“More Americans died between Monday and Saturday (8,800) than died from the wars in Afghanistan and Iraq combined.”
The US reported 2,108 deaths on Friday and passed 500,000 confirmed cases, but White House officials say the speed of the outbreak is easing off.
Join us for LIVE updates as Dr. Jacob Glanville and Sarah Ives give the world the latest news on the novel research being done in the fight against #Covid19.
- Today at 2:45PST — LEARN MORE about all of the amazing things happening in their world by clicking the links below!
www.distributedbio.com www.centivax.com — #Centivax #Dbio #DistributedBio #Biotechnology #Research #Antibodies #Pandemic
Professor Sarah Gilbert said a working vaccine by September was “just about possible if everything goes perfectly.”
Collaboration will always accelerate society faster than competition ever will:
https://www.google.com/amp/s/www.fool.com/amp/investing/2020…coali.aspx
“Biotest, BPL, LFB, and Octapharma have joined an alliance formed by CSL Behring (ASX: CSL/USOTC: CSLLY) and Takeda Pharmaceutical Company Limited (TSE:4502/NYSE: TAK) to develop a potential plasma-derived therapy for treating COVID-19. The alliance will begin immediately with the investigational development of one, unbranded anti-SARS-CoV-2 polyclonal hyperimmune immunoglobulin medicine with the potential to treat individuals with serious complications from COVID-19.”
RENO, Nev. (News 4 & Fox 11) — A Reno company has been awarded more than $550 million to help make ventilators during the coronavirus outbreak.
In a statement released on Friday, Rep. Mark Amodei, R-Nev., said Hamilton Medical would receive a five-month, $551 million contract as part of a national effort to stockpile 100,000 ventilators over the next 100 days.
Amodei states the money is coming in the form of a firm-fixed-price contract that began on March 31.
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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.
