Health New Coronavirus in China

the limit of humor and this year is cursed

year 2020, What else we should expect,

1, corovirus pandemia
2 mad weather, snowing at Greece at April (even today above 600 m)
3 a possible new 'hole of Ozon' at Antarctica
4 Chernobil abbandoned nuclear powerplant area is on fire, radiation from this fire is detected even to Athens
5 Oil has even negative prices (lower than cost of drilling)


what next?

maybe we see Batman in town?
250px-Gotham_City_Batman_Vol_3_14.png
 
Just some personal thoughts on [FONT=&quot]hydroxychloroquine and azythromycin: They should only be given to [/FONT][FONT=Helvetica Neue, Helvetica, Arial, sans-serif]Covid-19 patients with overactive immune systems. Remember the off label use for lupus and rheumatoid arthritis is to get the body's autoimmune response under control. If your body in fighting Covid-19 goes on an runaway auto-immune response the [/FONT] [FONT=Helvetica Neue, Helvetica, Arial, sans-serif]hydroxychloroquine will probably help. So before prescribing it test for excessive levels of cytokines. If over the threshold then go ahead and subscribe it to the patient. If you have a regular immune response, do not take it because it will lower your body's immune response and the Covid-19 virus will ravage your lungs. Not to mention that it can introduce arrhythmia. Now are there other immunosuppressant drugs with less side effects? I am sure.[/FONT]
 
Well, there goes that...

Preprint on patient group of 368 hospitalizedveterans with COVID-19. Hydroxychloroquine treatment: *higher* death rates thantreatment without HC. "Rates of death in the HC, HC+AZ, and no HC groupswere 27.8%, 22.1%, 11.4%, respectively."

Only if they're in the middle of a Cytokine storm, perhaps.


Also,
Dr. Fauci has announced that none of the anti-virals and other medications being tested have so far shown any promise.
 
Well, so much for freedom of speech on privately owned platforms...

#YouTube CEO Susan Wojcicki says anything that goes against the W.H.O. is a violation of YouTube policies. All content that isn't "medically substantiated," such as advising people take Vitamin C, will be removed by the platform.
YouTube should not be censoring videos that dispute WHO. They claimed no evidence for human-to-human transmission, airborne transmission, travel bans, masks. WHO isn’t always wrong. But they are humans, not oracles, and we must be allowed to rebut.
@SusanWojcicki
, please fix!

No buying of your films or tv lady.
 
So much for letting her rip:
Covid-19 deaths per million as off 4/22/20: Sweden, 191.8 USA, 137.3 Denmark: 66.1.

Sweden has 10 times the number of deaths of its "Nordic" neighbors. Guess they just are willing to absorb the hit; it's only older and sick people, after all.


Austria (and Germany)...handy indeed.

"Every deceased person who has previously been tested positive for COVID is listed in the statistics as “COVID dead person”"In Austria if you test positive and die, you're counted. Die without a positive test, you're not counted. Handy.

Croatia:"Close contact with a person with COVID-19 confirmed who does not have any signs of illness is routinely not tested."Croatia aren't even doing contact tracing. They only test if you need hospital and are not counting nursing home deaths.

 
Science & Society
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and the Central Nervous System


Fernanda G.De Felice(1,2,3)
Sérgio T.Ferreira(1,6)

https://doi.org/10.1016/j.tins.2020.04.004
Get rights and content


Emerging evidence indicates that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of coronavirus disease 2019 (COVID-19), can cause neurological complications. We provide a brief overview of these recent observations and discuss some of their possible implications. In particular, given the global dimension of the current pandemic, we highlight the need to consider the possible long-term impact of COVID-19, potentially including neurological and neurodegenerative disorders.

Keywords

COVID-19
neurological alterations
neurodegenerative diseases
encephalitis
anosmia
Parkinson’s disease

Coronaviruses, SARS-CoV-2, and Their Impact on Multiple Organ Systems

CoVs are the largest group of viruses that cause respiratory and gastrointestinal infections, and have been responsible for three pandemics in the past 18 years: SARS in 2002/2003, Middle East respiratory syndrome (MERS) in 2012 and, currently, COVID-19. SARS-CoV-2, the etiologic agent of COVID-19, is a novel member of the human CoV family that emerged in China in late 2019. The symptoms of COVID-19 can include fever, cough, loss of smell and taste, sore throat, leg pain, headache, diarrhea, and fatigue. Although most patients infected with SARS-CoV-2 are asymptomatic or develop mild to moderate symptoms, a subset of patients develop pneumonia and severe dyspnea, and require intensive care. Because acute respiratory syndrome is the hallmark feature of severe COVID-19, most initial studies on COVID-19 have focused on its impact on the respiratory system. However, accumulating evidence suggests that SARS-CoV-2 also infects other organs and can affect various body systems. As many scientists have already noted, these emerging findings call for investigations into the short- and long-term consequences of COVID-19 beyond the respiratory system. In the next sections we briefly discuss recent observations suggesting an association between SARS-CoV-2 infection and neurological complications. We place these findings in the context of previous studies demonstrating that various viruses, including CoVs, can have effects on the central nervous system (CNS). Lastly, we highlight the possibility that SARS-CoV-2 infection could promote or enhance susceptibility to other forms of CNS insults that may lead to neurological syndromes. Given scope limitations, we offer only a sample of the substantial literature on the CNS impact of viral infection, with the purpose of underscoring some of the sequelae and mechanisms that may be involved in the context of COVID-19, and that require further investigation.

Possible Neurotropism of SARS-CoV-2


Cerebrovascular diseases are among the comorbidities of patients with confirmed COVID-19 who develop severe respiratory complications [1]. For example, one study reported hypoxic/ischemic encephalopathy in ~20% of 113 deceased patients with COVID-19 [2]. A recent study evaluated 214 patients diagnosed with COVID-19 from China and found that 36% had neurological manifestations, including acute cerebrovascular disease and impaired consciousness [3]; a case of acute hemorrhagic necrotizing encephalopathy has also been reported [4]. Another recent study (from France) reported neurologic features in 58 of 64 patients with COVID-19, including encephalopathy, prominent agitation and confusion, and corticospinal tract signs [16]. Connections between viral infections and CNS pathologies are not new. The aforementioned observations on COVID-19 are in line with a report of severe neurological manifestations associated with MERS-CoV infection in Saudi Arabia [5]. With regards to SARS-CoV-2 specifically, current evidence remains scarce and additional work is needed on whether neurological manifestations occur in COVID-19 patient populations beyond those of the initial studies. It will also be important to determine whether SARS-CoV-2 is detected in the cerebrospinal fluid (CSF) of patients who develop neurological alterations, and/or whether other CSF alterations are present (see Outstanding Questions). CSF studies will be necessary, in part, to better understand the neurotropism of SARS-CoV-2 and to evaluate whether its impact on the CNS is through direct infection or via secondary effects relating to enhanced inflammatory/proinflammatory signaling.

Human CoVs and Other Neurotropic Viruses Affect the CNS


Although studies testing whether SARS-CoV-2 targets the brain in humans or in animal models are not yet available, it is well established in the literature that other viruses target the CNS and cause neurological alterations, including brain inflammation and encephalomyelitis [6]. For example, human CoV-OC43 has been associated with fatal encephalitis in children [7,8]. Detection of SARS-CoV RNA in the CSF of a patient with SARS has been reported [9]. Preclinical studies have further shown that human (e.g., HCoV-OC43) as well as animal CoVs reach the CNS and cause encephalitis [6]. In addition, CoV antigen and RNA have been found in human brain tissue and CSF in multiple sclerosis (MS) patients [10], and CoVs have been implicated as putative etiologic agents of CNS autoimmunity, including MS. There are also indications of possible relevance to neurodegenerative diseases. For example, CoV-OC43 and CoV-229E have been found in the CSF of Parkinson’s disease patients [11]. Of note, early preclinical studies showed that intranasal/intraocular inoculation in non-human primates [12] led to detection of CoV RNA or antigen in the brain, and post-mortem analyses indicated the presence of brain pathology, including inflammation and white matter edema. Future studies may reveal whether the intranasal route of infection is connected to anosmia (loss of sense of smell) that is described as a frequent and early symptom of COVID-19 [13].
Studies on CNS invasion by neurotropic viruses, and on the underlying mechanisms leading to neuroinflammation and neurological symptoms, have made significant strides in recent years (e.g., [14,15]). These studies may provide guidance on key areas of investigation to clarify whether and how SARS-CoV-2 affects the CNS. Notably, brain inflammation has been shown to underlie, at least in part, CNS damage associated with infection by West Nile, Zika, and herpes simplex viruses, conditions in which long-lasting inflammatory processes develop within the CNS. In addition, the intense systemic inflammatory response linked to viral infection can lead to blood–brain barrier (BBB) breakdown. This in turn can allow peripheral cytokines to gain access to the CNS, where they may trigger or exacerbate neuroinflammation leading to encephalitis [15].

Possible Long-Term CNS Consequences of SARS-CoV-2 Infection


Human neurodegenerative diseases often involve a gradual process that evolves, in some cases, over several decades. Large numbers of young adults worldwide are now infected, or will be infected in the near future, by SARS-CoV-2. For some, the severity of the disease will require hospitalization, opening up the possibility of detailed medical examination which could be leveraged for longitudinal studies, as discussed later. Literature on previously studied viruses raises the possibility that SARS-CoV-2 may affect the CNS. The inflammatory response elicited in acute or chronic infection may trigger or accelerate early and subclinical mechanisms that underlie the earliest stages of neurodegenerative disorders. Moreover, because findings in neurodegenerative diseases and other viral infections suggest that systemic inflammatory mediators may access the CNS and trigger damage via impaired BBB function, systemic inflammation triggered by SARS-CoV-2 infection may further contribute to neuroinflammatory processes and increase susceptibility to neurological syndromes. CNS infections may thus promote the development of neurodegenerative disease in individuals already at risk. There is an urgent need for longitudinal studies to determine whether the COVID-19 pandemic will lead to enhanced incidence of neurodegenerative disorders in infected individuals (Box 1).

Box 1A Roadmap for Research into the CNS Impact of SARS-CoV-2
There is a need to investigate whether and to what extent neurological alterations are observed in distinct COVID-19 patient groups, for example in immunocompetent/immunosuppressed individuals, as well as in patients with cardiovascular or metabolic disorders. In animal models, investigations should address whether infection by SARS-CoV-2 via different routes (intravenous, intranasal) induces neuroinflammation and neurodegeneration.
For patients under intensive care, who are likely to develop an intense systemic inflammatory response to viral infection, blood samples and CSF (whenever possible) should be collected longitudinally for evaluation of systemic and CNS inflammatory markers.
It will be crucial to conduct detailed cognitive testing on COVID-19 patients to detect possible cognitive impairments, as well as longitudinal studies that include brain imaging, neurological, and neuropsychological evaluation to examine multiple cognitive domains.
In patients who develop severe neurological complications, whenever possible, investigation of CSF samples for the presence of viral antigen/RNA and inflammatory mediators would be valuable to determine direct CNS infection. In addition, investigation of post-mortem brain and spinal cord tissue from deceased COVID-19 individuals (where possible) may provide evidence for parenchymal infection.

To conclude, emerging evidence suggests that SARS-CoV-2 is associated with neurological alterations in COVID-19 patients presenting with severe clinical manifestations. Three general scenarios are feasible. Specifically, the impact of SARS-CoV-2 on the CNS could (i) lead to neurological alterations directly, (ii) worsen pre-existing neurological conditions, and/or (iii) increase susceptibility to or aggravate damage caused by other insults. Given the global dimension of the current pandemic and the high transmissibility of SARS-CoV-2, the evidence discussed earlier raises concerns regarding the potential long-term CNS consequences of COVID-19 (Box 1). We propose that follow-up of severe COVID-19 patients should include careful clinical, imaging, and laboratory neurological assessment to determine to what extent the interplay between central and systemic infection drives CNS damage and neurological alterations. From where we now stand, it seems possible that, as currently infected individuals age in the coming years and decades, the systemic and/or brain inflammatory response elicited by SARS-CoV-2 infection may trigger long-term mechanisms leading to a widespread increase in the incidence of neurological and neurodegenerative disorders.

Outstanding QuestionsAre specific groups of COVID-19 patients more prone to developing neurological alterations?
Is SARS-CoV-2 present in post-mortem brain tissue or in the CSF of COVID-19 patients? Is there preferential targeting of CNS structures in patients who develop neurological alterations?
Is anosmia indicative of SARS-CoV-2 infection in the CNS. or does it reflect an impact on the peripheral nervous system (e.g., olfactory nerve)? Can SARS-CoV-2 be found in the olfactory or optic nerves as potential conduits for invasion of the CNS?

Considering potential neurological consequences, what strategies (clinical, imaging, biomarkers) should be adopted in the long-term neurological follow up of COVID-19 patients?

Acknowledgments

Work in the laboratories of the authors was supported by grants from Alzheimer’s Society Canada and the Weston Brain Institute (to F.G.D.F), the National Institute for Translational Neuroscience (INNT/Brazil)(to S.T.F., F.G.D.F, and J.M.), the Brazilian funding agencies Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) and Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) (to S.T.F., F.G.D.F, F.T-M., and J.M.), and from the Canadian Institutes of Health Research (CIHR) and Ontario Brain Institute (to D.P.M.).

nEbAbxr.jpg


MoKh7Ha.jpg

RJYMDbI.jpg
 
Science & Society
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and the Central Nervous System


Fernanda G.De Felice(1,2,3)
Sérgio T.Ferreira(1,6)

https://doi.org/10.1016/j.tins.2020.04.004
Get rights and content


Emerging evidence indicates that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of coronavirus disease 2019 (COVID-19), can cause neurological complications. We provide a brief overview of these recent observations and discuss some of their possible implications. In particular, given the global dimension of the current pandemic, we highlight the need to consider the possible long-term impact of COVID-19, potentially including neurological and neurodegenerative disorders.

Keywords

COVID-19
neurological alterations
neurodegenerative diseases
encephalitis
anosmia
Parkinson’s disease

Coronaviruses, SARS-CoV-2, and Their Impact on Multiple Organ Systems

CoVs are the largest group of viruses that cause respiratory and gastrointestinal infections, and have been responsible for three pandemics in the past 18 years: SARS in 2002/2003, Middle East respiratory syndrome (MERS) in 2012 and, currently, COVID-19. SARS-CoV-2, the etiologic agent of COVID-19, is a novel member of the human CoV family that emerged in China in late 2019. The symptoms of COVID-19 can include fever, cough, loss of smell and taste, sore throat, leg pain, headache, diarrhea, and fatigue. Although most patients infected with SARS-CoV-2 are asymptomatic or develop mild to moderate symptoms, a subset of patients develop pneumonia and severe dyspnea, and require intensive care. Because acute respiratory syndrome is the hallmark feature of severe COVID-19, most initial studies on COVID-19 have focused on its impact on the respiratory system. However, accumulating evidence suggests that SARS-CoV-2 also infects other organs and can affect various body systems. As many scientists have already noted, these emerging findings call for investigations into the short- and long-term consequences of COVID-19 beyond the respiratory system. In the next sections we briefly discuss recent observations suggesting an association between SARS-CoV-2 infection and neurological complications. We place these findings in the context of previous studies demonstrating that various viruses, including CoVs, can have effects on the central nervous system (CNS). Lastly, we highlight the possibility that SARS-CoV-2 infection could promote or enhance susceptibility to other forms of CNS insults that may lead to neurological syndromes. Given scope limitations, we offer only a sample of the substantial literature on the CNS impact of viral infection, with the purpose of underscoring some of the sequelae and mechanisms that may be involved in the context of COVID-19, and that require further investigation.

Possible Neurotropism of SARS-CoV-2


Cerebrovascular diseases are among the comorbidities of patients with confirmed COVID-19 who develop severe respiratory complications [1]. For example, one study reported hypoxic/ischemic encephalopathy in ~20% of 113 deceased patients with COVID-19 [2]. A recent study evaluated 214 patients diagnosed with COVID-19 from China and found that 36% had neurological manifestations, including acute cerebrovascular disease and impaired consciousness [3]; a case of acute hemorrhagic necrotizing encephalopathy has also been reported [4]. Another recent study (from France) reported neurologic features in 58 of 64 patients with COVID-19, including encephalopathy, prominent agitation and confusion, and corticospinal tract signs [16]. Connections between viral infections and CNS pathologies are not new. The aforementioned observations on COVID-19 are in line with a report of severe neurological manifestations associated with MERS-CoV infection in Saudi Arabia [5]. With regards to SARS-CoV-2 specifically, current evidence remains scarce and additional work is needed on whether neurological manifestations occur in COVID-19 patient populations beyond those of the initial studies. It will also be important to determine whether SARS-CoV-2 is detected in the cerebrospinal fluid (CSF) of patients who develop neurological alterations, and/or whether other CSF alterations are present (see Outstanding Questions). CSF studies will be necessary, in part, to better understand the neurotropism of SARS-CoV-2 and to evaluate whether its impact on the CNS is through direct infection or via secondary effects relating to enhanced inflammatory/proinflammatory signaling.

Human CoVs and Other Neurotropic Viruses Affect the CNS


Although studies testing whether SARS-CoV-2 targets the brain in humans or in animal models are not yet available, it is well established in the literature that other viruses target the CNS and cause neurological alterations, including brain inflammation and encephalomyelitis [6]. For example, human CoV-OC43 has been associated with fatal encephalitis in children [7,8]. Detection of SARS-CoV RNA in the CSF of a patient with SARS has been reported [9]. Preclinical studies have further shown that human (e.g., HCoV-OC43) as well as animal CoVs reach the CNS and cause encephalitis [6]. In addition, CoV antigen and RNA have been found in human brain tissue and CSF in multiple sclerosis (MS) patients [10], and CoVs have been implicated as putative etiologic agents of CNS autoimmunity, including MS. There are also indications of possible relevance to neurodegenerative diseases. For example, CoV-OC43 and CoV-229E have been found in the CSF of Parkinson’s disease patients [11]. Of note, early preclinical studies showed that intranasal/intraocular inoculation in non-human primates [12] led to detection of CoV RNA or antigen in the brain, and post-mortem analyses indicated the presence of brain pathology, including inflammation and white matter edema. Future studies may reveal whether the intranasal route of infection is connected to anosmia (loss of sense of smell) that is described as a frequent and early symptom of COVID-19 [13].
Studies on CNS invasion by neurotropic viruses, and on the underlying mechanisms leading to neuroinflammation and neurological symptoms, have made significant strides in recent years (e.g., [14,15]). These studies may provide guidance on key areas of investigation to clarify whether and how SARS-CoV-2 affects the CNS. Notably, brain inflammation has been shown to underlie, at least in part, CNS damage associated with infection by West Nile, Zika, and herpes simplex viruses, conditions in which long-lasting inflammatory processes develop within the CNS. In addition, the intense systemic inflammatory response linked to viral infection can lead to blood–brain barrier (BBB) breakdown. This in turn can allow peripheral cytokines to gain access to the CNS, where they may trigger or exacerbate neuroinflammation leading to encephalitis [15].

Possible Long-Term CNS Consequences of SARS-CoV-2 Infection


Human neurodegenerative diseases often involve a gradual process that evolves, in some cases, over several decades. Large numbers of young adults worldwide are now infected, or will be infected in the near future, by SARS-CoV-2. For some, the severity of the disease will require hospitalization, opening up the possibility of detailed medical examination which could be leveraged for longitudinal studies, as discussed later. Literature on previously studied viruses raises the possibility that SARS-CoV-2 may affect the CNS. The inflammatory response elicited in acute or chronic infection may trigger or accelerate early and subclinical mechanisms that underlie the earliest stages of neurodegenerative disorders. Moreover, because findings in neurodegenerative diseases and other viral infections suggest that systemic inflammatory mediators may access the CNS and trigger damage via impaired BBB function, systemic inflammation triggered by SARS-CoV-2 infection may further contribute to neuroinflammatory processes and increase susceptibility to neurological syndromes. CNS infections may thus promote the development of neurodegenerative disease in individuals already at risk. There is an urgent need for longitudinal studies to determine whether the COVID-19 pandemic will lead to enhanced incidence of neurodegenerative disorders in infected individuals (Box 1).

Box 1A Roadmap for Research into the CNS Impact of SARS-CoV-2
There is a need to investigate whether and to what extent neurological alterations are observed in distinct COVID-19 patient groups, for example in immunocompetent/immunosuppressed individuals, as well as in patients with cardiovascular or metabolic disorders. In animal models, investigations should address whether infection by SARS-CoV-2 via different routes (intravenous, intranasal) induces neuroinflammation and neurodegeneration.
For patients under intensive care, who are likely to develop an intense systemic inflammatory response to viral infection, blood samples and CSF (whenever possible) should be collected longitudinally for evaluation of systemic and CNS inflammatory markers.
It will be crucial to conduct detailed cognitive testing on COVID-19 patients to detect possible cognitive impairments, as well as longitudinal studies that include brain imaging, neurological, and neuropsychological evaluation to examine multiple cognitive domains.
In patients who develop severe neurological complications, whenever possible, investigation of CSF samples for the presence of viral antigen/RNA and inflammatory mediators would be valuable to determine direct CNS infection. In addition, investigation of post-mortem brain and spinal cord tissue from deceased COVID-19 individuals (where possible) may provide evidence for parenchymal infection.

To conclude, emerging evidence suggests that SARS-CoV-2 is associated with neurological alterations in COVID-19 patients presenting with severe clinical manifestations. Three general scenarios are feasible. Specifically, the impact of SARS-CoV-2 on the CNS could (i) lead to neurological alterations directly, (ii) worsen pre-existing neurological conditions, and/or (iii) increase susceptibility to or aggravate damage caused by other insults. Given the global dimension of the current pandemic and the high transmissibility of SARS-CoV-2, the evidence discussed earlier raises concerns regarding the potential long-term CNS consequences of COVID-19 (Box 1). We propose that follow-up of severe COVID-19 patients should include careful clinical, imaging, and laboratory neurological assessment to determine to what extent the interplay between central and systemic infection drives CNS damage and neurological alterations. From where we now stand, it seems possible that, as currently infected individuals age in the coming years and decades, the systemic and/or brain inflammatory response elicited by SARS-CoV-2 infection may trigger long-term mechanisms leading to a widespread increase in the incidence of neurological and neurodegenerative disorders.

Outstanding QuestionsAre specific groups of COVID-19 patients more prone to developing neurological alterations?
Is SARS-CoV-2 present in post-mortem brain tissue or in the CSF of COVID-19 patients? Is there preferential targeting of CNS structures in patients who develop neurological alterations?
Is anosmia indicative of SARS-CoV-2 infection in the CNS. or does it reflect an impact on the peripheral nervous system (e.g., olfactory nerve)? Can SARS-CoV-2 be found in the olfactory or optic nerves as potential conduits for invasion of the CNS?

Considering potential neurological consequences, what strategies (clinical, imaging, biomarkers) should be adopted in the long-term neurological follow up of COVID-19 patients?

Acknowledgments

Work in the laboratories of the authors was supported by grants from Alzheimer’s Society Canada and the Weston Brain Institute (to F.G.D.F), the National Institute for Translational Neuroscience (INNT/Brazil)(to S.T.F., F.G.D.F, and J.M.), the Brazilian funding agencies Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) and Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) (to S.T.F., F.G.D.F, F.T-M., and J.M.), and from the Canadian Institutes of Health Research (CIHR) and Ontario Brain Institute (to D.P.M.).

nEbAbxr.jpg


MoKh7Ha.jpg

RJYMDbI.jpg

Good God. I'd rather die of it than get a neurodegenerative disease or something like MS. One of my third cousins here in America had a really severe case of it. Her skunk of a husband left her and took the children because he said he couldn't watch her like that and didn't want the children to see her. I have a feeling the bimbo he married ten months later might have had something to do with it. Her blessed mother and brother cared for her. She prayed to die.

This thing is a scourge: neurological damage, irreversible lung damage, liver damage...what else?

Is it possible that the "light" cases have no lasting effect? Is the difference individual immune make up?
 
Good God. I'd rather die of it than get a neurodegenerative disease or something like MS. One of my third cousins here in America had a really severe case of it. Her skunk of a husband left her and took the children because he said he couldn't watch her like that and didn't want the children to see her. I have a feeling the bimbo he married ten months later might have had something to do with it. Her blessed mother and brother cared for her. She prayed to die.

This thing is a scourge: neurological damage, irreversible lung damage, liver damage...what else?

Is it possible that the "light" cases have no lasting effect? Is the difference individual immune make up?

Yes Angela. This disease is scary. A young doctor specialized in ICUs died yesterday in São Paulo. Young, handsome, healthy, 32 years old. I'm on alert for my 24-year-old son. :sad-2:
 
World News - El País (Spain) in English:

Coronavirus reverses the historical roles of northern and southern Italy | International

April 22, 2020

eoD3kkR.jpg


On March 8, after two in the morning, Milan’s train station was filled with Neapolitans, Calabreses and people from other southern regions, dragging suitcases at full speed to escape south. The images, captured by security cameras that day, represented an unexpected paradigm shift in the history of Italy. For the first time since the country’s unification, since the times of FIAT’s growth in Turin and mass immigration, the exodus was taking place in the opposite direction. A hyperbole that in the following weeks found replicas in different political and social formats. On the way to 13,000 deaths and dubious management of the coronavirus crisis, in Rome the idea is growing that Lombardy should undergo the intervention of a manager. The governor of Campania (Naples region) has warned that he will not allow his citizens to enter and the Executive sharpens his knives to settle the score with aggressive northern rhetoric.

The gap between north and south, the famous Italy at two speeds, widens every day at six in the afternoon, when data on contagions are published. This happens in the opposite direction of the clock in history, the virus reversed things. On Monday there were 60 new cases in Lazio, 45 in Campania and three in Calabria. In Lombardy, however, they reached 735; 292 in Piedmont, 307 in Emilia-Romagna. The death toll is also very uneven: in Lombardy, 12,376 people have officially died of coronavirus since the crisis began. In Lazio, the region of Rome, 349. Data that suggest that if Italy stopped counting the problem in Lombardy, which is not exclusively the result of the density and dynamism of Milan, it would go through a very different crisis.


The situation in Lombardy or Piedmont responds to different circumstances. But with each passing day, its health model and crisis management are also questioned. Mistakes have been made. Nursing homes were used to transfer patients with coronavirus, criticized on Monday the governor of Lazio and general secretary of the Democratic Party (PD), Nicola Zingaretti. Today the zunzunzum turns into political strategy and the Chigi Palace, where a long history of resentment accumulates with all the criticism recently received by the leader of the League, Matteo Salvini, sees the opportunity to reach the former interior minister where else It hurts. The “southern question”, thus named in 1873 by the radical Lombard deputy Antonio Billia and used by Antonio Gramsci in a text that addressed this kind of historical colonization of the north based on a reunification conceived in Piedmont, returns with the covid-19.


The geography traced by the virus, however, is very different for the first time. “The pandemic has raised a deep, buried Italy. As it happened after the Second World War ”, points out the historian Giovanni Luna. Today, the three regions with the most contagions and deaths in Italy are governed by the League or a member of its right-wing coalition. Piedmont, Lombardy and Veneto showed different approaches to the crisis, but they maintain worrying numbers, especially the first two, which represent the heart of the autonomous power of the old northern party. Salvini’s credibility is based on the successes of his home region and is partly linked to the fate of his governor, Attilio Fontana, who he himself put to liquidate the party’s old guard. To overthrow it, as the Italian Executive intends with the daily wear and tear and the hypothesis of an intervention by the region, would leave the former interior minister exposed to the political weather.


The collapse of a myth


Political scientist Piero Ignazi is very tough and believes that “the myth of Lombardy has collapsed”. “The narrative of the winning region, which takes on the leadership role. The disaster of his health system and his administrative officials, particularly the president of the region, liquidated his image. In terms of reputation it is a disaster. The arrogance and airs of superiority, historically interpreted by the League and by Silvio Berlusconi himself, now allow some to demand accountability. Furthermore, a very serious political problem is born for Salvini. Defending Lombard management can be a terrible boomerang. He will lose consensus in the south and divide his voters from the north, ”says Ignazi on the phone.

Entrepreneurs, a traditional stronghold of support for the League in northern Italy, are beginning to tire of the problems and the delay in reopening the industries that Lombard management will imply. “This is no time for criticism. But the reality is that many things have failed ”, says an employer director Confindustria. Research is also sending signals in this direction. The League has lost about five points since the start of the health crisis and Salvini has fallen from second to third place among the most appreciated leaders (behind Prime Minister Giuseppe Conte and right-wing coalition partner Giorgia Meloni). Immigration is no longer used to galvanize public opinion and the virus is too unpredictable to bet on. Everything will revolve around the economy in the coming months. And then maybe things will turn around again.


THE SOUTH VOICE IN THE CRISIS


Vincenzo De Luca, governor of the Campania (Naples) region, has in recent weeks become the proud voice of the south. President since June 2015, he was mayor of Salerno for four terms. Charismatic, with exaggerated and extremely ironic rhetoric, he was one of the strongholds of the country’s closure; he fiercely opposed the idea of ​​Lombardy to open before the others. In fact, this weekend his government closed a small town called Saviano, where a funeral was held that drew a crowd, to prevent it from becoming a new focus. That same Sunday, De Luca accused the League region of its intentions to accelerate the reopening. “If there were races to reopen in regions where contagion is still so strong, Campania would close its borders. We would do an ordinance to prohibit the entry of citizens from these regions. The ‘tweeters’ producers spent two months in a hearing crisis, ”he said in reference to Salvini. Campania data is very low compared to the north. However, the number of tests performed is also extremely small.

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https://www.time24.news/i/2020/04/coronavirus-reverses-the-historical-roles-of-northern-and-southern-italy-international.html

 
^^Let them enjoy their moment. I totally understand the genesis.

The facts are still the facts, however. They didn't get hit because they aren't inundated with Japanese tourists and business people, nor are they at the center of travel with the rest of continental Europe and internationally, so it could come in from anywhere. In addition, Lombardia had a superspreader event, the Atalanta/Valencia match, and it seems the first cases were young healthy people who passed under the radar, so it spread silently for a long time, as I maintained from the beginning. Lombardy and the north in general also have longer lived people than in the south.

I could also argue that the real "heart" of the separatist movement was the Veneto, and they have very good numbers in comparison.

Plus, with all due respect to my husband and the southern Italian members here, had the south been the first hit and where it spread, given the state of their infrastructure, and particularly their health care system, and the almost compete dearth of ICU units, Lombardia would seem like paradise compared to what would have happened there.

As for "mistakes", all the countries in the west have made "mistakes", many of them because they followed the recommendations of the WHO, and also because a lot of the data coming out of China was incorrect. Remember the WHO telling all countries first that there was no person to person transmission because China said so, and that restricting international travel was a mistake, and that masks wouldn't help, and on and on?

It was only the data coming out of Lombardia that started giving a more accurate picture, as Dr. Birks of Trump's council pointed out at one of the recent briefings.

The Chinese told us to send the infected who didn't need hospitalization home. Now, they say maybe that was a bad idea and they should be isolated in separate facilities. Meanwhile, in California they followed that advice at first, and also were sending the recovering Covid patients to care homes, thinking they could isolate them there. Bad idea which they later abandoned. The Mayor of New York now says infected people not needing hospitalization will be put in hotels, but what about any non-Covid people in the hotels? What about the air vents?

It has also turned out that intubation may have made matters worse, but that fact has only emerged in the last week or so. Intubation has always been the standard treatment for ARDS symptoms. Are we going to blame the doctors now?

I'm really tired of all the "Monday Morning Quarterbacking". Where were they when it was going on?

I know what I said from the beginning, but how about Nancy Pelosi telling everyone in California to go out to Chinatowns, that the closure of travel from China was just racism? Now she blames everyone in the administration for mishandling the crisis. The mayor of New York was the same. People have short memories for their own mistakes and stupidities. Is it so hard to say: I was wrong.

How many of those Southern Italians living in Northern Italy were devil may care about the whole thing, thinking it was nothing and wandering around having parties at cafes with their friends until the quarantine was announced? It would be nice to know the number and how many are now criticizing. Had a lot of them been infected they would have infected the whole south.

Enough of using this for political gain. Clean up your own houses; prepare your own hospitals and banked supplies.
 
Here are some thoughts on how to reopen the economy:


  1. Testing by the millions - also remember that a negative test does not mean you will be negative tomorrow or the next week. Also antibody tests - today you have immunity, in couple of months maybe not
  2. We will need billions of masks
  3. We still will need to wash hands
  4. Office workers will probably still need to work from home.
  5. Public facing service workers will need to wear masks - Think hairdressers. Maybe the customers should wear masks as well?
  6. Restaurants should be encouraged to move tables outside. In Florida maybe awnings to protect them from the sun and the afternoon rains. Indoor tables capacity should be cut to 1/3. Which leads me to the following major point
  7. Air conditioning and air handling systems need to be updated/redesigned. They can spread the virus by air movement. Filters must be upgraded to trap the virus and need to be changed much more often
  8. Courthouses should be provided with copious amounts of masks to provide to workers, lawyers, judges, witnesses, jurors. Defendants should appear by video for most of their appearances except for trials. Misdemeanors should be given a notice to appear except for DUIs and domestic violence. There's more but I will stop here.
  9. Factory's should provide PPEs to their workers. Work spaces should be isolated from each other
  10. Usage of delivery/pick up services should be encouraged
  11. Gyms - When you're huffing and puffing you're probably spreading the virus far and wide. Limit the number of people at the gym at any one time and space them out in the machines. Force them wear masks? You can't huff and puff if you're wearing masks. See point 7 above also. I love going to the gym but I am going to wait a bit.
  12. Movie theaters - Forget about it for a while. People are not going.
  13. Schools should re-open in the fall. Games should be played but at 1/2 to 1/3 capacity. Masks?
  14. Department Stores - Limit the number of people in the store and encourage them to wear masks
  15. Buses/subways - Everybody wear asks and gloves. Extensive de-con throughout the day?
  16. Antivirals/vaccines - As soon as possible
  17. Hydroxycloroquine/azythromycin and other immunosuppressive medicines should only be given if your body has a runaway immune response to the virus so you need to check your cytokines. Otherwise if your suppress your immune system the the virus will ravage your lungs. They should be monitored for serious side effects
  18. Beaches should be opened but with social distancing in place and no socializing between different families that don't live together. We also don't want half of Orlando to end up in Cocoa Beach on Saturday/Sunday.
  19. Theme Parks - You have seen how long and crowded those lines are. Do not open for a little while longer
  20. Cruise ships - Forget about it
  21. Airplanes - You can have flights but without the middle seat and everybody wears masks and possibly gloves. Something tells me people won't be flying voluntarily for a little while.
  22. Clubs/Bars - See restaurants above. Capacity severely reduced.

That's just off the top of my head. And that's for counties that are trending down and are well past their peaks. BTW the reason that our hospital system was not overwhelmed was that social distancing worked.
 
^^Let them enjoy their moment. I totally understand the genesis.

The facts are still the facts, however. They didn't get hit because they aren't inundated with Japanese tourists and business people, nor are they at the center of travel with the rest of continental Europe and internationally, so it could come in from anywhere. In addition, Lombardia had a superspreader event, the Atalanta/Valencia match, and it seems the first cases were young healthy people who passed under the radar, so it spread silently for a long time, as I maintained from the beginning. Lombardy and the north in general also have longer lived people than in the south.

I could also argue that the real "heart" of the separatist movement was the Veneto, and they have very good numbers in comparison.

Plus, with all due respect to my husband and the southern Italian members here, had the south been the first hit and where it spread, given the state of their infrastructure, and particularly their health care system, and the almost compete dearth of ICU units, Lombardia would seem like paradise compared to what would have happened there.

As for "mistakes", all the countries in the west have made "mistakes", many of them because they followed the recommendations of the WHO, and also because a lot of the data coming out of China was incorrect. Remember the WHO telling all countries first that there was no person to person transmission because China said so, and that restricting international travel was a mistake, and that masks wouldn't help, and on and on?

It was only the data coming out of Lombardia that started giving a more accurate picture, as Dr. Birks of Trump's council pointed out at one of the recent briefings.

The Chinese told us to send the infected who didn't need hospitalization home. Now, they say maybe that was a bad idea and they should be isolated in separate facilities. Meanwhile, in California they followed that advice at first, and also were sending the recovering Covid patients to care homes, thinking they could isolate them there. Bad idea which they later abandoned. The Mayor of New York now says infected people not needing hospitalization will be put in hotels, but what about any non-Covid people in the hotels? What about the air vents?

It has also turned out that intubation may have made matters worse, but that fact has only emerged in the last week or so. Intubation has always been the standard treatment for ARDS symptoms. Are we going to blame the doctors now?

I'm really tired of all the "Monday Morning Quarterbacking". Where were they when it was going on?

I know what I said from the beginning, but how about Nancy Pelosi telling everyone in California to go out to Chinatowns, that the closure of travel from China was just racism? Now she blames everyone in the administration for mishandling the crisis. The mayor of New York was the same. People have short memories for their own mistakes and stupidities. Is it so hard to say: I was wrong.

How many of those Southern Italians living in Northern Italy were devil may care about the whole thing, thinking it was nothing and wandering around having parties at cafes with their friends until the quarantine was announced? It would be nice to know the number and how many are now criticizing. Had a lot of them been infected they would have infected the whole south.

Enough of using this for political gain. Clean up your own houses; prepare your own hospitals and banked supplies.

^^ I understand you Angela. Far be it from me to want to do politics about something I never understood. The domestic policy in Brazil is already complicated for me to get involved a with foreign policy. I still have the risk of such bicycle mechanic will appear here again roaring like a real member of the royal family to get my attention, LOL. I am transcribing the news to show how COVID-19 has soured the internal and external relations of all countries.
 
^^ I understand you Angela. Far be it from me to want to do politics about something I never understood. The domestic policy in Brazil is already complicated for me to get involved a with foreign policy. I still have the risk of such bicycle mechanic will appear here again roaring like a real member of the royal family to get my attention, LOL. I am transcribing the news to show how COVID-19 has soured the internal and external relations of all countries.

I completely understand, Duarte. If I weren't out of juice I'd give you an upvote.

I had hoped this would bring people together but it isn't.

One little note as I know you're no Bolsonaro fan, so I won't be offending you. :)

I saw a little clip where he was out singing and coughing at a rally with no mask on. He may win for dumbest leader, although he has stiff competition. He should be challenged to walk around shaking hands with and singing with people on the streets of inner Brooklyn and Queens to show how brave he is...

If we come out of this all right it will be because Trump sort of listens, imo, after making a lot of dumb comments, and after God knows what careful handling, to the sometimes correct advice of the experts, and the fact that he's always been a germaphobe and hates China.
 
I completely understand, Duarte. If I weren't out of juice I'd give you an upvote.

I had hoped this would bring people together but it isn't.

One little note as I know you're no Bolsonaro fan, so I won't be offending you. :)

I saw a little clip where he was out singing and coughing at a rally with no mask on. He may win for dumbest leader, although he has stiff competition. He should be challenged to walk around shaking hands with and singing with people on the streets of inner Brooklyn and Queens to show how brave he is...

If we come out of this all right it will be because Trump sort of listens, imo, after making a lot of dumb comments, and after God knows what careful handling, to the sometimes correct advice of the experts, and the fact that he's always been a germaphobe and hates China.

Thank you Angela. I am also out of juice. There is a big difference between Trump and Bolsonaro. Even those who don't like Trump have to recognize. Trump is a very smart man and Bolsonaro is dumb. The difference between the two in private life says it all: Trump is a successful businessman and Bolsonaro is a military man who was retired at the age of 45 with the rank of captain, having been arrested and threatened with expulsion of the corporation for insubordination.

Cheers ;)
 
Thank you Angela. I am also out of juice. There is a big difference between Trump and Bolsonaro. Even those who don't like Trump have to recognize.
Trump is a very smart man and Bolsonaro is dumb.
The difference between the two in private life says it all: Trump is a successful businessman and Bolsonaro is a military man who was retired at the age of 45 with the rank of captain, having been arrested and threatened with expulsion of the corporation for insubordination.

Cheers ;)


Poor Duarte, if Trump is superbe smart compared to Bolsonaro.....

"In the land of the blind, the one-eyed man is king"???

:grin:

And the privat life of Trump is lily white?

:petrified:

Perhaps you have been too long in quarantine hahahahah :rolleyes:

IMO both have made at least big estimation errors and have put their countries in big danger.....just a view of an European on Eupedia....so taken with some salt....:innocent:
 
OK this is totally counterintuitive and it comes from France so...but it seems that nicotine protects against the coronavirus. Maybe it explains how well the Greeks have done :grin:!!

Frontline health workers and patients in France may be given nicotine patches after studies found that four times fewer smokers contracted Covid-19 than non-smokers.
It may sound counterintuitive that people who puff on Gauloises are less likely to catch a virus that can cause deadly attacks on the lungs. However, that was the statistical outcome of an in-depth study conducted by the Pasteur Institute, a leading French research centre into the disease.
The institute tested almost 700 teachers and pupils of a school in Crépy-en-Valois in one of the hardest-hit areas in France, as well as their families. The “highly accurate” tests found that only 7.2 per cent of smokers from among the adults tested were infected while four times as many non-smokers, some 28 per cent, were infected.
Arnaud Fontanet, an epidemiologist at the institute, warned that they were not encouraging people to take up smoking, remarking that those smokers who do catch the virus “risk suffering more complications” than others. Scientists suggested it could be the nicotine in cigarettes that was behind the surprising results regarding infection, although more research is needed.

https://www.yahoo.com/news/smokers-four-times-less-likely-151203823.html
 
Poor Duarte, if Trump is superbe smart compared to Bolsonaro.....

"In the land of the blind, the one-eyed man is king"???

:grin:

And the privat life of Trump is lily white?

:petrified:

Perhaps you have been too long in quarantine hahahahah :rolleyes:

IMO both have made at least big estimation errors and have put their countries in big danger.....just a view of an European on Eupedia....so taken with some salt....:innocent:

The King of Irony on Eupedia. Clap, clap, clap. Do you are happy now? :grin:

If you were British you could give some phlegm to your ironies. It would definitely look more elegant.:innocent:

Oh man, I don't die of loves by any of both.:petrified:

An European's vision at Eupedia. I loved that statement. :grin:

It is fair, it is very fair, it is very very fair. I’m just a poor Latin-American guy. :sad-2:

The profile flag is that of the country where you currently reside. If it were the flag of coutry of citizenship, I could use both the Brazilian flag and the Portuguese flag. It is that dual citizenship thing allowed by the Constitution of Brazil (and Portugal too). :cool-v:

Will be that I would be able to change the flag of Brazil for that of Portugal so that my opinions can also be given with a little salt as befits every good European at Eupedia? :unsure:

It's a shame that I don't have the courage to do that. I feel like an Eurodescendant, more specifically a Portuguese-Brazilian, but I don't feel myself an European. :disappointed:

Cheers my dear :)
 
OK this is totally counterintuitive and it comes from France so...but it seems that nicotine protects against the coronavirus. Maybe it explains how well the Greeks have done :grin:!!

Frontline health workers and patients in France may be given nicotine patches after studies found that four times fewer smokers contracted Covid-19 than non-smokers.
It may sound counterintuitive that people who puff on Gauloises are less likely to catch a virus that can cause deadly attacks on the lungs. However, that was the statistical outcome of an in-depth study conducted by the Pasteur Institute, a leading French research centre into the disease.
The institute tested almost 700 teachers and pupils of a school in Crépy-en-Valois in one of the hardest-hit areas in France, as well as their families. The “highly accurate” tests found that only 7.2 per cent of smokers from among the adults tested were infected while four times as many non-smokers, some 28 per cent, were infected.
Arnaud Fontanet, an epidemiologist at the institute, warned that they were not encouraging people to take up smoking, remarking that those smokers who do catch the virus “risk suffering more complications” than others. Scientists suggested it could be the nicotine in cigarettes that was behind the surprising results regarding infection, although more research is needed.

https://www.yahoo.com/news/smokers-four-times-less-likely-151203823.html

This bug is so bizarre that I'm willing to accept any hypothesis if it's supported by good data.

So, is that what this shows, however? Belgium has terrible death rates, but perhaps the infection rate is lower? England is high in both, I think. Germany is pretty high in infections, but low in deaths if you believe their figures.

It might have something to do with the Scandinavian countries, though. They don't smoke much, but the men, especially, who are more at risk for Covid 19 anyway, are constantly chewing it in SNUS form. A more disgusting habit is hard for me to imagine. Talk about imagining; imagine kissing a man who just had a mouthful of that juice! If he had a beard and spit it out he'd probably hit it. It must stain the teeth terribly too. I remember from my dating days that yellow or snaggly teeth and even a good night kiss on the cheek was out. I'd be celibate in a SNUS chewing world. :(

cigarette-consumption.jpg


Maybe when you're exhaling all that smoke you're dispersing the virus hanging around in the air, and maybe even some that made it into your nose???

I don't see why the nicotine itself would help, although I'm not a scientist. Could it have to do with the fact that it's a vasocontrictor?

There are a lot of benefits to nicotine: mood improvement for one, and more concentration for the other, along, paradoxically, with more relaxation.

They're even testing it for Alzheimer's and Parkinson's patients.
 

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