The Playground

  • Figures released by the Department of Health (DoH) showed that on Thursday this week, of those in Intensive Care Units (ICUs ) with Covid, 72% were unvaccinated, 8% had one dose and 20% had been double jabbed.

    Of course "we" know that the unvaccinated ones were only admitted to the ICU due to worms (ivermectin not allowed to be administered of course), not severe COVID. lol.

  • Glad to not live in Switzerland where all IPS patients seem to die anyway...

    In UK 50% of the relevant age group 50+ in ICU dies. The problem is the age group 80+ that makes up about 95% of all deaths in CH...


    So ICU deaths should only be discussed in view of no treatment. ICU = concentration camp = care to death or (rest-) live long handicapped.

  • Of course "we" know that the unvaccinated ones were only admitted to the ICU due to worms (ivermectin not allowed to be administered of course), not severe COVID. lol.


    No you fool! They secretly give Ivermectin to the ones that survive. Just give them the secret handshake and you’ll be fine.

  • In UK 50% of the relevant age group 50+ in ICU dies. The problem is the age group 80+ that makes up about 95% of all deaths in CH...


    So ICU deaths should only be discussed in view of no treatment. ICU = concentration camp = care to death or (rest-) live long handicapped.

    Great answer... you claimed earlier all swiss patients with Covid under ICU care will die anyway, seems only 25%? What is right and what is wrong?

  • Pathologists find evidence of pre-existing chronic lung disease in people with long COVID

    Some symptoms may be caused by damage developed before patients contracted the coronavirus.


    Pathologists find evidence of pre-existing chronic lung disease in people with long COVID
    Some symptoms may be caused by damage developed before patients contracted the coronavirus.
    labblog.uofmhealth.org


    For nearly two years, the collective attention of researchers worldwide has focused on understanding what infection with SARS-CoV-2, the coronavirus that causes COVID-19, does to the human body.


    As a result, scientists have amassed evidence of a wide range of effects on the heart, lungs, brain and various other organs. Much of that insight has been gathered from autopsies of people who died from COVID-19. Yet, for the millions of people who survived the infection only to experience lingering symptoms, referred to colloquially as long COVID, much remains unknown.


    Researchers at University of Michigan Health, part of Michigan Medicine, are examining lung biopsies from patients living with persistent respiratory symptoms, such as shortness of breath, to help better define the pattern of damage associated with COVID-19. Their work has led to a surprising finding: some patients’ symptoms could be due to damage that existed before getting COVID-19.


    “Some of the early publications and popular press around long COVID has implied or assumed that once you had COVID, everything that happens next is COVID-related,” said senior author Jeffrey Myers, M.D., professor of anatomic pathology. “Of course, that might or might not be true.


    Myers, along with Kristine E. Konopka, M.D., associate professor of thoracic pathology, and their Department of Pathology team, examined lung biopsies from 18 living patients who had ongoing respiratory symptoms or abnormal CT scans after recovering from COVID-19. Five patients were reported to have lung disease prior to their COVID-19 diagnosis. Fourteen patients had what is known as ground glass opacities on radiological scans, areas of the lungs that appear as a cloudy gray color as opposed to the dark color of normal air-filled lungs, on a chest X-ray or CT scan.



    The most common finding in this set of patients was a condition known to pathologists as usual interstitial pneumonia, or UIP, also known clinically as idiopathic pulmonary fibrosis, or IPF, a well-studied chronic lung disease. IPF is the most common type of pulmonary fibrosis and causes scarring and stiffening of the lungs.


    “We were seeing a lot of UIP, which isn’t the pattern we tend to associate with acute lung injury,” said Konopka, lead author on the study. “So, we think these are patients who had lung disease prior to COVID and maybe they just weren’t being followed by primary care physicians. They then had COVID, are still sick, and their UIP is finally being picked up.”


    The notion that a person could have chronic lung damage and not know it was unheard of until relatively recently, noted Myers.


    “The assumption was if you had UIP/IPF, you were sick and you would know you had it. We’ve learned for a variety of reasons, including the rate at which we use radiology of the chest, there are people walking around with UIP/IPF that aren’t sick. If you test with typical tests for lung function, they come back normal.”


    However, UIP/IPF is a progressive disease that gets worse with time and an infection, such as with SARS-CoV-2, can lead to accelerated illness or even death, what is known as an acute exacerbation of IPF, explained Myers. “SARS-CoV-2 comes along and does to the lung, from a pathology perspective, exactly what happens with an acute exacerbation.”

    .


    Biopsies from these patients show evidence of the underlying pre-existing lung scarring with, layered on top, evidence of diffuse alveolar damage, a pattern of lung tissue damage commonly seen in patients with acute respiratory distress syndrome of any cause.


    Myers and Konopka note that without full clinical histories, including tests from before the patients’ COVID diagnosis, it is impossible to say for certain that SARS-CoV-2 did not cause UIP. However, they hope their findings will encourage clinicians think twice about automatically attributing respiratory symptoms to long COVID.


    “You shouldn’t make assumptions but ask the right questions, the first of which would be ‘I wonder if this is really COVID?’,” said Myers. “What you do after that depends on the answer to that question.”


    Paper cited: “Usual Interstitial Pneumonia is the Most Common Finding in Surgical Lung Biopsies from Patients with Persistent Interstitial Lung Disease Following Infection with SARS-CoV-2,” EClinicalMedicine. DOI: 10.1016/j.eclinm.2021.101209


    DEFINE_ME

  • Disulfiram use is associated with lower risk of COVID-19: A retrospective cohort study


    Disulfiram use is associated with lower risk of COVID-19: A retrospective cohort study
    Effective, low-cost therapeutics are needed to prevent and treat COVID-19. Severe COVID-19 disease is linked to excessive inflammation. Disulfiram is an…
    journals.plos.org


    Abstract

    Effective, low-cost therapeutics are needed to prevent and treat COVID-19. Severe COVID-19 disease is linked to excessive inflammation. Disulfiram is an approved oral drug used to treat alcohol use disorder that is a potent anti-inflammatory agent and an inhibitor of the viral proteases. We investigated the potential effects of disulfiram on SARS-CoV-2 infection and disease severity in an observational study using a large database of clinical records from the national US Veterans Affairs healthcare system. A multivariable Cox regression adjusted for demographic information and diagnosis of alcohol use disorder revealed a reduced risk of SARS-CoV-2 infection with disulfiram use at a hazard ratio of 0.66 (34% lower risk, 95% confidence interval 24–43%). There were no COVID-19 related deaths among the 188 SARS-CoV-2 positive patients treated with disulfiram, in contrast to 5–6 statistically expected deaths based on the untreated population (P = 0.03). Our epidemiological results suggest that disulfiram may contribute to the reduced incidence and severity of COVID-19. These results support carefully planned clinical trials to assess the potential therapeutic effects of disulfiram in COVID-19.


    Discussion

    Our study is the largest using real world data to demonstrate a lower risk of SARS-CoV-2 infection in those taking disulfiram. Recently, in a preliminary report, Tamburin et al. [17] showed that patients taking disulfiram had a significantly lower incidence of symptoms compatible with COVID-19, such as fever and dyspnea, compared to a control group. However, their study was underpowered to discern a difference in actual risk of COVID-19 disease. Our study significantly extends these initial observations in two ways: (1) the VA patient population with relevant data is considerably larger, which enabled us to infer a statistically significant association between disulfiram use and risk of SARS-CoV-2 infection, and (2) we were able to document the clinical outcomes of those infected with COVID-19 taking disulfiram and estimate the risk of death. Other commonly used drugs have also been reported to reduce the risk of infection and disease severity [18]. Access to larger clinical datasets and meta-analysis across diverse health-care systems would be useful in future investigations on this topic.


    The principal limitation of our study, as is true even for studies with controlled cohorts, is that association does not prove causation and that even very likely causation does not guarantee the success of the corresponding therapeutic intervention. There are several additional limitations. Since Veterans can receive care outside of the VA, diagnoses and outcomes may be incompletely recorded and we do not know if patients actually took the prescribed disulfiram drug, or whether they were still taking the drug near the time of infection. We also cannot rule out the possibility that those prescribed disulfiram had other factors, such as behavioral differences or other confounding variables, that contributed to their protection against COVID-19. Additionally, we are unable to distinguish symptomatic from asymptomatic infection, as documentation of the relevant symptoms is inconsistent in the electronic health records used in our study. For inpatient settings, patients are routinely tested on admission. For outpatient settings, testing can occur for symptoms or concerns of exposure.


    Our epidemiological results suggest that disulfiram may be efficacious in combating COVID-19. Additional information is expected from two small ongoing Phase II clinical trials of disulfiram involving early mild-to-moderate symptomatic (NCT04485130, 60 participants) or hospitalized (NCT04594343, 200 participants) COVID-19 patients. Reduction in disease progression in the first trial, if observed, may be primarily due to inhibition of viral replication. This hypothesis is based on clear evidence from biochemical experiments that disulfiram inhibits several enzymes involved in viral replication (Mpro, PLpro, Nsp13 and Nsp14) via covalent modification of cysteine residues in the active site of the Mpro and PLpro proteases and via weakening of Cys-coordinated Zn2+ ion binding sites in the finger domain of PLpro and in the RNA-modifying enzymes Nsp13 and Nsp14 [3–11]. Better outcomes in the second trial, if observed, may be more influenced by the anti-inflammatory effects of disulfiram, as demonstrated in a mouse model of sepsis, via inhibition of the formation of the host gasdermin D pore and reduction of pyroptosis and inflammatory cytokine secretion [12].


    Given the urgent medical need, larger clinical trials stratified for early and late COVID-19 disease as well as in uninfected populations are highly desirable to test the impact of disulfiram across the entire COVID-19 continuum, from infection to disease progression and severe disease. A positive drug effect would most likely also extend to the constantly evolving SARS-CoV-2 variants and related coronaviruses, as the known viral target sites of disulfiram are highly conserved Cys residues. As a repurposing candidate, disulfiram has particular advantages given its low cost, both in production and distribution, and favorable safety profile [2, 19].


    We therefore propose that clinical trials should be pursued proactively, given the current limited access to vaccination and the lack of generally available, low-cost proven therapeutic agents against this pandemic disease. Our view is that such trials require governmental or philanthropic funding and that time is of the essence. If successful in clinical trials, disulfiram would be a good candidate as a COVID-19 therapeutic for world-wide distribution, including to low-income populations.

  • On a more trivial note (this is the playground after all) I just received a letter dated November the 5th from the gendarmerie in France. They say that a cat is trapped inside a house belonging to me, So, 19 days later I told them where to get a key.


    Nothing like an emergency response.

  • I don't know yet. I have organised somebody to take a key to the police station. I can't really understand how it got in there, the only access is via the courtyard behind - which is surrounded by high walls. Poor thing, at least there's water to drink, with water on hand cats can survice a very long fast.

  • Poor thing, at least there's water to drink, with water on hand cats can survice a very long fast.

    On college break many years ago I came back to my home town to see my dad. I asked him where Fireball was. Fireball was a beautiful orange shorthaired male cat, the fourth generation of a grey cat lineage we had in our house growing up. (Somehow, he, and he alone, turned out orange.) My dad said he hadn't seen him in about a month. I left immediately in search of him. Fireball knew my 'meow' sound, so I went around the neighbourhood meowing for him. Finally I came full circle, approaching our house and dejected that there was no sign of Fireball. Then I thought I heard the faintest meow, and then maybe again. I approached a neighbour's house across the street which appeared like it had been recently abandoned. I meowed some more. Nothing. But there was a hinged window to the basement that I saw was not secure, so I, ahem, lifted it up, squeezed through the opening, and landed on the basement floor. I looked around, and my last course was to look under a single bed that was up against a wall. Well lo and behold there was Fireball. He was curled up, very skinny and barely able to even lift his head. I picked him up and brought him home. It took two weeks to nurse him back to relative health. Frankly, one of the highlights of my life.

  • Isrrael reports: Yesterday 700+ today 600+ cases - from Israel health page. Cases are clearly raising!

    Typically fascist FUD. Inventing facts and comment them. Reichkristallnacht... Or may be just children Zeus46  zorud on the wrong playground.

    Let’s agree then, that your invented fact that all ICU covid patients in Switzerland will die, is fascist FUD as well? 😉

  • Critique of vaccine analysis (there is basically now discussins of his work and he can't get a preprint out, being wiell published before, WTF)


    Now look at this for the swedish cox regression study


    Covariates
    From Statistics Sweden, we obtained information on whether individuals were born in
    Sweden or not, birth year, birth month, and sex for all individuals24
    . From Statistics Sweden,
    we also obtained individual-level data on highest education during year 2019. Individual-level
    data regarding diagnoses, prescription medications, country of birth, and homemaker service
    were obtained from national registries managed by the Swedish National Board of Health and
    Welfare (http://www.socialstyrelsen.se). Homemaker services includes domestic services provided
    to individuals (primarily older individuals) who live at home but need help with shopping,
    cleaning, meal preparation, and similar tasks. Local governments are responsible for
    determining eligibility for these services. From the Swedish National Inpatient Register and
    National Outpatient Register for specialist care, diagnoses from 1998 and 2001 and later,
    respectively, were obtained, based on ICD-10 codes. Prescription medications from 2018 and
    later were obtained from the Prescribed Drug Register using Anatomic Therapeutic Chemical
    classification system codes. These three registers are complete for all specialist care and
    medications prescribed in Sweden for the years selected. The diagnoses and medications
    This preprint research paper has not been peer reviewed. Electronic copy available at: https://ssrn.com/abstract=3949410
    Preprint not peer reviewed
    selected as covariates for this study were based on the results from a previous nationwide
    study25
    . See Supplemental Table 1 for definitions.


    This list of covariates is why I like this study

  • What wrong with Wyttengod? Did I hit a nerve? You call for moderators, if someone asks a question or states something that is not in line with your philosophy?


    Barely a post or even a sentence without fascist, mafiosi, clown, Dr. Mengele, Auschwitz, Reichskristallnacht, Heil, concentration camp, fools, idiots, terror, criminals, cricket brains, blood suckers, Nazi, babies, children, fascism, euthanasia, crap, FM/R/%/B mafia, crime, killer, FUD, nonsens, brain farts,… (not complete…).


    You are the only one in this entire forum that obviously needs to use such primitive language to make a point…sad.

    Is this the language of a seriously skilled and educated person? Hard to believe…

Subscribe to our newsletter

It's sent once a month, you can unsubscribe at anytime!

View archive of previous newsletters

* indicates required

Your email address will be used to send you email newsletters only. See our Privacy Policy for more information.

Our Partners

Supporting researchers for over 20 years
Want to Advertise or Sponsor LENR Forum?
CLICK HERE to contact us.