rigorousintuition.ca

undead » Fri Apr 24, 2020 12:12 pm wrote:I would guess environmental factors - air pollution, electromagnetic fields of various kinds that exhaust the adrenal glands, all that asbestos from 9/11 that is still around being cleaned up by remediation companies, processed food, transgenic food, even organic food contains environmental pollutants, social stress, work stress, fear. There are so many factors that get swept under the rug as insignificant, but when they are added up they are very significant. It could also be an affliction of affluence that having more access to pharmaceutical medicine throughout life also means racking up more cumulative negative side effects.

JackRiddler » Fri Apr 24, 2020 10:44 am wrote:

liminalOyster » Fri Apr 24, 2020 12:00 am wrote:Jack is this compatible with the CA antibody data from earlier this week?

Doesn't .1 put us in swine flu territory?

I FUCKED UP the math - horribly.

17,000/1,700,000 = 1 percent

corrected post - yes it was late night but still! Sorry!

http://rigorousintuition.ca/board2/view ... 31#p686531

A nicotinic hypothesis for Covid-19 with preventive and therapeutic implications
jean-pierre CHANGEUX, Zahir Amoura1, Felix Rey2, Makoto Miyara1

Abstract
SARS-CoV-2 epidemics raises a considerable issue of public health at the planetary scale. There is a pressing urgency to find treatments based upon currently available scientific knowledge. Therefore, we tentatively propose a hypothesis which hopefully might ultimately help saving lives. Based on the current scientific literature and on new epidemiological data which reveal that current smoking status appears to be a protective factor against the infection by SARS-CoV-2 [1], we hypothesize that the nicotinic acetylcholine receptor (nAChR) plays a key role in the pathophysiology of Covid-19 infection and might represent a target for the prevention and control of Covid-19 infection.

https://www.qeios.com/read/article/581

Smokers 'four times less likely' to contract Covid-19, prompting nicotine patch trials on patients
Researchers in France will test nicotine patches on health workers and patients but reiterated smoking could also cause more severe illness
By Henry Samuel
23 April 2020 • 5:04pm

Frontline health workers and patients in France may be given nicotine patches after studies found that four times fewer smokers contracted Covid-19 than non-smokers.

It may sound counterintuitive that people who puff on Gauloises are less likely to catch a virus that can cause deadly attacks on the lungs. However, that was the statistical outcome of an in-depth study conducted by the Pasteur Institute, a leading French research centre into the disease.

The institute tested almost 700 teachers and pupils of a school in Crépy-en-Valois in one of the hardest-hit areas in France, as well as their families. The “highly accurate” tests found that only 7.2 per cent of smokers from among the adults tested were infected while four times as many non-smokers, some 28 per cent, were infected.

Arnaud Fontanet, an epidemiologist at the institute, warned that they were not encouraging people to take up smoking, remarking that those smokers who do catch the virus “risk suffering more complications” than others. Scientists suggested it could be the nicotine in cigarettes that was behind the surprising results regarding infection, although more research is needed.

A study from China prompted Public Health England and the Centers for Disease Control and Prevention in the United States to put smoking on the list of 'risk factors' for coronavirus earlier in the crisis.

Public Health England said: "Smoking tobacco is known to damage the lungs and airways causing a range of severe respiratory problems. The evidence clearly shows Covid-19 virus attacks the respiratory system, which explains why smokers are at greater risk. A small but highly impactful survey from China finds that smokers with Covid-19 are 14 times more likely to develop severe disease."

Cigarette butts in an ashtray
Smoking kills 75,000 people every year in France, which has suffered 21,000 deaths from the coronavirus CREDIT: Jenny Kane/AP
However, the Pasteur Institute results appear to tally with another study by the Pitié-Salpêtrière Hospital in Paris, which questioned 480 patients who tested positive for the virus.

According to their findings, among the 350 patients hospitalised, whose median age was 65, only 4.4 per cent were regular smokers. Among those released home, with a median age of 44, 5.3 per cent smoked.

The French health authority Santé Publique France puts the number of smokers in the general population at 32 per cent of people between 18 to 75 years old.

“Compared to the French general population, the Covid-19 population exhibited a significantly weaker current daily smoker rate by 80.3 per cent for outpatients and by 75.4 per cent for inpatients,” the researchers wrote in their study.

“Thus, current smoking status appears to be a protective factor against the infection by SARS-CoV-2.”

The researchers said that a “nicotinic acetylcholine receptor (nAChR)” plays a key role in infection from the coronavirus and that nicotine may act to protect this receptor from attack. It may also lessen the overreaction of the body’s immune system that has been found in the most severe cases of Covid-19 infection.


Clinical trials of nicotine patches on health workers and patients are awaiting the approval of the country’s health authorities.

Health minister Olivier Véran called the study "interesting", adding: "We will not be shutting any doors and certainly not that one."

Smoking causes 75,000 deaths in France and researchers were at pains to point out that nobody should take up the habit as a preventative measure.

“One should not forget that nicotine is a drug of abuse responsible for smoking addiction," they wrote.

“Smoking has severe pathological consequences and remains a serious danger for health. Yet under controlled settings, nicotinic agents could provide an efficient treatment for an acute infection such as Covid-19,” they concluded.

https://www.telegraph.co.uk/news/2020/0 ... -nicotine/

JackRiddler wrote: And what's the point to any of this? What's your big message?
.

https://www.nytimes.com/2019/05/23/health/candida-auris-hospitals-ny.html
[...]While C. auris is not the first drug-resistant germ to take hold, it is so dangerous and easily spread that it is putting new kinds of pressures on the health care system. One hallmark of C. auris is that it can be very difficult to clean from equipment or clothing, and it may spread through the air. Officials suspect that the spores can be shaken loose from bedding and they have been known to cling to walls and ceiling tiles.[...]

https://www.statnews.com/2019/07/23/the-superbug-candida-auris-is-giving-rise-to-warnings-and-big-questions/

The superbug Candida auris is giving rise to warnings — and big questions

By Helen Branswell
July 23, 2019

What’s known about the fungus Candida auris confounds the scientists who study it, the doctors who struggle to treat the persistent infections it causes, and the infection control teams that endeavor to clear it from hospital rooms after infected patients leave.

But the list of what’s not known about this highly unusual fungus is longer still — and fascinating. Experts say there’s an urgent need for answers and for funding with which to generate them.

Candida auris was first spotted a decade ago in Japan, and more recently has been popping up in far-flung parts of the globe. The fungus doesn’t behave like a fungus. It causes outbreaks like a bacterium and is generally highly resistant to available antifungal drugs. It’s a growing problem, and a deeply concerning one.

Recently STAT asked a number of scientists to describe what they see as the most pressing research questions facing the field. Here are their thoughts:

Where does the darn thing come from?

Most fungi — and there are multitudes — are found in a variety of places. In soil, in insects, in plants. But the only place C. auris has been found to date is in people.

It has to be somewhere else in nature, said Tom Chiller, chief of mycotic ( i.e. fungal) diseases at the Centers for Disease Control and Prevention.

“They didn’t just ‘poof!’ appear,” Chiller insisted. “They’ve been here for a while. And I wonder where they were hiding.”

Tejas Bouklas, an assistant professor in the department of biomedical sciences at Long Island University, Post, campus, would like to know what other species C. auris can infect.

Knowing where the fungus lives in nature and how people are picking it up might help to answer another very pressing question.

Why and how did different clones of the fungus pop up across the world in a very short time span?

A few years after its 2009 discovery, a number of countries around the globe started reporting C. auris cases. Initially the thinking was that travelers or medical tourists were responsible for the movement. But when the genetic sequences were compared, it was clear that was not the case.

Samples of C. auris circulating in South Africa all looked a lot alike. So did the samples from Asia and from South America. But none of them looked like each other. And they don’t always act like each other.

Chiller noted that the C. auris cases reported in Japan seemed to be mainly ear infections — the original finding of the fungus was from an ear infection, hence the “auris” of the name. In Japan, the fungus doesn’t seem to cause invasive disease; it doesn’t get into the bloodstream. But in South Korea, the same clone (think strain) of C. auris does.

“Wouldn’t it be fascinating to know what changes in that organism that make it go from external ear infection to an invader?” Chiller mused. “Is there something that changes in the genome? … I wish people would just jump on that and study it.”

Knowing the how and the why are crucial, said Dr. Luis Ostrosky, professor of infectious diseases at McGovern Medical School at the University of Texas Health Science Center at Houston.

That’s “the only way we’re going to control it. Because if we don’t know the source, we’re kind of fighting the fire a little bit at a time,” said Ostrosky, who is director of his hospital’s laboratory of mycology research. “If you don’t know the source of an infection, you’re never going to control it completely. And it’s going to keep happening.”

Why now?

The nearly simultaneous emergence on different continents of a highly drug resistant fungus that acts like a bacteria seems … well, kind of unsettling. What happened to allow this species of Candida to act in ways Candida fungi don’t normally act?

A related concern: If this fungal species learned this trick, can others? Is that what the future holds?

A just-published study in the journal mBio theorizes that climate change may have contributed in part to the emergence of C. auris. The authors say that historically the human body temperature has acted as protection against invasive fungal infections — in effect, we’re too hot for them to be able to grow well in us. But as the globe has warmed, they’ve adapted.

If the theory is correct, other fungi may follow C. auris’ path, posit Arturo Casadevall, of the Johns Hopkins Bloomberg School of Public Health, and his co-authors.

“Whether C. auris is the first example of new pathogenic fungi emerging from climate change … its emanation stokes worries that humanity may face new diseases from fungal adaptation to hotter climates,” they write.

Chiller said uncovering C. auris’ backstory is important. “These things are going to continue to emerge. And understanding how they emerge and where they emerge might lead us to prevention strategies or reactive strategies or preparation strategies for the next big thing.”

Could C. auris help other fungi adapt to be bigger threats to humans?

That’s a question Bouklas is wondering about. “The more ubiquitous it becomes, the more problematic. Because now it could potentially transmit DNA to other Candida species. And maybe even bacteria,” she said.

That idea is not far-fetched. Fungi can mate sexually, Chiller pointed out, allowing them to swap large amounts of DNA.

Where did it get its “Ironman suit”?

That’s the way Johanna Rhodes describes the drug-resistant superpowers of C. auris. Rhodes is an epidemiologist at Imperial College London who has worked on C. auris since a 2016 outbreak at London’s Royal Brompton Hospital.

Some of the patients in that outbreak developed resistance to an entire class of antifungal drugs within a month — “which is just unheard of,” she said.

Bouklas also has resistance questions. “Why does it have such a strong resistance to every known anti-fungal?” she asked. “All of them use a different mechanism of killing…. That’s the biggest question.”

Often pathogens that develop drug resistance pay for it in other ways — it’s called a “fitness cost.” Yes, Bacterium X can evade Drug Y, but in acquiring that skill it becomes less transmissible or weaker in some way.

Not C. auris.

“It seems that it’s got resistance at no fitness cost. It’s still able to form biofilms. It’s still able to persist [in an environment]. It’s still able to infect,” Rhodes said.

Biofilms are a layer of pathogens — in this case, fungi — that attach to a surface and effectively lay in wait there. Sometimes biofilms form in the drains or pipes leading from sinks in hospitals. Many like wet surfaces, but C. auris can form dry biofilms, lurking on surfaces like bed railings in a contaminated hospital room. These infectious residues can transmit C. auris from one patient to the next in a hospital room.

This fungus is really hard to get rid of. That’s something Dr. Anthony Fauci, director of the National Institute for Allergy and Infectious Diseases, thinks needs to be explored.

“Why is it so different from others that you could easily, by wiping it with whatever it is you wipe it with, it goes away? Whereas this just seems to stick there,” Fauci asked.

Ostrosky also wants to know why the fungus spreads so well in hospitals, which are not normally terribly hospitable to fungi.

What’s the best way to treat patients who develop C. auris infections?

That’s a question Ostrosky, who has treated patients with C. auris infections, would very much like answered.

Chiller has a related question: How often is C. auris causing death?

Between 30% and 60% of patients who develop C. auris infections die, the CDC estimates. But in the United States, anyway, C. auris infections occur in the sickest of patients: people whose immune systems have been compromised, who have spent prolonged periods on ventilators — machines that breathe for people whose lungs aren’t up to the task.

Are these people dying from their C. auris infections? Or are their other medical problems the cause of death? “Are they dying of C. auris or with C. auris? I still want to know that,” said Chiller, though he acknowledged that “those are really hard studies to do.”

JackRiddler » Fri Apr 24, 2020 10:45 am wrote:Wrote the below -- bad idea, big waste of time on people who aren't interested in knowing -- but then got the identity cross-post. Basically you can all screw off with your 9/11 disease fantasies. This has been very well tracked over the years and you are showing complete ignorance or indifference to the actual, horrific impact on the thousands caught up in the cloud and those who worked on the pile in 2001-2. You are exploiting those victims to suggest that somehow it now magically expresses itself in 20,000 additional deaths, within a short period 20 years later, which merely happen to mimic exactly the action of a contagion. You don't bother to know anything about it, it's pathetic. All so you can suggest the current contagion somehow isn't actually happening. And, in effect, you are covering for a government that actually IS lying about many aspects of the unfolding shitshow by implying it's lying about something else, a secret to which you are the only ones privy via your personal selection of youtube videos that speak to your longstanding obsessions. Who are you people?

undead » Fri Apr 24, 2020 7:02 pm wrote:So when this conveniently visible problem came along, of course all the people responsible for the horrendously dangerous and unhealthy conditions in medical facilities are eager to blame everything on this one pathogen, even though it is obvious to many people that there is much more contributing to all of these deaths.

identity » Fri Apr 24, 2020 7:21 pm wrote:Where do I argue that the blame for any excess deaths in NYC now rests squarely on the shoulders of 9/11's toxic clouds?

It was, frankly, the first thing that occurred to me that distinguishes NYC from other large urban areas in your country.

Is the crowding there really that much worse than other big cities? I am no authority on this subject; perhaps you can enlighten me.

I thought this place was open to points of view which diverted from official (both government and scientific)/mainstream/received ones. Perhaps I was mistaken?

JackRiddler wrote: Your statements show no interest in what contributes to these deaths. Much information on this has actually been shared. The comorbidities are well known and often discussed. These are most commonly: age over 80, obesity, heart disease, diabetes, and kidney disease. Each of the last four are to substantial degrees social illnesses, but not due to factors that interest you or that you dwell upon.

Healthcare facilities in several countries have reported that a type of yeast called Candida auris has been causing severe illness in hospitalized patients. In some patients, this yeast can enter the bloodstream and spread throughout the body, causing serious invasive infections. This yeast often does not respond to commonly used antifungal drugs, making infections difficult to treat. Patients who have been hospitalized in a healthcare facility a long time, have a central venous catheter, or other lines or tubes entering their body, or have previously received antibiotics or antifungal medications, appear to be at highest risk of infection with this yeast.

Specialized laboratory methods are needed to accurately identify C. auris. Conventional laboratory techniques could lead to misidentification and inappropriate management, making it difficult to control the spread of C. auris in healthcare settings.

Because of these factors, CDC is alerting U.S. healthcare facilities to be on the lookout for C. auris in their patients.

[...]

Who is at risk for infection from C. auris?

People who have recently spent time in nursing homes and have lines and tubes that go into their body (such as breathing tubes, feeding tubes and central venous catheters), seem to be at highest risk for C. auris infection. Limited data suggest that the risk factors for Candida auris infections are generally similar to risk factors for other types of Candida infections. These risk factors include recent surgery, diabetes, broad-spectrum antibiotic and antifungal use. Infections have been found in patients of all ages, from preterm infants to the elderly. Further study is needed to learn more about risk factors for C. auris infection.

8bitagent wrote: Been following the main Covid Reddit update page. People downplay it as "viruses mutate and become weaker", but from all the data I'm seeing with the Covid mutations, it seems really bizarre. Like a real life Freddy Krueger that presents wildly bizarre and different symptoms to different people, geographics, areas, etc. A biological trickster. Ultimately maybe it wont matter the "true "origins"...a Wuhan lab or wet market, meat tainted by bat contamination(the 2011 Contagion movie theory) or mother nature lashing out. This virus is acting like the Joker in 1989's Batman spreading toxins or 2008 Dark Knight causing random havoc to the entire system.