Research on Antimicrobial Resistance in the Last 15 Years, India: A Bibliometric Analysis.

SUMMARY: Effective antimicrobials play an important element in modern medicine's success in treating infections, without which the patients would be put at risk. Along with the naturally occurring process of antibiotic resistance, the misuse/overuse of these antibiotics also leads to them losing their effectiveness. It limits the treatment options as the microbe that had previously been sensitive becomes resistant. This bibliometric study was performed by searching the Scopus database according to a specific search strategy. A total of 4200 articles were retrieved from the search, and after applying inclusion and exclusion criteria, 1355 articles were included in the study. All of the bibliometric variables examined in this study revealed significant growth in this research field, especially during COVID-19, in terms of increasing scientific output and research collaboration. The study findings indicate an adequate quality and amount of antimicrobial resistance (AMR) research on microbiology and pharmacodynamics in India, whereas more research needs to be conducted on measures to tackle AMR, its public health, and policy aspects.

Plasma Membrane Ca2+ ATPase Activity Enables Sustained Store-operated Ca2+ Entry in the Absence of a Bulk Cytosolic Ca2+ Rise.

In many cell types, the rise in cytosolic Ca2+ due to opening of Ca2+ release-activated Ca2+ (CRAC) channels drives a plethora of responses, including secretion, motility, energy production, and gene expression. The amplitude and time course of the cytosolic Ca2+ rise is shaped by the rates of Ca2+ entry into and removal from the cytosol. However, an extended bulk Ca2+ rise is toxic to cells. Here, we show that the plasma membrane Ca2+ ATPase (PMCA) pump plays a major role in preventing a prolonged cytosolic Ca2+ signal following CRAC channel activation. Ca2+ entry through CRAC channels leads to a sustained sub-plasmalemmal Ca2+ rise but bulk Ca2+ is kept low by the activity of PMCA4b. Despite the low cytosolic Ca2+, membrane permeability to Ca2+ is still elevated and Ca2+ continues to enter through CRAC channels. Ca2+-dependent NFAT activation, driven by Ca2+ nanodomains near the open channels, is maintained despite the return of bulk Ca2+ to near pre-stimulation levels. Our data reveal a central role for PMCA4b in determining the pattern of a functional Ca2+ signal and in sharpening local Ca2+ gradients near CRAC channels, whilst protecting cells from a toxic Ca2+ overload.