There is growing awareness of a link between the gut and cardiovascular disease. Constipation is common among individuals who have had a stroke, and it negatively affects social functioning and quality of life. However, no systematic study on the incidence of constipation in stroke patients has been reported.We selected studies included in Medline, Embase, Cochrane database, and Web of Science. Studies were included if they reported the incidence in stroke patients. Two authors selected the studies, extracted the data independently, and assessed these. Subgroup analyses were conducted according to the stroke subtype and stage of stroke.After detailed evaluations, 8 studies (n = 1385 participants) were found that contained data that were suitable for meta-analytic synthesis. A forest plot showed that the incidence of constipation was 48% (95% confidence interval [CI] = 33%–63%). In the analysis of the type of stroke subgroup, the incidence of constipation in patients who had had a hemorrhagic stroke (66% [95% CI = 40–91%]) was higher than that in patients who had experienced an ischemic stroke (51% [95% CI = 27%–75%]). The incidence in the acute stage (45% [95% CI = 36%–54%]) was lower than that in the rehabilitation stage (48% [95% CI = 23%–73%]).Constipation after a stroke event occurs frequently. This finding may raise awareness about bowel complications to allow correct evaluation and proper management.
abstract:The azoospermia factor c (AZFc) region in the long arm of human Y chromosome is characterized by massive palindromes. It harbors eight multi-copy gene families that are expressed exclusively or predominantly in testis. To assess systematically the role of the AZFc region and these eight gene families in spermatogenesis, we conducted a comprehensive molecular analysis (including Y chromosome haplogrouping, AZFc deletion typing and gene copy quantification) in 654 idiopathic infertile men and 781 healthy controls in a Han Chinese population. The b2/b3 partial deletion (including both deletion-only and deletion-duplication) was consistently associated with spermatogenic impairment. In the subjects without partial AZFc deletions, a notable finding was that the frequency of DAZ and/or BPY2 copy number alterations in the infertile group was significantly higher than in the controls. Combined patterns of DAZ and/or BPY2 copy number abnormality were associated with spermatogenic impairment when compared with the pattern of all AZFc genes with common level copies. In addition, in Y chromosome haplogroup O1 (Y-hg O1), the frequency of copy number alterations of all eight gene families was significantly higher in the case group than that in the control group. Our findings indicate that the DAZ, BPY2 genes may be prominent players in spermatogenesis, and genomic rearrangements may be enriched in individuals belonging to Y-hg O1. Our findings emphasize the necessity of routine molecular analysis of AZFc structural variation during the workup of azoospermia and/or oligozoospermia, which may diminish the genetic risk of assisted reproduction.
The newest member of the Na(+)/H(+) exchanger (NHE) family, NHE8, is abundantly expressed at the apical membrane of the intestinal epithelia. We previously reported that mucin 2 expression was significantly decreased in the colon in NHE8(-/-) mice, suggesting that NHE8 is involved in intestinal mucosal protection. In this study, we further evaluated the role of NHE8 in intestinal epithelial protection after dextran sodium sulfate (DSS) challenge. Compared with wild-type mice, NHE8(-/-) mice have increased bacterial adhesion and inflammation, especially in the distal colon. NHE8(-/-) mice are also susceptible to DSS treatment. Real-time PCR detected a remarkable increase in the expression of IL-1β, IL-6, TNF-α, and IL-4 in DSS-treated NHE8(-/-) mice compared with DSS-treated wild-type littermates. Immunohistochemistry showed a disorganized epithelial layer in the colon of NHE8(-/-) mice. Periodic acid-Schiff staining showed a reduction in the number of mature goblet cells and the area of the goblet cell theca in NHE8(-/-) mice. Phyloxine/tartrazine staining revealed a decrease in functional Paneth cell population in the NHE8(-/-) small intestinal crypt. The expression of enteric defensins was also decreased in NHE8(-/-) mice. The reduced mucin production in goblet cells and antimicrobial peptides production in Paneth cells lead to disruption of the intestinal mucosa protection. Therefore, NHE8 may be involved in the establishment of intestinal mucosal integrity by regulating the functions of goblet and Paneth cells.
Steroid receptor coactivator 3 (SRC-3) is a multifunctional protein that plays an important role in regulation of bacterial lipopolysaccharide-induced inflammation. However, its involvement in host defense against bacterial infection remains unclear. Herein we used SRC-3 knockout mice to assess the role of SRC-3 in antibacterial defense in E. coli-induced septic peritonitis. After E. coli bacteria were injected intraperitoneally, SRC-3 deficient mice exhibited excessive local and systemic inflammatory responses and more severe bacterial burdens, leading to a significantly higher mortality compared with wild-type mice. Peritoneal macrophages of SRC-3 deficient mice showed a decrease in bacterial phagocytosis in culture and an increase in apoptosis, which was consistent with the defective bacterial clearance observed in SRC-3-deficient mice. Accordingly, SRC-3 null macrophages expressed much lower levels of the scavenger receptor A, the antioxidant enzyme catalase, and anti-apoptotic gene Bcl-2. Collectively, our data demonstrate that SRC-3 is important in not only modulating the local and systemic inflammation but also intensifying bacterial clearance, which highlights a pivotal role of SRC-3 in the host defense system against bacterial infection.
Multiple sodium/hydrogen exchanger (NHE) isoforms are expressed in the testes, and they play various roles in cell volume regulation, intracellular pH regulation, and fluid absorption. NHE8, the most recently characterized NHE family member, is detected in the Leydig cells in humans and mice in great abundance by immunohistochemistry in the current study. Male mice lacking NHE8 expression were infertile. Despite having intact male reproductive organs, male NHE8 Ϫ/Ϫ mice have smaller testes and lacked spermatozoon in the seminiferous tubules and the epididymis. At the age of 39 wk, few spermogonia were seen in the testis in NHE8 Ϫ/Ϫ mice. Although male NHE8 Ϫ/Ϫ mice have normal serum levels of luteinizing hormone and follicle-stimulating hormone, serum testosterone level was significantly reduced. These mice have decreased expression of luteinizing hormone receptor in the testes. In NHE8 small-interfering RNA-transfected mouse Leydig cells (MLTC-1), silencing of NHE8 decreased the expression of luteinizing hormone receptor by ϳ70%. Moreover, loss of NHE8 function in Leydig cells resulted in disorganized luteinizing hormone receptor membrane distribution. Therefore, male infertility in NHE8 Ϫ/Ϫ mice is at least partially due to the disruption of luteinizing hormone receptor distribution and consequent low testosterone production, which leads to Sertoli cell dysfunction. Our work identified a novel role of NHE8 in male fertility through its effect on modifying luteinizing hormone receptor function.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.