Pagesmith4074

We also found that among the various coping strategies, (a) watching television for entertainment, (b) social networking, (c) listening to music, (d) sleeping, (e) doing mundane house chores like cleaning, washing, etc. (f) eating well, and (g) clearing/finishing thepiled-up work were ranked among the most utilized coping strategies by all participants. This study identifies the need to provide the free professional and psychological services to help cope with stress during the disease-enforced lockdown.Killing someone directly is never morally right, but sometimes, choosing someone to save and leaving another to die is. The moral philosophy, law, and medical ethics have all wrestled with the problem of distinguishing between saving someone and leaving another to die. While this distinction might seem intuitively straightforward, it becomes far more complex when applied in treating patients of novel Coronavirus Disease pandemic (COVID-19). The World Health Organization reports more than eight million and half cases of infection and more than 450,000 deaths, 26% in USA. However, with the exponential rise in number of COVID-19 victims and the shortage of life-saving ventilators, the pandemic has imposed to health professionals an ethical medical triage decision-making based on the utilitarian theory to maximize total benefits and life expectancy. Moreover, the decision to put restrictions on treatment beneficence is not discretionary, but an indispensable response to the overwhelming impacts of COVID-19 pandemic. The main concern is not whether to underline priorities, but how to do so systematically and ethically, instead of building decisions on individualized institutional aspirations or health professionals' intuition. The serious glaring disequilibrium, in healthcare market, between supply and demand for scarce medical resources in several developed nations (including the USA, UK, France, Italy, Spain, etc.) imposes a fundamental question which COVID-19 patient to save when facing scarce resources?Coronavirus disease (COVID-19) is caused by a beta-coronavirus (SARS-CoV-2) that affects the lower respiratory tract and appears as pneumonia in humans. Metabolism agonist COVID-19 became apparent in December 2019 in Wuhan City of China, and has propagated profusely globally. Despite stringent global quarantine and containment drives, the incidence of COVID-19 keeps soaring high. Measures to minimize human-to-human transmission have been implemented to control the pandemic. However, special efforts to reduce transmission via efficient public health communications and dissemination of risks should be applied in susceptible populations including children, health care providers, and the elderly. In response to this global pandemic, this article summarizes proven strategies that could be employed to combat the COVID-19 disease outbreak, taking a cue from lessons learned from the Ebola virus disease response.The low cost lipase derived from Thermomyces lanugionous was chosen to conjugate with Fe3O4 nanoparitcles as a magnetic responsive lipase (MRL) biocatalyst. The structure of MRL was observed by atomic force microscopy (AFM). The Fourier transform infrared (FTIR) spectroscopy analysis confirmed the lipase conjugated to Fe3O4 nanoparticles. Optimized conditions for the process of biodiesel production by MRL were investigated by the response surface methodology (RSM) and the Box-Behnken design (BBD). The optimized conditions for biodiesel production by MRL were as follows. The molar ratio of methanol to oil was 4.0, water content was 1.5 % as oil weight, the dosage of MRL to oil was 9.0 % (W/W) under 41 °C for 28 h. Under the optimized conditions, the yield of FAMEs by MRL reached 82.20 %. Further experiments showed that the MRL could be used 10 cycles and the yield of FAMEs decreased slightly by 10.97 %. These results indicated that Fe3O4 nanoparticle carrier could efficiently improve the FAMEs synthesis and enhance the MRL stabilization and reusability in the biodiesel production.Superspreaders are critical infectious resources in multiple infectious diseases. They can be asymptomatic or present mild symptoms but can transmit pathogens to susceptible populations, leading to severe symptoms, and even death. Early identification of this population is extremely important to inhibit the spread of infectious diseases. Right now, the whole global world is suffering from a devastating infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In this article, a superspreader cluster event in coronavirus disease 2019 (COVID-19) was identified by tracking contacting histories of infected patients. This cluster was found to be originated from an asymptomatic SARS-CoV-2 carrier, which resulted in 13 secondary cases getting infected. All the secondary patients presented with non-typical symptoms of COVID-19, such as fever, dry cough, and myalgia, one of which died of respiratory failure at the end. From this cluster, we learn that people with older ages, low immunity, multiple underlying diseases, especially pulmonary diseases, can contribute to a poor prognosis. Thus, asymptomatic superspreaders of COVID-19 can be extremely dangerous and must be handled time-efficiently.Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative virus of the coronavirus disease 2019 (COVID-19) pandemic. To establish a safe and convenient assay system for studying entry inhibitors and neutralizing antibodies against SARS-CoV-2, we constructed a codon-optimized, full-length C-terminal mutant spike (S) gene of SARS-CoV-2. We generated a luciferase (Luc)-expressing pseudovirus containing the wild-type or mutant S protein of SARS-CoV-2 in the envelope-defective HIV-1 backbone. The key parameters for this pseudovirus-based assay, including the S mutants and virus incubation time, were optimized. This pseudovirus contains a Luc reporter gene that enabled us to easily quantify virus entry into angiotensin-converting enzyme 2 (ACE2)-expressing 293T cells. Cathepsin (Cat)B/L inhibitor E-64d could significantly block SARS-CoV-2 pseudovirus infection in 293T-ACE2 cells. Furthermore, the SARS-CoV-2 spike pseudotyped virus could be neutralized by sera from convalescent COVID-19 patients or recombinant ACE2 with the fused Fc region of human IgG1.