In late December 2019, a cluster of unexplained pneumonia cases has been reported in Wuhan, China. A few days later, the causative agent of this mysterious pneumonia was identified as a novel coronavirus. This causative virus has been temporarily named as severe acute respiratory syndrome coronavirus 2 and the relevant infected disease has been named as coronavirus disease 2019 (COVID‐19) by the World Health Organization, respectively. The COVID‐19 epidemic is spreading in China and all over the world now. The purpose of this review is primarily to review the pathogen, clinical features, diagnosis, and treatment of COVID‐19, but also to comment briefly on the epidemiology and pathology based on the current evidence.

Depression and transient ischaemic attack represent the common psychological and neurological diseases, respectively, and are tightly associated. However, studies of depression-affected ischaemic attack have been limited to epidemiological evidences, and the neural circuits underlying depression-modulated ischaemic injury remain unknown. Here, we find that chronic social defeat stress (CSDS) and chronic footshock stress (CFS) exacerbate CA1 neuron loss and spatial learning/memory impairment after a short transient global ischaemia (TGI) attack in mice. Whole-brain mapping of direct outputs of locus coeruleus (LC)-tyrosine hydroxylase (TH, Th:) positive neurons reveals that LC-CA1 projections are decreased in CSDS or CFS mice. Furthermore, using designer receptors exclusively activated by designer drugs (DREADDs)-based chemogenetic tools, we determine that Th:LC-CA1 circuit is necessary and sufficient for depression-induced aggravated outcomes of TGI. Collectively, we suggest that Th:LC-CA1 pathway plays a crucial role in depression-induced TGI vulnerability and offers a potential intervention for preventing depression-related transient ischaemic attack.

Background: Esophageal cancer (ESCA) is one of the most common cancers worldwide and has a very poor prognosis. Hypoxia-inducible factor 1 (HIF1) signaling pathway plays a critical role in tumorigenesis and is therefore considered a potential therapeutic target in the treatment of many cancers. Activating transcription factor 5 (ATF5) facilitates the expression of various genes and has been extensively studied for its potential role in cancer treatment. Methods: The expression level of ATF5 in clinic sample was detected by quantitative real time PCR and immunohistochemistry. ATF5 biological function was investigated by western blot, cell cycle analysis, cell viability assay, luciferase reporter assays, colony formation assay, transwell assay, wound healing assay, tube formation assay, and ELISA assay. CHIP and Re-CHIP assay, GST-pulldown, and RNA-sequencing were used to study the cross-talks between ATF5 and HIF1 complex. Mouse xenograft study was utilized to study the correlation of ATF5 and tumor growth in vivo. Student’s t-test or Chi-square test was used for statistical analysis. Results: Here, we first found ATF5 was dramatically upregulated in ESCA cancer and related with poor survival time. Next, we found that the expression level of ATF5 had a positive relationship with the proliferation, migration, and invasion ability of ESCA cells. Besides, we innovatively found that ATF5 functions as a novel coactivator in HIF1 transcription complex by binding to HIF1α. Further, we demonstrated that silencing ATF5 phenocopies HIF1α knockdown in tumorigenic properties in vitro and inhibited ESCA tumor angiogenesis and proliferation in vivo. Conclusion: Herein, we found ATF5 as a novel component of the HIF1 transcription complex. The findings of the present study may provide new insights into the development of a novel and more efficient therapeutic strategy against ESCA.

Background/Aims: The Wnt signaling pathway has essential functions in the central nervous system, where it regulates the major physiological functions of neurons, including development, differentiation, and plasticity. Wnt signaling controls these cellular events; however, how Wnt pathways integrate into a coherent developmental program remains unclear. Methods: The expression and secretion of different WNT ligands (Wnt-1, Wnt-3a, Wnt-4, Wnt-5a, Wnt-11), and the levels and activities of cyclin-dependent kinases (CDK2, CDK4, CDK6/cyclin D, cyclin E) or CDK5 (CDK5/p35 and p25) were measured in Rat cortex at different embryonic stages, and in RA/BDNF-induced differentiated SH-SY5Y cell model, by Quantitative real-time PCR (qPCR), western blotting, ELISA, and in vitro CDK5 kinase assays. MAP2-BrdU double staining was used to assess cell differentiation and cell cycle exit in an RA/BDNF-induced differentiated SH-SY5Y cell model. The effects of CDK5 and Ca²⁺/calpain signaling were assessed using specific chemical inhibitors. Results: We found that Wnt-1 was unchanged and Wnt-3a was attenuated, whereas Wnt-4, Wnt-5a, and Wnt-11 were markedly up-regulated, during the development of neurons and differentiated SH-SY5Y cells. Simultaneously, the activity of CDK5 was elevated. Furthermore, we describe crosstalk between non-canonical Wnt signaling and CDK5 in the development of neurons and differentiated SH-SY5Y cells. Wnt-5a, a non-canonical Wnt ligand, regulated CDK5 via Ca²⁺/calpain signaling in both neuronal development and differentiation. Inhibition of Wnt-5a diminished CDK5 kinase activity via the Ca²⁺/calpain pathway, thereby attenuating RA-BDNF induced SH-SY5Y cell differentiation. Conclusion: Wnt-5a signaling is a significant regulator of neuronal development and differentiation and upregulates CDK5 kinase activity via Ca²⁺/calpain signaling.

Esophageal adenocarcinoma (EAC) is one of the most common subtypes of esophageal cancer, and is associated with a low 5-year survival rate. The present study aimed to identify key genes and pathways associated with EAC using bioinformatics analysis. The gene expression profiles of GSE92396, which includes 12 EAC samples and 9 normal esophageal samples, were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) between the EAC and normal samples were identified using the limma package in R language. Gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the identified DEGs were conducted using the online analysis tool, the Database for Annotation, Visualization and Integrated Discovery. A protein-protein interaction (PPI) network of the DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes (STRING) database and Cytoscape software. Finally, module analysis was conducted for the PPI network using the MCODE plug-in in Cytoscape. Of the 386 DEGs identified, the 150 upregulated genes were mainly enriched in the KEGG pathways of complement and coagulation cascades, maturity onset diabetes of the young and protein digestion and absorption; and the 236 downregulated genes were mainly enriched in amoebiasis, retinol metabolism and drug metabolism-cytochrome P450. Based on information from the STRING database, a PPI network comprising of 369 nodes and 534 edges was constructed in Cytoscape. The top 10 hub nodes with the highest degrees were determined as interleukin-8, involucrin, tissue inhibitor of metalloproteinase 1, fibronectin 1, serpin family E member 1, serpin family A member 1, cystic fibrosis transmembrane conductance regulator, secreted phosphoprotein 1, collagen type I alpha 1 chain and angiotensinogen. A total of 6 modules were detected from the PPI network that satisfied the criteria of MCODE score >4 and number of nodes >4. KEGG pathways enriched for the module DEGs were mainly within arachidonic acid metabolism, complement and coagulation cascades and rheumatoid arthritis. In conclusion, identification of these key genes and pathways may improve understanding of the mechanisms underlying the development of EAC, and may be used as diagnostic and therapeutic targets in EAC.

Postoperative atrial fibrillation (POAF) is one of the most complications after esophagectomy. Thus, our study was conducted to explore risk factors that are associated with POAF following esophagectomy. In the current study, we retrospectively evaluated 511 patients with esophageal cancer who underwent esophagectomy at our center between May 2018 and December 2020. The incidence of POAF and clinical variables were collected and analyzed. POAF occurred in 62 (12.13%) of 511 patients. Increasing age (P = .004) and lower preoperative albumin level (P = .028) was significantly associated with POAF. The length of stay was significantly increased in patients with POAF when compared to patients without POAF (P = .003). Multivariate analysis suggested that age (odds ratio [OR] = 1.049, 95% confidence interval [CI] = 1.008–1.093, P = .020), hypertension (OR = 2.207, 95% CI = 1.221–3.987, P = .009), respiratory complications (OR = 2.015, 95% CI = 1.130–3.591, P = .018) and Ivor Lewis approach (OR = 3.001, 95% CI = 1.032–8.723, P = .044) were independent risk factors for POAF following esophagectomy. Increasing age, preoperative hypertension, respiratory complications and Ivor Lewis approach are independent risk factors for POAF after esophagectomy. POAF is associated with prolonged length of stay. This study suggests that older patients, patients with hypertension or patients underwent Ivor Lewis approach should be monitored more closely during the postoperative period.