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Immune thrombocytopenia (ITP) is an acquired bleeding disease due to immune-mediated destruction of antilogous platelets and ineffective thrombopoiesis. Although the etiology of ITP remains unknown, genetic variants are thought to predispose individuals to the disease. Several candidate gene analyses have identified several loci that increased ITP susceptibility, but no systematic genetic analysis on a genome-wide scope. To extend the genetic evidence and to identify novel candidates of ITP, we performed a pooling genome-wide association study (GWAS) by IlluminaHumanOmniZhongHua-8 combining pathway analysis in 200 ITP cases and 200 controls from Chinese Han population (CHP). The results revealed that 4 novel loci (rs117503120, rs5998634, rs4483616, and rs16866133) were strongly associated with ITP (P less then 1.0 × 10-7). Expect for rs4483616, other three loci were validated by the TaqMan probe genotyping assay (P less then 0.05) in another cohort including 250 ITP cases and 250 controls. And rs5998634 T allele was more sensitive to glucocorticoids for ITP patients (χ 2 = 7.30, P less then 0.05). Moreover, we identified three overrepresented signaling pathways including the neuroactive ligand-receptor interaction, pathways in cancer, and the JAK-STAT pathway, which involved in the etiology of ITP. In conclusion, our results revealed four novel loci and three pathways related to ITP and provided new clues to explore the pathogenesis of ITP. Copyright © 2020 Yanmei Xu et al.Aristolochic acid (AA) is a group of structurally related nitrophenanthrene carboxylic acids found in many plants that are widely used by many cultures as traditional herbal medicines. AA is a causative agent for Chinese herbs nephropathy, a term replaced later by AA nephropathy. Evidence indicates that AA is nephrotoxic, genotoxic, and carcinogenic in humans; and it also induces tumors in the forestomach, kidney, renal pelvis, urinary bladder, and lung of rats and mice. Therefore, plants containing AA have been classified as carcinogenic to humans (Group 1) by the International Agency for Research on Cancer. In our laboratories, we have conducted a series of genotoxicity and toxicogenomic studies in the rats exposed to AA of 0.1-10 mg/kg for 12 weeks. Our results demonstrated that AA treatments induced DNA adducts and mutations in the kidney, liver, and spleen of rats, as well as significant alteration of gene expression in both its target and nontarget tissues. AA treatments altered mutagenesis- or carcinogenesis-related microRNA expression in rat kidney and resulted in significant changes in protein expression profiling. We also applied benchmark dose (BMD) modeling to the 3-month AA-induced genotoxicity data. The obtained BMDL10 (the lower 95% confidence interval of the BMD10 that is a 10% increase over the background level) for AA-induced mutations in the kidney of rats was about 7 μg/kg body weight per day. This review constitutes an overview of our investigations on AA-induced genotoxicity and toxicogenomic changes including gene expression, microRNA expression, and proteomics; and presents updated information focused on AA-induced genotoxicity in rodents.BACKGROUND Giant paraesophageal hiatal hernias (HH) are very infrequent, and their spectrum of clinical manifestations is large. Giant HH mainly occurs in elderly patients, and its relationship with anemia has been reported. For the surgical treatment of large HH, Nissen fundoplication is the most common antireflux procedure, and the reinforcement of HH repair with a patch (either synthetic or biologic) is still debatable. CASE SUMMARY We report on a case of giant paraesophageal HH in a middle-aged male patient with reflux symptoms and severe anemia. After performing a series of tests and diagnostic approaches, results showed a complete intrathoracic stomach associated with severe iron deficiency anemia. The patient underwent successful laparoscopic hernia repair with mesh reinforcement and Nissen fundoplication. Postoperatively, reflux symptoms were markedly relieved, and the imaging study showed complete reduction of the hernia sac. More importantly, anemia was resolved, and hemoglobin, serum iron and ferritin level were returned to the normal range. The patient kept regular follow-up appointments and remained in a satisfactory condition. CONCLUSION This case report highlights the relationship between large HH and iron deficiency anemia. For the surgical treatment of large HH, laparoscopic repair of large HH combined with antireflux procedure and mesh reinforcement is recommended. ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.BACKGROUND The incidence of short stature in KBG syndrome is relatively high. Data on the therapeutic effects of growth hormone (GH) on children with KBG syndrome accompanied by short stature in the previous literature has not been summarized. CASE SUMMARY Here we studied a girl with KBG syndrome and collected the data of children with KBG syndrome accompanied by short stature from previous studies before and after GH therapy. The girl was referred to our department because of short stature. Physical examination revealed mild dysmorphic features. The peak GH responses to arginine and clonidine were 6.22 and 5.40 ng/mL, respectively. The level of insulin-like growth factor 1 (IGF-1) was 42.0 ng/mL. Genetic analysis showed a c.2635 dupG (p.Glu879fs) mutation in the ANKRD11 gene. She received GH therapy. During the first year of GH therapy, her height increased by 0.92 standard deviation score (SDS). click here Her height increased from -1.95 SDS to -0.70 SDS after two years of GH therapy. There were ten children with KBG syndrome accompanied by short stature who received GH therapy in reported cases. Height SDS was improved in nine (9/10) of them. The mean height SDS in five children with KBG syndrome accompanied by short stature increased from -2.72 ± 0.44 to -1.95 ± 0.57 after the first year of GH therapy (P = 0.001). There were no adverse reactions reported after GH treatment. CONCLUSION GH treatment is effective in our girl and most children with KBG syndrome accompanied by short stature during the first year of therapy. ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
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