Objective: To identify markers associated with in-hospital death in patients with coronavirus disease 2019 (COVID-19)eassociated pneumonia. Patients and Methods: A retrospective cohort study was conducted of 140 patients with moderate to critical COVID-19eassociated pneumonia requiring oxygen supplementation admitted to the hospital

BackgroundEnvironmental pollutants such as polycyclic aromatic hydrocarbons (PAHs), lead, and mercury are released by combustion of coal and other fossil fuels.ObjectivesIn the present study we evaluated the association between prenatal exposure to these pollutants and child development measured by the Gesell Developmental Schedules at 2 years of age.MethodsThe study was conducted in Tongliang, Chongqing, China, where a seasonally operated coal-fired power plant was the major source of ambient PAHs and also contributed lead and mercury to the air. In a cohort of nonsmoking women and their newborns enrolled between March 2002 and June 2002, we measured levels of PAH–DNA adducts, lead, and mercury in umbilical cord blood. PAH–DNA adducts (specifically benzo[a]pyrene adducts) provided a biologically relevant measure of PAH exposure. We also obtained developmental quotients (DQs) in motor, adaptive, language, and social areas.ResultsDecrements in one or more DQs were significantly associated with cord blood levels of PAH–DNA adducts and lead, but not mercury. Increased adduct levels were associated with decreased motor area DQ (p = 0.043), language area DQ (p = 0.059), and average DQ (p = 0.047) after adjusting for cord lead level, environmental tobacco smoke, sex, gestational age, and maternal education. In the same model, high cord blood lead level was significantly associated with decreased social area DQ (p = 0.009) and average DQ (p = 0.038).ConclusionThe findings indicate that exposure to pollutants from the power plant adversely affected the development of children living in Tongliang; these findings have implications for environmental health policy.

Full author information is available at the end of the article Xuefeng Zang and Qian Wang contributed equally to this work. Hua Zhou, Sanhong Liu and Xinying Xue contributed equally to this work. The members of the COVID-19 Early Prone Position Study Group are listed in the Acknowledgements.

Cell-based therapy represents a promising strategy in the treatment of neurological disorders. Human umbilical cord tissue has recently been recognized as an ideal source of mesenchymal stromal cells due to accessibility, vast abundance and safety. Here, an intracerebral hemorrhage (ICH) rat model was established by injection of bacterial collagenase VII and CM-DiI labeled human umbilical cord tissue derived mesenchymal stromal cells (UC-MSC) were intracerebrally transplanted into rat brain 24h after ICH. The results demonstrated that UC-MSC treatment significantly improved neurological function deficits and decreased injury volume of ICH rats. Leukocytes infiltration, microglial activation, ROS level and matrix metalloproteinases (MMPs) production were substantially reduced in peri-ICH area in cell-treated group as compared with PBS control at day 3 post-transplantation. In addition, UC-MSC treatment significantly increased vascular density in peri-ICH area and transplanted UC-MSC were found to be able to incorporate into cerebral vasculature in ipsilateral hemisphere at 14 days after transplantation. In summary, intracerebral administration of UC-MSC could accelerate neurological function recovery of ICH rat, the underlying mechanism may ascribe to their ability to inhibit inflammation and promote angiogenesis. Thus UC-MSC may provide a potential cell candidate for cell-based therapy in neurological disorders.

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Caffeic acid phenethyl ester, an active component of propolis, has been implicated in the regulation of cell growth and apoptosis, although the exact mechanism of this activity has not been elucidated. In this study, we explored the effects of caffeic acid phenethyl ester on growth, cell cycle, apoptosis and beta-catenin/T-cell factor signaling in human colon cancer cells. Using two human sporadic colon cancer cell lines (HCT116 and SW480), we assayed for cell growth inhibition, cell cycle and apoptosis induction. We also assayed for beta-catenin and downstream target genes (cyclin D1 and c-myc) mRNA and protein expression by reverse transcriptase-polymerase chain reaction and Western blot analysis. Beta-catenin localization was detected by indirect immunofluorescence. Beta-catenin/T-cell factor transcriptional activity was determined by transient transfection and reporter gene assay. Caffeic acid phenethyl ester completely inhibited growth, and induced G1 phase arrest and apoptosis in a dose-dependent manner in both HCT116 and SW480 cells. Treatment of human colon cancer cells with apoptotic concentrations of caffeic acid phenethyl ester resulted in a dose-dependent and time-dependent loss of total beta-Catenin protein, associated with decreased nuclear beta-catenin. Caffeic acid phenethyl ester reduced the expression of cyclin D1 and c-myc in a dose-dependent and time-dependent manner. We proved that caffeic acid phenethyl ester markedly suppressed the transcriptional activity of beta-catenin/T-cell factor in both HCT116 and SW480 cells depending on the concentration of caffeic acid phenethyl ester. These results indicate that caffeic acid phenethyl ester is an excellent inhibitor of beta-catenin/T-cell factor signaling in colon cancer cell lines and suggest that caffeic acid phenethyl ester merits further study as an agent against colorectal cancers.

UC-MSC transplantation could accelerate neurologic functional recovery of rats after stroke, which may be mediated by their ability to promote angiogenesis.

Recent studies have suggested that the etiology of autism spectrum disorder (ASD) may be caused by immunological factors, particularly abnormalities in the innate immune system. However, it is still unclear which specific cytokines may be of most importance. The current study therefore investigated which cytokines showed altered concentrations in blood in ASD compared with healthy control children and which were also correlated with symptom severity. Our study sample included 32 children diagnosed with ASD and 28 age and sex-matched typically developing children. Autism symptoms were measured using the Autistic Behavior Checklist (ABC) and blood samples were taken from all subjects. We used Milliplex cytokine kits to determine serum concentrations of 11 Th1, Th2 and Th17 related cytokines. Additionally, expression of THRIL (TNFα and hnRNPL related immunoregulatory LincRNA), a long non-coding RNA involved in the regulation of tumor necrosis factor- α (TNF-α), was determined using real–time PCR. Of the 11 cytokines measured only concentrations of TNF-α (p=0.002), IL-1β (p=0.02) and IL-17a (p=0.049) were significantly increased in ASD children compared to typically developing controls, but only TNF-α concentrations were positively correlated with severity of ASD symptoms on all 5 different ABC sub-scales and were predictive of an ASD phenotype (area under the curve = 0.74). Furthermore, THRIL RNA expression was significantly decreased in ASD children. Our results provide further support for altered innate immunity being an important autism pathogenic factor, with autistic children showing increased blood TNF-α concentrations associated with symptom severity, and decreased expression of the THRIL gene involved in regulating TNF-α.