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We demonstrate all-optical spatial mode-cleaning in non-Hermitian waveguides. The effect is accounted by a unidirectional coupling among the modes resulting from a simultaneous modulation of the refractive index and the gain/loss along graded index multimodal waveguides. Depending on the spatial delay between the real and imaginary part of the potential modulation, higher or lower order modes are favored, which in latter case eventually leads to an nearly-monomode propagation. In this way, for any arbitrary initial field distribution an antisymmetric non-Hermitian modulation results in an effective mode-cleaning. The effect is demonstrated analytically, based on coupled mode theory in 1D waveguides, and numerically proven by solving the wave propagation equation with the antisymmetric non-Hermitian potential. The proposal is also generalized to the more involved case of 2D waveguides, leading to a significant reduction of the beam quality factor and improvement of beam spatial quality.

The development of novel strategies to counteract diseases related to barrier dysfunction is a priority, since sepsis and acute respiratory distress syndrome are still associated with high mortality rates. In the present study, we focus on the effects of the unfolded protein response suppressor (UPR) 4-Phenylbutyrate (4-PBA) in Lipopolysaccharides (LPS)-induced endothelial injury, to investigate the effects of that compound in the corresponding damage. 4-PBA suppressed binding immunoglobulin protein (BiP) - a UPR activation marker - and potentiated LPS - induced signal transducer and activator of transcription 3 (STAT3) and extracellular signal-regulated protein kinase (ERK) 1/2 activation. In addition to those effects, 4-PBA enhanced paracellular hyperperme-ability in inflamed bovine pulmonary endothelial cells, and did not affect cell viability in moderate concentrations. Our observations suggest that UPR suppression due to 4-PBA augments LPS-induced endothelial injury, as well as the corresponding barrier disruption. [ABSTRACT FROM AUTHOR]

Reactive oxygen species are a group of cellular molecules that stand as double-edged swords, their good and bad being discriminated by a precise balance. Several metabolic reactions in the biological system generate these molecules that interact with cellular atoms to regulate functions ranging from cell homeostasis to cell death. A prooxidative state of the cell concomitant with decreased clearance of such molecules leads to oxidative stress, which contributes as a prime pathophysiological mechanism in various diseases including renal disorders, such as acute kidney injury. However, targeting the generation of oxidative stress in renal disorders by an antioxidant, resveratrol, is gaining considerable therapeutic importance and is known to improve the condition in preclinical studies. This review aims to discuss molecular mechanisms of oxidative stress in acute kidney injury and its amelioration by resveratrol. The major sources of data were PubMed and Google Scholar, with studies from the last five years primarily included, with significant earlier data also considered. Mitochondrial dysfunction, various enzymatic reactions, and protein misfolding are the major sources of reactive oxygen species in acute kidney injury, and interrupting these loci of generation or intersection with other cellular components by resveratrol can mitigate the severity of the condition. [ABSTRACT FROM AUTHOR]

T-activation polyagglutination can be caused by bacteria or viruses and has been associated with haemolytic anaemia. Coronavirus disease-19 (COVID-19) is also associated with haemolytic anaemia. The presented study aims to determine T activation polyagglutination in critically ill COVID-19 patients. Anti-T Arachis hypogaea lectin was incubated with the red blood cells of the COVID-19 patient and checked for agglutination. Thirty-four percent (34.3%) of COVID-19 patients in the intensive care unit (ICU) had potentially activated T cells and polyagglutinable red blood cells, as demonstrated by their cryptantigen exposure that caused agglutination. The study revealed a high prevalence of anti-T among ICU-admitted COVID-19 patients, suggesting that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may cause transient T activation, polyagglutination in critically ill COVID-19 patients in vitro and possibly haemolysis in vivo. [ABSTRACT FROM AUTHOR]