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    • On correlating acute rejection to different risk markers by

    2022-04-15

    On correlating acute rejection to different risk markers by multiple linear regression analysis, we found that serum FasL and serum creatinine were variables that were independently associated with AR. Carstens et al., reported that significant differences were present between acute rejection and zero-hour samples and acute rejection and non-rejection samples for FasL measured transcripts. No significant difference was found between acute borderline rejection (n=16) and non-rejection samples [49]. Also, the curative antirejection-therapy resistance of overt, acute-rejection episode was significantly linked with higher Fas Ligand gene simvastatin zocor (AUC=0.764, P<0.01, sensitivity [71%], specificity [99.5%]).They demonstrated that the coinciding measurement of the mRNA up-regulation of Fas Ligand might clarify an efficient good maker for the prediction of the pejorative outcome of acute rejection [19]. Post-transplant monitoring currently relies on surveillance of allograft function (e.g. serum creatinine levels and GFR, in kidney transplantation). An acute alteration in the functional parameter suggests acute rejection occurrence, but confirmation requires the invasive procedure of allograft biopsy. Moreover, this approach recognizes rejection at a relatively advanced stage of the immune process and tissue injury and fails to diagnose subclinical acute rejection: histological rejection in the absence of graft dysfunction. Protocol or scheduled biopsies have been executed mainly in recipients of kidney or heart allografts to detect acute rejection prior to graft dysfunction [50]. Moreover, the diagnosis of subclinical rejection requires multiple biopsies; the biopsy procedures are invasive, complications occur, and sampling errors may bias the histological diagnosis. The costs and timing of this procedure need to be considered as well. Gene/protein expression patterns of noninvasively collected biologic specimens have been investigated as biomarkers of allograft status [51]. A noninvasive tool has a number of potential advantages including frequent and sequential assessments of recipient's immune status. Molecular perturbations may precede not only graft dysfunction but also histological changes. Importantly, molecular parameters may serve to guide minimization of immunosuppression and individualization of immunosuppressive therapy. Clinicians with a more refined knowledge of the recipient's immune status may be able to adjust the immunosuppressive drug therapy that is often responsible for numerous side effects [50]. A molecular-based approach that incorporates a set of markers could function not only as a surrogate for the invasive biopsy procedure, but could also provide predictive, diagnostic, and prognostic information as well as provide mechanistic insights into the pathobiology of allograft dysfunction. Kinetic studies in three patients with AR revealed that increased perforin, granzyme B and FasL mRNA levels could precede or were concomitant with increased serum creatinine levels [52].
    Conflict of interest
    Introduction The placenta has a unique role in providing oxygen and nutrition for the developing fetus. In addition, the placenta protects the fetus from rejection by the maternal immune system. During normal human pregnancy, the fetal cytotrophoblast stem cells differentiate and invade the uterus and spiral arterioles. In pregnancies complicated by preeclampsia, cytotrophoblast differentiation is abnormal [1]. Studies have shown that there is increased placental trophoblastic apoptosis in pregnancies complicated by preeclampsia and intrauterine growth restriction, two phenomena which are often associated [1], [2], [3], [4]. The Fas–Fas ligand system is the major signal transduction pathway involved in apoptosis (programed cell death). Fas, also known as CD95, is a type I transmembrane protein that belongs to the tumor necrosis factor superfamily. The natural ligand of Fas is a type II protein known as Fas ligand. The Fas receptor protein interacts with its natural ligand, to initiate an irreversible sequence of reactions in the death signal cascade, ultimately resulting in cell death via apoptosis. Fas and Fas ligand are expressed in many tissues including human placental trophoblast and other tissues [5], [6]. Variations in the promoter area of the maternal Fas-670 gene may affect Fas gene expression and modulate apoptotic signaling, contributing to an increased risk of preeclampsia and intrauterine growth restriction [7]. We recently reported an association between maternal Fas-670 single nucleotide polymorphism and the development of intrauterine growth restriction [4]. Since preeclampsia is thought to be a disorder of trophoblastic invasion, we hypothesized that polymorphisms in the Fas–Fas ligand pathway of apoptosis in the placenta contribute to the pathogenesis of preeclampsia. The objective of this study was to determine if polymorphisms of the Fas and Fas ligand genotypes differed between patients with and without preeclampsia.