Lifeboat Foundation

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As authorities enforce social distancing in the battle against coronavirus, don’t be surprised if you hear reminders coming from the sky.

Police departments in Florida and New Jersey have drones with pre-recorded warnings that will be deployed if crowds are not following COVID-19 guidelines.

Ahhhhhh, these people scare me, more than the Virus.

Clearview AI, which has alarmed privacy experts, hired several far-right employees, a HuffPost investigation found.

Worth having a look, who knows.

Cytokines and chemokines are thought to play an important role in immunity and immunopathology during virus infections [3]. Patients with severe COVID-19 have higher serum levels of pro-inflammatory cytokines (TNF-α, IL-1 and IL-6) and chemokines (IL-8) compared to individuals with mild disease or healthy controls, similar to patients with SARS or MERS. The change of laboratory parameters, including elevated serum cytokine, chemokine levels, and increased NLR in infected patients are correlated with the severity of the disease and adverse outcome, suggesting a possible role for hyper-inflammatory responses in COVID-19 pathogenesis. Importantly, previous studies showed that viroporin E, a component of SARS-associated coronavirus (SARS-CoV), forms Ca2C-permeable ion channels and activates the NLRP3 inflammasome. In addition, another viroporin 3a was found to induce NLRP3 inflammasome activation. The mechanisms are unclear.

Colchicine, an old drug used in auto-inflammatory disorders (i.e., Familiar Mediterranean Fever and Bechet disease) and in gout, counteracts the assembly of the NLRP3 inflammasome, thereby reducing the release of IL-1b and an array of other interleukins, including IL-6, that are formed in response to danger signals. Recently, colchicine has been successfully used in two cases of life-threatening post-transplant capillary leak syndrome. These patients had required mechanically ventilation for weeks and hemodialysis, before receiving colchicine, which abruptly restored normal respiratory function and diuresis over 48 hrs [4].

Continue reading “Colchicine Efficacy in COVID-19 Pneumonia” »

This is a good one pass it on

This study aimed to explore whether the therapeutic effects of EPO rely on the suppression of the NLRP3 inflammasome and the specific mechanisms in an LPS-induced ALI mouse model. ALI was induced in C57BL/6 mice by intraperitoneal (i.p.) injection of LPS (15 mg/kg). EPO was administered intraperitoneally at 5 U/g after LPS challenge. The mice were sacrificed 8 h later. Our findings indicated that application of EPO markedly diminished LPS-induced lung injury by restoring histopathological changes, lessened lung wet/dry (W/D) ratio, protein concentrations in bronchoalveolar lavage fluid (BALF) and myeloperoxidase (MPO) levels. Meanwhile, EPO evidently decreased interleukin-1β (IL-1β) and interleukin-18 (IL-18) secretion, the expression of NLRP3 inflammasome components including pro-IL-1β, NLRP3, and cleaved caspase-1 as well as phosphorylation of nuclear factor-κB (NF-κB) p65, which may be associated with activation of EPO receptor (EPOR), phosphorylation of Janus-tyrosine kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3)

Taken together, this study indicates that EPO can effectively attenuate LPS-induced lung injury in mice by suppressing the NLRP3 inflammasome, which is dependent upon activation of EPOR/JAK2/STAT3 signaling and inhibition of the NF-κB pathway.

Continue reading “Suppression of NLRP3 Inflammasome” »

Even before the coronavirus, air pollution killed seven million people a year. Will today’s cleaner air inspire us to do better?

I rarely use the words transformative or breakthrough for neuroscience findings. The brain is complex, noisy, chaotic, and often unpredictable. One intriguing result under one condition may soon fail for a majority of others. What’s more, paradigm-shifting research trends often require revolutionary tools. When we’re lucky, those come once a decade.

But I can unabashedly say that the 2010s saw a boom in neuroscience breakthroughs that transformed the field and will resonate long into the upcoming decade.

In 2010, the idea that we’d be able to read minds, help paralyzed people walk again, incept memories, or have multi-layered brain atlases was near incomprehensible. Few predicted that deep learning, an AI model loosely inspired by neural processing in the brain, would gain prominence and feed back into decoding the brain. Around 2011, I asked a now-prominent AI researcher if we could automatically detect dying neurons in a microscope image using deep neural nets; we couldn’t get it to work. Today, AI is readily helping read, write, and map the brain.

Working around the clock for two weeks, a large team of Stanford Medicine scientists has developed a test to detect antibodies against the novel coronavirus, SARS-CoV-2, in blood samples.

In contrast to current diagnostic tests for COVID-19, which detect genetic material from the virus in respiratory secretions, this test looks for antibodies to the virus in plasma, the liquid in blood, to provide information about a person’s immune response to an infection.

The test was launched April 6 at Stanford Health Care. It differs from an externally developed test that Stanford researchers used for a prevalence study during recent community screening events.

New hope for stroke patients as scientists find way to restore mobility and touch using human stem cells to recreate nerve connections in damaged rat brain…

Scientists have found a way to restore mobility and touch in rats after a stroke using human stem cells to recreate nerve connections in damaged brains — offering patients a new hope.

Continue reading “Scientists restore mobility and touch in stroke-afflicted rats” »

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the infectious disease COVID-19, which was first reported in Wuhan, China in December, 2019. Despite the tremendous efforts to control the disease, COVID-19 has now spread to over 100 countries and caused a global pandemic. SARS-CoV-2 is thought to have originated in bats; however, the intermediate animal sources of the virus are completely unknown. Here, we investigated the susceptibility of ferrets and animals in close contact with humans to SARS-CoV-2. We found that SARS-CoV-2 replicates poorly in dogs, pigs, chickens, and ducks, but ferrets and cats are permissive to infection. We found experimentally that cats are susceptible to airborne infection. Our study provides important insights into the animal models for SARS-CoV-2 and animal management for COVID-19 control.

In late December 2019, an unusual pneumonia emerged in humans in Wuhan, China, and rapidly spread internationally, raising global public health concerns. The causative pathogen was identified as a novel coronavirus (1–16) that was named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) on the basis of a phylogenetic analysis of related coronaviruses by the Coronavirus Study Group of the International Committee on Virus Taxonomy (17); the disease it causes was subsequently designated COVID-19 by the World Health Organization (WHO). Despite tremendous efforts to control the COVID-19 outbreak, the disease is still spreading. As of March 11, 2020, SARS-CoV-2 infections have been reported in more than 100 countries, and 118,326 human cases have been confirmed, with 4,292 fatalities (18). COVID-19 has now been announced as a pandemic by WHO.

Although SARS-CoV-96.2% identity at the nucleotide level with the coronavirus RaTG13, which was detected in horseshoe bats (Rhinolophus spp) in Yunnan province in 2013 (3), it has not previously been detected in humans or other animals. The emerging situation raises many urgent questions. Could the widely disseminated viruses transmit to other animal species, which then become reservoirs of infection? The SARS-CoV-2 infection has a wide clinical spectrum in humans, from mild infection to death, but how does the virus behave in other animals? As efforts are made for vaccine and antiviral drug development, which animal(s) can be used most precisely to model the efficacy of such control measures in humans? To address these questions, we evaluated the susceptibility of different model laboratory animals, as well as companion and domestic animals to SARS-CoV-2.