Business resilience is essential for sustainable economic prosperity and growth. A company's ability to bounce back from adversity impacts the wider economic picture, shaping growth and employment trajectories. This study delves into the experiences and lessons learned by business leaders in 2020 and early 2021, aiming to capture the essence of business strategies during the global disruption caused by the COVID-19 pandemic. Rather than broad generalisations, the focus is on understanding real-world experiences and practical adaptations.
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Corona virus Radoslav Zilinsky/Getty Images hide caption
Corona virus
Scientists have uncovered a possible explanation for one of COVID-19's most vexing legacies: the stubborn neurological symptoms of long COVID, such as brain fog, memory loss and fatigue.
The first clue emerged when researchers scoured the blood of long COVID patients: It was serotonin specifically, a lack of the neurotransmitter circulating in the body that grabbed their attention.
Their analysis revealed that having low levels of that chemical predicted whether or not someone was suffering from persistent symptoms following an infection.
Next, the team of researchers at the University of Pennsylvania carefully recreated the chain of events that might be depleting serotonin and causing downstream consequences that could line up with some of the symptoms characteristic of long COVID.
Their findings, published in the journal Cell, point to an intriguing hypothesis that winds its way from the gut up through the vagus nerve and ultimately into the brain.
"Basically, we can explain some of the neurocognitive manifestations of long COVID through this pathway that leads to serotonin reduction," says Christoph Thaiss, a senior author on the study and an assistant professor of microbiology at the University of Pennsylvania.
The work has made an impression on those studying long COVID, a condition that still has no validated treatment or widely accepted biomarker that doctors can use to diagnose the condition.
The study weaves together several prominent lines of evidence on the potential drivers of the condition the ongoing presence of viral material, blood clotting and chronic inflammation and offers up possible targets for clinical trials that can test treatments in humans.
"I'm impressed by the study," says Dr. Michelle Monje, a professor of neurology at Stanford University. "I think they did a beautiful job showing the causality of these changes."
Given that much of the work was done on mice, the implications for long COVID patients still need to be fully explored in future studies, but the results tell a "very nice linear story," says Akiko Iwasaki, an immunologist at Yale University.
"Everyone who's engaged in this research should now be thinking about this serotonin pathway," says Iwasaki.
So what exactly did they find?
With serotonin on their minds, the researchers tried to start from the very beginning of the disease process, primarily using experiments on mice to trace its course.
Their hunch was that "viral persistence" a major suspect in long COVID could underlie the depletion of serotonin. Multiple studies show that well after the initial illness passes, some long COVID patients may have a lingering infection in certain parts of the body, sometimes called a "viral reservoir," which could be driving some of their symptoms.
Maayan Levy, a senior author, says they looked for evidence of viral persistence by checking the stool of their long COVID subjects for genetic material from the virus.
"In about 30% of patients, we could find viral RNA in their gastrointestinal tract, so we took this and tried to model it in mice," says Levy, an assistant professor of microbiology at the University of Pennsylvania.
Those experiments revealed that a chronic viral infection (they used lymphocytic choriomeningitis virus as a stand-in for SARS-CoV-2) also led to reductions in serotonin and that the body's own immune response seemed to be the culprit.
This led to further experiments focused on a cytokine, called type 1 interferon, revealing that this signaling protein was driving inflammation and interfering with serotonin levels in the bloodstream in several ways.
The gut produces 90% of serotonin in the body. The amino acid tryptophan is critical to this task it's a precursor to serotonin and gets absorbed in the gastrointestinal tract from the food we eat. Except, this inflammatory response in the gut actually impaired the absorption of tryptophan.
"If there's less tryptophan, there's less serotonin production," says Thaiss. On top of that, these cytokines also lead to clotting of blood platelets which store serotonin further reducing the amount of serotonin in circulation.
Here, the detective work moved away from the gut to the vagus nerve, which essentially acts like the brain's monitoring system of the body and connects to the gastrointestinal tract and many other organs.
Levy says they found this reduction in serotonin impairs communication between the vagus nerve and the brain, which then reduces some activity in a region of the brain known as the hippocampus.
What's promising, though, is that the cognitive symptoms the Penn researchers documented in mice could be reversed.
"We can make the animals remember perfectly again by just reactivating their vagus nerve or by restoring their serotonin signaling," says Thaiss, referring to a cognitive behavioral test they performed on their mouse models of long COVID.
"Whether the exact same thing is true in individuals with long COVID is something we don't know."
Because much of this work was done on mice, there are limitations to what conclusions can be drawn about humans. Levy points out that their data can't prove a viral reservoir is causing these events in humans and that a lack of good mouse models of long COVID still hampers research.
"To make any recommendations for patients, we need to perform a large clinical trial that is well-controlled," she says, "The obvious next step would be for us to to try an intervention that will increase serotonin levels or stimulate the vagus nerve in other ways or [to] supplement tryptophan."
In their experiment, they gave the mice a generic form of Prozac a class of medication known as an SSRI that's typically prescribed for depression and increases circulating serotonin in the brain.
The research offers new insights into how immune problems outside of the nervous system can have far-reaching consequences on the brain and other functions in the aftermath of COVID-19, says Stanford's Monje.
"It's not the whole puzzle and it's not meant to be the whole puzzle but it's a really important aspect of it," she says.
Indeed, scientists don't expect to find a single mechanism that, once unearthed, will resolve all these problems.
"There are many ways that COVID can influence the nervous system that are not mutually exclusive," says Monje. "Any individual might be suffering from some combination of those."
For example, her lab has found that, in mice, a mild COVID-19 infection in the lungs sets off an inflammatory cascade that impairs neuron production in the hippocampus.
The long COVID "brain fog" syndrome encompasses a constellation of symptoms, everything from problems with memory and attention to speed of information processing to executive function and fatigue.
Monje says research on the effects of COVID-19 have revealed neurobiological changes elsewhere in the brain, too. "It's broader than just the hippocampus, but certainly the hippocampus has been implicated."
As with all long COVID research, the challenge is figuring out how these findings fit into our ever-changing understanding of the disease.
"Long COVID is a heterogeneous disorder. There are many different manifestations," says Dr. Saurabh Mehandru, a professor of medicine at Mount Sinai in New York. "It's novel, exciting data. I would consider this as important but initial findings which have to be further studied."
Mehandru says "it makes sense the tryptophan-serotonin pathway is being affected" given that SARS-CoV-2 utilizes the ACE-2 receptor, which is widely expressed on the surface of the small intestines.
"It's expressed there because it plays a role in absorption of amino acids" like tryptophan, he says.
But he says there are still many open questions about this business of viral persistence in the gut of long COVID patients.
Because these cells renew every three to five days, "for anything to be persistently active in this layer, it would by definition imply there's some level of replication," he says. It's not clear, however, exactly what's replicating.
Multiple studies have found evidence of genetic material and viral proteins in different tissues. Yet, no one has actually cultured the virus from intestinal tissue, which is admittedly difficult to do, he says. "These are active and important scientific areas of interest."
While it's possible a chronic viral infection in the gut could be driving these symptoms in some patients, as the Penn study suggests, Yale's Iwasaki says the neurocognitive dysfunction in long COVID can be "downstream of many different things, including circulating inflammatory factors and autoantibodies."
"Even though the dots are very well connected with animal models and patient samples, whether this is happening in patients and what proportion might be suffering from this particular pathology, that still requires future studies," says Iwasaki, whose research has found that low levels of the stress hormone cortisol are also associated with long COVID symptoms.
Ultimately, this research may not explain all the neurological symptoms that surround long COVID and that's okay, says Monje.
"It's not that we have to put all the pieces of the puzzle together to begin to make meaningful therapeutic changes," she says. "I think it's worth further pursuing."
Children who tested positive for COVID-19 in 2022 were contagious for a median of 3 days, regardless of vaccination status, suggesting that 5-day school isolation policies are sufficient amid Omicron variant predominance, University of Southern California (USC) and Stanford University researchers report today in JAMA Pediatrics.
The study included 76 children aged 7 to 18 years infected with SARS-CoV-2 in Los Angeles County from April to September 2022. The researchers obtained throat swabs for culture and recorded demographic information and COVID-19 vaccination status during five visits to the children's homes over 10 days. The samples were examined in a lab for evidence of cell death, a sign of viral infectivity.
The researchers noted that a previous study found that nose-throat swabs from children diagnosed as having COVID-19 were half as likely to contain culturable virus than those from adults but that none had assessed viral shedding of the Omicron variant among children over time.
"COVID-19 quarantine and self-isolation policies continue to interrupt education," the study authors wrote. "These policies, while typically more stringent than for routine viral illnesses, are guided by few data."
Of the 76 participants, 52 (68.4%) were vaccinated, 41 (55.4%) were aged 7 to 12 years, and 38 (50.0%) were boys. The median duration of infectivity was 3 days, regardless of COVID-19 primary or booster vaccination status. Fourteen children (18.4%) were still infectious on day 5 and 3 (3.9%) remained so on day 10. A sensitivity analysis that used the date of symptom onset as the origin of observation produced similar results.
The authors said that school policies requiring students with COVID-19 stay at home for 5 days are probably appropriate and that return-to-school policies may not need to consider vaccination or booster status.
We want to protect the other children in the school who could potentially get infected, but at the same time, we don't want to disrupt education for the child who is infected, given the amount of disruption that's already happened.
"We're basically saying five days is more than sufficient; public-health and education leaders may consider shorter durations," coauthor Neeraj Sood, PhD, director of the COVID-19 Initiative and a senior fellow at the USC Schaeffer Center, said in a USC news release.
"We want to protect the other children in the school who could potentially get infected, but at the same time, we don't want to disrupt education for the child who is infected, given the amount of disruption that's already happened," he added.
Sood said future research is needed to enable policymakers to adjust school COVID-19 isolation policies as needed. "The virus will keep mutating," he said. "We need to continue doing studies like this because the next variant may have a longer or shorter duration of infectivity."
Fungi
Certain gut-dwelling fungi flourish in severe cases of COVID-19, amplifying the excessive inflammation that drives this disease while also causing long-lasting changes in the immune system, according to a new study.
Utilising patient samples and preclinical models, researchers at Weill Cornell Medicine and NewYork-Presbyterian in the US determined that the growth of fungi in the intestinal tract, particularly strains of Candida albicans yeast, trigger an upsurge in immune cells whose actions can exacerbate lung damage.
Their findings, published in the journal Nature Immunology, also elucidate that patients retain a heightened immune response and immune memory against these fungi for up to a year after the resolution of SARS-CoV-2 infection.
The research reveals a new dimension of the complex pathology unleashed by severe COVID-19, said Dr Iliyan Iliev, immunologist and Associate Professor in the Department of Medicine at Weill.
"Severe and long COVID were not thought to involve fungal blooms in the intestines that, in addition to the virus, can impact a patient's immunity," he said.
The team first made the connection when analysis of blood samples from patients diagnosed with severe COVID-19 unveiled the presence of antibodies tuned to attack fungi common to the gut. The researchers then found that populations of yeast, and one species in particular, Candida albicans, increased in the intestines of the patients during the course of severe COVID-19.
When they looked at the patients' immune systems, the researchers found a parallel increase in immune cells called neutrophils. In severe COVID-19, excessive numbers of neutrophils appear in the lungs, where their activity worsens the inflammatory response already damaging these organs.
Turning to preclinical models, the investigators found that mice bearing fungi from patients with severe COVID-19 produced more neutrophils in their blood and lungs, and had signs of heightened inflammation when infected with SARS-CoV-2.
However, giving them an antifungal drug reduced these effects.
From within patients' blood samples, researchers also uncovered evidence of persistent changes to the immune system they believe are related to a condition known as long COVID, in which symptoms linger, or new ones develop after an infection has cleared.
When the team examined patients' blood up to a year afterwards, they found it still contained anti-fungal antibodies. In addition, when they looked at the stem cells that give rise to neutrophils, the researchers found that these progenitors are primed to respond to fungi.
They found that an immune protein called IL-6 that these fungi induce, appears to bolster both the neutrophils and the antibodies.
Further experiments showed that blocking IL-6 in the patients or in mice dampened this immunological memory, causing the presence of neutrophils and antibodies to wane.
While these results do not have immediate implications for treating severe or long COVID, they suggest new opportunities to tailor therapy, according to Dr. Iliev.
**
The above article has been published from a wire agency with minimal modifications to the headline and text.
Children infected with the Omicron variant remain infectious for three days on average after testing positive for the SARS-CoV-2 virus, according to a study.
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Researchers at the University of Southern California (USC) and Stanford University in the U.S. noted that school policies that require students with COVID-19 to stay out of the classroom for five days are more than sufficient.
"We are basically saying five days is more than sufficient; public health and education leaders may consider shorter durations, said study co-author Neeraj Sood, Director of the COVID-19 Initiative and a senior fellow at the USC Schaeffer Center.
The study, published in the journal JAMA Pediatrics, found that the median time of infectivity was three days, with 18.4% and 3.9% of children still infectious on day five and day 10, respectively.
The researchers also found no association between how long children were infectious and whether they were vaccinated, suggesting return-to-school policies may not need discriminate by vaccine or booster status.
The study seeks to inform policymakers who grapple with how long children must isolate when they contract COVID-19. Such self-isolation policies, aimed at halting the spread of the virus, can negatively interrupt children's education.
"We want to protect other children in the school who could potentially get infected, but at the same time, we don't want to disrupt education for the child who is infected, given the amount of disruption that's already happened, said Mr. Sood.
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"The duration of infectivity is an important parametre into figuring out what the optimal duration of self-isolation should be," he added.
The researchers partnered with a virus testing company and examined nasal swabs from 76 children in Los Angeles County who were between the ages of seven and 18 and tested positive for COVID-19.
Survey participants provided samples during five home visits over a 10-day period and samples were examined in a lab to find evidence of cell death, a sign of infectivity. All participants were infected with the Omicron variant of COVID-19.
"We wanted to capture how infectivity changed over the 10-day window," said study lead author Nikhilesh Kumar, a Doctor of Medicine student at the USC Keck School of Medicine.
The findings are consistent with previous research on adults who contracted the Omicron variant, which showed no association between vaccination status and time of infectivity.
That research, published in the New England Journal of Medicine, showed adults with Omicron were infected for a slightly longer duration, with a median time of five days, the authors noted.
The team called for further research so that policymakers can consider adjusting the time students must stay out of the classroom.
The first-of-its-kind study was conducted in Israel byKSM - Maccabi's Research and Innovation Center. The results were published in the peer-reviewed journal Viruses.
TEL AVIV, Israel, Oct. 24, 2023 /PRNewswire/ -- A retrospective study undertaken by Maccabi KSM Research in Israel has revealed that the Pfizer COVID-19 vaccine offers the same level of protection against the virus for patients with Celiac Disease as it does for those without this chronic condition.
Throughout the pandemic, there were concerns surrounding whether individuals with Celiac Disease would generate an adequate immune response to COVID-19 vaccines. These concerns stemmed from earlier research, which indicated reduced vaccine responsiveness among children with Celiac Disease to the hepatitis B vaccine. Furthermore, the absence of data from COVID-19 vaccine clinical trials involving individuals with chronic conditions, including Celiac Disease, exacerbated these uncertainties.
Now, researchers in Israel and New York have concluded a real-world, population-based study to assess the effectiveness of the BNT162b2 mRNA COVID-19 vaccine (Pfizer vaccine) against SARS-CoV-2 (COVID-19). This study was carried out in 2021 during the pandemic peak when COVID-19 tests were readily accessible and often mandated by government authorities. The study's findings were recentlypublished in the journal Viruses.
The retrospective study, pulled on anonymous data from Maccabi Healthcare Services, included 5,381 Maccabi members over the age of 12 with Celiac Disease and 14,939 controls. All Celiac Disease patients had received two COVID-19 vaccine doses.
The results showed no difference in the vaccine effectiveness between the groups.There was also no significant difference between patients with controlled and uncontrolled Celiac Disease and in patients recently diagnosed with Celiac Disease.
The study was led by Dr. Tal Patalon and Dr. Amir Ben Tov from KSM Research and Innovation Center, Israel, in cooperation with Dr. Benjamin Lebwohl from the Celiac Disease Center at Columbia University Irving Medical Center, New York.
Dr.Patalon, head of KSM Research and Innovation Center, said, "This research proves the importance of real-world evidence in healthcare, where big-data studies can retrospectively focus on small and particular groups of individuals, often missed in clinical trials."
Media Contact Dvir Assouline, dvir@propr.us
View original content:https://www.prnewswire.com/news-releases/covid-19-vaccine-protects-against-the-corona-virus-in-patients-with-celiac-disease-301966302.html
SOURCE KSM Research and Innovation Center
A cruise operator that failed to cancel a voyage from Sydney that led to a COVID-19 outbreak has been ruled negligent in an Australian class-action case
By
ROD McGUIRK Associated Press
October 25, 2023, 2:51 AM ET
3 min read
CANBERRA, Australia -- A cruise operator that failed to cancel a voyage from Sydney that led to a major COVID-19 outbreak was ruled negligent in its duty of care to passengers in an Australian class-action case Wednesday.
The Ruby Princess ocean liner left Sydney on March 8, 2020, with 2,671 passengers aboard for a 13-day cruise to New Zealand but returned in 11 days as Australias borders were closing. COVID-19 spread to 663 passengers and claimed 28 lives.
Passenger Susan Karpik was the lead plaintiff in the case against British-American cruise operator Carnival and its subsidiary Princess Cruises, the ship's owner.
Federal Court Justice Angus Stewart ruled that Carnival had been negligent as defined by Australian consumer law by allowing the cruise to depart in the early months of the pandemic. He said Carnival had a duty to take reasonable care of her health and safety in regard to COVID-19.
I have found that before the embarkation of passengers on the Ruby Princess for the cruise in question, the respondents knew or ought to have known about the heightened risk of coronavirus infection on the vessel and its potentially lethal consequences and that their procedures for screening passengers and crew members for the virus were unlikely to screen out all infectious individuals, Stewart said.
Carnival had already experienced outbreaks on its cruises in the previous month aboard the Grand Princess off California and the Diamond Princess off Japan, the judge said.
Carnival had failed to explain why it offered free cancellation for all cruises worldwide leaving from March 9 the day after the Ruby Princess departed and suspended all cruises on March 13, he said.
To the respondents knowledge, to proceed with the cruise carried significant risk of a coronavirus outbreak with possible disastrous consequences, yet they proceeded regardless, Stewart said.
Susan Karpik had sued Carnival for more than 360,000 Australian dollars ($230,000).
However, she was only awarded her out-of-pocket medical expenses of AU$4,423.48 ($2,823.28) for reasons including that the judge did not accept she suffered from long COVID and that Carnival had refunded all the passengers fares.
But she said she was happy with the outcome.
I was very pleased with that finding. And I hope the other passengers are pleased with that finding too, she told reporters outside court.
I hope the finding brings some comfort to them because theyve all been through the mill and back, she added.
Her lawyer Vicky Antzoulatos said other passengers who suffered worse consequences from their sickness could expect larger payouts.
While Susan Karpik's symptoms were relatively mild, her husband Henry Karpik spent two months in hospital and almost died from his infection.
Susans husband was very catastrophically injured, so we expect that he will have a substantial claim, and that will be the same for a number of the passengers on the ship, Antzoulatos said.
Each passenger will have to prove their claims unless Carnival agrees to settle, she said.
Its been a long time coming and a very comprehensive victory for the passengers on the Ruby Princess, Antzoulatos said.
Carnival Australia said in a statement it was considering the judgment in detail.
The pandemic was a difficult time in Australias history, and we understand how heartbreaking it was for those affected, Carnival said.
CANBERRA, Australia (AP) A cruise operator that failed to cancel a voyage from Sydney that led to a major COVID-19 outbreak was ruled negligent in its duty of care to passengers in an Australian class-action case Wednesday.
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The Ruby Princess ocean liner left Sydney on March 8, 2020, with 2,671 passengers aboard for a 13-day cruise to New Zealand but returned in 11 days as Australias borders were closing. COVID-19 spread to 663 passengers and claimed 28 lives.
Passenger Susan Karpik was the lead plaintiff in the case against British-American cruise operator Carnival and its subsidiary Princess Cruises, the ship's owner.
Federal Court Justice Angus Stewart ruled that Carnival had been negligent as defined by Australian consumer law by allowing the cruise to depart in the early months of the pandemic. He said Carnival had a duty to take reasonable care of her health and safety in regard to COVID-19.
I have found that before the embarkation of passengers on the Ruby Princess for the cruise in question, the respondents knew or ought to have known about the heightened risk of coronavirus infection on the vessel and its potentially lethal consequences and that their procedures for screening passengers and crew members for the virus were unlikely to screen out all infectious individuals, Stewart said.
Carnival had already experienced outbreaks on its cruises in the previous month aboard the Grand Princess off California and the Diamond Princess off Japan, the judge said.
Carnival had failed to explain why it offered free cancellation for all cruises worldwide leaving from March 9 the day after the Ruby Princess departed and suspended all cruises on March 13, he said.
To the respondents knowledge, to proceed with the cruise carried significant risk of a coronavirus outbreak with possible disastrous consequences, yet they proceeded regardless, Stewart said.
Susan Karpik had sued Carnival for more than 360,000 Australian dollars ($230,000).
However, she was only awarded her out-of-pocket medical expenses of AU$4,423.48 ($2,823.28) for reasons including that the judge did not accept she suffered from long COVID and that Carnival had refunded all the passengers fares.
But she said she was happy with the outcome.
I was very pleased with that finding. And I hope the other passengers are pleased with that finding too, she told reporters outside court.
I hope the finding brings some comfort to them because theyve all been through the mill and back, she added.
Her lawyer Vicky Antzoulatos said other passengers who suffered worse consequences from their sickness could expect larger payouts.
While Susan Karpik's symptoms were relatively mild, her husband Henry Karpik spent two months in hospital and almost died from his infection.
Susans husband was very catastrophically injured, so we expect that he will have a substantial claim, and that will be the same for a number of the passengers on the ship, Antzoulatos said.
Each passenger will have to prove their claims unless Carnival agrees to settle, she said.
Its been a long time coming and a very comprehensive victory for the passengers on the Ruby Princess, Antzoulatos said.
Carnival Australia said in a statement it was considering the judgment in detail.
The pandemic was a difficult time in Australias history, and we understand how heartbreaking it was for those affected, Carnival said.
