(04-09-2020, 01:41 AM)Millhouse Wrote: Scored a big pack of Charmin earlier today from Lowes of all places, so if anyone is running low, might be worth to check one out.

Also was reading how sanitary products could take a long time to get back on the shelves. So if that is the case, probably a good thing to know or to look into to possibly start rationing what you have.

The secret is to hit grocery stores first thing in the morning... I came upon Lysol aerosol and cleaner Tuesday. They're stocked in the morning, but are picked clean pretty quickly.

Also my local CVS had hand sanitizer for sale at the register.

(04-10-2020, 08:55 PM)jason Wrote: The secret is to hit grocery stores first thing in the morning... I came upon Lysol aerosol and cleaner Tuesday. They're stocked in the morning, but are picked clean pretty quickly.

Also my local CVS had hand sanitizer for sale at the register.

Yep, they told us at one of the Kroger stores by us they get TP in on 3 trucks a week but it's gone within 30 minutes of opening every time. Rx and dollar stores is where we've found it lately, again early in the morning.

(04-10-2020, 07:37 PM)Millhouse Wrote: See I treat the gloves like if I didnt have them on. ALso I always park by a cart corral, as I put the cart in it, take a glove off to open car up and put groceries in, then throw gloves away without touching anything on and in the car, and my face as well. Then just to be extra sure, a bit of hand sanitizer. When I get home, I wash my hands after putting groceries away. The main thing is that the gloves keep my hands from having contact while also being extra careful while wearing them too.

Now I live in an area where there are hardly any cases we know of. If this was to be a hot spot, I would sanitize the groceries when I got them here. Hopefully it doesnt come to that.

ALso on the bleach solution you are using. I was reading up on it on the CDC website. They said the bleach shouldn't be more than a year old, and have been stored in a non-hot area. Something about it loses effectiveness in killing germs/bacteria the older it gets. Just a heads up on that in case you (and others) didn't know.

Like I said above, some thought is that wearing gloves might cross contaminate easier than bare hands.  I can't recall where I saw that.  Maybe I dreamed it or something as I have not been sleeping well for awhile.  But from what I recall they are not really necessary as long as as you practice proper hand hygiene, don't touch your face etc.  I don't know, there seems to be so much conflicting information these days and it is hard to keep track of it all. The main thing gloves or not seems to be just stop touching your face. It might be seen by many as extreme but I handle everything as if it potentially has Covid-19 on it. I wash my hands every time I handle my food, before and after preparing as well as regularly disinfecting things I touch often like sink handles, keys, doorknobs, keyboard and mouse and my cell phone. My house is defiantly the cleanest it has ever been.

As for the bleach, yeah it does expire to some degree.  I have 3 gallons that I bought in February when I saw things starting to get worse with Covid-19 as well as another used bottle that is less than 6 months old I use for laundry and used for my bleach solution. All stored in a cool dry place out of direct sunlight with my other supplies. As I posted some time ago, I'm a bit of a prepper just not at the same level as people in those TV shows.  So I'm good for awhile when it comes to having bleach that is effective.  

On a side note, once this is all over I will be good if I never have to hear, "in these uncertain times" and other variations used in commercials again.

(04-10-2020, 09:05 PM)George Cantstandya Wrote: On a side note, once this is all over I will be good if I never have to hear, "in these uncertain times" and other variations used in commercials again.  

There needs to be a COVID-19 drinking game. Whenever you hear things like "uncertain times" "new normal" and other buzzwords take a shot. 

That'll kill me long before COVID-19 probably does. 

(04-10-2020, 09:05 PM)George Cantstandya Wrote: Like I said above, some thought is that wearing gloves might cross contaminate easier than bare hands.  I can't recall where I saw that.  Maybe I dreamed it or something as I have not been sleeping well for awhile.  But from what I recall they are not really necessary as long as as you practice proper hand hygiene, don't touch your face etc.  I don't know, there seems to be so much conflicting information these days and it is hard to keep track of it all.  The main thing gloves or not seems to be just stop touching your face.  It might be seen by many as extreme but I handle everything as if it potentially has Covid-19 on it.  I wash my hands every time I handle my food, before and after preparing as well as regularly disinfecting things I touch often like sink handles, keys, doorknobs, keyboard and mouse and my cell phone.  My house is defiantly the cleanest it has ever been.

As for the bleach, yeah it does expire to some degree.  I have 3 gallons that I bought in February when I saw things starting to get worse with Covid-19 as well as another used bottle that is less than 6 months old I use for laundry and used for my bleach solution. All stored in a cool dry place out of direct sunlight with my other supplies.  As I posted some time ago, I'm a bit of a prepper just not at the same level as people in those TV shows.  So I'm good for awhile when it comes to having bleach that is effective.  

On a side note, once this is all over I will be good if I never have to hear, "in these uncertain times" and other variations used in commercials again.  

Wha....wait.. Bleach has an expiration date? You mean after 5 years you can drink it? C'mon man.. Unless you've been storing bleach since maybe 1834 it's still good to go.

(04-16-2020, 10:45 AM)grampahol Wrote: Wha....wait.. Bleach has an expiration date? You mean after 5 years you can drink it? C'mon man.. Unless you've been storing bleach since maybe 1834 it's still good to go.

Bleach starts to break down after about a year even when stored properly and becomes less effective.


From The Scripps Research Institute:  https://www.scripps.edu/newsandviews/e_20060213/bleach.html

Quote:Bleach can expire. After a shelf life of six months, bleach starts to degrade. Even in its original bottle, bleach becomes 20 percent less effective as each year goes by.

From the CDC on disinfecting with Bleach for Covid-19: https://www.cdc.gov/coronavirus/2019-ncov/prevent-getting-sick/disinfecting-your-home.html

Quote:Unexpired household bleach will be effective against coronaviruses when properly diluted.

From an article posted on the Michigan State University website:  https://www.canr.msu.edu/news/covid-19-disinfecting-with-bleach

Quote:

• Bleach expires 1 year from production.
• Bleach can start to lose potency quickly after opening if not stored correctly.
• Homemade cleaning solutions made with bleach lose efficacy after 24 hours.
  

Will expired, or old bleach still disinfect surfaces?

No, bleach loses efficacy with time and exposure to heat and light. So, after one year unopened on a shelf, if stored incorrectly in direct sunlight, or at a temperature above 77ºF, it begins to degrade and continues to deteriorate. 
Once the product loses potency, it can no longer disinfect properly, and you need to dispose of it properly by diluting the remaining bleach with a large amount of water before it pouring into a sink drain.

From Clorox:  https://www.clorox.com/how-to/laundry-basics/bleach-101/clorox-regular-bleach-should-be-replaced-every-year-and-stored-as-directed-for-optimum-performance/

Quote:When properly stored, a bottle of bleach has a one year shelf life. Beyond a year, it should be replaced because the sodium hypochlorite active begins to rapidly break down into salt and water

Some info I found on what (little) they know about the disease and how it ravages the body.

https://www.sciencemag.org/news/2020/04/how-does-coronavirus-kill-clinicians-trace-ferocious-rampage-through-body-brain-toes?fbclid=IwAR2IRzpTNK8yGuausZBL4UXpQk5Ke93XKPDYNNt5PxV5whIREbfRJj7qV9M#

Quote:How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes

Quote:On rounds in a 20-bed intensive care unit (ICU) one recent day, physician Joshua Denson assessed two patients with seizures, many with respiratory failure and others whose kidneys were on a dangerous downhill slide. Days earlier, his rounds had been interrupted as his team tried, and failed, to resuscitate a young woman whose heart had stopped. All shared one thing, says Denson, a pulmonary and critical care physician at the Tulane University School of Medicine. “They are all COVID positive.”

As the number of confirmed cases of COVID-19 surges past 2.2 million globally and deaths surpass 150,000, clinicians and pathologists are struggling to understand the damage wrought by the coronavirus as it tears through the body. They are realizing that although the lungs are ground zero, its reach can extend to many organs including the heart and blood vessels, kidneys, gut, and brain.

“[The disease] can attack almost anything in the body with devastating consequences,” says cardiologist Harlan Krumholz of Yale University and Yale-New Haven Hospital, who is leading multiple efforts to gather clinical data on COVID-19. “Its ferocity is breathtaking and humbling.”

Understanding the rampage could help the doctors on the front lines treat the fraction of infected people who become desperately and sometimes mysteriously ill. Does a dangerous, newly observed tendency to blood clotting transform some mild cases into life-threatening emergencies? Is an overzealous immune response behind the worst cases, suggesting treatment with immune-suppressing drugs could help? What explains the startlingly low blood oxygen that some physicians are reporting in patients who nonetheless are not gasping for breath? “Taking a systems approach may be beneficial as we start thinking about therapies,” says Nilam Mangalmurti, a pulmonary intensivist at the Hospital of the University of Pennsylvania (HUP).

What follows is a snapshot of the fast-evolving understanding of how the virus attacks cells around the body, especially in the roughly 5% of patients who become critically ill. Despite the more than 1000 papers now spilling into journals and onto preprint servers every week, a clear picture is elusive, as the virus acts like no microbe humanity has ever seen. Without larger, prospective controlled studies that are only now being launched, scientists must pull information from small studies and case reports, often published at warp speed and not yet peer reviewed. “We need to keep a very open mind as this phenomenon goes forward,” says Nancy Reau, a liver transplant physician who has been treating COVID-19 patients at Rush University Medical Center. “We are still learning.”

The infection begins

When an infected person expels virus-laden droplets and someone else inhales them, the novel coronavirus, called SARS-CoV-2, enters the nose and throat. It finds a welcome home in the lining of the nose, according to a preprint from scientists at the Wellcome Sanger Institute and elsewhere. They found that cells there are rich in a cell-surface receptor called angiotensin-converting enzyme 2 (ACE2). Throughout the body, the presence of ACE2, which normally helps regulate blood pressure, marks tissues vulnerable to infection, because the virus requires that receptor to enter a cell. Once inside, the virus hijacks the cell’s machinery, making myriad copies of itself and invading new cells.

As the virus multiplies, an infected person may shed copious amounts of it, especially during the first week or so. Symptoms may be absent at this point. Or the virus’ new victim may develop a fever, dry cough, sore throat, loss of smell and taste, or head and body aches.

If the immune system doesn’t beat back SARS-CoV-2 during this initial phase, the virus then marches down the windpipe to attack the lungs, where it can turn deadly. The thinner, distant branches of the lung’s respiratory tree end in tiny air sacs called alveoli, each lined by a single layer of cells that are also rich in ACE2 receptors.

Normally, oxygen crosses the alveoli into the capillaries, tiny blood vessels that lie beside the air sacs; the oxygen is then carried to the rest of the body. But as the immune system wars with the invader, the battle itself disrupts this healthy oxygen transfer. Front-line white blood cells release inflammatory molecules called chemokines, which in turn summon more immune cells that target and kill virus-infected cells, leaving a stew of fluid and dead cells—pus—behind. This is the underlying pathology of pneumonia, with its corresponding symptoms: coughing; fever; and rapid, shallow respiration. Some COVID-19 patients recover, sometimes with no more support than oxygen breathed in through nasal prongs.

But others deteriorate, often quite suddenly, developing a condition called acute respiratory distress syndrome (ARDS). Oxygen levels in their blood plummet and they struggle ever harder to breathe. On x-rays and computerized tomography scans, their lungs are riddled with white opacities where black space—air—should be. Commonly, these patients end up on ventilators. Many die. Autopsies show their alveoli became stuffed with fluid, white blood cells, mucus, and the detritus of destroyed lung cells (see graphic).

An invader’s impact

In serious cases, SARS-CoV-2 lands in the lungs and can do deep damage there. But the virus, or the body’s response to it, can injure many other organs. Scientists are just beginning to probe the scope and nature of that harm.

Some clinicians suspect the driving force in many gravely ill patients’ downhill trajectories is a disastrous overreaction of the immune system known as a “cytokine storm,” which other viral infections are known to trigger. Cytokines are chemical signaling molecules that guide a healthy immune response; but in a cytokine storm, levels of certain cytokines soar far beyond what’s needed, and immune cells start to attack healthy tissues. Blood vessels leak, blood pressure drops, clots form, and catastrophic organ failure can ensue.

Some studies have shown elevated levels of these inflammation-inducing cytokines in the blood of hospitalized COVID-19 patients. “The real morbidity and mortality of this disease is probably driven by this out of proportion inflammatory response to the virus,” says Jamie Garfield, a pulmonologist who cares for COVID-19 patients at Temple University Hospital.

But others aren’t convinced. “There seems to have been a quick move to associate COVID-19 with these hyperinflammatory states. I haven’t really seen convincing data that that is the case,” says Joseph Levitt, a pulmonary critical care physician at the Stanford University School of Medicine.

He’s also worried that efforts to dampen a cytokine response could backfire. Several drugs targeting specific cytokines are in clinical trials in COVID-19 patients. But Levitt fears those drugs may suppress the immune response that the body needs to fight off the virus. “There’s a real risk that we allow more viral replication,” Levitt says.

Meanwhile, other scientists are zeroing in on an entirely different organ system that they say is driving some patients’ rapid deterioration: the heart and blood vessels.



The coronavirus wreaked extensive damage (yellow) on the lungs of a 59-year-old man who died at George Washington University Hospital, as seen in a 3D model based on computerized tomography scans.
George Washington Hospital and Surgical Theater
How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes

By Meredith Wadman, Jennifer Couzin-Frankel, Jocelyn Kaiser, Catherine MatacicApr. 17, 2020 , 6:45 PM

Science’s COVID-19 reporting is supported by the Pulitzer Center.

On rounds in a 20-bed intensive care unit (ICU) one recent day, physician Joshua Denson assessed two patients with seizures, many with respiratory failure and others whose kidneys were on a dangerous downhill slide. Days earlier, his rounds had been interrupted as his team tried, and failed, to resuscitate a young woman whose heart had stopped. All shared one thing, says Denson, a pulmonary and critical care physician at the Tulane University School of Medicine. “They are all COVID positive.”

As the number of confirmed cases of COVID-19 surges past 2.2 million globally and deaths surpass 150,000, clinicians and pathologists are struggling to understand the damage wrought by the coronavirus as it tears through the body. They are realizing that although the lungs are ground zero, its reach can extend to many organs including the heart and blood vessels, kidneys, gut, and brain.

“[The disease] can attack almost anything in the body with devastating consequences,” says cardiologist Harlan Krumholz of Yale University and Yale-New Haven Hospital, who is leading multiple efforts to gather clinical data on COVID-19. “Its ferocity is breathtaking and humbling.”

Understanding the rampage could help the doctors on the front lines treat the fraction of infected people who become desperately and sometimes mysteriously ill. Does a dangerous, newly observed tendency to blood clotting transform some mild cases into life-threatening emergencies? Is an overzealous immune response behind the worst cases, suggesting treatment with immune-suppressing drugs could help? What explains the startlingly low blood oxygen that some physicians are reporting in patients who nonetheless are not gasping for breath? “Taking a systems approach may be beneficial as we start thinking about therapies,” says Nilam Mangalmurti, a pulmonary intensivist at the Hospital of the University of Pennsylvania (HUP).
Related story

A patient on a ventilator
For survivors of severe COVID-19, beating the virus is just the beginning

What follows is a snapshot of the fast-evolving understanding of how the virus attacks cells around the body, especially in the roughly 5% of patients who become critically ill. Despite the more than 1000 papers now spilling into journals and onto preprint servers every week, a clear picture is elusive, as the virus acts like no microbe humanity has ever seen. Without larger, prospective controlled studies that are only now being launched, scientists must pull information from small studies and case reports, often published at warp speed and not yet peer reviewed. “We need to keep a very open mind as this phenomenon goes forward,” says Nancy Reau, a liver transplant physician who has been treating COVID-19 patients at Rush University Medical Center. “We are still learning.”
The infection begins

When an infected person expels virus-laden droplets and someone else inhales them, the novel coronavirus, called SARS-CoV-2, enters the nose and throat. It finds a welcome home in the lining of the nose, according to a preprint from scientists at the Wellcome Sanger Institute and elsewhere. They found that cells there are rich in a cell-surface receptor called angiotensin-converting enzyme 2 (ACE2). Throughout the body, the presence of ACE2, which normally helps regulate blood pressure, marks tissues vulnerable to infection, because the virus requires that receptor to enter a cell. Once inside, the virus hijacks the cell’s machinery, making myriad copies of itself and invading new cells.

As the virus multiplies, an infected person may shed copious amounts of it, especially during the first week or so. Symptoms may be absent at this point. Or the virus’ new victim may develop a fever, dry cough, sore throat, loss of smell and taste, or head and body aches.

If the immune system doesn’t beat back SARS-CoV-2 during this initial phase, the virus then marches down the windpipe to attack the lungs, where it can turn deadly. The thinner, distant branches of the lung’s respiratory tree end in tiny air sacs called alveoli, each lined by a single layer of cells that are also rich in ACE2 receptors.

Normally, oxygen crosses the alveoli into the capillaries, tiny blood vessels that lie beside the air sacs; the oxygen is then carried to the rest of the body. But as the immune system wars with the invader, the battle itself disrupts this healthy oxygen transfer. Front-line white blood cells release inflammatory molecules called chemokines, which in turn summon more immune cells that target and kill virus-infected cells, leaving a stew of fluid and dead cells—pus—behind. This is the underlying pathology of pneumonia, with its corresponding symptoms: coughing; fever; and rapid, shallow respiration. Some COVID-19 patients recover, sometimes with no more support than oxygen breathed in through nasal prongs.

But others deteriorate, often quite suddenly, developing a condition called acute respiratory distress syndrome (ARDS). Oxygen levels in their blood plummet and they struggle ever harder to breathe. On x-rays and computerized tomography scans, their lungs are riddled with white opacities where black space—air—should be. Commonly, these patients end up on ventilators. Many die. Autopsies show their alveoli became stuffed with fluid, white blood cells, mucus, and the detritus of destroyed lung cells (see graphic).
An invader’s impact

In serious cases, SARS-CoV-2 lands in the lungs and can do deep damage there. But the virus, or the body’s response to it, can injure many other organs. Scientists are just beginning to probe the scope and nature of that harm.

Some clinicians suspect the driving force in many gravely ill patients’ downhill trajectories is a disastrous overreaction of the immune system known as a “cytokine storm,” which other viral infections are known to trigger. Cytokines are chemical signaling molecules that guide a healthy immune response; but in a cytokine storm, levels of certain cytokines soar far beyond what’s needed, and immune cells start to attack healthy tissues. Blood vessels leak, blood pressure drops, clots form, and catastrophic organ failure can ensue.

Some studies have shown elevated levels of these inflammation-inducing cytokines in the blood of hospitalized COVID-19 patients. “The real morbidity and mortality of this disease is probably driven by this out of proportion inflammatory response to the virus,” says Jamie Garfield, a pulmonologist who cares for COVID-19 patients at Temple University Hospital.

But others aren’t convinced. “There seems to have been a quick move to associate COVID-19 with these hyperinflammatory states. I haven’t really seen convincing data that that is the case,” says Joseph Levitt, a pulmonary critical care physician at the Stanford University School of Medicine.

He’s also worried that efforts to dampen a cytokine response could backfire. Several drugs targeting specific cytokines are in clinical trials in COVID-19 patients. But Levitt fears those drugs may suppress the immune response that the body needs to fight off the virus. “There’s a real risk that we allow more viral replication,” Levitt says.

Meanwhile, other scientists are zeroing in on an entirely different organ system that they say is driving some patients’ rapid deterioration: the heart and blood vessels.
Striking the heart

In Brescia, Italy, a 53-year-old woman walked into the emergency room of her local hospital with all the classic symptoms of a heart attack, including telltale signs in her electrocardiogram and high levels of a blood marker suggesting damaged cardiac muscles. Further tests showed cardiac swelling and scarring, and a left ventricle—normally the powerhouse chamber of the heart—so weak that it could only pump one-third its normal amount of blood. But when doctors injected dye in the coronary arteries, looking for the blockage that signifies a heart attack, they found none. Another test revealed why: The woman had COVID-19.

How the virus attacks the heart and blood vessels is a mystery, but dozens of preprints and papers attest that such damage is common. A 25 March paper in JAMA Cardiology documented heart damage in nearly 20% of patients out of 416 hospitalized for COVID-19 in Wuhan, China. In another Wuhan study, 44% of 138 hospitalized patients had arrhythmias.

The disruption seems to extend to the blood itself. Among 184 COVID-19 patients in a Dutch ICU, 38% had blood that clotted abnormally, and almost one-third already had clots, according to a 10 April paper in Thrombosis Research. Blood clots can break apart and land in the lungs, blocking vital arteries—a condition known as pulmonary embolism, which has reportedly killed COVID-19 patients. Clots from arteries can also lodge in the brain, causing stroke. Many patients have “dramatically” high levels of D-dimer, a byproduct of blood clots, says Behnood Bikdeli, a cardiovascular medicine fellow at Columbia University Medical Center.

“The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19,” Bikdeli says.

Infection may also lead to blood vessel constriction. Reports are emerging of ischemia in the fingers and toes—a reduction in blood flow that can lead to swollen, painful digits and tissue death.

In the lungs, blood vessel constriction might help explain anecdotal reports of a perplexing phenomenon seen in pneumonia caused by COVID-19: Some patients have extremely low blood-oxygen levels and yet are not gasping for breath. It’s possible that at some stages of disease, the virus alters the delicate balance of hormones that help regulate blood pressure and constricts blood vessels going to the lungs. So oxygen uptake is impeded by constricted blood vessels, rather than by clogged alveoli. “One theory is that the virus affects the vascular biology and that’s why we see these really low oxygen levels,” Levitt says.

If COVID-19 targets blood vessels, that could also help explain why patients with pre-existing damage to those vessels, for example from diabetes and high blood pressure, face higher risk of serious disease. Recent Centers for Disease Control and Prevention (CDC) data on hospitalized patients in 14 U.S. states found that about one-third had chronic lung disease—but nearly as many had diabetes, and fully half had pre-existing high blood pressure.

Mangalmurti says she has been “shocked by the fact that we don’t have a huge number of asthmatics” or patients with other respiratory diseases in HUP’s ICU. “It’s very striking to us that risk factors seem to be vascular: diabetes, obesity, age, hypertension.”

Scientists are struggling to understand exactly what causes the cardiovascular damage. The virus may directly attack the lining of the heart and blood vessels, which, like the nose and alveoli, are rich in ACE2 receptors. Or perhaps lack of oxygen, due to the chaos in the lungs, damages blood vessels. Or a cytokine storm could ravage the heart as it does other organs.

“We’re still at the beginning,” Krumholz says. “We really don’t understand who is vulnerable, why some people are affected so severely, why it comes on so rapidly … and why it is so hard [for some] to recover.”

Multiple battlefields

The worldwide fears of ventilator shortages for failing lungs have received plenty of attention. Not so a scramble for another type of equipment: dialysis machines. “If these folks are not dying of lung failure, they’re dying of renal failure,” says neurologist Jennifer Frontera of New York University’s Langone Medical Center, which has treated thousands of COVID-19 patients. Her hospital is developing a dialysis protocol with different machines to support additional patients. The need for dialysis may be because the kidneys, abundantly endowed with ACE2 receptors, present another viral target.

According to one preprint, 27% of 85 hospitalized patients in Wuhan had kidney failure. Another reported that 59% of nearly 200 hospitalized COVID-19 patients in and near Wuhan had protein and blood in their urine, suggesting kidney damage. Those with acute kidney injury (AKI), were more than five times as likely to die as COVID-19 patients without it, the same Chinese preprint reported.

“The lung is the primary battle zone. But a fraction of the virus possibly attacks the kidney. And as on the real battlefield, if two places are being attacked at the same time, each place gets worse,” says Hongbo Jia, a neuroscientist at the Chinese Academy of Sciences’s Suzhou Institute of Biomedical Engineering and Technology and a co-author of that study.

Viral particles were identified in electron micrographs of kidneys from autopsies in one study, suggesting a direct viral attack. But kidney injury may also be collateral damage. Ventilators boost the risk of kidney damage, as do antiviral drugs including remdesivir, which is being deployed experimentally in COVID-19 patients. Cytokine storms also can dramatically reduce blood flow to the kidney, causing often-fatal damage. And pre-existing diseases like diabetes can boost the risk of AKI. “There is a whole bucket of people who already have some chronic kidney disease who are at higher risk for acute kidney injury,” says Suzanne Watnick, chief medical officer at Northwest Kidney Centers.
Buffeting the brain

Another striking set of symptoms in COVID-19 patients centers on the brain and central nervous system. Frontera says neurologists are needed to assess 5% to 10% of coronavirus patients at her hospital. But she says that “is probably a gross underestimate” of the number whose brains are struggling, especially because many are sedated and on ventilators.

Frontera has seen patients with the brain inflammation encephalitis, with seizures, and with a “sympathetic storm,” an immune response that’s the brain’s version of a cytokine storm. Some people with COVID-19 briefly lose consciousness. Others have strokes. Many report losing their sense of smell. And Frontera and others wonder whether in some cases, infection depresses the brain stem reflex that senses oxygen starvation. This is another explanation for anecdotal observations that some patients aren’t gasping for air, despite dangerously low blood oxygen levels.

ACE2 receptors are present in the neural cortex and brain stem, says Robert Stevens, an intensive care physician at Johns Hopkins Medicine. But it’s not known under what circumstances the virus penetrates the brain and interacts with these receptors. That said, the coronavirus behind the 2003 severe acute respiratory syndrome (SARS) epidemic—a close cousin of today’s culprit—could infiltrate neurons and sometimes caused encephalitis. On 3 April, a case study in the International Journal of Infectious Diseases, from a team in Japan, reported traces of new coronavirus in the cerebrospinal fluid of a COVID-19 patient who developed meningitis and encephalitis, suggesting it, too, can penetrate the central nervous system.

But other factors could be damaging the brain. For example, a cytokine storm could cause brain swelling, and the blood’s exaggerated tendency to clot could trigger strokes. The challenge now is to shift from conjecture to confidence, at a time when staff are focused on saving lives, and even neurologic assessments like inducing the gag reflex or transporting patients for brain scans risk spreading the virus.

Last month, Sherry Chou, a neurologist at the University of Pittsburgh Medical Center, began to organize a worldwide consortium that now includes 50 centers to draw neurological data from care patients already receive. The early goals are simple: Identify the prevalence of neurologic complications in hospitalized patients and document how they fare. Longer term, Chou and her colleagues hope to gather scans, lab tests, and other data to better understand the virus’ impact on the nervous system, including the brain.

Chou speculates about a possible invasion route: through the nose, then upward and through the olfactory bulb—explaining reports of a loss of smell—which connects to the brain. “It’s a nice sounding theory,” she says. “We really have to go and prove that.”

Most neurological symptoms “are reported from colleague to colleague by word of mouth,” Chou adds. “I don’t think anybody, and certainly not me, can say we’re experts.”



The coronavirus wreaked extensive damage (yellow) on the lungs of a 59-year-old man who died at George Washington University Hospital, as seen in a 3D model based on computerized tomography scans.
George Washington Hospital and Surgical Theater
How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes

By Meredith Wadman, Jennifer Couzin-Frankel, Jocelyn Kaiser, Catherine MatacicApr. 17, 2020 , 6:45 PM

Science’s COVID-19 reporting is supported by the Pulitzer Center.

On rounds in a 20-bed intensive care unit (ICU) one recent day, physician Joshua Denson assessed two patients with seizures, many with respiratory failure and others whose kidneys were on a dangerous downhill slide. Days earlier, his rounds had been interrupted as his team tried, and failed, to resuscitate a young woman whose heart had stopped. All shared one thing, says Denson, a pulmonary and critical care physician at the Tulane University School of Medicine. “They are all COVID positive.”

As the number of confirmed cases of COVID-19 surges past 2.2 million globally and deaths surpass 150,000, clinicians and pathologists are struggling to understand the damage wrought by the coronavirus as it tears through the body. They are realizing that although the lungs are ground zero, its reach can extend to many organs including the heart and blood vessels, kidneys, gut, and brain.

“[The disease] can attack almost anything in the body with devastating consequences,” says cardiologist Harlan Krumholz of Yale University and Yale-New Haven Hospital, who is leading multiple efforts to gather clinical data on COVID-19. “Its ferocity is breathtaking and humbling.”

Understanding the rampage could help the doctors on the front lines treat the fraction of infected people who become desperately and sometimes mysteriously ill. Does a dangerous, newly observed tendency to blood clotting transform some mild cases into life-threatening emergencies? Is an overzealous immune response behind the worst cases, suggesting treatment with immune-suppressing drugs could help? What explains the startlingly low blood oxygen that some physicians are reporting in patients who nonetheless are not gasping for breath? “Taking a systems approach may be beneficial as we start thinking about therapies,” says Nilam Mangalmurti, a pulmonary intensivist at the Hospital of the University of Pennsylvania (HUP).
Related story

A patient on a ventilator
For survivors of severe COVID-19, beating the virus is just the beginning

What follows is a snapshot of the fast-evolving understanding of how the virus attacks cells around the body, especially in the roughly 5% of patients who become critically ill. Despite the more than 1000 papers now spilling into journals and onto preprint servers every week, a clear picture is elusive, as the virus acts like no microbe humanity has ever seen. Without larger, prospective controlled studies that are only now being launched, scientists must pull information from small studies and case reports, often published at warp speed and not yet peer reviewed. “We need to keep a very open mind as this phenomenon goes forward,” says Nancy Reau, a liver transplant physician who has been treating COVID-19 patients at Rush University Medical Center. “We are still learning.”
The infection begins

When an infected person expels virus-laden droplets and someone else inhales them, the novel coronavirus, called SARS-CoV-2, enters the nose and throat. It finds a welcome home in the lining of the nose, according to a preprint from scientists at the Wellcome Sanger Institute and elsewhere. They found that cells there are rich in a cell-surface receptor called angiotensin-converting enzyme 2 (ACE2). Throughout the body, the presence of ACE2, which normally helps regulate blood pressure, marks tissues vulnerable to infection, because the virus requires that receptor to enter a cell. Once inside, the virus hijacks the cell’s machinery, making myriad copies of itself and invading new cells.

As the virus multiplies, an infected person may shed copious amounts of it, especially during the first week or so. Symptoms may be absent at this point. Or the virus’ new victim may develop a fever, dry cough, sore throat, loss of smell and taste, or head and body aches.

If the immune system doesn’t beat back SARS-CoV-2 during this initial phase, the virus then marches down the windpipe to attack the lungs, where it can turn deadly. The thinner, distant branches of the lung’s respiratory tree end in tiny air sacs called alveoli, each lined by a single layer of cells that are also rich in ACE2 receptors.

Normally, oxygen crosses the alveoli into the capillaries, tiny blood vessels that lie beside the air sacs; the oxygen is then carried to the rest of the body. But as the immune system wars with the invader, the battle itself disrupts this healthy oxygen transfer. Front-line white blood cells release inflammatory molecules called chemokines, which in turn summon more immune cells that target and kill virus-infected cells, leaving a stew of fluid and dead cells—pus—behind. This is the underlying pathology of pneumonia, with its corresponding symptoms: coughing; fever; and rapid, shallow respiration. Some COVID-19 patients recover, sometimes with no more support than oxygen breathed in through nasal prongs.

But others deteriorate, often quite suddenly, developing a condition called acute respiratory distress syndrome (ARDS). Oxygen levels in their blood plummet and they struggle ever harder to breathe. On x-rays and computerized tomography scans, their lungs are riddled with white opacities where black space—air—should be. Commonly, these patients end up on ventilators. Many die. Autopsies show their alveoli became stuffed with fluid, white blood cells, mucus, and the detritus of destroyed lung cells (see graphic).
An invader’s impact

In serious cases, SARS-CoV-2 lands in the lungs and can do deep damage there. But the virus, or the body’s response to it, can injure many other organs. Scientists are just beginning to probe the scope and nature of that harm.

Some clinicians suspect the driving force in many gravely ill patients’ downhill trajectories is a disastrous overreaction of the immune system known as a “cytokine storm,” which other viral infections are known to trigger. Cytokines are chemical signaling molecules that guide a healthy immune response; but in a cytokine storm, levels of certain cytokines soar far beyond what’s needed, and immune cells start to attack healthy tissues. Blood vessels leak, blood pressure drops, clots form, and catastrophic organ failure can ensue.

Some studies have shown elevated levels of these inflammation-inducing cytokines in the blood of hospitalized COVID-19 patients. “The real morbidity and mortality of this disease is probably driven by this out of proportion inflammatory response to the virus,” says Jamie Garfield, a pulmonologist who cares for COVID-19 patients at Temple University Hospital.

But others aren’t convinced. “There seems to have been a quick move to associate COVID-19 with these hyperinflammatory states. I haven’t really seen convincing data that that is the case,” says Joseph Levitt, a pulmonary critical care physician at the Stanford University School of Medicine.

He’s also worried that efforts to dampen a cytokine response could backfire. Several drugs targeting specific cytokines are in clinical trials in COVID-19 patients. But Levitt fears those drugs may suppress the immune response that the body needs to fight off the virus. “There’s a real risk that we allow more viral replication,” Levitt says.

Meanwhile, other scientists are zeroing in on an entirely different organ system that they say is driving some patients’ rapid deterioration: the heart and blood vessels.
Striking the heart

In Brescia, Italy, a 53-year-old woman walked into the emergency room of her local hospital with all the classic symptoms of a heart attack, including telltale signs in her electrocardiogram and high levels of a blood marker suggesting damaged cardiac muscles. Further tests showed cardiac swelling and scarring, and a left ventricle—normally the powerhouse chamber of the heart—so weak that it could only pump one-third its normal amount of blood. But when doctors injected dye in the coronary arteries, looking for the blockage that signifies a heart attack, they found none. Another test revealed why: The woman had COVID-19.

How the virus attacks the heart and blood vessels is a mystery, but dozens of preprints and papers attest that such damage is common. A 25 March paper in JAMA Cardiology documented heart damage in nearly 20% of patients out of 416 hospitalized for COVID-19 in Wuhan, China. In another Wuhan study, 44% of 138 hospitalized patients had arrhythmias.

The disruption seems to extend to the blood itself. Among 184 COVID-19 patients in a Dutch ICU, 38% had blood that clotted abnormally, and almost one-third already had clots, according to a 10 April paper in Thrombosis Research. Blood clots can break apart and land in the lungs, blocking vital arteries—a condition known as pulmonary embolism, which has reportedly killed COVID-19 patients. Clots from arteries can also lodge in the brain, causing stroke. Many patients have “dramatically” high levels of D-dimer, a byproduct of blood clots, says Behnood Bikdeli, a cardiovascular medicine fellow at Columbia University Medical Center.

“The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19,” Bikdeli says.

Infection may also lead to blood vessel constriction. Reports are emerging of ischemia in the fingers and toes—a reduction in blood flow that can lead to swollen, painful digits and tissue death.

The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19.
Behnood Bikdeli, Columbia University Irving Medical Center

In the lungs, blood vessel constriction might help explain anecdotal reports of a perplexing phenomenon seen in pneumonia caused by COVID-19: Some patients have extremely low blood-oxygen levels and yet are not gasping for breath. It’s possible that at some stages of disease, the virus alters the delicate balance of hormones that help regulate blood pressure and constricts blood vessels going to the lungs. So oxygen uptake is impeded by constricted blood vessels, rather than by clogged alveoli. “One theory is that the virus affects the vascular biology and that’s why we see these really low oxygen levels,” Levitt says.

If COVID-19 targets blood vessels, that could also help explain why patients with pre-existing damage to those vessels, for example from diabetes and high blood pressure, face higher risk of serious disease. Recent Centers for Disease Control and Prevention (CDC) data on hospitalized patients in 14 U.S. states found that about one-third had chronic lung disease—but nearly as many had diabetes, and fully half had pre-existing high blood pressure.

Mangalmurti says she has been “shocked by the fact that we don’t have a huge number of asthmatics” or patients with other respiratory diseases in HUP’s ICU. “It’s very striking to us that risk factors seem to be vascular: diabetes, obesity, age, hypertension.”

Scientists are struggling to understand exactly what causes the cardiovascular damage. The virus may directly attack the lining of the heart and blood vessels, which, like the nose and alveoli, are rich in ACE2 receptors. Or perhaps lack of oxygen, due to the chaos in the lungs, damages blood vessels. Or a cytokine storm could ravage the heart as it does other organs.

“We’re still at the beginning,” Krumholz says. “We really don’t understand who is vulnerable, why some people are affected so severely, why it comes on so rapidly … and why it is so hard [for some] to recover.”
Multiple battlefields

The worldwide fears of ventilator shortages for failing lungs have received plenty of attention. Not so a scramble for another type of equipment: dialysis machines. “If these folks are not dying of lung failure, they’re dying of renal failure,” says neurologist Jennifer Frontera of New York University’s Langone Medical Center, which has treated thousands of COVID-19 patients. Her hospital is developing a dialysis protocol with different machines to support additional patients. The need for dialysis may be because the kidneys, abundantly endowed with ACE2 receptors, present another viral target.

According to one preprint, 27% of 85 hospitalized patients in Wuhan had kidney failure. Another reported that 59% of nearly 200 hospitalized COVID-19 patients in and near Wuhan had protein and blood in their urine, suggesting kidney damage. Those with acute kidney injury (AKI), were more than five times as likely to die as COVID-19 patients without it, the same Chinese preprint reported.

Medical staff work to help a COVID-19 patient in an intensive care unit in Italy.
Antonio Masiello/Getty Images

“The lung is the primary battle zone. But a fraction of the virus possibly attacks the kidney. And as on the real battlefield, if two places are being attacked at the same time, each place gets worse,” says Hongbo Jia, a neuroscientist at the Chinese Academy of Sciences’s Suzhou Institute of Biomedical Engineering and Technology and a co-author of that study.

Viral particles were identified in electron micrographs of kidneys from autopsies in one study, suggesting a direct viral attack. But kidney injury may also be collateral damage. Ventilators boost the risk of kidney damage, as do antiviral drugs including remdesivir, which is being deployed experimentally in COVID-19 patients. Cytokine storms also can dramatically reduce blood flow to the kidney, causing often-fatal damage. And pre-existing diseases like diabetes can boost the risk of AKI. “There is a whole bucket of people who already have some chronic kidney disease who are at higher risk for acute kidney injury,” says Suzanne Watnick, chief medical officer at Northwest Kidney Centers.
Buffeting the brain

Another striking set of symptoms in COVID-19 patients centers on the brain and central nervous system. Frontera says neurologists are needed to assess 5% to 10% of coronavirus patients at her hospital. But she says that “is probably a gross underestimate” of the number whose brains are struggling, especially because many are sedated and on ventilators.

Frontera has seen patients with the brain inflammation encephalitis, with seizures, and with a “sympathetic storm,” an immune response that’s the brain’s version of a cytokine storm. Some people with COVID-19 briefly lose consciousness. Others have strokes. Many report losing their sense of smell. And Frontera and others wonder whether in some cases, infection depresses the brain stem reflex that senses oxygen starvation. This is another explanation for anecdotal observations that some patients aren’t gasping for air, despite dangerously low blood oxygen levels.

ACE2 receptors are present in the neural cortex and brain stem, says Robert Stevens, an intensive care physician at Johns Hopkins Medicine. But it’s not known under what circumstances the virus penetrates the brain and interacts with these receptors. That said, the coronavirus behind the 2003 severe acute respiratory syndrome (SARS) epidemic—a close cousin of today’s culprit—could infiltrate neurons and sometimes caused encephalitis. On 3 April, a case study in the International Journal of Infectious Diseases, from a team in Japan, reported traces of new coronavirus in the cerebrospinal fluid of a COVID-19 patient who developed meningitis and encephalitis, suggesting it, too, can penetrate the central nervous system.

A 58-year-old woman with COVID-19 developed encephalitis, resulting in tissue damage in the brain (arrows).
N. Poyiadji et al., Radiology, (2020) doi.org/10.1148/radiol.2020201187

But other factors could be damaging the brain. For example, a cytokine storm could cause brain swelling, and the blood’s exaggerated tendency to clot could trigger strokes. The challenge now is to shift from conjecture to confidence, at a time when staff are focused on saving lives, and even neurologic assessments like inducing the gag reflex or transporting patients for brain scans risk spreading the virus.

Last month, Sherry Chou, a neurologist at the University of Pittsburgh Medical Center, began to organize a worldwide consortium that now includes 50 centers to draw neurological data from care patients already receive. The early goals are simple: Identify the prevalence of neurologic complications in hospitalized patients and document how they fare. Longer term, Chou and her colleagues hope to gather scans, lab tests, and other data to better understand the virus’ impact on the nervous system, including the brain.

Chou speculates about a possible invasion route: through the nose, then upward and through the olfactory bulb—explaining reports of a loss of smell—which connects to the brain. “It’s a nice sounding theory,” she says. “We really have to go and prove that.”

Most neurological symptoms “are reported from colleague to colleague by word of mouth,” Chou adds. “I don’t think anybody, and certainly not me, can say we’re experts.”
Reaching the gut

In early March, a 71-year-old Michigan woman returned from a Nile River cruise with bloody diarrhea, vomiting, and abdominal pain. Initially doctors suspected she had a common stomach bug, such as Salmonella. But after she developed a cough, doctors took a nasal swab and found her positive for the novel coronavirus. A stool sample positive for viral RNA, as well as signs of colon injury seen in an endoscopy, pointed to a gastrointestinal (GI) infection with the coronavirus, according to a paper posted online on in The American Journal of Gastroenterology (AJG).

Her case adds to a growing body of evidence suggesting the new coronavirus, like its cousin SARS, can infect the lining of the lower digestive tract, where the crucial ACE2 receptors are abundant. Viral RNA has been found in as many as 53% of sampled patients’ stool samples. And in a paper in press at Gastroenterology, a Chinese team reported finding the virus’ protein shell in gastric, duodenal, and rectal cells in biopsies from a COVID-19 patient. “I think it probably does replicate in the gastrointestinal tract,” says Mary Estes, a virologist at Baylor College of Medicine.

Recent reports suggest up to half of patients, averaging about 20% across studies, experience diarrhea, says Brennan Spiegel of Cedars-Sinai Medical Center in Los Angeles, co–editor-in-chief of AJG. GI symptoms aren’t on CDC’s list of COVID-19 symptoms, which could cause some COVID-19 cases to go undetected, Spiegel and others say. “If you mainly have fever and diarrhea, you won’t be tested for COVID,” says Douglas Corley of Kaiser Permanente, Northern California, co-editor of Gastroenterology.

The presence of virus in the GI tract raises the unsettling possibility that it could be passed on through feces. But it’s not yet clear whether stool contains live, infectious virus, not just RNA and proteins. To date, “We have no evidence” that fecal transmission is important, says coronavirus expert Stanley Perlman of the University of Iowa. CDC says that based on experiences with SARS and with the virus that causes Middle East respiratory syndrome, another dangerous cousin of the new coronavirus, the risk from fecal transmission is probably low.

The intestines are not the end of the disease’s march through the body. For example, up to one-third of hospitalized patients develop conjunctivitis—pink, watery eyes—although it’s not clear that the virus directly invades the eye. Other reports suggest liver damage: More than half of COVID-19 patients hospitalized in two Chinese centers had elevated levels of enzymes indicating injury to the liver or bile ducts, according to two preprints. But several experts told Science that direct viral invasion isn’t likely the culprit. They say other events in a failing body, like drugs or an immune system in overdrive, are more likely driving the liver damage.

This map of the devastation that COVID-19 can inflict on the body is still just a sketch. It will take years of painstaking research to sharpen the picture of its reach, and the cascade of cardiovascular and immune effects it might set in motion. As science races ahead, from probing tissues under microscopes to testing drugs on patients, the hope is for treatments more wily than the virus that has stopped the world in its tracks.

The University of Louisville coming up HUGE!

I don't pay attention to Twitter too much, but this was a headline in an email from them, so I had to check it out.

Quote:University of Louisville researchers have developed a technology that is believed to block the novel coronavirus SARS-CoV-2 from infecting human cells.

The technology is based on a piece of synthetic DNA – an “aptamer” – which targets and binds with a human protein called nucleolin. Early tests show that this aptamer may stop viruses, including novel coronavirus, from “hijacking” nucleolin to replicate inside the body.

UofL is seeking to fast-track development, including application to the Food and Drug Administration for approval to start treating patients seriously affected with COVID-19.

The aptamer was discovered by UofL’s Paula Bates, John Trent and Don Miller, who have applied it in a variety of ways, most notably as a potential therapeutic drug against multiple types of cancer. With the current global pandemic of coronavirus and the COVID-19 disease it causes, Bates partnered with fellow researcher Kenneth Palmer to apply the technology once again.

“Like many scientists, as soon as I heard about the new coronavirus, I wanted to help and started to think about how my area of research might intersect with coronavirus research efforts,” said Bates, a professor of medicine. “I am fortunate to be at UofL, which is one of the few places in the country where we have the facilities to do experiments using the SARS-CoV-2 virus.”

Palmer, director of UofL’s Center for Predictive Medicine for Biodefense and Emerging Infectious Diseases (CPM), conducted proof-of-concept experiments showing the aptamer was effective against the virus at doses previous research has shown to be safe in patients. Palmer also is working on another potential COVID-19 treatment, Q-Griffithsin, developed at UofL in partnership with the National Cancer Institute and the University of Pittsburgh.

The CPM houses UofL’s Regional Biocontainment Laboratory, one of only 12 regional and two national biocontainment labs in the United States and the only one in Kentucky. Established with support from the NIH to conduct research with infectious agents, the lab includes Biosafety Level 3 facilities built to the most exacting federal safety and security standards. The stringently secure facilities protect researchers and the public from exposure to the pathogens being investigated.

After I just posted about a vaccine probably being 18 months to two years away, this pops up.

It sounds like a vaccine, but they don't say vaccine and pretty much make it sound like a treatment, which, if it stops the coronavirus from infecting other cells, why wouldn't they just inject everyone before they get the coronavirus and use it as a vaccine?

I haven't checked out Yahoo! or any news sites today, so is this being reported anywhere else?

I'm probably going to go and get one of the drive-thru tests on Monday. I go back to work soon and want to know. They have the antibody test, so if I've had it and it passed, I should be able to find out.

I have asthma, so am technically at risk, although the tests are officially open to anyone that wants them come Monday. I've had a dry cough for about 2 months that I'd like to know about. My allergies suck, and tis the season for that sort of drainage, but you never know.

I venture a guess that I'm fine. I run several times a week, lift weights on the regular, and eat tons of greens. I'm still able to do all of my normal exercise with no real issue. If I have/have had it I'm one of the asymptomatics.

(04-22-2020, 07:22 PM)BFritz21 Wrote: The University of Louisville coming up HUGE!

I don't pay attention to Twitter too much, but this was a headline in an email from them, so I had to check it out.




After I just posted about a vaccine probably being 18 months to two years away, this pops up.

It sounds like a vaccine, but they don't say vaccine and pretty much make it sound like a treatment, which, if it stops the coronavirus from infecting other cells, why wouldn't they just inject everyone before they get the coronavirus and use it as a vaccine?

I haven't checked out Yahoo! or any news sites today, so is this being reported anywhere else?

Vaccines are technically dead versions of viruses that trigger similar immune responses as live ones, thus giving the vaccinated subject an immunity.  That's how I've always understood it.  If it's not using that method, then it's a treatment and not a vaccine.

(04-22-2020, 07:22 PM)BFritz21 Wrote: The University of Louisville coming up HUGE!

I don't pay attention to Twitter too much, but this was a headline in an email from them, so I had to check it out.




After I just posted about a vaccine probably being 18 months to two years away, this pops up.

It sounds like a vaccine, but they don't say vaccine and pretty much make it sound like a treatment, which, if it stops the coronavirus from infecting other cells, why wouldn't they just inject everyone before they get the coronavirus and use it as a vaccine?

I haven't checked out Yahoo! or any news sites today, so is this being reported anywhere else?

Vaccines cause your immune system to produce antibodies. When your body needs those antibodies it ramps up production even years after being vaccinated.

This treatment doesn’t cause your body to produce antibodies thus it isn’t a vaccine.

Scary week for me.

My company arguably falls in the essential category. While we could have easily closed down due to limited work, the powers that be elected to go to a 40 hour week of 10 hour days Monday - Thursday, allowing the entire facility to be closed and empty for 3 days to hopefully have a clean building come Monday mornings.

Monday morning we got word that a coworker was out the last two days of last week because a family member got tested. The family member works in a correctional facility with a big outbreak, so there was definite concern the employee would be infected if the result was positive. It turns out the family member received a positive result on Saturday, so the employee was tested and everyone was holding their breath Monday and Tuesday awaiting results. They came back negative, and everyone had a sigh of relief. Suddenly word came out late last night that a different employee, who had not been in this week, has in fact tested positive and we would be closed today for his area to be deep cleaned. The message ended with a statement that there has not yet been a determination on Monday and beyond.

To me, that sounds like the intent is to call "all clear" and get everyone back in the building without having any idea of who else may have been infected by the individual, rather than shutting down for two weeks and having everyone who is symptom free return after the 14 days. For the first time since the beginning of the pandemic I feel like going to work is going to become a game of Russian Roulette.

From everything I've been able to gather one essential piece of equipment everyone should probably have is a oxygen/pulse sensor, those little dohickies that go on your finger. One of the tell tale signs is your oxygen level drops way off for no explained reason. Just about anything under 90 means you better seek medical attention quickly. Without oxygen in your blood stream you die. That's pretty basic stuff, but most people wait until it's really too late..The cough gets bad, high fever, etc.  Check your oxygen level daily if you can find a pulse/oxygen sensor. They are still available online so don't wait to get one. 

This idea of essential seems ambiguous at best anymore. It's essential if it's how you earn your living, but is it essential to the public at large? Here in South Carolina they're gambling with everyone's lives every day and opening almost everything again despite the risks. The day I start believing a politician who suggest people inject themselves with poison is the day I just give up and go ahead and drown myself. 

(04-24-2020, 10:39 AM)grampahol Wrote: From everything I've been able to gather one essential piece of equipment everyone should probably have is a oxygen/pulse sensor, those little dohickies that go on your finger. One of the tell tale signs is your oxygen level drops way off for no explained reason. Just about anything under 90 means you better seek medical attention quickly. Without oxygen in your blood stream you die. That's pretty basic stuff, but most people wait until it's really too late..The cough gets bad, high fever, etc.  Check your oxygen level daily if you can find a pulse/oxygen sensor. They are still available online so don't wait to get one. 

I think if you are relatively healthy, anything under 95 should be looked into. I’m sure Breech can give us some insight.

(04-24-2020, 10:46 AM)grampahol Wrote: This idea of essential seems ambiguous at best anymore. It's essential if it's how you earn your living, but is it essential to the public at large? Here in South Carolina they're gambling with everyone's lives every day and opening almost everything again despite the risks. The day I start believing a politician who suggest people inject themselves with poison is the day I just give up and go ahead and drown myself. 

Yup.  Despite a Stay At Home order here in VA, people are out and about continuously.  And there was an order to close all businesses which are not essential, but the same statement said stores which adhere to 10 or less patrons can stay open.  I have a coworker whose wife owns a brick and mortar store that buys and sells knick knacks and such, as well as rents space to vendors to peddle homemade goods and such.  There is absolutely nothing about what is done there that can come close to complying with what is deemed essential according to the available lists, and yet they can remain open for people to come in and browse because there are less than 10 customers inside at a given time.

(04-24-2020, 10:48 AM)michaelsean Wrote: I think if you are relatively healthy, anything under 95 should be looked into. I’m sure Breech can give us some insight.

You’re right, 95 and above is normal. If your oxygen level drops below 90 you won’t need a pulse oximeter because you will definitely feel short of breath. That’s someone with severe pneumonia, an asthma attack, or a life long smoker with a COPD flare up. If it’s that low you need an evaluation in the ER to determine the cause and if you need to be admitted.

Most people feel short of breath if it dips to 93.

I think a pulse oximeter a better tool to help determine how severe someone’s shortness of breath is and their response to treatment. But, your body will let you know if you’re short of breath or not.

An ice cream truck came through the neighborhood yesterday in Cleveland, and you can imagine what happened. A facebook post was made in our neighborhood group about it and loads of people said "let the kids be kids!" which I just couldn't ignore, lol. It resulted in an ER nurse getting into a "discussion" with me, or maybe argument. I don't like most of my neighbors anyway (who could like a Browns fan?), so I don't care if I look like an idiot trying to protect their own kids or my own family.

If both parties wear a mask, it's better than if both parties don't, just try not to touch your face during that short period of time. If I do have to get out of the house, I wear a mask and I try to get in and out as quickly as possible, mainly because I can sense myself wanting to touch the mask lol.

One big discussion I had was with their "we have to get back to normalcy". I want the Bengals to win a championship, just because I want to, doesn't mean it will happen, and it doesn't mean it will happen right now. You have to act based on data, not just willy nilly. For an ER Nurse to tell me data doesn't come into play, is odd, considering that's basically all they do - diagnoses and react to data.

The other big discussion surrounded wearing a mask. If you hear an ice cream truck the kids are going to automatically congregate and 95% of them over here are not wearing masks. Being an asymptomatic carrier at their age, it's probably not a good thing. They're petri dishes.

This nurse also told me she's at higher risk because she's a nurse but with all proper precautions she is fine, and she doesn't wear a mask in public. I told her that's interesting, but if I walk through a minefield and I come out fine, it doesn't mean the minefield was safe. It's very easy for me to see people who give personal experience and try to apply it to everyone, unfortunately that's not how it works but it's the way our brain works. "This is my experience, so it must be true" is an immature view.

Some of the stronger of us need to just wear the mask at the store. When I go to the store, I see 75% of people and employees wearing. It' sa shock at first, yes. But if you want to get back to a small percentage of normalcy, we have to do things we didn't before. It doesn't take long for people to be forced to new social norms, like, wearing a mask.

I see united airlines is going to give free masks ot passengers, but won't ask anyone to wear them. I think if they're breathable (which in my personal experience has been tough to find), you will be looked down upon if you're *not* wearing it. It's free (in that scenario). It's too bad in USA we can't give them out for free.

I visited Tokyo 15 years ago, and they had disposable umbrellas. I found that insane but it rains so much there (and in spurts, not all day necessarily), you could find a $1 umbrella on the street that probably didn't last longer than a day.

(04-29-2020, 07:18 AM)reuben.ahmed Wrote: An ice cream truck came through the neighborhood yesterday in Cleveland, and you can imagine what happened. A facebook post was made in our neighborhood group about it and loads of people said "let the kids be kids!" which I just couldn't ignore, lol. It resulted in an ER nurse getting into a "discussion" with me, or maybe argument. I don't like most of my neighbors anyway (who could like a Browns fan?), so I don't care if I look like an idiot trying to protect their own kids or my own family.

If both parties wear a mask, it's better than if both parties don't, just try not to touch your face during that short period of time. If I do have to get out of the house, I wear a mask and I try to get in and out as quickly as possible, mainly because I can sense myself wanting to touch the mask lol.

One big discussion I had was with their "we have to get back to normalcy". I want the Bengals to win a championship, just because I want to, doesn't mean it will happen, and it doesn't mean it will happen right now. You have to act based on data, not just willy nilly. For an ER Nurse to tell me data doesn't come into play, is odd, considering that's basically all they do - diagnoses and react to data.

The other big discussion surrounded wearing a mask. If you hear an ice cream truck the kids are going to automatically congregate and 95% of them over here are not wearing masks. Being an asymptomatic carrier at their age, it's probably not a good thing. They're petri dishes.

This nurse also told me she's at higher risk because she's a nurse but with all proper precautions she is fine, and she doesn't wear a mask in public. I told her that's interesting, but if I walk through a minefield and I come out fine, it doesn't mean the minefield was safe. It's very easy for me to see people who give personal experience and try to apply it to everyone, unfortunately that's not how it works but it's the way our brain works. "This is my experience, so it must be true" is an immature view.

Some of the stronger of us need to just wear the mask at the store. When I go to the store, I see 75% of people and employees wearing. It' sa shock at first, yes. But if you want to get back to a small percentage of normalcy, we have to do things we didn't before. It doesn't take long for people to be forced to new social norms, like, wearing a mask.

I see united airlines is going to give free masks ot passengers, but won't ask anyone to wear them. I think if they're breathable (which in my personal experience has been tough to find), you will be looked down upon if you're *not* wearing it. It's free (in that scenario). It's too bad in USA we can't give them out for free.

I visited Tokyo 15 years ago, and they had disposable umbrellas. I found that insane but it rains so much there (and in spurts, not all day necessarily), you could find a $1 umbrella on the street that probably didn't last longer than a day.

What did she say exactly? Because it sounds like she is full of BS.

Things certainly are different now as opposed to 3 months ago. I ventured out to Kroger to get a few things while wearing my mask. All the employees are wearing masks now but some of them not properly. A few had their masks over their mouth but under their nose. And one person had his on his chin not covering his mouth or nose at all. A news article the other day stated Kroger employees are now required to wear them. So maybe it is a training issue to get them to use them properly.

My dog was due for his heartworm prevention medication. He usually gets a shot that is good for 6 months. This time after calling the vet for advice he was put on a monthly tablet so he didn't have to go in for the injection. I had to call them from the parking lot, give them my card number for billing, and then they brought the medication out. As a precaution I popped the trunk and had them put it in there with my receipt. I'm glad my dog is still getting the preventive care he needs though and his veterinary clinic is using caution. So it worked out. He's due for his other shots in July so I hope things are better by then.

On another note, talk about bad timing, it seems I have a tooth that is going bad due to pain when chewing. I think it is an old filling that has started to break down from what I saw when I looked at it. I'm not too thrilled about the idea of going to a dentist even if I can find one that is willing to do the work. Having people with their hands and face that close to my mouth during this isn't something I would prefer. So I guess I'll have to see how bad it gets over time.

Anyway, things are certainly much different than they were a few months ago. I think for the most part we are getting used to it. We will probably be practicing social distancing for quite some time and wearing masks when in community places like grocery stores.