Isatin base Schiff bases (1-20) were synthesized, characterized by (1)H NMR and EI/MS and evaluated for α-glucosidase inhibitory potential. Out of these twenty (20) compounds only six analogs showed potent α-glucosidase inhibitory potential with IC50 value ranging in between 2.2±0.25 and 83.5±1.0μM when compared with the standard acarbose (IC50=840±1.73μM). Among the series compound 2 having IC50 value (18.3±0.56μM), 9 (83.5±1.0μM), 11 (3.3±0.25μM), 12 (2.2±0.25μM), 14 (11.8±0.15μM), and 20 (3.0±0.15μM) showed excellent inhibitory potential many fold better than the standard acarbose. The binding interactions of these active analogs were confirmed through molecular docking.
A pneumonia-like disease of unknown origin caused a catastrophe in Wuhan city, China. This disease spread to 215 countries affecting a wide range of people. World health organization (WHO) called it a pandemic and it was officially named as Severe Acute Respiratory Syndrome Corona virus 2 (SARS CoV-2), also known as Corona virus disease (COVID-19). This pandemic compelled countries to enforce a socio-economic lockdown to prevent its widespread. This paper focuses on how the particulate matter pollution was reduced during the lockdown period (23 March to April 15, 2020) as compared to before lockdown. Both ground-based and satellite observations were used to identify the improvement in air quality of Pakistan with primary focus on four major cities of Lahore, Islamabad, Karachi and Peshawar. Both datasets have shown a substantial reduction in PM2.5 pollution levels (ranging from 13% to 33% in case of satellite observations, while 23%-58% in ground-based observations) across Pakistan. Result shows a higher rate of COVID-19 spread in major cities of Pakistan with poor air quality conditions. Yet more research is needed in order to establish linkage between COVID-19 spread and air pollution. However, it can be partially attributed to both higher rate of population density and frequent exposure of population to enhanced levels of PM2.5 concentrations before lockdown period.
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.