SteroidsBro
Banned
It doesn't even exist whatsoever, and even if it did, more of us are going to die from responding to it like this than if we had just gone on like we normally do. This shit is rediculous. We deserve what we get.
MESO-Rx
Anabolic Steroids
Can touching a barbell in the gym get you sick with the coronavirus?
- Thread starter Michael Scally MD
- Start date
It doesn't even exist whatsoever, and even if it did, more of us are going to die from responding to it like this than if we had just gone on like we normally do. This shit is rediculous. We deserve what we get.
4Figgy
Member
I just find it kind of funny that people are freaked out about it still. These same people don’t say a single word when flu season hits and children die. Average age of death is around 80-ish with covid. You make it to 80 you lived a long life.
I’m willing to put down real money on the November thing. If Biden won (not a chance in hell) I would guarantee you don’t hear about it on leftist media.
SteroidsBro
Banned
It's a worldwide takeover. It's a lot bigger than just this election. Making trump look bad is just a bonus. He is bad anyway.
Theworm
Well-known Member
Completely agree, that’s why is was a ZERO concern during the riots (aka “mostly peaceful protests”).
In mid-May, the Food and Drug Administration issued a rare public warning about an Abbott Laboratories COVID-19 test that for weeks had received high praise from the White House because of its speed: Test results could be wrong.
The agency at that point had received 15 “adverse event reports” about Abbott’s ID NOW rapid COVID test suggesting that infected patients were wrongly told they did not have the coronavirus, which had led to the deaths of tens of thousands of Americans. The warning followed multiple academic studies showing higher “false negative” rates from the Abbott device, including one from New York University researchers who found it missed close to half of the positive samples detected by a rival company’s test.
But then, in a move that confounded lab officials and other public health experts, a senior FDA official later that month said coronavirus tests provided outside lab settings would be considered useful in fighting the pandemic even if they miss 1 in 5 positive cases — a worrisome failure rate.
The FDA has now received a total of 106 reports of adverse events for the Abbott test, a staggering increase. The agency has not received a single adverse event report for any other point-of-care tests meant to diagnose COVID-19, an agency spokesperson said.
In its own COVID-19 testing policy for labs and commercial manufacturers, the FDA says a diagnostic test should correctly identify at least 95% of positive samples.
But medical professionals are split over the lower 80% threshold for the Abbott and other point-of-care tests’ “sensitivity” — a metric showing how often a test correctly generates a positive result. They are debating whether it’s sufficient, given the risks that an infected person unwittingly spreads COVID-19 after receiving a negative result.
Horby P, Lim WS, Emberson J, et al. Effect of Dexamethasone in Hospitalized Patients with COVID-19: Preliminary Report. medRxiv 2020:2020.06.22.20137273. Effect of Dexamethasone in Hospitalized Patients with COVID-19: Preliminary Report
Background: Coronavirus disease 2019 (COVID-19) is associated with diffuse lung damage. Corticosteroids may modulate immune-mediated lung injury and reducing progression to respiratory failure and death.
Methods: The Randomised Evaluation of COVID-19 therapy (RECOVERY) trial is a randomized, controlled, open-label, adaptive, platform trial comparing a range of possible treatments with usual care in patients hospitalized with COVID-19. We report the preliminary results for the comparison of dexamethasone 6 mg given once daily for up to ten days vs. usual care alone. The primary outcome was 28-day mortality.
Results: 2104 patients randomly allocated to receive dexamethasone were compared with 4321 patients concurrently allocated to usual care. Overall, 454 (21.6%) patients allocated dexamethasone and 1065 (24.6%) patients allocated usual care died within 28 days (age-adjusted rate ratio [RR] 0.83; 95% confidence interval [CI] 0.74 to 0.92; P<0.001).
The proportional and absolute mortality rate reductions varied significantly depending on level of respiratory support at randomization (test for trend p<0.001): Dexamethasone reduced deaths by one-third in patients receiving invasive mechanical ventilation (29.0% vs. 40.7%, RR 0.65 [95% CI 0.51 to 0.82]; p<0.001), by one-fifth in patients receiving oxygen without invasive mechanical ventilation (21.5% vs. 25.0%, RR 0.80 [95% CI 0.70 to 0.92]; p=0.002), but did not reduce mortality in patients not receiving respiratory support at randomization (17.0% vs. 13.2%, RR 1.22 [95% CI 0.93 to 1.61]; p=0.14).
Conclusions: In patients hospitalized with COVID-19, dexamethasone reduced 28-day mortality among those receiving invasive mechanical ventilation or oxygen at randomization, but not among patients not receiving respiratory support.
Background: Coronavirus disease 2019 (COVID-19) is associated with diffuse lung damage. Corticosteroids may modulate immune-mediated lung injury and reducing progression to respiratory failure and death.
Methods: The Randomised Evaluation of COVID-19 therapy (RECOVERY) trial is a randomized, controlled, open-label, adaptive, platform trial comparing a range of possible treatments with usual care in patients hospitalized with COVID-19. We report the preliminary results for the comparison of dexamethasone 6 mg given once daily for up to ten days vs. usual care alone. The primary outcome was 28-day mortality.
Results: 2104 patients randomly allocated to receive dexamethasone were compared with 4321 patients concurrently allocated to usual care. Overall, 454 (21.6%) patients allocated dexamethasone and 1065 (24.6%) patients allocated usual care died within 28 days (age-adjusted rate ratio [RR] 0.83; 95% confidence interval [CI] 0.74 to 0.92; P<0.001).
The proportional and absolute mortality rate reductions varied significantly depending on level of respiratory support at randomization (test for trend p<0.001): Dexamethasone reduced deaths by one-third in patients receiving invasive mechanical ventilation (29.0% vs. 40.7%, RR 0.65 [95% CI 0.51 to 0.82]; p<0.001), by one-fifth in patients receiving oxygen without invasive mechanical ventilation (21.5% vs. 25.0%, RR 0.80 [95% CI 0.70 to 0.92]; p=0.002), but did not reduce mortality in patients not receiving respiratory support at randomization (17.0% vs. 13.2%, RR 1.22 [95% CI 0.93 to 1.61]; p=0.14).
Conclusions: In patients hospitalized with COVID-19, dexamethasone reduced 28-day mortality among those receiving invasive mechanical ventilation or oxygen at randomization, but not among patients not receiving respiratory support.
Blagov, Pavel S., PhD. 2020. “Adaptive and Dark Personality Traits in the Covid-19 Pandemic: Predicting Health-behavior Endorsement and the Appeal of Public-health Messages.” PsyArXiv. March 28. doi:10.31234/osf.io/chgkn. https://psyarxiv.com/chgkn/
Who embraces directions to socially distance, boost hygiene, and protect others during a pandemic of contagious respiratory disease? Do differently phrased public-health messages appeal to different people?
I based predictions on the five-factor, triarchic psychopathy, and Dark Triad models of normal-range and dark traits; the extended parallel process model (EPPM); and schema-congruence theory.
In a survey of 502 online participants, normal-range traits (esp. agreeableness and conscientiousness) predicted endorsement of social distancing and hygiene, as well as the appeal of health messages in general.
Consistent with the EPPM, conscientiousness and neuroticism had an interaction. Dark traits (esp. psychopathy, meanness, and disinhibition) predicted low endorsement of health behaviors and the intent to knowingly expose others to risk.
Most participants preferred a message appealing to compassion (“Help protect the vulnerable...”), but dark traits predicted lower appeal of that message. Personality appears relevant to epidemiology and public-health communication in a contagious-disease context.
Who embraces directions to socially distance, boost hygiene, and protect others during a pandemic of contagious respiratory disease? Do differently phrased public-health messages appeal to different people?
I based predictions on the five-factor, triarchic psychopathy, and Dark Triad models of normal-range and dark traits; the extended parallel process model (EPPM); and schema-congruence theory.
In a survey of 502 online participants, normal-range traits (esp. agreeableness and conscientiousness) predicted endorsement of social distancing and hygiene, as well as the appeal of health messages in general.
Consistent with the EPPM, conscientiousness and neuroticism had an interaction. Dark traits (esp. psychopathy, meanness, and disinhibition) predicted low endorsement of health behaviors and the intent to knowingly expose others to risk.
Most participants preferred a message appealing to compassion (“Help protect the vulnerable...”), but dark traits predicted lower appeal of that message. Personality appears relevant to epidemiology and public-health communication in a contagious-disease context.
[OA] Screening for Low Testosterone Is Needed for Early Identification and Treatment of Men at High Risk of Mortality from Covid-19
A repeated observation that disease severity and mortality rate of Covid-19 is significantly higher in male rather than female sufferers [1] has led researchers to investigate the role of sex hormones in disease progression. Recent reports of case series from China [2], Germany [3] and Italy [4] have highlighted strong associations between serum testosterone levels, inflammatory cytokines, disease progression and clinical outcomes in male Covid-19 patients, independent of patient age and comorbidities.
In a cohort of 31 Italian male hospital inpatients, a significant stepwise decline in calculated free (cFT) and total testosterone (TT) levels was strongly correlated with need for escalation of care from general ward based to specialist respiratory and intensive care [4].
There was significant negative correlation between both total and free testosterone with inflammatory markers such as neutrophil count, LDH and PCT, CRP and ferritin and a positive correlation with lymphocyte count.
The probability of being transferred to the ICU or dying below and above a TT level of 5 nmol/L was 14.18% [8.89–17.03] vs 0.60% [0.12–3.32] (p < 0.0001) and 12.40% [6.77–16.43] vs 0.39% [0.07–2.26] (p < 0.0001) respectively.
Similar observations were made in a cohort of 45 German patients with approximately 70% having low testosterone on admission to ICU with 7 of the 9 subsequent mortalities having significantly reduced TT levels [3].
Low testosterone levels in men admitted to hospital with acute illness have previously been described in published data and have similarly been directly associated with risk of admission to intensive care and severity of disease, as measured by likelihood of development of ARDS, length of ICU stay and mortality [5].
Expert commentators have however put forward hypothesise for disease-specific processes to suggest a potentially causative effect of low testosterone on adverse clinical outcomes in Covid-19. One theory is that low testosterone levels could theoretically be detrimental because of the role of testosterone in inducing the angiotensin-converting enzyme 2 (ACE2) expression, which is an important lung protective enzyme.
Further research is needed to define the cause and effect relationship between testosterone and severe acute illness from Covid-19; however, the importance of low testosterone as a prognostic marker of severe disease is clear and as yet underrecognised in men with Covid-19.
We call for wider screening of testosterone levels in men admitted to hospital with symptoms of Covid-19 as a strategy to identify those at highest risk of severe disease leading to ICU admission and mortality.
Rowland, S.P., O’Brien Bergin, E. Screening for low testosterone is needed for early identification and treatment of men at high risk of mortality from Covid-19. Crit Care 24, 367 (2020). Screening for low testosterone is needed for early identification and treatment of men at high risk of mortality from Covid-19
A repeated observation that disease severity and mortality rate of Covid-19 is significantly higher in male rather than female sufferers [1] has led researchers to investigate the role of sex hormones in disease progression. Recent reports of case series from China [2], Germany [3] and Italy [4] have highlighted strong associations between serum testosterone levels, inflammatory cytokines, disease progression and clinical outcomes in male Covid-19 patients, independent of patient age and comorbidities.
In a cohort of 31 Italian male hospital inpatients, a significant stepwise decline in calculated free (cFT) and total testosterone (TT) levels was strongly correlated with need for escalation of care from general ward based to specialist respiratory and intensive care [4].
There was significant negative correlation between both total and free testosterone with inflammatory markers such as neutrophil count, LDH and PCT, CRP and ferritin and a positive correlation with lymphocyte count.
The probability of being transferred to the ICU or dying below and above a TT level of 5 nmol/L was 14.18% [8.89–17.03] vs 0.60% [0.12–3.32] (p < 0.0001) and 12.40% [6.77–16.43] vs 0.39% [0.07–2.26] (p < 0.0001) respectively.
Similar observations were made in a cohort of 45 German patients with approximately 70% having low testosterone on admission to ICU with 7 of the 9 subsequent mortalities having significantly reduced TT levels [3].
Low testosterone levels in men admitted to hospital with acute illness have previously been described in published data and have similarly been directly associated with risk of admission to intensive care and severity of disease, as measured by likelihood of development of ARDS, length of ICU stay and mortality [5].
Expert commentators have however put forward hypothesise for disease-specific processes to suggest a potentially causative effect of low testosterone on adverse clinical outcomes in Covid-19. One theory is that low testosterone levels could theoretically be detrimental because of the role of testosterone in inducing the angiotensin-converting enzyme 2 (ACE2) expression, which is an important lung protective enzyme.
Further research is needed to define the cause and effect relationship between testosterone and severe acute illness from Covid-19; however, the importance of low testosterone as a prognostic marker of severe disease is clear and as yet underrecognised in men with Covid-19.
We call for wider screening of testosterone levels in men admitted to hospital with symptoms of Covid-19 as a strategy to identify those at highest risk of severe disease leading to ICU admission and mortality.
Rowland, S.P., O’Brien Bergin, E. Screening for low testosterone is needed for early identification and treatment of men at high risk of mortality from Covid-19. Crit Care 24, 367 (2020). Screening for low testosterone is needed for early identification and treatment of men at high risk of mortality from Covid-19
Sex Hormones Signal Why Virus Hits Men Harder
In January, one of the first publications on those sickened by the novel coronavirus in Wuhan, China, reported that three out of every four hospitalized patients were male. Data from around the world have since confirmed that men face a greater risk of severe illness and death from COVID-19 than women, and that children are largely spared. Now, scientists investigating how the virus does its deadly work have zeroed in on a possible reason: Androgens—male hormones such as testosterone—appear to boost the virus' ability to get inside cells.
A constellation of emerging data supports this idea, including COVID-19 outcomes in men with prostate cancer and lab studies of how androgens regulate key genes. And preliminary observations from Spain suggest that a disproportionate number of men with male pattern baldness—which is linked to a powerful androgen—end up in hospitals with COVID-19. Researchers are rushing to test already approved drugs that block androgens' effects, deploying them early in infection in hopes of slowing the virus and buying time for the immune system to beat it back.
Wadman M. Sex hormones signal why virus hits men harder. Science. 2020;368(6495):1038-1039. doi:10.1126/science.368.6495.1038 Sex hormones signal why virus hits men harder
In January, one of the first publications on those sickened by the novel coronavirus in Wuhan, China, reported that three out of every four hospitalized patients were male. Data from around the world have since confirmed that men face a greater risk of severe illness and death from COVID-19 than women, and that children are largely spared. Now, scientists investigating how the virus does its deadly work have zeroed in on a possible reason: Androgens—male hormones such as testosterone—appear to boost the virus' ability to get inside cells.
A constellation of emerging data supports this idea, including COVID-19 outcomes in men with prostate cancer and lab studies of how androgens regulate key genes. And preliminary observations from Spain suggest that a disproportionate number of men with male pattern baldness—which is linked to a powerful androgen—end up in hospitals with COVID-19. Researchers are rushing to test already approved drugs that block androgens' effects, deploying them early in infection in hopes of slowing the virus and buying time for the immune system to beat it back.
Wadman M. Sex hormones signal why virus hits men harder. Science. 2020;368(6495):1038-1039. doi:10.1126/science.368.6495.1038 Sex hormones signal why virus hits men harder
A federal judge on Monday denied a request from Michigan Gov. Gretchen Whitmer and state attorneys asking the judge to delay the reopening of gyms and fitness centers.
They’re currently slated to reopen to the public on Thursday, June 25.
U.S. District Judge Paul L. Maloney on Friday struck down portions of Michigan Gov. Gretchen Whitmer’s executive orders, including a blanket ban on the reopening of gyms and workout facilities statewide.
“This court must uphold the governor’s executive orders as long as they are supported by some relation to the public health,” Maloney’s opinion said. “Unfortunately ... the court has not been presented with any evidence that shows a rational relation between the continued closure of indoor gyms and the preservation of public health.”
Shortly after Maloney’s ruling, Assistant Attorney General John G. Fedynsky filed a request asking the judge to halt his order allowing gyms and fitness centers to reopen until after the appeals process had run its course.
Fedynsky wrote in a 20-page brief supporting the request for a stay that the judge’s order “is premised on a heightened form of rational basis review that is not rooted in the law,” and “the idea that gyms – with their high levels of heavy respiratory activity, shared indoor spaces, and shared surfaces – might be one of the later businesses to come back online in the midst of this global pandemic is hardly surprising and highly sensible.”
If the ruling isn’t delayed, “it will present irreparable harm to (the state) and not serve the public interest,” he wrote. ...
was wondering where your bitch ass has been. Feel better man, that sounds miserable. Reflux is the worst.
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