Abstract Light is a dominant zeitgeber for biological clocks, and its regulatory mechanism for sleep-wake activity has been extensively studied. However, the molecular pathways through which the Antarctic unique photoperiod, i.e. polar days in summer and polar nights in winter, affects human sleep and circadian rhythm remain largely unidentified, despite previous studies have observed delayed circadian rhythm and sleep disruptions of expeditioners during polar nights. In this study, we conducted comprehensive dynamic research of the expeditioners during their residence in Antarctica for over one year. By integrating the phenotypic changes with multi-omics data, we tried to identify the novel candidate regulators and their correlation networks involved in circadian and sleep disorders under the extreme photoperiod. We found that during the austral winter, expeditioners exhibited delayed bedtime and get up time, reduced sleep efficiency, and increased sleep fragmentation. Meanwhile, serum dopamine metabolite levels significantly increased, while serotonin metabolites and antioxidants decreased. These changes were accompanied by altered expression of genes and proteins associated with neural functions, cellular activities, transcriptional regulation, and so on. Through the correlation and causal mediation analysis, we identified several potential pathways modulating human sleep-wake activity, involving genes and proteins related to neural function, glucose metabolism, and extracellular matrix homeostasis, as well as some lncRNAs. Based on the identified causal mediators, LASSO regression analysis further revealed a novel candidate gene, Shisa Family Member 8 (SHISA8), as a potential key regulatory hub in this process. These findings shed light on the probable molecular mechanisms of sleep disorders in Antarctica and suggested SHISA8 as a novel candidate target for the medical intervention of sleep disorders under changed light-dark cycle.
Atrial fibrillation (AF) is a relatively common arrhythmia in clinical practice. Although significant progress has been achieved in the treatment of AF and its associated complications, research on AF prevention lags behind, mainly due to the lack of a deep understanding of AF pathogenesis. In recent years, as our knowledge has grown, the role of the inflammatory/immune response in the occurrence and progression of AF has gradually gained attention. In this paper, based on existing gene expression data in the Gene Expression Omnibus database, a detailed description of immune infiltration status in AF is presented using a series of analytical methods, including differential analysis, Gene Ontology categorization, Kyoto Encyclopedia of Genes and Genomes enrichment analysis, and weighted gene coexpression network analysis, and analysis tools such as CIBERSORTx and Cytoscape. Several new AF/immune infiltrations-related signature genes were identified, and the AF/immune infiltration pathology was classified based on these immune signature genes, thus providing novel insights into the pathogenesis of AF based on the inflammatory response.
Light is the dominant zeitgeber for biological clocks, and its regulatory mechanism for sleep–wake activity has been extensively studied. However, the molecular pathways through which the unique Antarctic light environment, with polar days in summer and polar nights in winter, affects human sleep and circadian rhythm remain largely unidentified, although previous studies have observed delayed circadian rhythm and sleep disruptions among expeditioners during polar nights. In this study, we conducted comprehensive dynamic research on the expeditioners residing in Antarctica for over one year. By integrating the phenotypic changes with multi-omics data, we tried to identify the novel candidate regulators and their correlation networks involved in circadian and sleep disorders under abnormal light exposure. We found that during the austral winter, expeditioners exhibited delayed bedtime and getting up time, reduced sleep efficiency, and increased sleep fragmentation. Meanwhile, serum dopamine metabolite levels significantly increased, while serotonin metabolites and antioxidants decreased. These changes were accompanied by altered expression of genes and proteins associated with neural functions, cellular activities, transcriptional regulation, and so on. Through the correlation and causal mediation analysis, we identified several potential pathways modulating human sleep–wake activity, involving genes and proteins related to neural function, glucose metabolism, extracellular matrix homeostasis, and some uncharacterized lncRNAs. Based on the identified causal mediators, LASSO regression analysis further revealed a novel candidate gene, Shisa Family Member 8 (SHISA8), as a potential key regulatory hub in this process. These findings shed light on the probable molecular mechanisms of sleep disorders in Antarctica and suggest SHISA8 as a novel candidate target for medical intervention in sleep disorders under unique light environments.
Objective To study the clinical application value of the low forceps in vaginal delivery. Methods To retrospectively analyze the clinical data of 280 cases of the low forceps in vaginal delivery,and randomly selected 140 cases pregnant women who cesarean section, as the control group. To compare the influence of maternal and neonatal morbidity in the two groups. Results There were no statistically significant differences between the two groups for the incidence of the postdelivery hemorrage,birth trauma infectious, asphyxia neonatorum associated with delivery from low forceps when compared with cesarean section. The incidenc of the postdelivery sick rate was significantly lower in the low forceps group( 3.2% ) than that in the control group ( 10.0% ) ( x2 = 8.30, P ＜ 0.05 ). Conclusion Low forceps may be a valuable instrument and safety or efficacy in vaginal delivery and that it should be more widely used in appropriate clinical situations.
Key words:
Obstetrical forceps; Labor; Labor complications
BackgroundPancreatic fibrosis is a pathophysiological process associated with excessive deposition of extracellular matrix in pancreas, leading to reduced insulin secretion and derangement of glucose metabolism. X/A-like cells, a group of unique endocrine cells in gastric oxyntic mucosa, produce and secret ghrelin to influence energy balance. Whether gastric X/A-like cells affect pancreatic fibrosis and subsequent glucose homeostasis remains unclear.MethodsWe established a Ghrl-cre transgene in which the cre enzyme is expressed in X/A-like cells under the control of ghrelin-promoter. TSC1flox/flox mice were bred with Ghrl-cre mice to generate Ghrl-TSC1−/− (TG) mice, within which mTORC1 signaling was activated in X/A-like cells. Pancreatic fibrosis and insulin secretion were analyzed in the TG mice.FindingsActivation of mTORC1 signaling by deletion of TSC1 gene in gastric X/A-like cells induced spontaneous pancreatic fibrosis. This alteration was associated with reduced insulin expression and secretion, as well as impaired glucose metabolism. Activation of mTORC1 signaling in gastric X/A-like cells reduced gastric and circulating ghrelin levels. Exogenous ghrelin reversed pancreatic fibrosis and glucose intolerance induced by activation of mTORC1 signaling in these cells. Rapamycin, an inhibitor of mTOR, reversed the decrease of ghrelin levels and pancreatic fibrosis.InterpretationActivation of mTORC1 signaling in gastric X/A-like cells induces spontaneous pancreatic fibrosis and subsequently impairs glucose homeostasis via suppression of ghrelin.
To identify the clinical and anatomical presentations and to discuss the guidelines for surgical management of anomalies of the first branchial cleft.Twenty-one patients with first branchial cleft anomalies were treated in our department between January 1994 and December 2004, their clinical data were retrospectively analysed.Surgery was performed on all patients. Among them 13 were males and 8 females, ranging in age from 1.5 to 33 years with an average of 15 years. Anatomically, 3 types of first branchial cleft anomalies were identified: fistulas (n = 17), cysts (n = 2), and fistula combined with cyst (n = 2). Before definitive surgery, soma patients (n = 4) underwent incision and drainage for infection owing to the difficulties in diagnosing this anomaly. Methylthioninium Chloride was used in almost all cases for tracking the fistulous during operation. Wide exposure is necessary in many cases,and a standard parotidectomy incision allows adequate exposure of the anomaly and preservation of the facial nerve.Complete removal without complications depends on a good understanding of regional embryogenesis, an awareness of the different anatomical presentations, and a readiness to identify and protect the facial nerve during resection.
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