Background: Drug-refractory secondary hyperparathyroidism (SHPT) is the most common complication in patients with chronic renal failure (CRF). Although surgery is the most effective and safe method for drug-refractory SHPT, the condition may persist or recur after the primary surgery, and reoperation is often required in these patients. The purpose of our current study was to evaluate the safety and effectiveness of reoperation for drug-refractory SHPT. Methods:The clinical data of 15 patients requiring reoperation after a surgery for drug-refractory SHPT in our hospital from 2010 to 2019 were retrospectively analyzed. Changes in biochemical markers including intact parathyroid hormone (iPTH), blood calcium (Ca), blood phosphorus (P), alkaline phosphatase (ALP), and blood calcium phosphorus product (Ca*P) were compared before and after the surgery, and the effectiveness and complications of the reoperation were summarized. Results:The reoperation was successful in all the 15 patients after a single attempt. Routine pathological examinations identified a total of 25 parathyroid glands, of which 10 were in the neck in situ, 5 were ectopic in the neck, and 10 were in the forearm. The ectopic parathyroid glands were located inside the thyroid gland (n=1), anterior superior mediastinum (n=1), or thymus (n=3). Surgical treatment significantly improved clinical symptoms such as skin pruritus and bone pain. Blood iPTH, Ca, P, ALP, and Ca*P were significantly reduced (P<0.05 or P<0.01) after surgery. Hypothyroidism occurred in 1 patient; 4 patients undergoing orthotopic neck surgery developed transient hoarseness, which were alleviated within 6 months; no severe complications such as bleeding or death were noted. No recurrence occurred during the 6-month follow-up.Conclusions: Reoperation is safe and effective for drug-refractory SHPT. Preoperative imaging should be performed to achieve accurate positioning, and the recurrent laryngeal nerve should be closely monitored during surgery. The purpose of the reoperation is to remove all possible parathyroid tissues to avoid recurrence.

Purpose This study aimed to investigate the effects of body mass index (BMI) on infertility in women of childbearing age. Patients and Methods We performed a cross-sectional study using data from 3624 participants from the National Health and Nutrition Examination Survey (NHANES). We used BMI and fertility status in the survey as independent and dependent variables, respectively. We evaluated their relationship and used smoothed curve fitting and multivariate logistic regression analysis as well as a generalized additive model (GAM) to determine the effect of BMI. Results Logistic regression model analysis linked BMI and infertility after adjusting for potential confounders OR 1.03, 95%Cl: 1.02–1.05). There was a non-linear relationship between BMI and infertility, with each unit increase in BMI reducing the risk of infertility by 33% when BMI was <19.5 kg/m 2 . In contrast, when BMI ≥19.5 kg/m 2 , each unit increase in BMI predicted a 3% increase in the risk of infertility. Conclusion The relationship between infertility and BMI presented a U-shaped curve. Therefore, a BMI that lay at the extremes of the spectrum tended to predict infertility. We believe that this study will support the maintenance of suitable BMI levels in women preparing for pregnancy.

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CD127 expression in T cells is decreased in patients with HIV-1 and is related to recovery of CD4T-cell counts and to naïve subsets.

Background Schizophrenia is a complex and heterogeneous disorder involving multiple regions and types of cells in the brain. Despite rapid progress made by genome-wide association studies (GWAS) of schizophrenia, the mechanisms of the illness underlying the GWAS significant loci remain less clear. Study Design We investigated schizophrenia risk genes using summary-data-based Mendelian randomization based on single-cell sequencing data, and explored the types of brain cells involved in schizophrenia through the expression weighted cell-type enrichment analysis. Results We identified 54 schizophrenia risk genes (two-thirds of these genes were not identified using sequencing data of bulk tissues) using single-cell RNA-sequencing data. Further cell type enrichment analysis showed that schizophrenia risk genes were highly expressed in excitatory neurons and caudal ganglionic eminence interneurons, suggesting putative roles of these cells in the pathogenesis of schizophrenia. We also found that these risk genes identified using single-cell sequencing results could form a large protein-protein interaction network with genes affected by disease-causing rare variants. Conclusions Through integrative analyses using expression data at single-cell levels, we identified 54 risk genes associated with schizophrenia. Notably, many of these genes were only identified using single-cell RNA-sequencing data, and their altered expression levels in particular types of cells, rather than in the bulk tissues, were related to the increased risk of schizophrenia. Our results provide novel insight into the biological mechanisms of schizophrenia, and future single-cell studies are necessary to further facilitate the understanding of the disorder.