Analysis of mitochondrial membrane potential is the most sensitive test by which to determine sperm quality. These findings promise development of a test that may help to predict successful IVF.
Profound anaemia may occur in adult patients with chronic osteomyelitis on prolonged linezolid therapy, and often necessitates linezolid cessation. These patients are likely to be aged >58 years and to have low pre-treatment haemoglobin. The results for the present series might help physicians to identify patients who should not be given long-term linezolid treatment for chronic osteomyelitis.
We provide here new insights into rotavirus (RRV) pathogenicity by showing that RRV infection promotes structural and functional injuries localized at the tight junctions (TJ) in the cell-cell junctional complex of cultured polarized human intestinal Caco-2 cells forming monolayers. RRV infection resulted in a progressive increase in the paracellular permeability to [ 3 H]mannitol as a function of the time postinfection. We observed a disorganization of the TJ-associated protein occludin as a function of the time postinfection, whereas distribution of the zonula adherens associated E-cadherin was not affected. These structural and functional RRV-induced TJ injuries were not accompanied by alteration in cell and monolayer integrity, as assessed by the lack of change in transepithelial membrane resistance and lactate dehydrogenase release. Finally, using the stabilizer of actin filaments Jasplakinolide, we demonstrated that the RRV-induced structural and functional alterations in TJ are independent of the RRV-induced apical F-actin rearrangements.Rotaviruses (RRV), nonenveloped double-stranded RNA viruses, are recognized as the most important worldwide cause of viral gastroenteritis in infants (for reviews see references 7 and 16). There is increasing information on their replication and maturation processes. Currently, the pathophysiological mechanisms by which RRV induce diarrhea remain unclear. RRV diarrhea might be due to enterocyte destruction from the top of intestinal villi. In agreement with this, extensive studies of animal models have reported the presence of histopathologic changes and functional abnormalities in infected intestinal mucosae that varied from mild to severe depending on the RRV strain virulence. However, this mechanism cannot explain situations in which mild histopathologic changes without enterocyte destruction are associated with low disaccharidase level. Indeed, whatever the severity of histopathologic changes, the activity of functional intestinal proteins is frequently decreased by RRV infection. Recently, we have gained consistent data which lead us to propose a alternate RRV pathophysiological model in which alteration of enterocytic functions depends on perturbation in protein trafficking and the cytoskeleton (3, 13).In the present study we have investigated the mechanisms by which RRV impair the structural and functional organization of the intestinal epithelial cell monolayers. In epithelia, the permeability barrier between different environments results from the assembly and maintenance of different junctional domains in the polarized cells; that the regulation of the paracellular pathway by its well-defined structures is a complex process is now apparent (for reviews see references 1, 4, and 18). In order to approach in vitro the situation in vivo and to gain further insights into the pathophysiological mechanisms of RRV infection, we have used the human polarized intestinal epithelial Caco-2 cells (23). These cells, established from a human colon adenocarcinoma, spontaneously...
Myocardial depression can be demonstrated following administration of endotoxin. Proposed mechanisms of endotoxin-induced myocardial dysfunction include the release of proinflammatory mediators, focal myocardial ischemia, and the presence of activated leukocytes within the myocardium. Recently, myocardial caspase activation and mitochondria-related apoptotic events (i.e., release of cytochrome c) were demonstrated in the failing septic heart. Here, we tested the hypothesis that immunosuppressors, cyclosporin A and tacrolimus (FK 506), would improve inflammation, heart nuclear apoptosis, and myocardial dysfunction in endotoxin-treated rats. Myocardial contractility was assessed using an isolated heart preparation. Heart leukocyte infiltration was assessed by measurement of heart myeloperoxidase activity. Leukocyte activation was studied using the intravital microscopy of the mesenteric venule. Apoptosis was detected as myocardial DNA fragmentation, downstream caspase activation, and mitochondrial cytochrome c release. Both cyclosporin A and FK 506 reduced heart leukocyte sequestration and venular adhesion in endotoxin-treated rats. Cyclosporin A, which blocks mitochondrial cytochrome c release, was able to reduce endotoxin-induced myocardial end-stage nuclear apoptosis and heart dysfunction, whereas tacrolimus had no such effects. These effects could be related to the unique properties of cyclosporin A to act on mitochondria.
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.