Phenotypic evolution of SARS-CoV-2 spike during the COVID-19 pandemic.

SARS-CoV-2 variants are mainly defined by mutations in their spike. It is therefore critical to understand how the evolutionary trajectories of spike affect virus phenotypes. So far, it has been challenging to comprehensively compare the many spikes that emerged during the pandemic in a single experimental platform.

Reaction of 4-(Alkynyloxy)cyclohexa-2,5-dienones with Dimethyl Sulfoxide: A Catalyst-Free Formation of 6/5/3-Fused Tricyclic Enones.

6/5/3-Fused tricyclic enones were obtained when 4-(alkynyloxy)cyclohexa-2,5-dienones were treated with DMSO at 150 °C. The reaction proceeded via a four-membered oxathietene intermediate. The protocol developed is atom economical, has a broad substrate scope, and is amenable to gram-scale synthesis.

A highly sensitive facile plasmonic scheme for assessment of melamine in raw milk.

This work presents two novel devices with a microcontroller and two different light sensors, namely, Light Dependent Resistor (LDR) and Ambient Light Sensor (ALS), which can provide a quantitative output from the colorimetric variations of citrate capped borohydride reduced silver nanoparticles (AgNPs) and citrate capped gold nanoparticles (AuNPs) upon addition of melamine adulterated milk. The limit of detection (LOD) of the LDR setup with AgNPs and AuNPs was found to be 1.24 ppm and 1.

Concomitant suppression of COX-1 and COX-2 is insufficient to induce enteropathy associated with chronic NSAID use.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most widely used medications for the management of chronic pain; however, they are associated with numerous gastrointestinal (GI) adverse events. Although many mechanisms have been suggested, NSAID-induced enteropathy has been thought to be primarily due to inhibition of both cyclooxygenases (COX) -1 and -2, which results in suppression of prostaglandin synthesis. Yet surprisingly, we found that concomitant postnatal deletion of and over 10 months failed to cause intestinal injury in mice unless they were treated with naproxen or its structural analog, phenylpropionic acid, which is not a COX inhibitor.