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Can touching a barbell in the gym get you sick with the coronavirus?
- Thread starter Michael Scally MD
- Start date
Researchers have long known that masks can prevent people from spreading airway germs to others — findings that have driven much of the conversation around these crucial accessories during the coronavirus pandemic.
But now, as cases continue to rise across the country, experts are pointing to an array of evidence suggesting that masks also protect the people wearing them, lessening the severity of symptoms, or in some instances, staving off infection entirely.
Different kinds of masks “block virus to a different degree, but they all block the virus from getting in,” said Dr. Monica Gandhi, an infectious disease physician at the University of California, San Francisco. If any virus particles do breach these barriers, she said, the disease might still be milder.
Dr. Gandhi and her colleagues make this argument in a new paper slated to be published in the Journal of General Internal Medicine. Drawing from animal experiments and observations of various events during the pandemic, they contend that people wearing face coverings will take in fewer coronavirus particles, making it easier for their immune systems to bring any interlopers to heel. Box
[OA] Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. Published online July 27, 2020. Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From COVID-19
Key Points
Question What are the cardiovascular effects in unselected patients with recent coronavirus disease 2019 (COVID-19)?
Findings In this cohort study including 100 patients recently recovered from COVID-19 identified from a COVID-19 test center, cardiac magnetic resonance imaging revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), which was independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis.
Meaning These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.
Importance Coronavirus disease 2019 (COVID-19) continues to cause considerable morbidity and mortality worldwide. Case reports of hospitalized patients suggest that COVID-19 prominently affects the cardiovascular system, but the overall impact remains unknown.
Objective To evaluate the presence of myocardial injury in unselected patients recently recovered from COVID-19 illness.
Design, Setting, and Participants In this prospective observational cohort study, 100 patients recently recovered from COVID-19 illness were identified from the University Hospital Frankfurt COVID-19 Registry between April and June 2020.
Exposure Recent recovery from severe acute respiratory syndrome coronavirus 2 infection, as determined by reverse transcription–polymerase chain reaction on swab test of the upper respiratory tract.
Main Outcomes and Measures Demographic characteristics, cardiac blood markers, and cardiovascular magnetic resonance (CMR) imaging were obtained. Comparisons were made with age-matched and sex-matched control groups of healthy volunteers (n = 50) and risk factor–matched patients (n = 57).
Results Of the 100 included patients, 53 (53%) were male, and the median (interquartile range [IQR]) age was 49 (45-53) years. The median (IQR) time interval between COVID-19 diagnosis and CMR was 71 (64-92) days. Of the 100 patients recently recovered from COVID-19, 67 (67%) recovered at home, while 33 (33%) required hospitalization.
At the time of CMR, high-sensitivity troponin T (hsTnT) was detectable (3 pg/mL or greater) in 71 patients recently recovered from COVID-19 (71%) and significantly elevated (13.9 pg/mL or greater) in 5 patients (5%).
Compared with healthy controls and risk factor–matched controls, patients recently recovered from COVID-19 had lower left ventricular ejection fraction, higher left ventricle volumes, higher left ventricle mass, and raised native T1 and T2.
A total of 78 patients recently recovered from COVID-19 (78%) had abnormal CMR findings, including raised myocardial native T1 (n = 73), raised myocardial native T2 (n = 60), myocardial late gadolinium enhancement (n = 32), and pericardial enhancement (n = 22).
There was a small but significant difference between patients who recovered at home vs in the hospital for native T1 mapping (median [IQR], 1122 [1113-1132] ms vs 1143 [1131-1156] ms; P = .02) but not for native T2 mapping or hsTnT levels.
None of these measures were correlated with time from COVID-19 diagnosis (native T1: r = 0.07; P = .47; native T2: r = 0.14; P = .15; hsTnT: r = −0.07; P = .50). High-sensitivity troponin T was significantly correlated with native T1 mapping (r = 0.35; P < .001) and native T2 mapping (r = 0.22; P = .03).
Endomyocardial biopsy in patients with severe findings revealed active lymphocytic inflammation. Native T1 and T2 were the measures with the best discriminatory ability to detect COVID-19–related myocardial pathology.
Conclusions and Relevance In this study of a cohort of German patients recently recovered from COVID-19 infection, CMR revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), independent of preexisting conditions, severity and overall course of the acute illness, and time from the original diagnosis. These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.
[OA] Yancy CW, Fonarow GC. Coronavirus Disease 2019 (COVID-19) and the Heart—Is Heart Failure the Next Chapter? JAMA Cardiol. Published online July 27, 2020. Coronavirus Disease 2019 (COVID-19) and the Heart
Multiple data sets now confirm the increased risk for morbid and mortal complications due to coronavirus disease 2019 (COVID-19) in individuals with preexisting cardiovascular diseases including hypertension, coronary artery disease, and heart failure.1,2 These salient observations have strengthened preventive strategies and undoubtedly have resulted in lives saved. Although episodes of clinical myocarditis have been suspected and a few cases have been reported in the literature,3 direct cardiac involvement due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been difficult to confirm.
Key Points
Question What are the cardiovascular effects in unselected patients with recent coronavirus disease 2019 (COVID-19)?
Findings In this cohort study including 100 patients recently recovered from COVID-19 identified from a COVID-19 test center, cardiac magnetic resonance imaging revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), which was independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis.
Meaning These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.
Importance Coronavirus disease 2019 (COVID-19) continues to cause considerable morbidity and mortality worldwide. Case reports of hospitalized patients suggest that COVID-19 prominently affects the cardiovascular system, but the overall impact remains unknown.
Objective To evaluate the presence of myocardial injury in unselected patients recently recovered from COVID-19 illness.
Design, Setting, and Participants In this prospective observational cohort study, 100 patients recently recovered from COVID-19 illness were identified from the University Hospital Frankfurt COVID-19 Registry between April and June 2020.
Exposure Recent recovery from severe acute respiratory syndrome coronavirus 2 infection, as determined by reverse transcription–polymerase chain reaction on swab test of the upper respiratory tract.
Main Outcomes and Measures Demographic characteristics, cardiac blood markers, and cardiovascular magnetic resonance (CMR) imaging were obtained. Comparisons were made with age-matched and sex-matched control groups of healthy volunteers (n = 50) and risk factor–matched patients (n = 57).
Results Of the 100 included patients, 53 (53%) were male, and the median (interquartile range [IQR]) age was 49 (45-53) years. The median (IQR) time interval between COVID-19 diagnosis and CMR was 71 (64-92) days. Of the 100 patients recently recovered from COVID-19, 67 (67%) recovered at home, while 33 (33%) required hospitalization.
At the time of CMR, high-sensitivity troponin T (hsTnT) was detectable (3 pg/mL or greater) in 71 patients recently recovered from COVID-19 (71%) and significantly elevated (13.9 pg/mL or greater) in 5 patients (5%).
Compared with healthy controls and risk factor–matched controls, patients recently recovered from COVID-19 had lower left ventricular ejection fraction, higher left ventricle volumes, higher left ventricle mass, and raised native T1 and T2.
A total of 78 patients recently recovered from COVID-19 (78%) had abnormal CMR findings, including raised myocardial native T1 (n = 73), raised myocardial native T2 (n = 60), myocardial late gadolinium enhancement (n = 32), and pericardial enhancement (n = 22).
There was a small but significant difference between patients who recovered at home vs in the hospital for native T1 mapping (median [IQR], 1122 [1113-1132] ms vs 1143 [1131-1156] ms; P = .02) but not for native T2 mapping or hsTnT levels.
None of these measures were correlated with time from COVID-19 diagnosis (native T1: r = 0.07; P = .47; native T2: r = 0.14; P = .15; hsTnT: r = −0.07; P = .50). High-sensitivity troponin T was significantly correlated with native T1 mapping (r = 0.35; P < .001) and native T2 mapping (r = 0.22; P = .03).
Endomyocardial biopsy in patients with severe findings revealed active lymphocytic inflammation. Native T1 and T2 were the measures with the best discriminatory ability to detect COVID-19–related myocardial pathology.
Conclusions and Relevance In this study of a cohort of German patients recently recovered from COVID-19 infection, CMR revealed cardiac involvement in 78 patients (78%) and ongoing myocardial inflammation in 60 patients (60%), independent of preexisting conditions, severity and overall course of the acute illness, and time from the original diagnosis. These findings indicate the need for ongoing investigation of the long-term cardiovascular consequences of COVID-19.
[OA] Yancy CW, Fonarow GC. Coronavirus Disease 2019 (COVID-19) and the Heart—Is Heart Failure the Next Chapter? JAMA Cardiol. Published online July 27, 2020. Coronavirus Disease 2019 (COVID-19) and the Heart
Multiple data sets now confirm the increased risk for morbid and mortal complications due to coronavirus disease 2019 (COVID-19) in individuals with preexisting cardiovascular diseases including hypertension, coronary artery disease, and heart failure.1,2 These salient observations have strengthened preventive strategies and undoubtedly have resulted in lives saved. Although episodes of clinical myocarditis have been suspected and a few cases have been reported in the literature,3 direct cardiac involvement due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been difficult to confirm.
[OA] Crosstalk Between COVID-19 and Prostate Cancer
A new coronavirus, named SARS-CoV-2, emerged in Wuhan city, China, in December 2019 causing atypical pneumonia and affecting multiple body organs. The rapidly increasing numbers of infected patients and deaths due to COVID-19 disease necessitated declaring it as a global pandemic.
Efforts were combined since then to rapidly develop a treatment and/or a vaccine to combat the deadly virus. Drug repurposing approach has been pursued as a temporary management tactic to treat COVID-19 patients. However, reports about the efficacy of many of the used drugs had been controversial with a dire need to keep the ongoing efforts for rapid development of new treatments.
Promising data came out pointing to a possible hidden liaison between prostate cancer (PCa) and COVID-19, where androgen-deprivation therapies (ADT) used in PCa had been shown to instigate a protective role against COVID-19. Delving into the possible mechanisms underlying the crosstalk between COVID-19 and PCa alludes a potential association between SARS-CoV-2 targets on host epithelial cells and PCa genetic aberrations and molecular signatures, including AR and TMPRSS2. The question remains: Can PCa treatments serve as potential therapeutic options for COVID-19 patients?
Bahmad HF, Abou-Kheir W. Crosstalk between COVID-19 and prostate cancer [published online ahead of print, 2020 Jul 24]. Prostate Cancer Prostatic Dis. 2020;10.1038/s41391-020-0262-y. doi:10.1038/s41391-020-0262-y https://www.nature.com/articles/s41391-020-0262-y
A new coronavirus, named SARS-CoV-2, emerged in Wuhan city, China, in December 2019 causing atypical pneumonia and affecting multiple body organs. The rapidly increasing numbers of infected patients and deaths due to COVID-19 disease necessitated declaring it as a global pandemic.
Efforts were combined since then to rapidly develop a treatment and/or a vaccine to combat the deadly virus. Drug repurposing approach has been pursued as a temporary management tactic to treat COVID-19 patients. However, reports about the efficacy of many of the used drugs had been controversial with a dire need to keep the ongoing efforts for rapid development of new treatments.
Promising data came out pointing to a possible hidden liaison between prostate cancer (PCa) and COVID-19, where androgen-deprivation therapies (ADT) used in PCa had been shown to instigate a protective role against COVID-19. Delving into the possible mechanisms underlying the crosstalk between COVID-19 and PCa alludes a potential association between SARS-CoV-2 targets on host epithelial cells and PCa genetic aberrations and molecular signatures, including AR and TMPRSS2. The question remains: Can PCa treatments serve as potential therapeutic options for COVID-19 patients?
Bahmad HF, Abou-Kheir W. Crosstalk between COVID-19 and prostate cancer [published online ahead of print, 2020 Jul 24]. Prostate Cancer Prostatic Dis. 2020;10.1038/s41391-020-0262-y. doi:10.1038/s41391-020-0262-y https://www.nature.com/articles/s41391-020-0262-y
Joe Morgan
Member
“Hydroxychloroquine lowers COVID-19 death rate, Henry Ford Health study finds”
Hydroxychloroquine lowers COVID-19 death rate, Henry Ford Health study finds
Hydroxychloroquine lowers COVID-19 death rate, Henry Ford Health study finds
A San Diego County official has confirmed there is an outbreak of COVID-19 tied to a popular San Diego gym that was operating in violation of the county's public health order last week.
At least three people affiliated with The Gym in Pacific Beach have tested positive for the novel coronavirus, a San Diego County spokesperson said.
The county would not confirm exactly how many people connected with The Gym have tested positive, but confirmed that a community outbreak occurs when three or more people from different households are linked to the same setting or location test positive for COVID-19.
If you are refusing to wear a mask due to concern your brain won’t get enough oxygen, I’m here to tell you; that ship has already sailed.
Oldschool
Member
[OA] Sex-Derived Attributes Contributing To SARS-Cov-2 Mortality
Epidemiological data in COVID-19 mortality indicate that men are more prone to die of SARS-CoV2 infection than women, but biologic causes for this sexual dimorphism are unknown. We discuss the prospective behavioral and biological differences between the sexes that could be attributed to this gender-based differentiation.
The female sex hormones and the immune stimulatory genes including toll-like receptors, interleukins, micro-RNAs present on X-chromosome may impart lesser infectivity and mortality of the SARS-CoV-2 in females over males. The sex hormone estrogen interacts with the Renin-Angiotensin-Aldosterone System, one of the most critical pathways in COVID-19 infectivity, and modulate the vasomotor homeostasis.
Testosterone on the contrary enhances the levels of the two most critical molecules angiotensin converting enzyme 2 (ACE2) and the transmembrane protease, serine-type 2 (TMPRSS2), transcriptionally and post-translationally, thereby increasing viral load and delaying viral clearance in men as compared to women.
We propose that modulating sex hormones, either by increasing estrogen or anti-androgen, may be a therapeutic option to reduce mortality from SARS-CoV-2.
Chanana N, Palmo T, Sharma K, Kumar R, Graham BB, Pasha Q. Sex-derived attributes contributing to SARS-CoV-2 mortality [published online ahead of print, 2020 Jul 29]. Am J Physiol Endocrinol Metab. 2020;10.1152/ajpendo.00295.2020. doi:10.1152/ajpendo.00295.2020 https://journals.physiology.org/doi/abs/10.1152/ajpendo.00295.2020
Epidemiological data in COVID-19 mortality indicate that men are more prone to die of SARS-CoV2 infection than women, but biologic causes for this sexual dimorphism are unknown. We discuss the prospective behavioral and biological differences between the sexes that could be attributed to this gender-based differentiation.
The female sex hormones and the immune stimulatory genes including toll-like receptors, interleukins, micro-RNAs present on X-chromosome may impart lesser infectivity and mortality of the SARS-CoV-2 in females over males. The sex hormone estrogen interacts with the Renin-Angiotensin-Aldosterone System, one of the most critical pathways in COVID-19 infectivity, and modulate the vasomotor homeostasis.
Testosterone on the contrary enhances the levels of the two most critical molecules angiotensin converting enzyme 2 (ACE2) and the transmembrane protease, serine-type 2 (TMPRSS2), transcriptionally and post-translationally, thereby increasing viral load and delaying viral clearance in men as compared to women.
We propose that modulating sex hormones, either by increasing estrogen or anti-androgen, may be a therapeutic option to reduce mortality from SARS-CoV-2.
Chanana N, Palmo T, Sharma K, Kumar R, Graham BB, Pasha Q. Sex-derived attributes contributing to SARS-CoV-2 mortality [published online ahead of print, 2020 Jul 29]. Am J Physiol Endocrinol Metab. 2020;10.1152/ajpendo.00295.2020. doi:10.1152/ajpendo.00295.2020 https://journals.physiology.org/doi/abs/10.1152/ajpendo.00295.2020
Freedom to not wear a mask
Welcome to the Freedom Cafe!
We trust you to make your own choices if you want to wear a face mask. And, in the same spirit of individual liberty, we allow our staff to make their own choices about the safety procedures they prefer to follow as they prepare and serve your food.
We encourage employees to wash their hands after using the bathroom, but understand that some people may be allergic to certain soaps or may simply prefer not to wash their hands. It is not our place to tell them what to do.
We understand that you may be used to chicken that has been cooked to 165 degrees. We do have to respect that some of our cooks may have seen a meme or a YouTube video saying that 100 degrees is fine and we do not want to encroach on their beliefs.
Some servers may wish to touch your food as they serve it. There is no reason that a healthy person with clean hands can’t touch your food. We will take their word for it that they are healthy and clean.
Water temperature and detergent are highly personal choices, and we allow our dishwashing team to decide how they’d prefer to wash the silverware you will put in your mouth.
Some of you may get sick, but almost everyone survives food poisoning. We think you’ll agree that it’s a small price to pay for the sweet freedom of no one ever being told what to do – and especially not for the silly reason of keeping strangers healthy.
Welcome to the Freedom Cafe!
We trust you to make your own choices if you want to wear a face mask. And, in the same spirit of individual liberty, we allow our staff to make their own choices about the safety procedures they prefer to follow as they prepare and serve your food.
We encourage employees to wash their hands after using the bathroom, but understand that some people may be allergic to certain soaps or may simply prefer not to wash their hands. It is not our place to tell them what to do.
We understand that you may be used to chicken that has been cooked to 165 degrees. We do have to respect that some of our cooks may have seen a meme or a YouTube video saying that 100 degrees is fine and we do not want to encroach on their beliefs.
Some servers may wish to touch your food as they serve it. There is no reason that a healthy person with clean hands can’t touch your food. We will take their word for it that they are healthy and clean.
Water temperature and detergent are highly personal choices, and we allow our dishwashing team to decide how they’d prefer to wash the silverware you will put in your mouth.
Some of you may get sick, but almost everyone survives food poisoning. We think you’ll agree that it’s a small price to pay for the sweet freedom of no one ever being told what to do – and especially not for the silly reason of keeping strangers healthy.
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