BackgroundCoronavirus disease 2019 (COVID-19) has produced a significant health burden worldwide, especially in patients with cardiovascular comorbidities. The aim of this systematic review and meta-analysis was to assess the impact of underlying cardiovascular comorbidities and acute cardiac injury on in-hospital mortality risk.MethodsPubMed, Embase and Web of Science were searched for publications that reported the relationship of underlying cardiovascular disease (CVD), hypertension and myocardial injury with in-hospital fatal outcomes in patients with COVID-19. The ORs were extracted and pooled. Subgroup and sensitivity analyses were performed to explore the potential sources of heterogeneity.ResultsA total of 10 studies were enrolled in this meta-analysis, including eight studies for CVD, seven for hypertension and eight for acute cardiac injury. The presence of CVD and hypertension was associated with higher odds of in-hospital mortality (unadjusted OR 4.85, 95% CI 3.07 to 7.70; I2=29%; unadjusted OR 3.67, 95% CI 2.31 to 5.83; I2=57%, respectively). Acute cardiac injury was also associated with a higher unadjusted odds of 21.15 (95% CI 10.19 to 43.94; I2=71%).ConclusionCOVID-19 patients with underlying cardiovascular comorbidities, including CVD and hypertension, may face a greater risk of fatal outcomes. Acute cardiac injury may act as a marker of mortality risk. Given the unadjusted results of our meta-analysis, future research are warranted.

The combination of high atomic number and high oxidation state in U materials gives rise to both high X-ray attenuation efficiency and intense green luminescence originating from ligand-to-metal charge transfer. These two features suggest that U materials might act as superior X-ray scintillators, but this postulate has remained substantially untested. Now the first observation of intense X-ray scintillation in a uranyl-organic framework (SCU-9) that is observable by the naked eye is reported. Combining the advantage in minimizing the non-radiative relaxation during the X-ray excitation process over those of inorganic salts of uranium, SCU-9 exhibits a very efficient X-ray to green light luminescence conversion. The luminescence intensity shows an essentially linear correlation with the received X-ray intensity, and is comparable with that of commercially available CsI:Tl. SCU-9 possesses an improved X-ray attenuation efficiency (E>20 keV) as well as enhanced radiation resistance and decreased hygroscopy compared to CsI:Tl.

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Updated scar management recommendations will benefit practitioners making decisions regarding optimal, evidence-based treatment strategies for their patients.

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Perfluorooctane sulfonate (PFOS) is a persistent and bio-accumulative pollutant ubiquitous in wildlife and humans, which receives many concerns on the fate, transport, distribution, and toxicity. Studies have shown that PFOS-induced neurotoxicity in experimental animals; however, little is known about the potential mechanism of PFOS exposure on the central nervous system (CNS). Ca(2+)/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha), cAMP-response element binding protein (CREB), c-fos, and c-jun, which are important down-stream molecules of calcium signaling in describing neuron cells structure and function in the CNS, were examined in the paper with the purpose to evaluate the effect of PFOS exposure on brain and approach the molecular mechanisms involved in the neurotoxicity induced by PFOS. Adult male Sprague-Dawley rats were administered with PFOS at dosages of 1.7, 5.0, and 15.0 mg/L in drinking water for 91 consecutive days. LC/MS was used for PFOS analysis in brain tissues, and western blot was employed to determine the expression of CaMKIIalpha and pCREB in the isolated cortex and hippocampus. The expression of c-fos and c-jun was detected by real-time reverse transcription polymerase chain reaction. The results showed that the expression of CaMKIIalpha and pCREB exhibits a significant increase in cortex and hippocampus after treatment with PFOS, compared with the control. The transcription factor c-fos was up-regulated in hippocampus, and c-jun was elevated both in cortex and hippocampus in PFOS-treated groups. These results indicated that, at least in part, the neurotoxic effect induced by PFOS is mediated by the Ca(2+)-dependent molecules in calcium signaling.

Searching for new host materials tailored for the high proton conductivity is highly desirable for the new generation of fuel cell system. We report here an anion-exchangeable cationic metal organic framework with the formula of [Ce­(Ccbp)2]­Br0.25Cl0.75·​6H2O·​2DMF (compound 1), which is constructed through the self-assembly of zwitterionic-based ligands H2Ccbp­Br (H2Ccbp­Br = 4-carboxy-1-(4-carboxy­benzyl)­pyridinium bromide) and (NH4)2­Ce­(NO3)6. During the investigation of humidity-dependent proton conduction behavior, we observed a rare case of rapid water-induced single-crystal-to-single-crystal phase transformation from compound 1 to a neutral chain [Ce­(Ccbp)3­(H2O)3]·​8H2O (compound 2). This structural transformation originates from the coordination of water to Ce­(III) metal centers, distortion of ligands, and the soft nature of the cationic framework 1, as probed and confirmed by a variety of investigations including color change, water vapor adsorption measurement, powder X-ray diffraction, single-crystal X-ray diffraction, humidity-dependent proton-conducting measurements, IR and UV–vis spectroscopies, and thermogravimetric analysis. As a consequence, this process introduces significant amounts of both coordinated and lattice water molecules into the structure, further giving rise to a decent water-assisted proton conductivity of 1.104 × 10–4 S cm–1 at 368 K and 95% relative humidity.

Perfluorooctane sulfonate (PFOS) and 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) are two persistent environmental contaminants that are toxic to developing nervous systems, particularly via their disruption of thyroid hormone (TH) function. To investigate whether an interaction existed between PFOS and BDE-47 on TH-mediated pathways, adult female Wistar rats were exposed to 3.2 and 32 mg/kg of PFOS or BDE-47 in their diet and co-exposed to a combination of each chemical (3.2 mg/kg) from gestational day 1 to postnatal day (PND) 14. Serum and brain tissues from both male and female neonates were collected on PNDs 1, 7, and 14 to examine TH-regulated gene and protein expression. The results revealed that (1) a significant accumulation difference occurred between the two chemicals; (2) On a equimolar basis, BDE-47 and PFOS affected serum total triiodothyronine and total thyroxine differently in adults and offspring; (3) there were region-specific and exposure- and time-dependent alterations in TH concentrations and tested gene and protein expression levels; and (4) interaction for the combined chemicals was only observed for brain-derived neurotrophic factor (BDNF), which exhibited a synergistic effect on PND 1 in the cortex and an antagonistic effect on PND 14 in the hippocampus. Our results suggest a complex TH-mediated gene and protein response to BDE-47 and/or PFOS exposure that seems little related to TH homeostasis and that little combined interaction of co-exposures was observed except on BDNF. The underlying mechanisms remain uncertain but seem to involve more actions than just TH-regulated pathway.