle: If colleges and universities lead to Covid-19 spikes, they could make it more difficult for K-12 schools to reopen. That, some experts argued, would be a backward outcome. “It’s much easier to do virtual learning for universities and for high schools,” Popescu argued.

So it’s the problem of community transmission, experts say, that must take priority over all other safety precautions within schools. As long as the US doesn’t get its whole coronavirus epidemic under control — whether due to incompetence from the Trump administration or other officials — schools are, just like other public settings, going to be at risk for Covid-19.

That’s not to say schools can’t take steps to make themselves safer. They can still embrace social distancing, masking, testing, and tracing. They can try to have fewer people on their campuses — by staggering schedules, or reducing the numbers of people in classrooms or dorms. They can encourage or mandate students to only socialize within a small group of people — by establishing a pod or cohorting, or by limiting students to people that they live or go to class with. They could try to improve ventilation in buildings, or hold more classes and events outside.

But these precautions aren’t going to be consistently effective if the virus is raging in the broader community.

If this isn’t taken seriously, it could, when paired with the holidays and people going inside to avoid the cold, contribute to a surge in coronavirus cases this fall and winter. America’s already bad Covid-19 epidemic, then, would get even worse.

Click Here:

As record daily Covid-19 hospitalizations and deaths this month in the US have pushed the pandemic to new crisis levels, senior government health officials have lamented that many patients are not getting the drugs — including monoclonal antibodies, antivirals, and corticosteroids — available to treat the disease, leaving many doses unused.

There are still questions about how well many of these drugs work. One recent report found that a mix of monoclonal antibodies developed by Eli Lilly could reduce Covid-19 hospitalizations and deaths by 70 percent, though some researchers cautioned that the findings were drawn from a small number of events.

And with the new, potentially more contagious variants of the virus that causes Covid-19 now spreading, a few of these therapies could prove even less effective.

After some stumbles earlier with drugs like hydroxychloroquine, regulators have authorized monoclonal antibodies, antivirals, and corticosteroids. Doctors say these drugs have helped them save lives, putting them in a far better position than they were last year and cushioning the blow of this pandemic.

Yet US health officials say hospitals are still struggling to get them administered, and to get patients to the hospital in time to take advantage of them. In particular, they noted earlier this month that less than 25 percent of available doses of monoclonal antibodies have been administered.

Click Here:

“Even with a vaccine, we know we will not prevent every infection,” said US Surgeon General Jerome Adams on January 14 during a press conference. “So today we want to remind everyone that for those of you who do contract Covid, we have excellent treatments to keep you out of the hospital, to keep you out of the ICU, to help you recover quickly.”

Administering these treatments most effectively also requires good timing. Some, like corticosteroids, work best in later stages of the disease; others, like monoclonal antibodies, need to be administered to patients early in the course of their illness, often before someone is even sick enough to go to the hospital.

That means testing to confirm that someone is carrying the virus and getting the results quickly is crucial, particularly for people at the highest risk of severe disease, like those over the age of 65. Then those patients need to get to a hospital that has the capacity to treat them in time. Many of these treatments also need medical supervision, adding further stress to hospitals reaching capacity. And as health facilities get overwhelmed, fatality rates are rising.

The Department of Health and Human Services has put together a website highlighting the tools available to control the pandemic and where people can receive treatments near them.

Here is how doctors think about treating Covid-19 patients, some of the most common treatments they have at their disposal, and their drawbacks.

Several tools and strategies for treating Covid-19 have emerged, with varying effectiveness

There are two main approaches for dealing with Covid-19. One is to constrain the virus, and the other is to temper the immune system’s response to it.

In the early stages of the disease, the SARS-CoV-2 virus itself is the main culprit behind the damage, leading to symptoms like coughing and a loss of smell. But as the disease progresses, the body’s immune system starts to overreact, causing problems like inflammation and, later, organ damage.

Figuring out what works to tamp down this often deadly disease has been tricky. Ideally, scientists would conduct randomized controlled trials, but in the face of an overwhelming pandemic, it’s been hard to recruit people into these studies and get adequate results in time. Much of the evidence for drugs to treat Covid-19 comes from weaker observational studies, leaving some therapies under a frustrating cloud of uncertainty. And doctors have been inclined to prescribe drugs that have already been approved for other uses and have an established safety record.

“We don’t have time to find a new drug in a test tube and do years of studying to make sure it’s safe,” said Matthew McCarthy, an associate professor at Weill Cornell Medicine who has been treating Covid-19 patients since the start of the pandemic. “We want to take drugs that we know are safe and see if they can help with Covid.”

But research is still underway to find better treatment options, and more therapies, from repurposed existing drugs to novel drugs, could become available soon.

Treatments include the following:

Convalescent plasma: The idea here is to use plasma, the liquid part of blood plus the proteins used for clotting, harvested from patients who survived Covid-19. During an infection, the immune system generates proteins called antibodies. They stick to a part of the virus or to an infected cell. That attachment can then block the virus from invading hosts, or it can flag the virus or infected cell for destruction by other immune cells.

After a patient successfully defeats the virus, their blood contains a variety of antibodies that stick to all different parts of the virus. Doctors then transfer those remaining antibodies via plasma to a patient with an active infection. Without outside help, the immune system can take several days to produce antibodies, so getting some from outside can bolster defenses, particularly for people at high risk.

This technique has been used in the past to treat other infections, but the evidence of how well it works against SARS-CoV-2 is mixed. The Food and Drug Administration granted an emergency use authorization to convalescent plasma last year, but the National Institutes of Health reported at the time that the evidence for its effectiveness was weak. Subsequent studies seemed to show that it helps slow the disease when administered early, particularly in older adults. More recent results have also been conflicting, with one study in the UK reporting no benefit and another finding that convalescent plasma rich in antibodies lowered the risk of death. Revised FDA guidelines allow convalescent plasma to be used to treat hospitalized patients.

The supply of convalescent plasma is limited by the number of patients who donate. And it’s infused intravenously, so it has to be administered by a professional. The main concerning side effects are allergic reactions and circulation problems associated with transfusion.

Monoclonal antibodies: This approach takes the idea behind convalescent plasma one step further. Some antibodies are more effective than others at corralling a given pathogen, so if one clones the best antibodies, they could be used as the basis for a targeted drug.

There are now two monoclonal antibody therapies for Covid-19 that have received emergency use authorizations from the FDA. One is called bamlanivimab, developed by the pharmaceutical company Eli Lilly. The other is a cocktail of two monoclonal antibodies, casirivimab and imdevimab, created by Regeneron (the -mab suffix stands for “monoclonal antibody”). President Trump famously received a course of the Regeneron therapy when he was ill with Covid-19 last year.

Under Operation Warp Speed, more than 500,000 doses of these therapies have been distributed across the US. Only about 25 percent of these doses have been used, despite high levels of Covid-19 transmission.

Like convalescent plasma, these drugs require transfusion. But monoclonal antibodies are most effective in the early stages of the illness, rather than in patients who are already hospitalized.

“By the time you’re hospitalized, your immune system is kicked into high gear and it may simply be too late,” McCarthy said. Some hospitals around the country have reported good results using monoclonal antibodies, with the treatment reducing the likelihood of a high-risk patient needing hospitalization.

However, NIH has been more skeptical of the evidence provided to date. For both the Eli Lilly therapy and the Regeneron therapy, the agency said “there are insufficient data to recommend either for or against the use” of these drugs and that they “should not be considered the standard of care.” That doesn’t necessarily mean that these drugs don’t work — just that the research to date hasn’t yielded a definitive answer.

Side effects are similar to those of convalescent plasma, with allergic reactions being the main concern.

Antivirals: These are drugs that directly interfere with the reproductive cycle of a virus. Since viruses like SARS-CoV-2 use human cells to make copies of themselves, it’s tricky to come up with a drug that hampers the virus without causing any collateral damage.

Remdesivir has emerged as a leading antiviral drug against Covid-19. Sold under the brand name Veklury by Gilead Sciences, it was the first drug to receive full FDA approval to treat Covid-19, becoming the new standard of care. It works by imitating one of the molecules the virus uses to encode the instructions for making copies of itself. The impostor molecule causes the viral replication process to stall, but it doesn’t fool human cells, giving it a targeted effect.

It was initially developed to treat the Ebola virus. There are concerns about how well it works with Covid-19. The World Health Organization conducted one of the largest studies to date on antiviral drugs for Covid-19 and found that remdesivir had little to no effect on mortality. However, several smaller studies found that it could reduce the length of hospital stays in patients.

McCarthy said that means the drug can still be useful. Shorter hospital stays mean fewer beds occupied, which in turn allows health workers to treat more patients. The drug is mainly administered to Covid-19 patients who are hospitalized.

Side effects of remdesivir include elevated liver enzymes, which could indicate liver damage, as well as allergic reactions leading to fever, shortness of breath, wheezing, swelling, low blood oxygen, and changes in blood pressure. This is also a transfused drug, so the same concerns about circulation problems apply here, as well as the challenge of administering it under medical supervision.

Corticosteroids: As Covid-19 progresses, it can throw the immune system way off balance. Immune cells can start attacking healthy cells, and the strain of being on high alert can trigger dangerous immunological conditions like cytokine storms, even after the virus has been cleared from the body.

So drugs that tamp down on the immune system can help patients in more advanced stages of the disease. This seems to be the case with dexamethasone, a generic corticosteroid. It’s one of the few drugs that has been shown to actually reduce the mortality rate of Covid-19, and it costs as little as $1 per dose, administered orally.

That’s why it’s quickly become one of the most common drugs used to treat hospitalized Covid-19 patients who are ill enough to need oxygen support.

However, because it can slow the immune system, it could actually backfire in early stages of Covid-19 when the virus itself is the main concern. Dexamethasone can also leave patients vulnerable to other infections and may cause dizziness, an irregular heartbeat, and psychiatric problems like anxiety and suicidal ideation.

Other emerging treatments: So far, there is still no surefire way to knock out Covid-19 the way an antibiotic can wipe away a bacterial infection. That’s why many doctors often use several of these therapies in conjunction to treat Covid-19 patients, like remdesivir and dexamethasone for hospitalized patients. “Those two things are given so frequently together that some people as a shorthand call it ‘remdexavir,’” said McCarthy.

But researchers are also investigating other drugs, both off-the-shelf varieties and new designs, to see if they can make more gains against the virus. Clinical trials are underway for drugs that act as immune system modulators like abatacept and infliximab, for instance, which are already used for rheumatoid arthritis, to deal with immunological imbalances wrought by Covid-19. A small randomized trial found that fluvoxamine, an antidepressant, prevented symptoms from getting worse in Covid-19 patients within seven days of symptoms appearing. Large scale trials are also beginning for generic drugs like the anti-inflammatory drug colchicine and the anti-parasitic drug ivermectin.

Doctors are also developing protocols to deal with patients experiencing lasting problems from Covid-19, the so-called long-haulers. “I think what you’re going to see six months or a year from now, long Covid is not going to be one diagnosis but a series or collection of different conditions,” McCarthy said. Persistent fatigue, neurological problems, and breathing trouble can linger, and each set of symptoms may require its own course of treatment. Some Covid-19 patients have had strokes, while others are reeling from blood clotting disorders.

“It’s become clear to me that I’m going to be dealing with coronavirus and the sequelae of it for years and years,” McCarthy said. And more research is still needed to determine what will work best for these many survivors who are still suffering.

Why it’s still so hard to deploy treatments for Covid-19

Despite the growing variety of options, health officials are concerned that not enough people are getting them. “These medications, these therapeutics, are not being used as much as I, or the doctors on the task force, or the career experts here at HHS feel that they should be,” Adams said. “Tools that never leave the toolbox don’t get the work done.”

Officials say part of the problem is public awareness — people don’t know that these options are available to them. Many public health agencies are also not conveying that there are treatments that can help people before they are hospitalized.

Another issue is that many of these drugs have to be administered early in the course of the disease. That means people need to get tested for the virus and get results quickly. People in high-risk groups in particular should then seek treatment right away, especially if they begin to notice breathing issues.

Hospitals are also filling up with patients, and many can’t spare the personnel to treat people with less severe symptoms, particularly with drugs that require transfusions. “The antibodies are not in shortage,” said Janet Woodcock, director of the Center for Drug Evaluation and Research at the FDA, during a press call this month. “We have a shortage of ability to administer these to patients.”

There are other options, however. Patients can receive these therapies at dedicated transfusion centers, or can have nurses administer the therapy at home, but both of these alternatives pose their own logistical challenges.

Cost is another barrier. While off-the-shelf therapies like dexamethasone are cheap, and the government is fronting the cost of the drugs for monoclonal antibodies, health providers can still charge for using their facilities. Transfusions in particular can cost hundreds to more than $1,000 out of pocket, depending on insurance coverage.

The Covid-19 pandemic is also throwing some curveballs. New variants of the virus are now spreading in the United States. These variants contain mutations that could weaken prior immunity to the virus and may elude targeted therapies like monoclonal antibodies.

“We are actively looking at that question,” Woodcock said. “We can’t predict what variants will arise and will become prevalent, so we have to rely on sampling and testing that’s done across the United States” to continue studying the efficacy of these drugs.

A spokesperson for Regeneron told Vox that the company’s combination of two monoclonal antibodies still seems to be effective against the apparently more contagious B.1.1.7 variant first identified in the United Kingdom. The 501.V2 variant first detected in South Africa seems to elude one of the antibodies in the treatment regimen, but not the other.

“We’ll continue to test/replicate our data to confirm that is the case,” the spokesperson wrote in an email.

Drugs that aren’t specific to a given version of the virus like corticosteroids or antivirals are likely to remain as effective against the new SARS-CoV-2 variants.

To keep treatments viable, the full suite of public health tools to control the pandemic must be used. Relieving the stress on hospitals requires reducing transmission of the virus, which in turn demands social distancing, masking, and rigorous hand-washing. Reducing transmission also lowers the chances of mutations that could render treatments less effective.

Administering care away from hospitals whenever possible could also lift the burden on hospitals and allow them to focus on the most critically ill patients.

Though the coming weeks are likely to remain grim, with high levels of hospitalizations and deaths, the combination of treatments and vaccines does offer hope. Progress against the pandemic will continue to be slow, hard-fought, and fragile, but we now have tools that we didn’t before. It’s a matter of whether and how we wield them.

Click:CNC machining

TIPPERARY STAR HURLER Pádraic Maher says that his decision to retire from the sport was made to ensure a greater quality of life going forward.

Paudie Maher on the ball for Tipperary.

Source: Ryan Byrne/INPHO

The three-time All-Ireland winner made the shock announcement during the week, saying that he had received medical advice to step away from contact sport due to a neck injury.

Maher had previously indicated his intentions to return for a 14th season with the Premier County, but will now be bringing the curtain down on his decorated career with both Tipperary and his club Thurles Sarsfields.

Speaking to the media today, the six-time All-Star elaborated on some of the details of his neck injury. He began by explaining how he was prompted to seek medical advice after he mistook some headaches and neck pain for possible having Covid-19 symptoms.

“I still have to meet one or two more lads about it to determine how old it is but at the moment from what I know I only got the symptoms from around the time of the county final when my neck was at me and I was getting a few headaches.

“That’s when it arose but again it could have been an accumulation of things, I don’t know. That’s why I’m hoping to meet one or two more specialists tomorrow and at the start of next week and hopefully they’ll be able to give me a bit more information as regards how old it is, how it happened, but there is a fair chance from what I told it happened in training or something between the county semi-final and final because the symptoms arose a few days before the county final.

Click Here:

“I said I wasn’t feeling great. At the time, I thought ‘am I getting Covid?’, I didn’t know what was going on. But then we got to the root of it recently and thankfully we did because if the doc didn’t send me for a scan I could be in training and could have been making it a lot worse unbeknownst to myself. Very unlucky but very lucky at the same time.

“So there is a fair chance I took a knock at training, noticed it myself. The way we train with Sarsfields is fairly physical so there is a fair chance I got a knock there and whether it ruptured something then or made an old injury worse I don’t know but hopefully I’ll get a lot of answers in the following weeks.”

Maher added that he was reassured by the doctor that eliminating the risk now means he can look forward to a healthy life away from hurling. He’s also clear to continue working for An Garda Síochána.

All forms of contact sport are no longer available to him, but individual pursuits like running, swimming and cycling are still safe options.

He has also recently opened the Heyday coffee house in Thurles with his Tipp team-mate Séamus Callanan, which will give him a new focus.

“He [the doctor] only listed off what the damage could be,” says Maher, “especially when you are working in the head and neck area, he put it to me, do you want your girlfriend lifting you off the couch to put you to bed every night? It was that extreme so when he started talking like that, I said, this is a fairly black and white decision for me.

“Thankfully, the risk has been taken away, please God, and with the bit of guidance from the medics going forward I will have a perfectly healthy life to live.

“It’s going to be some void to fill alright, being gone four or five nights a week and building up to big games at the weekend. So it’s going to be strange.

“I don’t know if I can be twisting or turning or moving my neck too sharply but there’s still loads for me to do between work and the coffee shop.”

Source: James Crombie/INPHO

Maher departs as one of Tipperary’s greatest ever players, who won three senior All-Ireland titles throughout the course of a decade. He also enjoyed success at underage level and was part of an exciting group of emerging talents that broke through to the senior ranks in 2010.

He added that the outpouring of appreciation for his contribution to hurling has been “amazing” and that he didn’t expect the huge volume of messages.

Tipperary will get their Division 1B campaign underway this weekend when they travel to face Laois in Portlaoise. Maher’s brother Ronan is still a key player for the county, and he wants to get started on adjusting to the role of supporter.

“I’m actually thinking this morning I might go down to Portlaoise to get it out of the system. It will be strange alright but get to the first one or two games and I’ll be as much a supporter as anyone.

“Ronan is involved there as well and I need to support him as well and yeah, sure, we’ll see we might go down to Portlaoise on Saturday evening and a few pints on the way home. Life has changed a lot in the last few days, it’s very strange.”

– First published 13.59, 3 February

The42 is on Instagram! Tap the button below on your phone to follow us!

MARK KEANE FELT the timing was right to pursue a hurling career with Cork after his decision last month to bring his time in the AFL to a close.

Source: Seb Daly/SPORTSFILE

The 21-year-old departed his Aussie Rules club Collingwood after being based with the Melbourne side since 2018.

His sporting focus has returned to his GAA roots in Ireland but despite starring for Cork football underage sides and famously scoring the goal for the senior team that secured a dramatic win over Kerry in November 2020, he has linked up with Kieran Kingston’s hurling squad for the year ahead.

Mark Keane is focused on Cork hurlers in 2022.

Source: Laszlo Geczo/INPHO

“Football was always kind of my love, I played hurling all the way up as well,” says Keane.

“I played minor and U20 at football level, would’ve played both if I could have. I just thought it was the right time to give hurling a go. It’s a dream for everyone really to play both codes, play Cork hurling and football. Since I’ve done the football, I just wanted to give hurling a go. I just feel like it’s the right time.

“I’ve been working closely with the selectors above in Cork senior hurling. They’ve been great and very supportive, trying to get the best out of me.

“It’s a very young crop of good players coming through, training sessions are very high intensity and very enjoyable. That’s all thanks I suppose to Kieran with Noel Furlong and Pat Mulcahy, they’ve been super. Even the training sessions are a great buzz, going up and meeting all the lads.”

Keane has a strong underage hurling track record and will link up with some colleagues from those teams now on the senior stage with Cork.

“I’ve a Munster medal and All-Ireland medal in hurling from U15 and U16 under John Meyler. Winning with the likes of Darragh Connery, Tommy O’Connell, Sean Twomey, and seeing them playing with Cork senior hurling. Seeing the Cork footballers win the U20 final (in 2019), my fellow clubmate Cathal O’Mahony win the U20 title as well. That was devastating for me as well, and I felt I could have been a part of it, if I was at home.”

Cork’s league campaign may be commencing on Saturday against Clare but Keane has a more significant assignment. His form for his club Ballygiblin has rekindled his interest in hurling, a series of powerful displays have helped propel them into the AIB All-Ireland junior final against Kilkenny’s Mooncoin.

He may have played at the MCG in Australia but this will be his first time gracing the Croke Park stage.

Mark Keane in action for Collingwood.

Source: AAP/PA Images

“It’s everyone’s dream to be in Croke Park with your club, definitely (didn’t think I would) with Ballygiblin. It’s an unbelievable buzz in fairness, it’s only a small country club outside of Mitchelstown. I couldn’t speak highly enough of Brian Molan and Liam Doc (O’Doherty), our chairman and secretary, they’ve been unreal. They’re just great characters and you just want to play and win for them any day of the week.”

After opting to close out his AFL days, Keane has no regrets at the end of a sporting chapter that saw him make five appearances for Collingwood.

“I went back over for five or six weeks for a pre-season (at the end of 2021). When I came home I just wasn’t ready to go back. Just in my own head, I’ve always went back without a bother but this time just felt it wasn’t the same and wasn’t ready to go back and commit to it.

“I suppose I always wanted to come home and play for Cork in either hurling or football. I just felt like it was the right time to come home.

“It’s always a tough decision when you’re leaving the AFL. I just had to ring the head coach and general manager and had a few conversations with them and they were very supportive of it as well, looked after me very well with my transition back to home.

“When I was over there I was always invested in it, whenever I was training, I trained to the best of my ability and stuff like that, but in the back of my mind GAA was always there. I’ve tried loads of times to ignore the GAA back here at home, but unfortunately I couldn’t get it out of my head.”

Mark Keane.

Source: AAP/PA Images

The restrictions enforced by Covid-19 made life difficult off the pitch over the past couple of years.

“I wasn’t able to get my parents and girlfriend over for my AFL debut. There were special moments like that you weren’t able to do. You weren’t able to come home as easy as you were.

“There were restrictions put on the AFL boys, even though there weren’t in Melbourne – you weren’t ablet to go to restaurants and stuff like, just to keep the AFL season up and running.

“AFL PA, and the Gaelic Players Association, have been super with helping me. AFL PA, even though you are retired, they’ll still help you for three years post-retirement, which is very good.

“The transiton has been good. It’s definitely been easier with there being a good buzz around the place, around Mitchelstown and Ballygiblin.”

When living in Australia, hurling was initially parked in Keane’s list of priorities. He then availed of an O’Neills depot in Adelaide to get himself a hurley so he could puck around with his housemate, Meath’s Cian McBride, and took in the odd training session with Melbourne club Garryowen.

Since last autumn he has become immersed in the sport again, only missing one of Ballygiblin’s matches when they played a Munster semi-final. He’s keeping an eye on Cork’s league trip to Tullamore on Sunday week against Offaly and gearing himself up for an All-Ireland club final.

The aim is achieve more than just that memorable goal for Cork in Páirc Uí Chaoimh in 2020.

Click Here:

“It’s always good when you’re knocking Kerry out of championship – you can’t beat them enough. I was just glad that we got to the Munster final, but we didn’t finish it off when we should have. I don’t want to be remembered just for that.

“I want to be remembered for other things: Playing with Cork hurling this year, aiding and helping Ballygiblin to get to an All-Ireland final, being around Mitchelstown in county finals, playing in the AFL as well.”

Buy The42’s new book, Behind The Lines, here:

DAITHÍ BURKE HAS been appointed as the Galway senior hurling captain for 2022.

The five-time All-Star and 2017 All-Ireland champion succeeds Padraic Mannion in the role, with Joseph Cooney named vice-captain. 

The news was announced in a Galway GAA statement, which reads: “We are delighted to announce that Daithí Burke, Turloughmore GAA, will captain the Galway senior hurling team for 2022 with Joseph Cooney, Sarsfields GAA, named as vice-captain.”

“Wishing Daithí, Joseph, the senior hurling panel, Henry Shefflin and management a successful year.”

📢PRESS RELEASE
We are delighted to announce that Daithí Burke @turloughmorehc will captain the Galway Senior Hurling team for 2022 with Joseph Cooney @SarsfieldsGAA named as Vice-Captain.
Wishing Daithí, Joseph, the Senior Hurling panel, Henry Shefflin & mgmt a successful year. pic.twitter.com/76KvhemONa

— Galway GAA (@Galway_GAA) February 3, 2022

Turloughmore defender Burke has been a mainstay for the county since making his debut eight years ago, and the 29-year-old dual star previously captained his club to the 2020 county final.

Shefflin’s Tribe open their 2022 National Hurling League campaign against Offaly at Pearse Stadium on Sunday.

Their Walsh Cup campaign saw them beat Michael Fennelly’s Faithful county and Antrim, and lose heavily to Dublin.

Galway exited the 2021 Liam MacCarthy race after defeat to Waterford in the qualifiers.

THE MULLINAHONE LADIES team is uniquely composed of players from two different counties.

Mullinahone’s Molly Walsh [right] ahead of the All-Ireland final against St Jude’s.

Source: Seb Daly/SPORTSFILE

Situated about halfway between Clonmel and Kilkenny city, the village sits right alongside the border between the two counties. Its official address is in the Premier region. On the other side of that line, a short drive away into Kilkenny territory, is the village of Windgap.

Both clubs belong to hurling country.

But football has been progressing in Mullinahone and both localities have formed an unusual alliance over the years, allowing players from both sides of the fence to play both codes.

The longevity of that relationship has resulted in Mullinahone reaching the currentaccount.ie All-Ireland junior club final against St Jude’s of Dublin this Saturday.

The squad will that will contest the decider includes seven camogie players from Windgap.

“Yeah, I’m from Windgap,” Mullinahone defender Molly Walsh tells the media ahead of that showdown with St Jude’s in Baltinglass.

“I’ve been playing football over in Mullinahone since I was 10. I’m here long enough anyway. When I started playing football, Mullinahone was the closest football team to me, so that’s where I went. A few more of the girls have joined in the last few years. It’s brilliant.

“The football has been really getting going this year. We’ve been working away for years but this was the first year that we won a junior county final. 

“It’s great to have Mullinahone to play football in because I would have had nowhere to play football in Windgap. It was only in primary school. I came over to Mullinahone then. There’s always been a few going over and back playing football there. We have a few playing camogie with us in Windgap.”

One of the Windgap seven that’s serving for Mullinahone is Kilkenny camogie star Denise Gaule. Gaule is a four-time All-Star in the small ball game, and was also crowned Camogie Association/WGPA Senior Players’ Player of the Year for the 2020 season.

A reliable free-taker for the Cats, Gaule converted a crucial last-minute penalty in the All-Ireland final that year which delivered a second O’Duffy Cup triumph for the county since 2016.

She’s a new recruit for the Mullinahone footballers, but Walsh says there’s been no struggle in making the transition.

“I’d say she’d adapt fairly quickly to anything she put her hand to,” Walsh says in praise of Gaule.

Click Here:

“She just came on board this year. The camogie finished up early. She was looking for a bit more to do. I’d be used to playing with her in Windgap.

“It’s probably good that we’re not in the same county. There’s not as much rivalry between each other. We all went out as one the other day. The supporters were brilliant. There were loads from Windgap and from Mullinahone.”

At the outset of the season, Mullinahone’s objective was to win the county final. They surpassed that goal by claiming Munster honours after defeating MKL Gaels of Kerry before earning a place in the All-Ireland final after getting the better of Galway’s St Brendan’s in last month’s semi-final.

A win over St Jude’s would be historic for Mullinahone and would make them the first Tipperary club to win an All-Ireland title at this grade.

“We’re delighted to be there,” says Walsh.

“It’s a Dublin team, they’d be much more known for their football than we would be down here. They will be a brilliant side, there’s no doubt about that.

“All the teams we’ve played are brilliant, all very close matches. [St] Brendans really put us under pressure, especially in the last few minutes.”

The42 is on Instagram! Tap the button below on your phone to follow us!

University of Limerick 2-12
Queens University Belfast 0-13

UNIVERSITY OF LIMERICK’S hopes for a first-ever Sigerson Cup title continue after goals in either half from Kerry sharpshooter David Clifford helped them to a 2-12 to 0-13 quarter-final victory over a spirited Queens Belfast side in Abbotstown.

Clifford finished as top scorer with 2-4 (2-3 from play) and along with Donal O’Sullivan and Emmet McMahon proved to be a constant threat as the Munster outfit prevailed despite being behind at half-time.

Clifford showed the attacking firepower he possesses for his opening goal after 10 minutes as he used all his strength and skill to finish expertly to the net after getting his hands on the ball for the first time in the game. This goal put UL two points in front.

However, in the remaining 20 minutes of the half, Queens would outscore UL by 0-6 to 0-3 to go in with a one-point lead at the break. The excellent Conor Turbitt showed his accuracy from frees and play during this time with the Armagh attacker kicking seven out of his team’s eight first-half scores.

UL’s Paul Towey and Conor Turbitt of Queen’s University.

Source: Ryan Byrne/INPHO

UL needed to respond after the break and they did so very impressively, scoring 1-6 without reply between the 34th and 52nd minute. Clifford scored 1-4 of this total with his goal coming as he punched to the net after being set-up by O’Sullivan.

To their credit, Queens never gave up and they scored four points in the final five minutes. This wasn’t enough, however, to deny Declan Brouder’s side a place in the semi-finals with UL running out five-point winners.

If Clifford and co.continue to hit top form, you wouldn’t be surprised to see the Limerick college going all the way and creating history.

Scorers for UL: D Clifford 2-4 ( 1 45), D O’Sullivan 0-6 (5 f) and E McMahon 0-2.

Scorers for Queens: C Turbett 0-8 (6 f), K Hughes 0-2 (1f), P Brooks, P Finnegan, C Love (f) all 0-1.

University of Limerick

1. C Flaherty (Claregalway/Carnmore – Galway)

2. P Towey (Charlestown – Mayo), 3. C Donnelly (Bracknagh – Offaly), 4. P Maher (Adare – Limerick)

5. J Coyne (Ballyhaunis – Mayo) 6. S Powter (Douglas – Cork) 7. E McLaughlin (Westport – Mayo)

8. C Dempsey (Knockmore – Mayo), 9. D Walsh (Kilmurry-Ibrickane – Clare)

10. C Downes (Kilmhil – Clare), 11. E McMahon (Kildysart – Clare), 12. O Looney (Miltown Malbay – Clare)

13. D Clifford (Fossa – Kerry), 14. D Gray (Castledermot – Kildare), 15. D O’Sullivan (Kilgarvan – Kerry).

Substitutes:

• C Igoe (Bonniconlon – Mayo) for D Gray (Half-time)
• P Walsh (Brosna – Kerry) for D O’Sullivan (56)
• S McDonnell (Mallow – Cork) for O Looney (62).

Queens University Belfast

1. E Mulholland (Clann Eireann – Armagh)

2. S Bolger (Killeshin – Laois), 3. R Conroy (Tír na nÓg Moy – Tyrone), 4. P Fagan (St Mary’s Burren – Down)

5. G Brown (Na Piarsaigh – Limerick), 6. M Murnaghan (Killyclogher Tyrone), 7. P Brooks (Glenn – Down)

8. R Donnolly (Carrickmore – Tyrone), 9. T Bogue (Tempo Maguire’s – Fermanagh)

10. F Canavan (Bryansford – Down), 11. O Mallon (Dungannon Thomas Clarkes – Tyrone), 12. B Campbell (Ballyholland – Down)

Click Here:

13. K Hughes (Ballymacnab – Armagh), 14. C Turbett (Clann Eireann – Armagh), 15. A McAvoy (St Marys Burren – Down).

Substitutes:

• S McCarthy (Clann Eireann – Armagh) for R Conroy (6, inj.)
• C Gorman (Newry Shamrocks) for K Hughes (42)
• C Love (Enniskillen Gaels – Fermanagh) for O Mallon (44)
• P Finnegan (Naomh Bríd Belfast – Antrim) for F Canavan (52).

Referee: David Gough (Meath).

MAYO GAA HAVE confirmed that star forward Tommy Conroy suffered a cruciate ligament injury, while in action in the Sigerson Cup last night.

A statement released this evening has outlined the injury suffered by The Neale forward, who went off injured while playing for NUI Galway in last night’s quarter-final tie against Letterkenny IT.

Click Here:

The Mayo GAA medical team did a full assessment and examination today, which confirmd Conroy’s knee injury setback.

“Tommy is such a great person and player,” said Mayo boss James Horan.

“We all wish him well during his rehabilitation. Tommy will still play a huge part in Mayo’s season and will remain very much part of the panel. Unfortunately, injuries like this are part of sport.

“I know all the players will rally around Tommy and I am sure it will galvanise the entire team, but I know his injury will inspire other players to drive forward, step up and follow in his boots.”

“It is such an unfortunate injury at this time of year,” said Mayo GAA chairperson Seamus Touhy.

“Mayo GAA however, will provide whatever it takes to support Tommy and ensure he gets the best medical care during his recovery.”

Tommy Conroy celebrates during last year’s win for Mayo against Dublin.

Source: Laszlo Geczo/INPHO

Conroy burst to prominence for Mayo in the last two seasons as he helped them reach two All-Ireland finals. He was particularly impressive in their memorable All-Ireland semi-final win over Dublin last August, scoring 0-3 from play in Croke Park. 

His absence removes a major attacking option for Mayo this season, although long-serving star Cillian O’Connor is due to return from injury this spring after tearing his Achilles tendon last year.

Buy The42’s new book, Behind The Lines, here:

Click:korean novel
NUI Galway 0-23
UCC 0-14

John Fallon reports from Dangan

NUI GALWAY SECURED home advantage for the quarter-finals of the Fitzgibbon Cup after an impressive victory over UCC at Dangan in Galway.

Both sides had already qualified for the knockout stages so home advantage was the prize on offer on a wet afternoon in Galway and Jeff Lynskey’s side delivered a solid performance in a game where they never trailed.

It helps, of course, to have the Hurler of the Year on board and the deft touches of Cian Lynch, especially in the opening half, were decisive and he could be poised to follow up his successes with Mary Immaculate in this competition with the Galway university where he is studying a Masters in Education.

But once again it was the accuracy of Galway’s Evan Niland which provided the scores as the Clarinbridge man landed twelve frees and one from play, while another who will be key to Henry Shefflin’s plans, Killimordaly’s Brian Concannon, was again impressive.

UCC were just unable to break down a rock solid Galway defence where Jack Fitzpatrick was again outstanding along with 2017 All-Ireland minor winning captain Darren Morrissey, while the 2019 successful captain Ian McGlynn was prominent in midfield.

That gave NUIG, looking for their first Fitzgibbon since 2010, a big platform and UCC were chasing the game from early on as the hosts opened up a 0-10 to 0-2 lead at the end of the opening quarter when they had the wind and rain behind them.

Three William Henn frees and points from the hard-working Shane Barrett and Mark Kehoe gave UCC hope but they turned around trailing by 0-15 to 0-6.

They needed a big start to the second-half but NUIG matched them point for point in the third quarter to lead by 0-19 to 0-10 and with UCC never looking like they would chisel their way through a resolute defence for a goal, the Galway college eased into a home quarter-final.

Scorers for NUI Galway: Evan Niland 0-13 (0-12f), Brian Concannon 0-3, Conor Walsh 0-2, Mark Gill 0-1, Ian McGlynn 0-1, Cian Lynch 0-1, John Fleming 0-1, Mark Kennedy 0-1.

Scorers for UCC: Shane Barrett 0-6 (0-5f, 0-1 ’65), William Henn 0-3f, Mark Kehoe 0-3, Conor Bowe 0-1, Simon Kennefick 0-1.

NUI Galway

1. Liam O’Reilly (Castlegar, Galway)

Click Here:

2. Eoin Lawless (Athenry, Galway), 3 Jack Fitzpatrick (Killimordaly, Galway), 4. Conor Caulfield (Kilconieron, Galway)

5. Caimin Killeen (Loughrea, Galway), 6. Darren Morrissey (Sarsfields, Galway), 7 Mark Gill (Castlegar, Galway)

8. Ian McGlynn (Kilconieron, Galway), 9. Diarmuid Kilcommins (Annaghdown, Galway)

10. Conor Walsh (Turloughmore, Galway), 11, Cian Lynch (Patrickswell, Limerick), 12. Brian Concannon (Killimordaly, Galway)

15. Phillip Hickey (Nenagh Éire Óg, Tipperary) 14. John Fleming (Meelick-Eyrecourt, Galway), 13. Evan Niland (Clarinbridge, Galway)

Subs

26. Mark Kennedy (Clarinbridge, Galway) for Hickey (50)

18. Sean Burke (Kilconieron, Galway) for Kilcommins (50)

19. Adam Brett (Galway) for Gill (53)

23. Liam Forde (Galway) for Fleming (53)

17. Eoin O’Donnell (Galway) for Killeen (57)

UCC

1. Ian Butler (Kildorrery, Cork)

3. Niall O’Leary (Castlelyons, Cork), 9. Ger Millerick (Fr O’Neills, Cork), 4 Killian O’Dwyer (Killenaule, Tipperary)

17. Rob Downey (Glen Rovers, Cork), 5. Ronan Connolly (Adare, Limerick) 22 Ciaran Barry (Ahane, Limerick)

6. Tommy O’Connell (Midleton, Cork), 7. Daire Connery (Na Piarsaigh, Cork)

10. Conor Boylan (Na Piarsaigh, Limerick), 8. Conor Cahalane (St Finbarr’s, Cork), 14. Shane Barrett (Blarney, Cork)

18. Simon Kennefick (Glen Rovers, Cork), 11. William Henn (Na Piarsaigh, Limerick), 12 Mark Kehoe (Kilsheelan-Kilcash, Tipperary)

Subs

21. Padraig Power (Blarney, Cork) for Barry (27)

13. Conor Bowe (Moyne-Templetuohy, Tipperary) for Henn (half-time)

15. Jack O’Connor (Sarsfields, Cork) for O’Connell (half-time)

33. Cormac O’Brien (Newtownshandrum, Cork) for Cahalane (46)

28. Eoin Roche (Bride Rovers, Cork) for Connery (52)

Referee: Johnny Murphy (Limerick)

Today’s other Fitzgibbon Cup results

Group A

• Mary Immaculate College 6-15 UCD 6-15

Group B

• DCU 2-13 IT Carlow 3-10
• Waterford IT 5-17 Maynooth University 0-20

Buy The42’s new book, Behind The Lines, here: