Bastard Tetris posted:

the novel coronavirus disrespected the NAP

Glumwheels posted:

I went to the doctor today for a check on my cholesterol and overheard the nurse inform the doctor my case and at the end say “oh he’s wearing a mask”. Now why would she say that?

mawarannahr posted:

mid 19th c
"oh he washed his hands"
*doctor rolls eyes*

gently caress COREY PERRY posted:

ibid posted:

https://twitter.com/pedsmd2b/status/1692319357333037385
https://twitter.com/pedsmd2b/status/1692323957733814296

harrygomm posted:

are you even allowed to emptyquote posts this recent?

mawarannahr posted:

mid 19th c
"oh he washed his hands"
*doctor rolls eyes*

Steve Yun posted:

my roommate went back to urgent care because one of his mastectomy stitches isn’t healing properly

luckily despite the hospital mask mandate being lifted last Friday in LA county, almost everyone is still wearing masks at Kaiser. both health care and patients. roommate only saw three people without masks

not sure if it’s inertia or people noticing there’s a wave going on, hoping it lasts

ibid posted:

https://twitter.com/pedsmd2b/status/1692319357333037385
https://twitter.com/pedsmd2b/status/1692323957733814296

Zugzwang posted:

my mom's oncologist and his staff stopped masking in May, lol

https://www.sciencedirect.com/science/article/abs/pii/S0925443923001849 posted:

Functional characterisation of the ACE2 orthologues in Drosophila provides insights into the neuromuscular complications of COVID-19

Highlights
• A large percentage of patients with COVID-19 have neuromuscular manifestations.
• Loss of Drosophila ACE2 orthologues Ance or Ance3 impaired motoric ability.
• Ance or Ance3 knockdown induced unique and overlapping transcriptional changes.
• Genes with a synaptic function were particularly vulnerable to splicing alterations.
• Findings favour ACE2 interference as a cause of COVID-19 neuromuscular disturbances.

Abstract
SARS-CoV-2, the virus responsible for the coronavirus disease of 2019 (COVID-19), gains cellular entry via interaction with the angiotensin-converting enzyme 2 (ACE2) receptor of host cells. Although SARS-CoV-2 mainly targets the respiratory system, the neuromuscular system also appears to be affected in a large percentage of patients with acute or chronic COVID-19. The cause of the well-described neuromuscular manifestations resulting from SARS-CoV-2 infection remains unresolved. These may result from the neuromuscular-invasive capacity of the virus leading to direct injury. Alternatively, they may be the consequence of ACE2 inactivation either due to viral infection, ACE2 autoantibodies or both. Here, we made use of the Drosophila model to investigate whether ACE2 downregulation is sufficient to induce neuromuscular phenotypes. We show that moderate gene silencing of ACE2 orthologues Ance or Ance3 diminished survival on exposure to thermal stress only upon induction of neuromuscular fatigue driven by increased physical activity. A strong knockdown of Ance or Ance3 directed to muscle reduced or abolished adult viability and caused obvious motoric deficits including reduced locomotion and impaired flight capacity. Selective knockdown of Ance and Ance3 in neurons caused wing defects and an age-dependent decline in motor behaviour, respectively, in adult flies. Interestingly, RNA sequencing allowed us to discover several differentially spliced genes that are required for synaptic function downstream of Ance or Ance3 depletion. Our findings are therefore supportive of the notion that loss of a RAS-independent function for ACE2 contributes to the neuromuscular manifestations associated with SARS-CoV-2 infection.

https://scitechdaily.com/unmasking-the-long-covid-mystery-new-study-reveals-cause-of-muscle-weakness/#google_vignette posted:

Unmasking the Long COVID Mystery: New Study Reveals Cause of Muscle Weakness
(..)
Around one in three individuals who recover from COVID-19 continue to experience life-disrupting symptoms, such as persistent fatigue, shortness of breath, ‘brain fog’ (a term used to describe concentration difficulties), and muscle weakness. The origin of long COVID, despite its increasing global impact on daily life, has remained a mystery.

SARS-CoV-2, the coronavirus responsible for COVID-19, latches onto the ACE2 (angiotensin-converting enzyme 2) receptor, which acts as the doorway through which the virus infects cells. In a pioneering study, researchers at the University of Malta exploited fruit flies to curb down the levels of the ACE2 receptor. In the absence of the virus, this was enough to induce fatigue and diminished mobility.

“Our research clearly shows that depletion of ACE2 is central to the neuromuscular complications experienced by a significant percentage of COVID-19 patients,” said Professor Ruben Cauchi, who heads the Motor Neuron Disease Laboratory at the University of Malta.
(..)
When analyzing molecular defects in organisms with downregulated ACE2 levels, the Maltese scientists discovered a breakdown in communication between nerves and muscles. Several key molecules required for nerves to send messages to muscles were found compromised.

Various paths are thought to coalesce to bring down ACE2 levels or dampen its function in humans following a coronavirus infection. “In addition to being hijacked by the virus, the ACE2 receptor on the cell’s surface can also be targeted by autoantibodies, with the immune system attacking the body as it does in Multiple Sclerosis,” added Dr. Paul Herrera, who performed the intricate experiments that were crucial to the study. There have also been reports of virus persistence long after the initial infection.
(..)

Pingui posted:

Zugzwang posted:

Fun fact, your use of the opening quote tag made this quote of your post empty too

I think 3 seems good, since it provides a way to find the original content without taking up much space. Thanks for all the great stuff you post.

Zugzwang posted:

Fun fact, your use of the opening quote tag made this quote of your post empty too

I think 3 seems good, since it provides a way to find the original content without taking up much space. Thanks for all the great stuff you post.

Insanite posted:

We can’t live our dramatically shortened lives in fear

Lib and let die posted:

yeah, I wanna die cramped in a climate refugee concentration temporary relocation camp!

Bastard Tetris posted:

I will never get over how funny the duck masks are, I love them

NeonPunk posted:

Burning man? More like Soaked man after Hilary comes through the place

Poppers posted:

Like TB and influenza have orders of magnitude difference in how likely they are to infect you if you’re in the room with a surg mask vs a respirator

https://www.ncbi.nlm.nih.gov/books/NBK143710/ posted:

No cases of TB disease have so far been reported among those known to have been infected with M. tuberculosis during air travel. From 1992 to 1994, the United States Centers for Disease Control and Prevention (CDC), together with state and local health departments, conducted contact investigations for seven index cases, involving one cabin-crew member and six passengers with infectious TB disease who had flown during this period. The concern was that the closed aircraft cabin environment may have facilitated transmission of M. tuberculosis (6–11). The total number of potentially exposed passengers and cabin crew exceeded 2600 on 191 flights involving nine different types of aircraft.

All index cases were identified as highly infectious, i.e. smears from spontaneous sputum specimens from all index cases were grossly positive for acid-fast bacilli (AFB) and all were culture-positive and had evidence of extensive pulmonary disease on chest radiography. In addition, one patient had biopsy- and culture-confirmed laryngeal TB, the most infectious form of TB.

Strains of M. tuberculosis resistant to isoniazid and rifampicin, i.e. multidrug-resistant TB (MDR-TB), were isolated in two of these episodes (6, 10). Organisms isolated from the other index cases were sensitive to all anti-TB drugs. Two passengers, who were flying to the United States for medical care, knew that they had active TB disease at the time of their flights but did not inform the airline of their status. In the other five instances, TB was diagnosed after the flights.

Investigation of close contacts found evidence of transmission of M. tuberculosis infection during a flight in only two of the seven episodes. In one event, transmission from a cabin flight attendant was detected in 2 of 212 crew members who had worked in close proximity with the index case during a 6-month period; both of those infected were exposed to the infectious source for at least 12 hours. In the other event, there was probable transmission from an infectious case to 4 passengers (seated in close proximity to the index case in the same cabin section), out of a total of 257 passengers tested on a flight longer than 8 hours (6, 10). These results suggest that the risk of infection with M. tuberculosis during air travel is similar to that associated with exposure during other activities in which prolonged contact with potentially infectious individuals may occur (e.g. train or bus travel, any gathering in enclosed spaces).

The average lifetime risk of untreated latent TB infection progressing to active disease at some time during life is <10% and not all persons infected as a result of exposure during air travel may receive effective preventive antibiotic treatment. Therefore, although no cases of TB disease have yet been reported among the infected contacts in the seven studies carried out by CDC, the possibility that future cases of TB disease due to TB infection acquired during air travel may occur cannot be excluded.

Subsequent published case reports of other instances of infectious TB in passengers on long-haul flights (12–16), reviewed in 2005 (17) and with a further case presently under investigation (18), have also suggested that the risk of transmission of infection on board appears to be low. According to an international airline analysis of in-flight TB on long-haul flights, 34 cases of infectious TB were notified to the airlines during a five-year period (2000–2004), giving an overall notification rate of 0.05 per 100 000 long-haul passengers (19).

https://doi.org/10.1097%2FEDE.0000000000000438 posted:

We identified 14 peer-reviewed publications describing contact tracing of passengers after possible exposure to influenza virus aboard an aircraft. Contact tracing during the initial phase of the influenza A(H1N1)pdm09 pandemic was described in 11 publications. The studies describe the follow-up of 2,165 (51%) of 4,252 traceable passengers. Altogether, 163 secondary cases were identified resulting in an overall secondary attack rate among traced passengers of 7.5%. Of these secondary cases, 68 (42%) were seated within two rows of the index case.

https://doi.org/10.1093/oxfordjournals.aje.a112781 posted:

A jet airliner with 54 persons aboard was delayed on the ground for three hours because of engine failure during a takeoff attempt. Most passengers stayed on the airplane during the delay. Within 72 hours, 72 per cent of the passengers became ill with symptoms of cough, fever, fatigue, headache, sore throat and myalgia. One passenger, the apparent index case, was ill on the airplane, and the clinical attack rate among the others varied with the amount of time spent aboard. Virus antigenically similar to A/Texas/1/77(H3N2) was isolated from 8 of 31 passengers cultured, and 20 of 22 ill persons tested had serologic evidence of infection with this virus. The airplane ventilation system was inoperative during the delay and this may account for the high attack rate.

Zantie posted:

[…]We don't know yet how quickly BA.2.86 is spreading or just how immune evasive it is because it's too early to tell. In general though it's a lot harder for our immune system to recognize and mount a quick response, whether it be from prior infection or vaccination or both, when a new one looks this different.

I'm like totally uninterested in EG.5.1/Eris now because of BA.2.86. EG.5.1 is one of many heading up our current wave but I'm looking past that at what will likely be the one after it.

NeonPunk posted:

Remember when that scientist said that with the continuing evolution of the virus, we would see a major Omicron-like shift in the virus about every 3-5 years? Lmao

Platystemon posted:

A fifth case has now been found, in London.

StratGoatCom posted:

https://twitter.com/shay_fleishon/status/1692531498576916878

Tl;dr: the guy who I think spotted this one thinks it no longer qualifies as Omicron.

make sure you get your swab technique right more then ever, with this sort of highly derived variant you want to get it done as correctly as possible to get good results.

https://twitter.com/DrEricLevi/status/1473185815597510656?t=h8U2Lbu8DG5sS4cf8nvwoQ&s=19

NeonPunk posted:

Burning man? More like Soaked man after Hilary comes through the place

posted:

Phylogenetic analyses further suggest that several introductions from birds to the fur animals may have taken place but are also consistent with possible transmission among the fur animals themselves and potentially even between species. Transmission between fur animals is also supported by the general epidemiological pattern of several hundreds of sick and dead animals on the 20 farms (mortality on affected farms has been 2–4 times the normal rate and, at the peak of the outbreak, a large farm recorded almost 400 deaths in one day, which is 10 times the normal rate). The exact mechanism of the transmission within and between farms is, however, not yet known. Some evidence for adaptation to replication in mammals is evident, as the PB2 gene E627K change was detected in samples from one farm and the T271A change in a sample from another farm.

StratGoatCom posted:

There's also some potentially very bad news on the influenza front:

https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2023.28.31.2300400