162 research outputs found

    Comparative study of bin and bulk microphysical schemes in simulating a heavy snowfall event that occurred in Beijing during the 2022 Winter Olympic Games

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    A heavy snowfall event that struck Beijing during February 12-13, 2022, affected some of the training sessions and events of the Winter Olympic Games. This heavy snowfall event was simulated using the Advanced Research Weather Research and Forecasting Model with both the two-moment bulk scheme (BULK) and the spectral bin microphysics scheme (BIN), and the differences in surface precipitation, radar reflectivity, and cloud microphysics processes were compared and analyzed. It was found that surface precipitation was dominated by solid precipitation particles. The 24-h accumulated precipitation of the BULK simulation was larger than that of the BIN simulation, but both were smaller than that observed. The BIN simulation was closer to the observations in terms of the trends of variation in precipitation rate and radar reflectivity during the period of heavy precipitation. The maximum and minimum vertical velocities of the BIN simulation were notably higher than those of the BULK simulation, and the water vapor content of the BIN scheme at the heights of the −10 to −20°C levels and above the −38°C level was substantially higher than that of the BULK scheme. The contents of cloud water and snow simulated by the BIN scheme were much higher than those simulated by the BULK scheme. The nucleation of ice crystals in the middle and high layers of the BULK scheme was obvious, whereas such a process was not evident in the BIN scheme. The net production rate of ice crystals and snow simulated by the BULK scheme was stronger near the surface than that simulated by the BIN scheme, and a second peak in the conversion rate existed at heights very close to the surface below 1 km, which might account for the greater intensity of precipitation in the BULK scheme. The latent heat simulated by the BULK scheme was larger (smaller) than that simulated by the BIN scheme below (above) the height of 2 km

    A prospective self-controlled study on shortening the time before taking delayed radiographs with iodized oil hysterosalpingography

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    Objectives: To verify the feasibility of walking to shorten the time before obtaining delayed radiographs after iodized oil hysterosalpingography (HSG). Material and methods: One hundred women with infertility were selected for HSG from June 2018 to December 2018 at the Women’s Hospital of Nanjing Medical University; the subjects were randomly divided into walking and control groups. The walking group was required to walk more than 12,000 steps within 6 hours after HSG, while the control group was prohibited from performing high-intensity exercise. The degree of pelvic adhesion was diagnosed with delayed radiographs acquired at 6 and 24 hours, and the diagnostic consistency of the radiographs at the two time points was evaluated. Results: No significant difference was observed in the baseline data between groups (p > 0.05). The delayed radiograph results in the walking group showed good agreement (p = 0.255 > 0.05, Kappa value 0.781 > 0.75), while those in the control group showed general agreement (p = 0.002 < 0.05, Kappa value 0.493 > 0.40 < 0.75). Conclusions: The time for acquiring delayed radiographs can be shortened by instructing patients to walk after HSG. This method improves the diagnostic efficiency of Iodized oil, saves time and costs, and may contribute to the popularization of HSG for female infertility screening, while offering good clinical application prospects

    CRISPR dynamics during the interaction between bacteria and phage in the first year of life

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    Gut microbiomes in infancy have a profound impact on health in adulthood. CRISPRs play an essential role in the interaction between bacteria and phages. However, the dynamics of CRISPRs in gut microbiomes during early life are poorly understood. In this study, using shotgun metagenomic sequencing data from 82 Swedish infants' gut microbiomes, 1882 candidate CRISPRs were identified, and their dynamics were analysed. We found large-scale turnover of CRISPRs and their spacers during the first year of life. As well as changes in relative abundance of the bacteria containing CRISPR, acquisition, loss and mutation of spacers were observed within the same CRISPR array sampled over time. Accordingly, the inferred interaction network of bacteria and phage was distinct at different times. This research underpins CRISPR dynamics and their potential role in the interaction between bacteria and phage in early life.</p

    Associations of vitamin D-related single nucleotide polymorphisms with post-stroke depression among ischemic stroke population

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    ObjectiveTo investigate the relationship between single nucleotide polymorphisms (SNPs) related to vitamin D (VitD) metabolism and post-stroke depression (PSD) in patients with ischemic stroke.MethodsA total of 210 patients with ischemic stroke were enrolled at the Department of Neurology in Xiangya Hospital, Central South University, from July 2019 to August 2021. SNPs in the VitD metabolic pathway (VDR, CYP2R1, CYP24A1, and CYP27B1) were genotyped using the SNPscan™ multiplex SNP typing kit. Demographic and clinical data were collected using a standardized questionnaire. Multiple genetic models including dominant, recessive, and over-dominant models were utilized to analyze the associations between SNPs and PSD.ResultsIn the dominant, recessive, and over-dominant models, no significant association was observed between the selected SNPs in the CYP24A1 and CYP2R1 genes and PSD. However, univariate and multivariate logistic regression analysis revealed that the CYP27B1 rs10877012 G/G genotype was associated with a decreased risk of PSD (OR: 0.41, 95% CI: 0.18–0.92, p = 0.030 and OR: 0.42, 95% CI: 0.18–0.98, p = 0.040, respectively). Furthermore, haplotype association analysis indicated that rs11568820-rs1544410-rs2228570-rs7975232-rs731236 CCGAA haplotype in the VDR gene was associated with a reduced risk of PSD (OR: 0.14, 95% CI: 0.03–0.65, p = 0.010), whereas no significant association was observed between haplotypes in the CYP2R1 and CYP24A1 genes and PSD.ConclusionOur findings suggest that the polymorphisms of VitD metabolic pathway genes VDR and CYP27B1 may be associated with PSD in patients with ischemic stroke

    Lipopolysaccharide-Induced Dephosphorylation of AMPK-Activated Protein Kinase Potentiates Inflammatory Injury via Repression of ULK1-Dependent Autophagy

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    AMP-activated protein kinase (AMPK) is a crucial metabolic regulator with profound modulatory activities on inflammation. Although the anti-inflammatory benefits of AMPK activators were well documented in experimental studies, the pathological significance of endogenous AMPK in inflammatory disorders largely remains unknown. This study investigated the phosphorylation status of endogenous AMPK and the potential roles of AMPK in mice with lipopolysaccharide (LPS)-induced lethal inflammation. The results indicated that LPS dose-dependently decreased the phosphorylation level of AMPK and its target protein acetyl-CoA carboxylase (ACC). Reactivation of AMPK with the AMPK activator A-769662 suppressed LPS-induced elevation of interleukin 6, alleviated histological abnormalities in lung and improved the survival of LPS-challenged mice. Treatment with A-769662 restored LPS-induced suppression of autophagy, inhibition of autophagy by 3-MA reversed the beneficial effects of A-769662. Treatment with A-769662 suppressed LPS-induced activation of mammalian target of rapamycin (mTOR), co-administration of mTOR activator abolished the beneficial effects of A-769662, and the suppressive effects of A-769662 on uncoordinated-51-like kinase 1 (ULK1) phosphorylation. Inhibition of ULK1 removed the beneficial effects of A-769662. These data indicated that LPS-induced dephosphorylation of AMPK could result in weakened inhibition of mTOR and repression of ULK1-dependent autophagy, which might potentiate the development of LPS-induced inflammatory injury. These data suggest that pharmacological restoration of AMPK activation might be a beneficial approach for the intervention of inflammatory disorders

    The role of indoleamine 2,3-dioxygenase 1 in early-onset post-stroke depression

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    BackgroundThe immune-inflammatory response has been widely considered to be involved in the pathogenesis of post-stroke depression (PSD), but there is ambiguity about the mechanism underlying such association.MethodsAccording to Diagnostic and Statistical Manual of Mental Disorders (5th edition), depressive symptoms were assessed at 2 weeks after stroke onset. 15 single nucleotide polymorphisms (SNPs) in genes of indoleamine 2,3-dioxygenase (IDO, including IDO1 and IDO2) and its inducers (including pro-inflammatory cytokines interferon [IFN]-γ, tumor necrosis factor [TNF]-α, interleukin [IL]-1β, IL-2 and IL-6) were genotyped using SNPscan™ technology, and serum IDO1 levels were detected by double-antibody sandwich enzyme-linked immune-sorbent assay.ResultsFifty-nine patients (31.72%) were diagnosed with depression at 2 weeks after stroke onset (early-onset PSD). The IDO1 rs9657182 T/T genotype was independently associated with early-onset PSD (adjusted odds ratio [OR] = 3.008, 95% confidence interval [CI] 1.157-7.822, p = 0.024) and the frequency of rs9657182 T allele was significantly higher in patients with PSD than that in patients with non-PSD (χ2 = 4.355, p = 0.037), but these results did not reach the Bonferroni significance threshold (p &gt; 0.003). Serum IDO1 levels were also independently linked to early-onset PSD (adjusted OR = 1.071, 95% CI 1.002-1.145, p = 0.044) and patients with PSD had higher serum IDO1 levels than patients with non-PSD in the presence of the rs9657182 T allele but not homozygous C allele (t = -2.046, p = 0.043). Stroke patients with the TNF-α rs361525 G/G genotype had higher serum IDO1 levels compared to those with the G/A genotype (Z = -2.451, p = 0.014).ConclusionsOur findings provided evidence that IDO1 gene polymorphisms and protein levels were involved in the development of early-onset PSD and TNF-α polymorphism was associated with IDO1 levels, supporting that IDO1 which underlie strongly regulation by cytokines may be a specific pathway for the involvement of immune-inflammatory mechanism in the pathophysiology of PSD
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