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ObjectiveStudies have shown a high incidence of subclinical hypothyroidism in pregnancy, but the adverse pregnancy outcomes caused by it are not clear. Therefore, we conducted a systematic review and meta-analysis to evaluate the relationship between subclinical hypothyroidism in pregnancy and hypertensive disorders of pregnancy(HDP) to guide clinical practice.MethodWe searched the MEDLINE (PubMed), Cochrane Central, EMBASE, Web of Science, and SCOPUS databases and screened all studies evaluating the relationship between subclinical hypothyroidism in pregnancy and hypertensive disorders of pregnancy. Two researchers independently evaluated the quality of all eligible original studies using the Newcastle-Ottawa Scale (NOS). We also performed a meta-analysis using STATA15.1. Sensitivity analyses were also performed by examining the effects of individual studies as well as using different effect models and detecting any publication bias using the harbord test.ResultsTwenty-two studies were included in the final meta-analysis. Our results indicated that pregnant women with subclinical hypothyroidism had an increased risk of HDP (OR = 1.54(95% CI: 1.21-1.96) I²=67.1%), compared with euthyroidism. Subclinical hypothyroidism in pregnancy was not associated with hypertensive disorders of pregnancy at TSH diagnostic cut-off of less than 3.0 mIU/L (P = 0.077). Curiously, the risk of HDP increases when the TSH diagnostic cut-off value is higher or lower than 4 mIU/L. Although only 9 studies were above the threshold, the risk of developing HDP was still 1.69 times, which was highest in all subgroup analyses. This is consistent with the newly recommended diagnostic cut-off value of 4 mIU/L for TSH by the ATA. Our results consider that the risk of hypertensive disorder complicating pregnancy is increased regardless of the diagnosis of subclinical hypothyroidism at any stage of pregnancy. Unfortunately, there is insufficient evidence to support that patients can benefit from treatment with levothyroxine.ConclusionThe results of this meta-analysis indicate that subclinical hypothyroidism in pregnancy is associated with an increased risk of developing HDP, and this association exists regardless of the gestational period. However, the available evidence cannot support these patients receiving thyroxine intervention can benefit from it, so routine screening is only recommended for pregnant women with risk factors for hypothyroidism. Further research is needed to validate more scientific and rigorous clinical studies to clarify the relationship between subclinical hypothyroidism and HDP to improve patient prognosis.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/, PROSPERO (CRD42021286405)

Background Given antisense long noncoding RNAs (lncRNAs) poly C binding protein-1 antisense RNA1 (PCBP1-AS1) was significantly co-expressed with tumor necrosis factor receptor associated factor 5 (TRAF5) mRNA in vulvar squamous cell carcinoma (VSCC). TRAF5 could mediate nuclear factor kappa B (NF-κB) activation and regulate biological behaviors of tumor cells. Herein, we determined whether PCBP1-AS1 could affect the tumor behaviors of VSCC by regulating TRAF5 and NF-κB expression. Methods The expression of PCBP1-AS1 and TRAF5 mRNA in VSCC tissues and cells was detected via quantitative real-time polymerase chain reaction, while the protein expression levels of TRAF5, p65, p-p65, c-Rel, and IκBα were examined by immunoblotting. After the overexpression of PCBP1-AS1 and RNA interference knockdown of TRAF5 in SW954 cells, NF-κB activation-nuclear translocation fluorescence, the CCK-8 assay, Annexin V-FITC & PI fluorescent staining, the wound healing assay, and the Transwell invasion assay were performed to evaluate the activity of NF-κB, cellular proliferation, apoptosis, migration, and invasion. Results PCBP1-AS1 and TRAF5 mRNA expression were downregulated in VSCC tissues and were correlated with patient clinicopathological characteristics. The protein expression of TRAF5, p65, p-p65, c-Rel, and IκBα protein in VSCC tissues was significantly decreased. We demonstrated that PCBP1-AS1 positively regulated the expression of TRAF5. PCBP1-AS1 overexpression or knockdown of TRAF5 regulated the activity of the NF-κB pathway. Increase of PCBP1-AS1 significantly inhibited proliferation and enhanced apoptosis via TRAF5-mediated regulation of the NF-κB signaling pathway. Additionally, PCBP1-AS1 can suppress migration and invasion in an NF-κB-independent manner. Conclusions As a tumor suppressor gene, PCBP1-AS1 regulates the proliferation and apoptosis of VSCC via TRAF5-mediated expression of the NF-κB.

Bo Li,1 Qianqian Jiang,1 Shitai Zhang,1 Yang Zhou,1 Qing-Fu Zhang,2 Ling OuYang1 1Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, 2Department of Pathology, the First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, People’s Republic of China Abstract: Yolk sac tumor (YST) is a common malignant primitive germ cell tumor that often exhibits differentiation into endodermal structures. They most commonly occur in childhood and adolescence and are rare after the age of 40 years. Derived from the yolk sac during the embryonic period, YSTs can occur in the gonads and germ cells because the tumor cells migrate from the yolk sac toward the gonads. Here, we present a rare case of primary gluteus YST in a 3-year-old girl. She received BEP chemotherapy (bleomycin + etoposide + cisplatin) after surgical resection. There was no evidence of recurrence 7 months after primary treatment. Keywords: immunohistochemistry, yolk sac tumor, germ cell tumor

Objective: This study attempted to examine the methylation status of SH3GL2 gene in different types of human vulvar lesions and its correlation with clinicopathological parameters. Methods: Immunohistochemical analysis was used to identify the expression status of SH3GL2 in vulvar squamous cell carcinoma (VSCC), vulvar intraepithelial neoplasia (VIN) and benign vulvar squamous epithelium tissues. Bisulfite genomic sequencing method was used to detect methylation status of the SH3GL2 gene. Clinicopathological correlation of the alterations was analysed by the chi-square tests. Results: Immunohistochemical analysis showed expression of SH3GL2 in VSCC was significantly downregulated than that in VIN and normal vulvar tissues. In accordance with higher frequency of methylation status in SH3GL2, statistical analysis showed methylation status of SH3GL2 was closely related to tumor TNM stage (P=0.003), but not related to age, tumor volume, tumor differentiation, lymph node metastasis and VIN grade. High-methylation status of SH3GL2 showed significant association with HPV infection status. Conclusions: Our results indicated that the methylation status of SH3GL2 gene was associated with the TNM staging and HPV infection status of VSCC, suggesting that it might play a synergistic role in the development of VSCC.