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yonza bam

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  1. It's early days, but 2020 is shaping up to be the warmest year, globally, since records began in the 19th century, and very probably the warmest year Earth has experienced since the end of the last Ice Age, 11,500 years ago. Usually, when a new record is set, it coincides with an above average intensity El Nino, which is a periodic warming of the tropical Pacific. This was the case during the record intensity 2016 El Nino (on a par with the then record 1997-98 event). 2016 is the current global temperature record year. El Ninos usually last for several months, straddling the end of one year, and the start of the following year. The global temperature anomalies for the first four months of the following year are almost always the most extreme, and this was the case in 2016. According to the NASA GISS data, 2016 was 1.02 C warmer than the average for 1951-80. The Jan-Apr anomaly averaged 1.26 C, but only some of this large anomaly would have been due to El Nino. Something else is going on, which I'll get to later. For comparison, the weak or non El Nino (ENSO neutral) years of 2017, 2018 and 2019 had global temperature anomalies of 0.92 C, 0.85 C and 0.98 C, respectively. The Jan-Apr average for those three years was 0.98C. The May-Dec average for 2017-19 was 0.89 C, or 0.09 C less than the Jan-Apr average. Despite no El Nino, the average anomaly for the first four months of 2020 was a whopping 1.19 C. If we assume that May-Dec monthly anomalies average the same 0.09 C less, this would give an annual global temperature anomaly of 1.13 C, obliterating the 2016 record in an ENSO neutral year. This is quite dramatic stuff, and the questions that arise are 1) is this the start of a global warming surge, probably due to positive feedback effects starting to kick in, and 2) if so, what's causing it? Most of the warming caused by greenhouse gases (GHGs) is not due to the direct reradiation of outgoing infrared radiation back to the surface. It's caused by positive feedback effects. For example, water vapour is a much more potent greenhouse gas than carbon dioxide, and the relatively modest amount of direct warming caused by CO2, methane, and other greenhouse gases, causes more water to evaporate from the ocean, greatly enhancing the initial warming. Cloud formation prevents this feedback effect from becoming 'runaway' global warming, which is what's believed to have happened on Venus. Other positive feedback effects include the reduction of snow and ice cover, decreasing Earth's albedo, so that more sunlight is absorbed, and the release of CO2 and methane from melting permafrost, and from warmer soils due to increased bacterial activity. The release of methane from methane ice below the sea bed as the sea temperature rises, particularly under the Arctic Ocean, has also received much attention, but this is more conjectural, although there's no doubt that vast amounts of methane in ice exist there. The ocean is the 'sleeping giant' of climate change. It's an enormous heat sink, and it's estimated that 94% of the extra energy trapped by GHGs is absorbed by the ocean, and most of that is transported to the depths. There is enormous potential for various positive feedback effects to kick in as a result of warming in the ocean, which are poorly handled by the computer models, so we don't hear much about them. It seems very likely that the recent strong anomalies in the early months of the year are due to heat being given off by the Arctic Ocean in winter. At first glance, this seems counter intuitive. Although the September minimum ice cover area in the Arctic Ocean has decreased considerably in recent years, winter cover has not changed much, but what has changed is the depth of the ice. Although satellite pictures show little change in winter area of Arctic Ocean sea ice, what they don't reveal is how much it has thinned. And, it's thinned a lot. Typically, it may only be a metre thick, when it was several metres thick in the past. Syukuro Manabe is a retired Japanese climatologist who spent most of his career working in the US, and was an early pioneer of computer modelling of greenhouse gas effects on climate, particularly in the area of coupled ocean-atmosphere modelling. A few years ago, I watched a Youtube video of him explaining how thinning Arctic Ocean ice in winter could have a profound effect on global climate. Annoyingly, I haven't been able to find it, since. When the ice is thick, the heat from the ocean can't get through to warm the air above. But, when the ice thins appreciably, it can permeate through to warm the air above. The water below the ice is about -2 C, while the air above may be -40 C or lower in winter. So, there is enormous potential for a positive feedback effect involving warming of the air above the Arctic Ocean in winter as the sea ice thins. And what goes on in the Arctic doesn't stay in the Arctic. This may be responsible for the high monthly global temperature anomalies in the Jan-Apr period in recent years. If it is, then the extremely high 2020 anomalies is cause for concern, as it might be an early indication that this largely unheralded, but potentially large, positive feedback effect may be about to take off. Many ice core studies in recent years have replaced the previous misconception that climate change is always a gradual process. Analysis of Greenland ice core samples have shown that there have been very rapid sustained temperature changes in Greenland of around 10 C in the past, occurring in just a few years. The ocean surface water mixes with water at depth. If it didn't, there would be no oxygen, and no life, in the deeper parts of the ocean. This mixing is dependent on salinity and temperature differences. Warmer surface water expands due to the heat, so is less dense than deeper water, and therefore less able to mix. But, the evaporation at the surface makes it more saline, and this makes it more likely to sink. Recent research concludes that, as the surface of the ocean gets warmer, it will become more stratified, and less prone to sinking. Presumably, this will mean that the 94% figure for the amount of energy trapped by GHGs that is absorbed by the ocean will drop, and there will be a surge in atmospheric warming as a result. Yet another potentially large feedback effect that you don't hear much about. Much of the CO2 produced by man goes into the ocean. This is dependent on the temperature of the ocean surface, and the amount of CO2 already dissolved. The colder regions absorb CO2, while the warmer regions actually outgas it. Therefore, as the oceans warm, there will be less uptake, and more outgassing. In theory, the ocean could eventually become a net emitter of CO2 to the atmosphere, a nightmare scenario. The same thing happens with oxygen. Marine phytoplankton and seaweeds produce oxygen, but it is also absorbed from the air. As with CO2, this is temperature dependent, and some warmer regions may outgas oxygen to the point where they become anoxic 'dead zones'. Such zones are often seen close to shore, as a result of fertiliser runoff, but anoxic dead zones are increasingly being identified in warmer oceanic regions far from the influence of agriculture. In the distant past, mass extinction events were associated with high atmospheric CO2 levels, global warming, anoxia in the oceans, and a mysterious terrestrial charcoal layer, indicating that the world burned. High levels of atmospheric oxygen, due to outgassing from warmer oceans, and increased lightning due to a warmer climate is a plausible explanation for the charcoal layer. https://data.giss.nasa.gov/gistemp/tabledata_v4/GLB.Ts+dSST.txt
  2. This is interesting - very. Someone is suggesting that the MMR vaccine may be the reason why so few younger people are being seriously affected by COVID-19. Correlation is not causation, of course, and I'm sceptical, but definitely something worth looking into. Here's a cut and paste. MMR Vaccine Link to COVID-19: Fewer Deaths and Milder Cases from SARS-CoV-2 in Measles-Rubella Vaccinated Populations v4.0 MMR vaccine studied as possible way to protect vulnerable people from COVID-19 Principal Investigator: Jeff Gold; Co-Investigator: Dr. Larry P. Tilley, Diplomate, ACVIM (Internal Medicine) Correspondence: Text/Phone: 202-642-4445; Email: media@world.org Widely deployed measles-rubella containing vaccines (MRCV) including MMR, MR, and MMRV are theorized by the Principal Investigator to be why children, teenagers and other young adults often have few severe symptoms from COVID-19, and few deaths are attributed to COVID-19 in young age groups. We believe it is possible MRCV are responsible for widely varying outcomes related to COVID-19 in different age groups and different countries. COVID-19 has what appears to be a clearly defined fatality rate pivot point close to 50 years old. From birth to age 49 the fatality rate from COVID-19 increases only slightly with each year of age. After age 50 the fatality rate from COVID-19 climbs quickly and steadily. This is very different from most other diseases. The MMR (measles, mumps, rubella) vaccine was introduced in 1971. It was most commonly given as a single vaccination from 1971-1978 then as a set of two vaccinations at least 28 days apart starting in 1979. Based upon its year of introduction, most people today aged 49 and under would likely have had at least one MMR vaccination, and those 41 and under would most likely have had two MMR vaccinations. This vaccine history may be a possible explanation for a COVID-19 death rate pivot point close to age 50. The fact that some aged 40-49 only received a single MRCV dose is a possible reason why this age range has a marginally higher death rate than those under 40. In countries where vaccination "catch up" programs have been instituted in recent decades there appears to be the lowest incidence of death from COVID-19, and in a few countries no deaths at all. In many of these countries, two doses of MRCV were given to older teenagers, and in some cases also to young adults, in addition to children. Full article here https://world.org/COVID-19-MMR.pdf PS Looks like page 5 has disappeared.
  3. In 1918-19, Spanish flu infected around 500 million people, almost a third of the world population at the time. It's believed to have killed an estimated 20 to 50 million people, although the often quoted case fatality rate of 2.5% would give a figure of 12.5 million. The first wave, in the spring of 1918, was generally mild, affecting mainly old people. As with typical flu, people recovered after about a week. The second wave, in autumn, was very different. People sometimes died within hours of developing symptoms, their skin turning blue, and their lungs filling with fluid. Others would hang on for longer, eventually succumbing to secondary bacterial infection. It was before the discovery of antibiotics.The third wave in the spring of 1919, had twice the mortality of the first wave, but was much less deadly than the second wave. In the deadly second wave, nearly half of all deaths were in young adults aged 20-40, whereas in the first wave, young, healthy adults recovered easily. Something had changed big time, but what? If you read up on the subject, you'll frequently come across the assertion that the virus mutated to a more deadly form, and mutation is something that flu viruses do best. But, there's actually no evidence for the deadly second wave being due to the virus mutating. It's an assumption. Moreover, when such viruses mutate, they almost always mutate to a less deadly form, but 'fitter' in the Darwinian sense. Viruses are not 'interested' in killing the host, because that also kills the virus. They are only 'interested' in proliferating and spreading, and that is best achieved by only causing mild illness. Not causing any illness would be even better from the virus's point of view. So, what actually changed? In the current COVID-19 pandemic, it's becoming more and more clear that the severe hospitalised cases are just a tiny tip of a much larger iceberg of mild and asymptomatic cases. There may have been many mild and asymptomatic cases during the first wave of the Spanish flu also, particularly among the fitter younger population. It's known that those who had a typical bad case of flu during the first wave were immune to infection during the second wave. The more severe illness would have resulted in them producing lots of antibodies, which would have prevented future infection. Now, this is where things start to get a bit speculative. I've read a suggestion that those who had a mild or asymptomatic infection in the first wave would probably not have made enough antibodies to protect them from future infection. Moreover, the initial infection may have sensitised their immune systems, so that subsequent infection resulted in what's commonly referred to as a 'cytokine storm'. This is similar to an extreme allergic reaction. For example, there's a tiny number of people who, when stung by a bee for the first time, have no adverse immune response. But, this initial provocation changes the immune system in a way that, if they are stung by a bee in the future, even if the second bee sting is decades later, they could have what's called an 'anaphylactic shock' reaction, and could die as a result. I'm more inclined to believe that the explanation for the second wave being so much more deadly than the first wave, is that the immune system of those mildly affected in the first wave was sensitised in a way that made it overreact to future infection, than that the flu virus mutated to a much more deadly strain. If that's the case, is it possible that something similar might happen with COVID-19? This pandemic has been ongoing for four months now, and children have been largely immune to its effects, although there have probably been many asymptomatic infections among children. Now, we are seeing the emergence of a disease in the UK, in children infected by SARS-CoV-2, driven by a systemic overreaction of the immune response, resulting in what doctors are calling toxic shock syndrome, or atypical Kawasaki disease. When I first heard about it, I assumed that it was something that had probably been around since the beginning of the pandemic in the UK, but had not been identified. That idea now seems to be wrong. This is a very recent development. Doctors are saying that the situation with COVID-19 is 'fluid and rapidly changing'. So, what do they actually mean by 'fluid'? That the virus is mutating, or that our immune systems are 'mutating' after exposure to it? I think the children who are suffering from toxic shock syndrome, or atypical Kawasaki disease, are either being reinfected, or the virus is reactivating from a previous infection, after lying dormant inside cells, and causing an extreme systemic immune hypersensitivity reaction. It's possible that the virus is changing our immune systems, and that there is going to be a 'second wave' in which previously mild or asymptomatic cases who are reinfected will have serious symptoms, but it will be a small minority of people who are genetically predisposed, who will be most at risk from this.
  4. From The Independent: An urgent alert has been issued to doctors about a new coronavirus-related condition seen emerging in children. The warning says there has been an “apparent rise in the number of children of all ages presenting with a multi-system inflammatory state requiring intensive care across London and also other regions of the UK” over the last three weeks. The NHS England alert, shared by the Paediatric Intensive Care Society on Sunday evening, adds: “There is a growing concern that a [Covid-19] related inflammatory syndrome is emerging in children in the UK, or that there may be another, as yet unidentified, infectious pathogen associated with these cases.” It is not known how many children have been affected, however the illness has been seen in children who have tested positive for the novel coronavirus, as well as those who have not had the disease. The condition has the characteristics of severe Covid-19, and also shares certain features of toxic shock syndrome and atypical Kawasaki Disease, according to the alert. Abdominal pain and gastrointestinal symptoms “have been a common feature” of the illness, as has cardiac inflammation. Doctors have been asked to urgently refer any patients showing signs of these.
  5. Yet another Guardian article claiming systemic racism in the US health system, because black people make up a majority of COVID-19 deaths in some places, despite being a minority in the community. As an example, 64% of patients in St Louis are black, despite only being 45% of the population. Here's a quote from today's article: "COVID-19 has begun to divide the country between those ready to explore the structural racism ingrained in America's public health care outcomes, and those who are not". https://www.theguardian.com/world/2020/apr/25/coronavirus-racial-disparities-african-americans The London mayor, Sadiq Khan, had a similar article imputing systemic racism in health care printed in the Guardian last week. This is a cut & paste from a post I made elsewhere. Saves me typing it all out again. For some reason, it's posting with the blue cut & paste background. The virus also takes a more deadly toll in males, irrespective of ethnicity, which is almost certainly due to genes. Obesity is very strongly associated with more severe COVID-19, and black Americans are more prone to obesity. They also have a higher incidence of the metabolic syndrome diseases - diabetes, hypertension, cardiovascular disease, kidney disease - that are associated with obesity, and are the underlying health conditions seen in severe COVID-19. Although black American males actually smoke slightly less than white American males, they are three times more likely to get lung cancer. All of these conditions - obesity, metabolic syndrome and cancer - are associated with chronic activation of the NF-kB driven immune response, which is also activated in COVID-19. It seems that they are more genetically predisposed to chronic activation, and some genetic differences associated with increased NF-kB activation include immune system, receptor, and enzyme polymorphisms, particularly enzymes in the cytochrome P450 superfamily. It's the overly strong immune system activation that causes the disease symptoms. Also, they tend to have less vitamin D, which has been shown in some research to have a protective effect against the virus, and probably live in more air polluted regions, which has also been identified as a risk factor.
  6. Evidence continues to mount that smoking helps to prevent COVID-19 infection, or that it prevents severe disease, requiring hospitalisation. This was first seen in China, where there is a very high smoking rate among males, but the number of daily smokers was under represented by more than half in hospitalised cases. The same thing has been seen in France, and trials are now underway there with nicotine patches, although I tend to think patches may not be a good substitute for nicotine absorbed directly into the lungs. https://news.sky.com/story/coronavirus-nicotine-patches-to-be-tested-on-patients-after-study-suggests-smokers-less-likely-to-catch-covid-19-11977460 Smoking is pro-inflammatory, so you might expect it to worsen the harmful effects of COVID-19. I've a pretty convoluted hypothesis for what may be happening, so here goes. Nicotine binds to the acetylcholine NACH receptor as an agonist (activating it). The 'N' stands for nicotinic. This appears to cause narrowing of the arteries and hypertension. One way for the body to try to correct this would be to increase the number of ACE-2 receptors, and smokers are known to have more ACE-2 expression. The function of ACE-2 is to act as a counterbalance to the vasoconstricting angiotensin-2, by converting it to the vasodilating angiotensin-(1-7). So, it could also be used to counter the effects of nicotine. ACE-2 is also the receptor that the virus uses to enter cells, so you would expect increased expression to result in a higher risk of becoming infected. However, in patients severely affected by COVID-19, blood vessels are constricted in the lungs and elsewhere, resulting in reduced oxygen transport from the lungs and systemic hypertension. This probably results from the NF-kB driven immune response attempting to prevent infection by decreasing the expression of ACE-2. Since smokers have increased ACE-2 expression, they would be more resistant to the harmful effects of this decrease.
  7. New study, published in The Lancet, suggests that COVID-19 infection may cause diabetes: https://7news.com.au/news/health/coronavirus-may-trigger-diabetes-study-c-997082 It has been known for some time that underlying medical conditions, such as obesity, diabetes, hypertension, cardiovascular and kidney disease make the development of severe COVID-19 more likely. It's now becoming clear that this is a two way street. For example, the virus elicits the NF-kB driven immune response, which attempts to reduce infection by decreasing the expression of the ACE-2 receptor it uses to get into cells. This causes blood vessels to narrow, resulting in hypertension and increased risk of heart attacks. This is a quote from a 2010 paper: "In ACE2 deficient mice, alterations in glucose tolerance and reduced first phase insulin secretion have been described, suggesting a potential role of ACE2 in the development of diabetes". https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2992757/
  8. This is a big surprise. Similar studies in Europe reveal more like a 3% infection rate, and the WHO spokeswoman expressed disappointment at the low rate. The more people in the community who have been infected, the lower the case fatality, which is beginning to look like it's below 1%, maybe even 0.5%. Also, a great many of these positive antibody tests have been asymptomatic, which is also good news. Cut & paste Preliminary results from New York's first coronavirus antibody study show nearly 14 percent tested positive, meaning they had the virus at some point and recovered, Gov. Andrew Cuomo said Thursday. That equates to 2.7 million infections statewide -- more than 10 times the state's confirmed cases. The study, part of Cuomo's "aggressive" antibody testing launched earlier this week, is based on 3,000 random samples from 40 locations in 19 counties. While the preliminary data suggests much more widespread infection, it means New York's mortality rate is much lower than previously thought. As of Thursday, nearly 16,000 people in New York have died of virus-related complications. With 250,000-plus confirmed cases, the mortality rate would be as high as 16 percent. With 2.7 million cases, it would be around 0.5 percent -- much lower, though still much higher than the seasonal flu. Cuomo was quick to caution, though, that that the death toll was higher than even the state's own official report -- it counts deaths in hospitals and nursing homes, but not at-home deaths or other "probable" cases. In other words, the mortality rate is still hard to determine properly. New York City had a higher rate of antibodies (21.2 percent) than anywhere else in the state and accounted for 43 percent of the total tested. Long Island had a 16.7 percent positivity rate, while Westchester and Rockland counties saw 11.7 percent of their samples come up with the antibody. The rest of the state, which accounted for about a third of those studied, had a 3.6 percent positivity rate.
  9. That would be great, but I'm not optimistic. I just don't see any exit strategy. We're still at well over 700 deaths a day. Even if there were an easing of the lockdown, it would be piecemeal, and the last thing that would be allowed would be tourist bus trips. In addition, the timetables for the skeleton services aren't the regular summer timetables, so useless for planning.
  10. Why the US outsourced bat virus research to Wuhan (Cut & paste) The US National Institutes of Health (NIH) funded bat-coronavirus research in the Wuhan Institute of Virology in China to the tune of US$3.7 million, a recent article in the British newspaper Daily Mail revealed. Back in October 2014, the US government had placed a federal moratorium on gain-of-function (GOF) research – altering natural pathogens to make them more deadly and infectious – as a result of rising fears about a possible pandemic caused by an accidental or deliberate release of these genetically engineered monster germs. This was in part due to lab accidents at the US Centers for Disease Control and Prevention (CDC) in July 2014 that raised questions about biosafety at US high-containment labs. At that time, the CDC had closed two labs and halted some biological shipments in the wake of several incidents in which highly pathogenic microbes were mishandled by US government laboratories: an accidental shipment of live anthrax, the discovery of forgotten live smallpox samples and a newly revealed incident in which a dangerous influenza strain was accidentally shipped from the CDC to another lab. A CDC internal report described how scientists failed to follow proper procedures to ensure samples were inactivated before they left the lab, and also found “multiple other problems” with operating procedures in the anthrax lab. As such in October 2014, because of public health concerns, the US government banned all federal funding on efforts to weaponize three viruses – influenza, Middle East respiratory syndrome (MERS) and severe acute respiratory syndrome (SARS). It is understandable that the Chinese lab likely struggled with safety issues given the fact US labs share similar problems, and indeed in January 2018 the US Embassy in Beijing sent cables warning about the safety of the Wuhan lab and asked for help. Additionally, the embassy warned that researchers “showed that various SARS-like coronaviruses can interact with ACE2, the human receptor identified for SARS-coronavirus,” meaning bat coronaviruses can be transmitted to humans to cause SARS-like diseases.
  11. I mentioned in a previous post that Sweden was conducting an 'experiment' by having no lockdown like other countries. They've taken some measures, like closing secondary schools, while keeping primary schools open, but nothing like as strict as we're doing here and elsewhere. I'm getting the feeling that they may be about to pay the price. They have the same problem with the reporting of COVID-19 deaths that we have in the UK, in that deaths are under reported at the weekend and Mondays, while Tuesday sees an upsurge due to weekend deaths being added. Bearing that in mind, today (Tuesday) saw 185 deaths reported. For a country with a population of just 10.23 million, that's proportionately larger than the highest daily death tolls from Italy (919 March 27) and the UK (980 April 10), but still lower than Spain's (961 April 2).
  12. Something very 'fishy' going on in Japan. Reports of ambulances with very sick patients going to many hospitals and being told there's no room BBC article: Japan doctors warn of health system 'break down' as cases surge. https://www.bbc.co.uk/news/world-asia-52336388 Yet, here are the official figures for Japan (pop. 127 million), compared with the UK (pop. 67 million) Japan total cases 9,787 total deaths 190 UK total cases 114,217 Total deaths 15,464 Deaths in last 24 hours 888. Makes China look like a model of honesty and transparency.
  13. BBC article and video on the situation in Ecuador. The video is a shocker, but worth watching to get a feel for what might be going to happen on a much grander scale in Brazil, since president Bolsonaro doesn't think a 'little flu' is much to be concerned about. The WHO has warned about the potential effect of the virus in Africa, and I think Ecuador is a foretaste of what will happen there. https://www.bbc.co.uk/news/world-latin-america-52324218
  14. Had a meet with the manager about my retirement, again. He said he'd assumed that I had received all the figures from the relevant council dept, when he got my letter. Turns out retiring is a bit complicated, and you don't just hand in 4 weeks notice, as it takes at least 12 weeks before it gets processed, and I'd lose some serious money by leaving 8 weeks before it had all gone through. So, I'm handing in a new letter, asking to retire on 31 July, although it'll be before that, as I haven't taken any holidays this year.
  15. Huge increase in cardiac arrest deaths in New York City. This will be due to the same mechanism mentioned in the post about ventilation deaths, above. SARS-CoV-2 enters cells through the ACE-2 receptor. The immune system reduces expression of ACE-2 to prevent infection. The function of ACE-2 is to act as a counterbalance to the vasoconstrictive effects of angiotensin-2, by converting it to the vasodilator, angiotensin-(1-7). Greatly reduced expression of ACE-2 will therefore result in severe vasoconstriction, leading to hypertension (high blood pressure), and an increased incidence of cardiac arrest. A small amount of the increase may also be due to hospitals being overworked, resulting in reduced care for non COVID-19 patients.
  16. I'll be 67 in May, and made the decision to hand in 4 weeks notice to the council to finally retire. As I work on my own outdoors, I'm considered low risk, so have been working while other workers who work as a squad have been off work. Anyway, the manager said that, as I hadn't used up any of my annual leave this year, I'd be finished before the 4 weeks, which suits okay. I've been in the job 19 years. I've ordered new tyres for my bike, which is my preferred exercise. Age and slightly arthritic hips rule out jogging, but cycling doesn't aggravate hip arthritis. My current tyres are worn, and the extra friction that causes with the road surface, makes for heavy going up the hills, so I'm looking forward to flying up them with the new tyres.
  17. Fascinating graphic here, which shows daily death tolls in the UK from all the leading causes changing on a daily basis since early on in the COVID-19 epidemic to the present. The 2 leading causes of death are cancer and heart disease, and deaths from the virus now equal both categories combined. That's just hospital deaths. You get an impression of how bad it might have been without the lock down. https://public.flourish.studio/visualisation/1865109/
  18. Pneumonia, caused by inflammation of the lungs, typically as a result of infection with a virus, such as influenza, results in low blood levels of oxygen, which can become life threatening. Doctors who treat these patients in intensive care units (ICUs) are used to seeing patients unable to breathe, and use ventilators to force oxygen into their lungs at high pressure, thus oxygenating the blood. Using a ventilator is not a procedure that is taken lightly. The high pressure can damage the delicate small air sacs in the lungs. Some people who recover from pneumonia, have lasting damage to their lungs as a result of being ventilated. The blood of COVID-19 patients who end up in ICUs is also dangerously low in oxygen, resulting in them being put on ventilators. However, some doctors are now beginning to question whether this is appropriate in cases of COVID-19, because they do not present with typical pneumonia symptoms. Although their blood oxygen levels are low, they do not appear to have difficulty breathing. They can hold a conversation with a doctor, while a typical pneumonia patient can't finish a sentence. Two doctors who are trying to raise awareness about this are Dr. Cameron Kyle-Sidell, who works in intensive care in Brooklyn, and Dr. Luciano Gattinoni, a leading expert in mechanical ventilation who treated many COVID-19 patients in northern Italy. Both are of the opinion that, although it is imperative to oxygenate the blood of patients , high pressure ventilation may be doing more harm than good. It may actually be killing patients. An analogy that is made is two balloons , one made with thick rubber, and the other with thin rubber. Typical pneumonia patients with inflamed lungs containing fluid can be likened to the thick rubber balloon, which requires more pressure to inflate it. However, the same amount of pressure applied to the thin rubber lungs of COVID-19 patients may cause irreparable, sometimes fatal, damage. Dr. Gattinoni said that around 30% of COVID-19 patients were 'thick balloon' typical pneumonia types, while 70% were 'thin balloon' atypical types, and that one centre in central Europe, that had begun using different treatments for different types of COVID-19 patients, had not seen any deaths among those patients in its ICUs. But, a nearby hospital that was treating all patients with the standard ventilation procedures, had a 60% death rate. Dr. Kyle-Sidell said the atypical cases looked more like altitude sickness than the pneumonia cases that they were used to seeing. As if a plane full of Americans flying at 30,000 ft suddenly suffered catastrophic decompression. Within a few minutes, the passengers would resemble the COVID-19 patients he was dealing with. Dr. Gattinoni thinks the trouble with the atypical patients may lie with the web of small blood vessels (capillaries) in the lungs. "Is it possible that there's a problem with how the blood vessels regulate blood flow? That is, I guess, a possibility, which would be different to what we see in acute respiratory distress syndrome (ARDS)", he said. https://www.webmd.com/lung/news/20200407/doctors-puzzle-over-covid19-lung-problems I think he may be right about that. First, some background. I'm a layman, but I've been a science nerd all my life. I'm extra nerdy about subjects that interest me more, but on the subject of disease causation, I'm supernerd. There's an illness that runs in my family, and I became interested in researching it in libraries long before the Internet was a thing. The research snowballed into many other areas, and I wrote an online blog 10 years ago titled 'Integrative Theory of the Causation of Non-Communicable Diseases: Immune Mimicry Disease (IMD) Theory'. It's a 3 hour read, but that's without clicking on any of the 900+ PubMed links. http://www.imdtheory.blogspot.com It's hard to summarise, but here's the gist for the part that's relevant for this particular subject. Nuclear Factor-kappa Beta (NF-kB) is a 'master molecule' found inside cells, which has many important functions. One of these functions is the control of viruses and bacteria which establish latency inside cells, such as the herpes family. Human coronaviruses are not known to do this , but recent research confirms that bat coronaviruses do establish intracellular latency. Now, many researchers are convinced that cases of apparent reinfection of people who had been given the all clear, may instead be due to to the virus establishing intracellular latency, thus becoming undetectable, then reactivating, and bursting out of the cells again. Such pathogens are dealt with by the NF-kB driven immune response. A novel finding of my research is that this immune response attempts to prevent pathogens entering cells by closing down receptors used by the pathogen to enter cells. This can take three forms - reduced expression of receptors, reduced sensitivity of receptors (usually by phosphorylation), and receptor blockade by antibodies. I'll use the word 'suppression' for all three. When this suppression becomes chronic, illness can result. I believe that this is what's happening to the COVID-19 patients with atypical hypoxia. SARS-CoV-2 enters cells through the ACE-2 receptor. The NF-kB response to this will be to suppress the ACE-2 receptor. ACE-2 is both a receptor and an enzyme attached to the membranes of cells in the lungs, arteries, heart, kidney and intestines. Its main function is to act as a vasodilator, by countering the vasoconstricting effect of angiotensin 2, by reducing the amount of angiotensin 2 by cleaving it into the vasodilator, angiotensin (1-7). Therefore, chronic suppression of ACE-2 by NF-kB in order to prevent infection by SARS-CoV-2 will result in extreme vasoconstriction of the oxygen carrying small blood vessels of the lungs, resulting in the hypoxia seen in COVID-19 patients. Youtube video from Dr Cameron Kyle Sidell
  19. Scottish fishermen turn to food banks as COVID-19 devastates industry. Just another thing that no one saw coming. Bad weather and poor winter catches have contributed, but now the virus appears to have squashed demand, particularly for exports. Some UK supermarkets have also closed their fresh fish counters. https://www.theguardian.com/environment/2020/apr/10/scottish-fishermen-turn-to-food-banks-as-covid-19-devastates-industry
  20. Thanks, Tam. I never expected the thread to get as many visits, but maybe some googlers came across it, and decided to bookmark it. Good to see, anyway.
  21. Biggest UK daily death toll, yet, at 938. However, there's always a surge in UK deaths reporting on Tuesdays. It diminishes due to reduced manpower at the weekends, and this persists into Monday. Come Tuesday, there's a large increase due to the backlog of uncounted cases. Still, 938 is a lot. The UK has started counting 'community' deaths, but isn't including them in the hospital death stats. They're being counted in a separate database, which is updated once a week. France has also started counting community deaths, but has chosen to add them to the hospital deaths, which has resulted in a big increase in the daily death count. Sweden is 'interesting'. They decided not to follow the lock downs and social distancing that have been implemented elsewhere. They have taken some measures. For example, secondary schools are closed, but primary schools aren't. The latest daily death toll is 96, with 114 reported yesterday. The population of Sweden is around 10 million, so these numbers are quite big, but not as big as you might expect. Do the Swedes know something the rest of us don't? Probably not. This is terra incognita for everyone, but they're an independently minded lot, and like to do their own thing. I think the plan is to introduce more social isolation measures, but to do it more slowly. In my view, that's a gamble, but I'm really glad they're doing it. We need to know what works, and that means different countries trying out different strategies. Personally, I think they're in for a terrible time, because even if they were to implement the same lock down strategy as other countries tomorrow, the fact that they're almost on a par with UK daily deaths, relative to population, means that in the weeks it takes to see the curve begin to flatten, they'd be dealing with the UK equivalent of thousands of deaths a day. The plus side is that they'll get to the point where most people have been infected with it, and presumably become immune to it, more quickly than other countries. That means that normal life can resume again, or something like it. So, we might end up envying them, but probably not in the short term.
  22. A few days ago, epidemiologists at Imperial College London were predicting 7,000 to 20,000 UK COVID-19 deaths. We'll pass the 7,000 mark today or tomorrow. In today's Guardian, the Institute of Health Metrics and Evaluation, based in Seattle, and regarded as one of the foremost authorities in this field in the world, are predicting 66,314 UK deaths, more than Italy, Spain and France combined, and not far short of the 81,766 US deaths they predict. Frankly, I'm bamboozled. https://www.theguardian.com/world/2020/apr/07/how-can-coronavirus-models-get-it-so-wrong
  23. 60% of Antarctic cruise ship passengers test positive for COVID-19. Frankly, I find it appalling that people are still going on cruises after all that has happened. They are floating petri dishes. This one sailed from Australia on March 15, so it's not as if they didn't know what they might be getting into. 128 of 217 passengers and crew are infected, and the ship is currently sitting off Uruguay. No one is being allowed off, unless very ill, although it looks as if Australian and New Zealand nationals might be flying home, where they'll go into quarantine for 14 days. The second article on the link says that more than a dozen cruise ships are currently stuck at sea due to the virus. https://edition.cnn.com/2020/04/07/americas/greg-mortimer-cruise-ship-coronavirus-intl-hnk/index.html
  24. Good Scientific American article on what's involved in developing a vaccine for COVID-19. https://blogs.scientificamerican.com/observations/can-we-really-develop-a-safe-effective-coronavirus-vaccine/
  25. COVID-19 patients now being found to develop heart damage, and die of cardiac arrest. https://khn.org/news/mysterious-heart-damage-not-just-lung-troubles-befalling-covid-19-patients/ I'd guess that this happens because the heart expresses a lot of ACE-2 receptors, which is the entry point used by SARS-CoV-2 to enter cells. If that's right, we might be hearing about intestinal effects soon, as the intestines also express a lot of ACE-2 receptors.
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