Quantifying depressive symptoms on incidence of common chronic diseases and multimorbidity patterns in middle-aged and elderly Chinese adults.

BACKGROUND: Depressive symptoms are highly prevalent and increase risks of various morbidities. However, the extent to which depressive symptoms could account for incidence of these chronic conditions, in particular multimorbidity patterns, remains to be examined and quantified. METHODS: For this cohort analysis, we included 9024-14,093 participants aged 45 years and older from the China Health and Retirement Longitudinal Study (CHARLS). Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the longitudinal associations between depressive symptoms and 13 common chronic diseases and 4 multimorbidity patterns. Population attributable fractions (PAFs) combining the information on both exposure prevalence and risk association were estimated to quantify the magnitude of the burden of these conditions attributable to depressive symptoms. RESULTS: Depressive symptoms were associated with increased risks of liver disease, stroke, heart problem, asthma, diabetes, arthritis, kidney disease, chronic lung disease, digestive disease, dyslipidemia, and memory-related disease, and the adjusted HRs (95% CIs) and PAFs (95% CIs) ranged from 1.15 (1.05-1.26) to 1.64 (1.38-1.96) and 5% (0-10%) to 17% (6-28%), respectively. In addition, individuals with depressive symptoms had elevated risks of the cardiometabolic-cancer pattern, the cerebrovascular-memory pattern, the articular-visceral organ pattern, and the respiratory pattern, with respective HRs (95% CIs) of 1.26 (1.11-1.42), 1.34 (1.07-1.69), 1.45 (1.29-1.63), and 2.01 (1.36-2.96), and respective PAFs (95% CIs) of 5% (0-10%), 8% (-4-21%), 12% (7-17%), and 20% (5-35%). CONCLUSION: Depressive symptoms contribute substantially to the burden across a broad range of chronic diseases as well as different multimorbidity patterns in middle-aged and older Chinese.

Uterine rupture in patients with a history of hysteroscopy procedures: Case series and review of literature.

RATIONALE: Uterine rupture during pregnancy poses significant risks to both the fetus and the mother, resulting in high mortality and morbidity rates. While awareness of uterine rupture prevention after a cesarean section has increased, insufficient attention has been given to cases caused by pregnancy following hysteroscopy surgery. PATIENT CONCERNS: We report 2 cases here, both of whom had a history of hysteroscopy surgery and presented with severe abdominal pain during pregnancy. DIAGNOSES: Both patients had small uterine ruptures, with no significant abnormalities detected on ultrasonography. The diagnosis was confirmed by a CT scan, which showed hemoperitoneum. INTERVENTIONS: We performed emergency surgeries for the 2 cases. OUTCOMES: We repaired the uterus in 2 patients during the operation. Both patients recovered well. The children survived. No abnormalities were detected during their follow-up visits. LESSONS: Attention should be paid to the cases of pregnancy after hysteroscopy.

Advances in the relationship between ferroptosis and epithelial-mesenchymal transition in cancer.

Epithelial-mesenchymal transition (EMT) is a cellular reprogramming process that converts epithelial cells into mesenchymal-like cells with migratory and invasive capabilities. The initiation and regulation of EMT is closely linked to a range of transcription factors, cell adhesion molecules and signaling pathways, which play a key role in cancer metastasis and drug resistance. The regulation of ferroptosis is intricately linked to various cell death pathways, intracellular iron homeostasis, and the protein network governing iron supply and storage. The ability of ferroptosis to disrupt cancer cells and overcome drug resistance lies in its control of intracellular iron ion levels. EMT process can promote the accumulation of iron ions, providing conditions for ferroptosis. Conversely, ferroptosis may impact the regulatory network of EMT by modulating transcription factors, signaling pathways, and cell adhesion molecules. Thus, ferroptosis related genes and signaling pathways and oxidative homeostasis play important roles in the regulation of EMT. In this paper, we review the role of ferroptosis related genes and their signaling pathways in regulating cancer EMT to better understand the crosstalk mechanism between ferroptosis and EMT, aiming to provide better therapeutic strategies for eradicating cancer cells and overcoming drug resistance.

[Bioinformatics-based identification of key genes CDC5L and related pathways in osteosarcoma and Ewing's sarcoma].

OBJECTIVE: Osteosarcoma(OS) and Ewing's sarcoma (EWS) are the two most common primary malignant bone tumors in children. The aim of the study was to identify key genes in OS and EWS and investigate their potential pathways. METHODS: Expression profiling (GSE16088 and GSE45544) were obtained from GEO DataSets. Differentially expressed genes were identified using GEO2R and key genes involved in the occurrence of both OS and EWS were selected using venn diagram. Gene ontology and pathway enrichment analyses were performed for the ensembl. Protein-protein interaction (PPI) networks were established by STRING. Further, UCSC was used to predict the transcription factors of the cell division cycke 5-like(CDC5L) gene, and GEPIA was used to analyze the correlation between the transcription factors and the CDC5L gene. RESULTS: The results showed that CDC5L gene was the key gene involved in the pathogenesis of OS and EWS. The gene is mainly involved in mitosis, and is related to RNA metabolism, processing of capped intron-containing pre-mRNA, mRNA and pre-mRNA splicing. CONCLUSION: CDC5L, as a key gene, plays a role in development of OS and EWS, which may be reliable targets for diagnosis and treatment of these primary malignant tumors.

Tanshinone IIA alleviates ovalbumin-induced allergic rhinitis symptoms by inhibiting Th2 cytokine production and mast cell histamine release in mice.

CONTEXT: Studies have shown that tanshinone IIA (TIIA) has an anti-inflammatory effect, but the effect on allergic rhinitis (AR) is unclear. OBJECTIVE: In this study, we explore the effect of TIIA on AR. MATERIALS AND METHODS: AR mice model was established by the intraperitoneal (ip) injection of 50 µg ovalbumin (OVA). AR mice in the dose tested groups were treated with TIIA (10 mg/kg/d, ip) or dexamethasone (Dex) (2.5 mg/kg/d, oral). The number of nasal rubbing in mice was counted. Inflammatory, goblet and mast cells in nasal mucosal tissue were detected. The contents of histamine, OVA-immunoglobulin E (IgE), OVA-immunoglobulin G1 (IgG1), tumour necrosis factor-α (TNF-α), interleukin-4 (IL-4), IL-5, interferon-γ (IFN-γ) and IL-12 in nasal lavage fluid (NALF) or serum were measured. Human mast cells (HMC-1) were treated with C48/80 to release histamine or TIIA for therapeutic effect, and the cell viability, histamine content and mast cell degranulation were examined. RESULTS: OVA promoted the number of nasal rubbings in mice (78 times/10 min, p< 0.001), increased the inflammatory, goblet and mast cells in nasal mucosal tissue, and significantly (p< 0.001) elevated the levels of histamine (120 ng/mL), OVA-IgE (2 pg/mL), OVA-IgG1 (90 ng/mL), TNF-α (2.3 pg/mL), IL-4 (150 pg/mL) and IL-5 (65 pg/mL) in serum or NALF of OVA-induced AR mice. However, both TIIA and Dex inhibited the effect of OVA on AR mice. Besides, TIIA reversed the promotion of histamine release (30%) and mast cell degranulation induced by C48/80. DISCUSSION AND CONCLUSIONS: TIIA alleviates OVA-induced AR symptoms in AR mice, and may be applied as a therapeutic drug for patients with Th2-, or mast cell-allergic disorders.

Uterine tumor resembling ovarian sex-cord tumor: case report and review of the literature.

Background: We report the clinicopathological characteristics, immunohistochemical features, ultrastructure, tissue source, differential diagnosis, treatment, and prognosis of a patient with a uterine tumor resembling ovarian sex-cord tumor (UTROSCT). Case report: A 40-year-old woman had a uterine myoma with enlargement for 2.5 years. An ultrasound examination showed a mixed echogenic mass at the posterior wall of the uterus and a dark cyst in the right adnexal area, which suggested a suspected uterine myoma with liquefaction and a suspected chocolate cyst. The patient underwent transabdominal tumor resection with removal of the right adnexal mass. Through postoperative pathological examination, the patient was diagnosed with UTROSCT. No recurrence was observed after a follow-up of 1 year. Conclusion: Although UTROSCT is usually benign, it can relapse or metastasize, and patients with UTROSCT need comprehensive diagnosis and treatment.

The diagnostic performance of magnetic resonance imaging for differentiating the nature of cardiac masses: A systematic review protocol.

BACKGROUND: Cardiac masses are rare, but lead to high risk of stroke and death. Because of the different treatment methods, it is significant for clinicians to differentiate the nature of masses. Cardiac magnetic resonance (CMR) imaging has high intrinsic soft-tissue contrast and high spatial and temporal resolution and can provide evidence for differential diagnosis of cardiac masses. However, there is no evidence-based conclusion as to its accuracy. Therefore, the purpose of our study is to perform a systematic review on this issue and provide useful information for clinical diagnosis and treatment. METHODS: We will perform a systematic search in EMBASE, Cochrane Library, PubMed and Web of Science for diagnostic studies using CMR to detect cardiac masses from inception to October, 2019. Two authors will independently screen titles and abstracts for relevance, review full texts for inclusion and conduct detail data extraction. The methodological quality will be assessed using the QUADAS-2 tool. If pooling is possible, we will use bivariate model for diagnostic meta-analysis to estimate summary sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio of CMR, as well as different sequences of CMR. Estimates of sensitivity and specificity from each study will be plotted in summary receive operating curve space and forest plots will be constructed for visual examination of variation in test accuracy. If enough studies are available, we will conduct sensitivity analysis and subgroup analysis. RESULTS: The results of this systematic review and meta-analysis will be published in a peer-reviewed journal. CONCLUSION: To our knowledge, this will be the first systematic review on the accuracy of CMR in the differential diagnosis of cardiac masses. This study will provide evidence and data to form a comprehensive understanding of the clinical value of CMR for cardiac masses patients. ETHICS AND DISSEMINATION: Ethics approval and patient consent are not required, as this study is a systematic review. PROSPERO REGISTRATION NUMBER: CRD42019137800.

Knockdown of miR-629 Inhibits Ovarian Cancer Malignant Behaviors by Targeting Testis-Specific Y-Like Protein 5.

Ovarian cancer (OC) is the most lethal gynecological cancer. The molecular mechanism of it is complicated, and numerous researches suggest that microRNAs are key regulators for it. This study was to investigate the pivotal role of miR-629 in the progression of OC and to reveal the possible molecular mechanism of its action. Testis-specific Y-like protein 5 (TSPYL5) is a tumor suppressor gene in various cancers, but there is little for its role in OC. OC OVCAR3 cells were transfected with the miR-629 vector, miR-629 inhibitor, and/or small interfering RNA (siRNA) targeting TSPYL5 (si-TSPYL5), respectively. After transfection, cell apoptosis, the ability of migration, and invasion were explored, as well as the level of miR-629 and TSPYL5 protein expression were detected by quantitative polymerase chain reaction and western blot. Compared with the control, there was increasing of miR-629, and decreasing of TSPYL5 and caspase 3 in OC tissue. Overexpression of miR-629 promoted the cell ability of migration and invasion and reduced OC cell apoptosis. In addition, elevated cancer inhibition ability of TSPYL5 induced by the miR-629 inhibitor was significantly blocked by inhibition of TSPYL5 (si-TSPYL5). All the above results suggested that miR-629 could promote OC proliferation, migration, and invasion by directly suppressing TSPYL5 expression, and inhibition of miR-629 might serve as a therapeutic target for OC.

HBx-induced MiR-1269b in NF-κB dependent manner upregulates cell division cycle 40 homolog (CDC40) to promote proliferation and migration in hepatoma cells.

BACKGROUND: Occurrence and progression of hepatocellular carcinoma (HCC) are associated with hepatitis B virus (HBV) infection. miR-1269b is up-regulated in HCC cells and tissues. However, the regulation of miR-1269b expression by HBV and the mechanism underlying the oncogenic activity of miR-1269b in HCC are unclear. METHODS: Reverse transcription quantitative PCR (RT-qPCR) was used to measure the expression of miR-1269b and target genes in HCC tissues and cell lines. Western blot analysis was used to assess the expression of miR-1269b target genes and related proteins. Using luciferase reporter assays and EMSA, we identified the factors regulating the transcriptional level of miR-1269b. Colony formation, flow cytometry and cell migration assays were performed to evaluate the phenotypic changes caused by miR-1269b and its target in HCC cells. RESULTS: We demonstrated that the expression levels of pre-miR-1269b and miR-1269b in HBV-positive HepG2.2.15 cells were dramatically increased compared with HBV-negative HepG2 cells. HBx was shown to facilitate translocation of NF-κB from the cytoplasm to the nucleus, and NF-κB binds to the promoter of miR-1269b to enhance its transcription. miR-1269b targets and up-regulates CDC40, a cell division cycle 40 homolog. CDC40 increases cell cycle progression, cell proliferation and migration. Rescue experiment indicated that CDC40 promotes malignancy induced by miR-1269b in HCC cells. CONCLUSION: We found that HBx activates NF-κB to promote the expression of miR1269b, which augments CDC40 expression, contributing to malignancy in HCC. Our findings provide insights into the mechanisms underlying HBV-induced hepatocarcinogenesis.

Downregulation of miR-7 upregulates Cullin 5 (CUL5) to facilitate G1/S transition in human hepatocellular carcinoma cells.

MicroRNAs (miRNAs) are small, non-coding RNAs that participate in the regulation of gene expression. In this study, we demonstrate that miR-7 was downregulated in hepatocellular carcinoma (HCC) tissues compared to adjacent non-tumor tissue. Over-expression of miR-7 in QGY-7703 and HepG2 cell lines inhibited colony formation and induced G1/S phase arrest, whereas knockdown of miR-7 produced the opposite phenotype. A tumor suppressor gene, CUL5, was identified as a direct target of miR-7, and CUL-5 is upregulated upon the binding of miR-7 to its 3'UTR. Furthermore, suppression of CUL5 also suppressed cell colony formation and induced cell cycle arrest. Ectopic expression of CUL5 abrogated the effects of miR-7 inhibition on QGY-7703 and HepG2 cell lines. These results indicate that miR-7 suppresses colony formation and causes cell cycle arrest via upregulation of CUL5, and it may function as a tumor suppressor in HCC.