Lopezforrest1521

Thermoelectric effects of ice play an important role in many natural and engineering phenomena. We investigate, numerically and analytically, the electrification of finite-thickness ice slabs due to an imposed temperature difference across them. When exposed to a temperature gradient, thermoelectrification involves a fast initial stage dominated by Bjerrum defects and a subsequent slow stage driven by ionic defects. The time scales of the first and second stages are derived analytically and correspond to the Debye time scales based on the density of Bjerrum and ionic defects, respectively. For a given ice slab, at the steady state, the thermovoltage across it and the charge accumulation near its two ends depend strongly on its thickness, with the sensitivity of the thermovoltage being more pronounced. The discrepancy between the computed thermovoltage and experimental measurements is analyzed. The analysis shows that, although thermoelectric effects in ice were discovered 50 years ago, significant gaps, ranging from the bulk and interfacial properties of defects to the measurement of thermovoltage, exist in the quantitative understanding of these effects. Filling these gaps requires further experimental, theoretical, and computational studies.Malignant tumors are one of the main causes for human death and are tightly associated with overexpression of reactive oxygen species (ROS) in pathological processes. Therefore, in vivo monitoring of ROS, especially ONOO-, remains of great significance for diagnosis and therapy of tumors to improve the survival rate. Herein, we designed and constructed a reliable near-infrared (NIR) ratiometric fluorescent biosensor CDMS for monitoring the fluctuations of ONOO- in the process of tumor progression. CDMS featured outstanding stability to photoirradiation, substantial quantum yields, rapid response ( less then 5 s), high selectivity and excellent biocompatibility. Moreover, CDMS exhibited distinct ratiometric fluorescence signal changes after reacting with ONOO-. Fluorescence imaging in immune stimulated cells indicated that CDMS was competent to determine the levels of ONOO- in the cellular level. Remarkably, CDMS was further applied in monitoring the expression of ONOO- in a peritonitis mouse model and tumor-bearing mouse model. Based on the excellent properties of CDMS, the probe exhibited the potential for noninvasive in vivo visualization of ONOO- in the occurrence and process of tumor development. It is envisioned that CDMS can be employed as a promising tool for monitoring the ONOO- fluxes in tumor pathological progression, especially for tumor diagnosis and therapy.Steroid saponins are the medicinal compounds and nutrition ingredients of medicine food homology (MFH) Dioscorea zingiberensis C. H. Wright (D. zingiberensis) yam. Our phytochemical investigation of the edible rhizomes resulted in 9 new furostanol steroid saponins named dioscins A-I (1-9), together with 11 known steroid saponins. Their chemical structures were elucidated based on spectroscopic and chemical analyses. The new dioscins were evaluated for their anti-inflammatory and beneficial effects against cerebral ischemia reperfusion (I/R) injury on RAW264.7 and PC12 cells in vitro, respectively. Dioscins A, B, and G revealed considerable anti-I/R effect through an anti-inflammatory mechanism based on the decreasing concentration of pro-inflammatory (TNF-α and IL-6) and down-regulating the NF-κB expression. The present research demonstrated that daily consumption of this yam plant probably prevented the I/R occurrence via the anti-inflammatory property of steroid saponins, and it also enriched the steroid saponin library, providing the possibility to develop MFH-containing steroid saponins into functional foods for maintenance of human health or drugs for the treatment of I/R disease.Lack of long-term patency has hindered the clinical use of small-diameter prosthetic vascular grafts with the majority of these failures due to the development of neointimal hyperplasia. Previous studies by our laboratory revealed that small-diameter expanded polytetrafluoroethylene (ePTFE) grafts coated with antioxidant elastomers are a promising localized therapy to inhibit neointimal hyperplasia. This work is focused on the development of poly(diol-co-citrate-co-ascorbate) (POCA) elastomers with tunable properties for coating ePTFE vascular grafts. A bioactive POCA elastomer (@20  20  8, [citrate]  [diol]  [ascorbate]) coating was applied on a 1.5 mm diameter ePTFE vascular graft as the most promising therapeutic candidate for reducing neointimal hyperplasia. Surface ascorbate density on the POCA elastomer was increased to 67.5 ± 7.3 ng mg-1 cm-2. The mechanical, antioxidant, biodegradable, and biocompatible properties of POCA demonstrated desirable performance for in vivo use, inhibiting human aortic smooth muscle cell proliferation, while supporting human aortic endothelial cells. POCA elastomer coating number was adjusted by a modified spin-coating method to prepare small-diameter ePTFE vascular grafts similar to natural vessels. A significant reduction in neointimal hyperplasia was observed after implanting POCA-coated ePTFE vascular grafts in a guinea pig aortic interposition bypass graft model. POCA elastomer thus offers a new avenue that shows promise for use in vascular engineering to improve long-term patency rates by coating small-diameter ePTFE vascular grafts.

Increasing reports of long-term symptoms following COVID-19 infection, even among mild cases, necessitates systematic investigation into the prevalence and type of lasting illness. Notably, there is limited data regarding the influence of social determinants of health, like perceived discrimination and economic stress, which may exacerbate COVID-19 health risks. The primary goals of this study are to test the bearing of subjective experiences of discrimination, financial security, and quality of care on illness severity and lasting symptom complaints.

1,584 recovered COVID-19 patients that experienced mild to severe forms of the disease provided information about their illness, medical history, lasting symptoms, and psychosocial information. Prevalence data isolated differences in patients infected early versus late in the pandemic. click here Path analyses examined hypothesized associations between discrimination, illness severity, and lasting symptoms.

logistic regressions tested social determinants hypothesizeortantly, psychosocial factors (perceived discrimination and perceived SES) can exacerbate individual health risk. This study provides actionable directions for improved health outcomes by establishing that sociodemographic risk and medical care influence near and long-ranging health outcomes.

Lasting symptoms after recovery from COVID-19 are highly prevalent and neural systems are significantly impacted. Importantly, psychosocial factors (perceived discrimination and perceived SES) can exacerbate individual health risk. This study provides actionable directions for improved health outcomes by establishing that sociodemographic risk and medical care influence near and long-ranging health outcomes.Cellular entry of coronaviruses depends on binding of the viral spike (S) protein to a specific cellular receptor, the angiotensin-converting enzyme 2 (ACE2). Furthermore, the viral spike protein expresses an RGD motif, suggesting that cell surface integrins may be attachment co-receptors. However, using infectious SARS-CoV-2 requires a biosafety level 3 laboratory (BSL-3), which limits the techniques that can be used to study the mechanism of cell entry. Here, we UV-inactivated SARS-CoV-2 and fluorescently labeled the envelope membrane with octadecyl rhodamine B (R18) to explore the role of integrin activation in mediating both cell entry and productive infection. We used flow cytometry and confocal fluorescence microscopy to show that fluorescently labeled SARS-CoV-2 R18 particles engage basal-state integrins. Furthermore, we demonstrate that Mn 2+ , which activates integrins and induces integrin extension, enhances cell binding and entry of SARS-CoV-2 R18 in proportion to the fraction of integrins activated. We also show that one class of integrin antagonist, which binds to the αI MIDAS site and stabilizes the inactive, closed conformation, selectively inhibits the engagement of SARS-CoV-2 R18 with basal state integrins, but is ineffective against Mn 2+ -activated integrins. At the same time, RGD-integrin antagonists inhibited SARS-CoV-2 R18 binding regardless of integrin activity state. Integrins transmit signals bidirectionally 'inside-out' signaling primes the ligand binding function of integrins via a talin dependent mechanism and 'outside-in' signaling occurs downstream of integrin binding to macromolecular ligands. Outside-in signaling is mediated by Gα 13 and induces cell spreading, retraction, migration, and proliferation. Using cell-permeable peptide inhibitors of talin, and Gα 13 binding to the cytoplasmic tail of an integrin's β subunit, we further demonstrate that talin-mediated signaling is essential for productive infection by SARS-CoV-2.SARS-CoV-2 has made >190-million infections worldwide, thus it is pivotal to understand the viral impacts on host cells. Many viruses can significantly alter host chromatin 1 , but such roles of SARS-CoV-2 are largely unknown. Here, we characterized the three-dimensional (3D) genome architecture and epigenome landscapes in human cells after SARS-CoV-2 infection, revealing remarkable restructuring of host chromatin architecture. High-resolution Hi-C 3.0 uncovered widespread A compartmental weakening and A-B mixing, together with a global reduction of intra-TAD chromatin contacts. The cohesin complex, a central organizer of the 3D genome, was significantly depleted from intra-TAD regions, supporting that SARS-CoV-2 disrupts cohesin loop extrusion. Calibrated ChIP-Seq verified chromatin restructuring by SARS-CoV-2 that is particularly manifested by a pervasive reduction of euchromatin modifications. Built on the rewired 3D genome/epigenome maps, a modified activity-by-contact model 2 highlights the transcriptional weakening of antiviral interferon response genes or virus sensors (e.g., DDX58 ) incurred by SARS-CoV-2. In contrast, pro-inflammatory genes (e.g. IL-6 ) high in severe infections were uniquely regulated by augmented H3K4me3 at their promoters. These findings illustrate how SARS-CoV-2 rewires host chromatin architecture to confer immunological gene deregulation, laying a foundation to characterize the long-term epigenomic impacts of this virus.The increasing prevalence of SARS-CoV-2 variants has raised concerns regarding possible decreases in vaccine efficacy. Here, neutralizing antibody titers elicited by mRNA-based and an adenoviral vector-based vaccine against variant pseudotyped viruses were compared. BNT162b2 and mRNA-1273-elicited antibodies showed modest neutralization resistance against Beta, Delta, Delta plus and Lambda variants whereas Ad26.COV2.S-elicited antibodies from a significant fraction of vaccinated individuals were of low neutralizing titer (IC 50 less then 50). The data underscore the importance of surveillance for breakthrough infections that result in severe COVID-19 and suggest the benefit of a second immunization following Ad26.COV2.S to increase protection against the variants.