Background And Objectives: Treg and TH17 cells influence the inflammatory process in periodontal diseases and could also play in a similar pattern, an essential role in immune-inflammatory mechanisms involved in the destruction of the peri-implant tissues, peri-implantitis. Therefore, this study evaluated the levels of RORγT and FOXP3 gene expression in subjects with peri-implantitis and healthy peri-implant tissues.
Methods: A total of 35 subjects with implant-supported restorations in both diseased and healthy clinical conditions (n = 15 healthy; n = 20 peri-implantitis) were included in this study.
Introduction: Currently, the shortage of organs available for kidney transplantation and a change in donors' and recipients' profiles (elderly, with cardiovascular risk, donors after cardiac death), it is becoming necessary to assess grafts from expanded-criteria donors (ECD) in order to have methods that allow us to predict viability and graft survival.
Objective: The aim of this study was to analyze the different methods of renal donor assessment (estimated glomerular filtration rate [eGFR], preimplantation biopsy, and Kidney Donor Profile Index [KDPI] score) as predictors of graft survival and renal function of our recipient at 1 year.
Methods: We performed a descriptive and retrospective study of 183 deceased donor kidney transplantations performed at our center between 2011 and 2015.
NGF diminishes dendrite complexity in cultured hippocampal neurons by decreasing the number of primary and secondary dendrites, while increasing the length of those that remain. The transduction pathway used by NGF to provoke dendrite elongation involves the activation of NF-kappa-B and the expression of the homologues of Enhancer-of-split 1 gene. Here, we define important steps that link NGF with NF-kappa-B activation, through the activity of protein tyrosine phosphatase 1B (PTP1B).
View Article and Find Full Text PDFAdministration of 4 mg of the antiprogestagen RU486 to 4-day-cyclic rats over 8 consecutive days starting on the day of estrus (Day 1) induced and anovulatory cystic ovarian condition with endocrine and morphological features similar to those exhibited in polycystic ovarian disease (PCO). To determine whether the RU486-treated rat responds in an analogous fashion to therapies similar to those that have been used to treat human PCO, RU486-treated rats were injection on Days 5 and 7 with 1) 1 mg of an LHRH antagonist (LHRHa), 2) 5 IU of human FSH (hFSH), 3) 2 mg of the antiandrogen flutamide (FLU), 4) 1 mg of the antiestrogen tamoxifen (TMX), or 5) 1 mg of the dopamine agonist bromocriptine (BRC). Controls were intact cyclic rats decapitated on estrus and rats injected with RU486 and the corresponding vehicles (saline or 70% ethanol) used with LHRHa, hFSH, FLU, TMX, and BRC injections.
View Article and Find Full Text PDFThe inhibitors histidine and AMP cause the enzyme ATP phosphoribosyltransferase of E. coli to associate into a hexamer from its initial dimeric form. The behaviour of these inhibitors has been studied by three different methods.
View Article and Find Full Text PDFCovalently bound bromoacetamide nitroxides have been used to detect the conformational changes and enzyme association induced by its feedback inhibitor, histidine.
View Article and Find Full Text PDFThe reversible reaction catalyzed by ATP phosphoribosyltransferase favors the pyrophosphorolysis of phosphoribosyl-ATP (PR-ATP). The enzyme is inhibited by PR-ATP. To avoid this problem and measure with confidence initial rates of the transferase, we have purified more than one hundred fold the enzyme PR-ATP pyrophosphohydrolase, which irreversibly converts PR-ATP to PR-AMP.
View Article and Find Full Text PDFThiazolealanine, a false feedback inhibitor, causes transient repression of the his operon previously derepressed by a severe histidine limitation in strains with a wild-type or feedback-hypersensitive first enzyme but not in feedback-resistant mutants. Since experiments reported here clearly demonstrate that thiazolealanine is not transferred to tRNAHis, it is proposed that this "transient repression" is effected through the interaction of thiazolealanine with the feedback site of the enzyme. Experiments in the presence of rifampin indicate that this thiazolealanine-mediated effect is exerted at the level of translation.
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