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Loosing DHX15 affects endothelial vitality metabolism, lymphatic water flow as well as tumour metastasis within rodents.
In both PBMCs and CSE-exposed U937 cells, andrographolide restored dexamethasone inhibition of IL-8 production, accompanied by the up-regulation of Nrf2 and HDAC2 levels. In the U937 cells, andrographolide was able to block CSE-induced Akt and reduce the level of c-Jun. Besides, andrographolide also augmented dexamethasone actions on lowering total and neutrophil counts, cytokine levels and oxidative damage markers in bronchoalveolar lavage fluid from CS-exposed mice. CONCLUSION AND IMPLICATIONS We report here for the first time a novel corticosteroid re-sensitization property of andrographolide in human PBMCs, and provide mechanistic evidence to support clinical evaluation of andrographolide in reversing steroid resistance in COPD. This article is protected by copyright. All rights reserved.BACKGROUND Cesarean delivery is one of the most common surgical procedures performed by obstetricians. Infectious morbidity after cesarean delivery can have a tremendous impact on the postpartum woman's return to normal function and her ability to care for her baby. Despite the widespread use of prophylactic antibiotics, postoperative infectious morbidity still complicates cesarean deliveries. This is an update of a Cochrane Review first published in 2010 and subsequently updated in 2012, twice in 2014, in 2017 and 2018. OBJECTIVES To determine if cleansing the vagina with an antiseptic solution before a cesarean delivery decreases the risk of maternal infectious morbidities, including endometritis and wound complications. We also assessed the side effects of vaginal cleansing solutions to determine adverse events associated with the intervention. SEARCH METHODS We searched the Cochrane Pregnancy and Childbirth's Trials Register, ClinicalTrials.gov, the World Health Organization (WHO) International Clinical Tll reported outcomes, with downgrading decisions based on limitations in study design or imprecision. As a simple intervention, providers may consider implementing preoperative vaginal cleansing with povidone-iodine or chlorhexidine before performing cesarean deliveries. Future research on this intervention being incorporated into bundles of care plans for women receiving cesarean delivery will be needed. TRIAL REGISTRATION ClinicalTrials.gov NCT00386477 NCT01437228 NCT02915289 NCT03133312 NCT03925155 NCT03442218 NCT03640507 NCT02495753 NCT02693483 NCT03093194 NCT03397615 NCT03423147. Copyright © 2020 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.OBJECTIVE Our aim was to evaluate the relationship between evening chronotype, a proxy marker of circadian system dysfunction, and disordered eating behavior and poor dietary habits in individuals with bipolar disorder (BD). METHODS In this cross-sectional study, we evaluated 783 adults with BD. Chronotype was determined using Item 5 from the reduced Morningness-Eveningness Questionnaire. The Eating Disorder Diagnostic Scale (EDDS) and the Rapid Eating Assessment for Participants - Shortened Version (REAPS-S) were used to assess disordered eating behavior and dietary habits, respectively. General linear models and logistic regression models were utilized to evaluate differences between chronotype groups. RESULTS Two hundred and eight (27%) BD participants self-identified as having evening chronotypes. Compared to non-evening types, evening types were younger (p less then 0.01), and, after controlling for age, had higher mean EDDS composite z-scores (p less then 0.01), higher rates of binge eating (BE) behavior (p=0.04), bulimia nervosa (p less then 0.01), and nocturnal eating binges (p less then 0.01), and a higher body mass index (p=0.04). Compared to non-evening types, evening chronotypes had a lower REAP-S overall score (p less then 0.01) and scored lower on the "healthy foods" and "avoidance of unhealthy food" factors. Evening types also skipped breakfast more often (p less then 0.01), ate less fruit (p=0.02) and vegetables (p=0.04), and consumed more fried foods (p less then 0.01), unhealthy snacks (p=0.02), and soft drinks (p=0.01). CONCLUSIONS Our findings suggest that the circadian system plays a role in the disordered eating and unhealthy dietary behaviors observed in BD patients. The circadian system may therefore represent a therapeutic target in BD-associated morbidity that warrants further investigation. This article is protected by copyright. All rights reserved.BACKGROUND AND PURPOSE Evidence indicates that the entire kallikrein-kinin system is present in the skin, and it is thought to exert a relevant role in cutaneous diseases, including psoriasis. Thus, the present study was designed to evaluate the relevance of kinin receptors in the development and progression of a psoriasis mice model. EXPERIMENTAL APPROACH Kinin B1 and B2 receptor knockout mice as well as C57BL/6 wild type (WT) mice treated with kinin receptor antagonists (SSR240612C or FR173657) were submitted to the Imiquimod (IMQ)-induced psoriasis model. KEY RESULTS Both kinin receptors were upregulated following 6 days of IMQ treatment. Kinin B1 and B2 receptor deficiency as well as the use of selective antagonists, show morphological and histological improvement of the psoriasis hallmarks. This protective effect was associated with a decrease in undifferentiated and proliferating keratinocytes, decreased cellularity (neutrophils, macrophages, CD4+ T lymphocytes), reduced γδ T cells as well as lower accumulation of IL-17. The lack of B2 receptors resulted in reduced CD8+ T cells in the psoriatic skin. Relevantly, blocking kinin receptors reflected the improvement of psoriasis disease in the well-being behaviour of the mice. CONCLUSIONS AND IMPLICATIONS The present results have provided clear experimental evidence that kinins exert a critical role in IMQ-induced psoriasis. Both B1 and B2 kinin receptors exacerbate the disease development, influencing keratinocyte proliferation and immunopathology. Therefore, the use of antagonists for one or even both kinin receptors might constitute a new strategy for psoriasis clinical treatment. This article is protected by copyright. All rights reserved.With the application of BACs-on-BeadsTM (BoBs) and array-comparative genome hybridization (aCGH) technologies in prenatal diagnosis, microdeletion/microduplications at Xp22.3 have been frequently detected. However, the relatively high prevalence and lack of knowledge of such disorders have brought difficulties for clinical genetic counseling. Here, recent progress of research on microdeletion/microduplications at Xp22.3, including epidemiology, pathogenesis, clinical manifestation, and prenatal diagnosis, is reviewed.Charcot-Marie-Tooth disease (CMT) is the commonest form of inherited neuropathy and has an incidence of 1/2500. CMT1A is the commonest subtype of CMT, which is caused by duplication of peripheral myelin protein 22 (PMP22) gene and accounts for approximately 50% of CMT diagnosed by genetic testing. Duplication of PMP22 may influence the production of PMP22 mRNA and protein, and interfere with the proliferation, differentiation and apoptosis of Schwann cells. In addition, deregulation of NRG1/ErbB pathway and lipid metabolism can also lead to dysfunction of Schwann cells. Such factors may disturb the myelination process, leading to axon degeneration, muscle weakness, and atrophy subsequently. Accordingly, drug therapies for CMT1A are developed by targeting such factors. PXT3003, antisense oligonucleotides (ASOs) and small interfering RNA (siRNA) are supposed to down-regulate the level of PMP22 mRNA, while recombinant human NRG-1 (rhNRG1) and neurotrophin-3 (NT-3) may enhance Schwann cells survival and differentiation. In addition, lipid-supplemented diet may remedy the defect of lipid metabolism and maintain the proper structure of myelin. Other targeting drugs include ascorbic acid, progesterone antagonists, IFB-088, ADX71441, and ACE-083. This review is to sum up the pathogenesis of CMT1A and promising targeting drug therapies for further research.Bartter syndrome is an inherited metabolic disorder characterized by hypokalemic alkalosis and high rennin-angiotensin-aldosteronism which can occur at all ages but mainly in childhood. Classical Bartter syndrome is caused by loss-of-function variants in the gene encoding basolateral chloride channel ClC-Kb (CLCNKB), which is a common type of Bartter syndrome characterized with diverse clinical manifestations ranging from severe to very mild. This article reviews the function and mechanism of CLCNKB variants in Chinese population and the genotype-phenotype correlation of CLCNKB variants in classical Bartter syndrome.OBJECTIVE To explore the molecular basis for an A subtype of the ABO blood group. METHODS The forward and reverse typing of the ABO blood group were identified by gel card and test tube methods. The ABO gene of the patient was detected by PCR-sequence specific primer (PCR-SSP). Exons 1 to 7 of the ABO gene was amplified by PCR and sequenced. The ABO gene was also subjected to subclone sequencing for haplotype analysis. RESULTS The patient's red cells showed weak agglutination with anti-A but non-agglutination with anti-B. The patient's serum showed 1+ agglutination with A cells and 4+ agglutination with B cells. Based on above serological characteristics, the patient was defined as Aw subtype of the ABO blood group. Sequencing analysis showed that the patient was heterozygous for c.106G>T, c.188G>A, c.189C>T, c.220C>T, c.297A>G, c.467C>T, c.543G>C, c.646T>A, c.681G>A, c.771C>T, c.829G>A, in addition with a c.261G deletion. Combined with the result of subclone sequencing, the ABO genotype of the patient was determined as ABO*AW.33. new/O.01.02, which harbored c.467C>T and c.543G>C variants compared with ABO*A1.01 and c.543G>C variant compared with ABO*A1.02. The novel allele has been submitted to GenBank with an accession number of MK302122. CONCLUSION A novel allele of Aw33 subtype has been identified with its GTA transferase gene harboring c.467C>T and c.543G>C variants compared with A1.01.OBJECTIVE To explore the genotype-phenotype correlation of Cardio-facio-cutaneous syndrome (CFCS) caused by MAP2K1 gene variants. METHODS Genomic DNA was extracted from peripheral blood sample from a child patient and his parents. Whole exome sequencing (WES) was carried out for the patient. Suspected variant was verified by Sanger sequencing. RESULTS The patient was a 1-year-8-month old Chinese male who manifested short stature, psychomotor retardation, relative macrocephaly, distinctive facial features, and congenital heart disease. WES test revealed a heterozygous missense c.389A>G (p.Tyr130Cys) variant in the MAP2K1 gene. Sanger sequencing has confirmed the variant as de novo. According to ACMG/AMP guidelines, the variant was classified as pathogenic. CONCLUSION Compared with previously reported CFCS cases due to MAP2K1 variants. The patient showed obvious behavioral problems, good appetite and tricuspid regurgitation, which may to be novel features for CFCS.OBJECTIVE To assess the value of preimplantation genetic test (PGT) based on next generation sequencing (NGS) for achieving pregnancy for 71 couples with one partner carrying a reciprocal or Robertsonian translocation. METHODS Following blastocyst biopsy, whole genome of single cell was amplified, and PGT was performed by NGS. The subjects included 60 couples with one partner carrying a reciprocal translocation and 11 with one partner carrying a Robertsonian translocation. The results of PGT, implantation and prenatal diagnosis for all of the couples were analyzed. RESULTS In total 301 embryos were obtained for the 71 couples through 92 ovulation cycles, 287 (95.3%) of which were successfully diagnosed by NGS. Eighty-five euploidy embryos were identified for the reciprocal translocation carrier group. In 18 cycles, no euploid embryo was obtained. Cancellation rate for the cycles was 19.5%. learn more For reciprocal translocation carrier group and Robertsonian translocation carrier group, the rates for implantation, early abortion, and clinical pregnancy were 89.
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