Evaluation of endometrial activin A secretion for prediction of pregnancy after intrauterine insemination

n/

Evaluation of Endometrial Urocortin Secretion for Prediction of Pregnancy after Intrauterine Insemination

Abstract Background: Urocortin is a neuropeptide produced by the human endometrium and has biological effects putatively important for promoting blastocyst implantation. We measured urocortin concentrations in samples of endometrial wash fluid collected from women with unexplained infertility who underwent intrauterine insemination (IUI). Methods: Patients 28–42 years of age (n = 71) were consecutively enrolled after a complete clinical evaluation. Endometrial wash fluid was retrieved before IUI, at the time of ultrasound evaluation of endometrial thickness. Urocortin concentrations were assayed with a specific ELISA. Results: After IUI, 28 patients (39%) became pregnant. Urocortin concentrations were significantly higher in women who became pregnant than in those who did not (0.38 μg/L vs 0.13 μg/L, P <0.0001). At a cutoff of 0.321 μg/L, urocortin results were positive in 61% [95% confidence interval (CI), 41%–78%] of women who had successful implantation and negative in 98% (95% CI, 88%–99.6%) of those who did not. The pregnancy rate for women with urocortin concentrations >0.32 μg/L was 94%, which differed significantly (P <0.05) from the overall pregnancy rate of 39% in the study population. Conclusions: Urocortin is measurable in endometrial wash fluid, and its concentrations before IUI are higher in women who subsequently achieve pregnancy. These data suggest that the probability of having a successful pregnancy-producing IUI may be better estimated by measuring urocortin in endometrial wash fluid

Virus Infections: Lessons from Pancreas Histology

Type 1 diabetes mellitus is a chronic autoimmune disease resulting from the progressive immune-mediated destruction of pancreatic β cells in genetically susceptible individuals, with the likely contribution of environmental factors, among which viruses have been extensively studied. The pathologic hallmark of the disease is insulitis—a process characterized by islet infiltration of immunocompetent cells that has been well characterized in animal models of islet autoimmunity, and to a lesser extent, in humans. Insulitis characterization has provided valuable information to gain insights into the disease pathogenesis. We review the recent literature on the viral contribution to β-cell destruction and dysfunction in type 1 diabetes, with particular reference to the pathology of the pancreatic islet in humans and in animal models of the disease

Viral infections and diabetes.

Type 1 diabetes mellitus (T1DM) is a multi-factorial autoimmune disease determined by the interaction of genetic, environmental and immunologic factors. One of the environmental risk factors identified by a series of independent studies is represented by viral infection, with strong evidence showing that viruses can indeed infect pancreatic beta cells with consequent effects ranging from functional damage to cell death. In this chapter we review the data obtained both in man and in experimental animal models in support of the potential participation of viral infections to Type 1 diabetes pathogenesis, with a particular emphasis on virus-triggered islet inflammation, beta-cell dysfunction and autoimmunity.info:eu-repo/semantics/publishe

Estrogen receptor gene polymorphisms are associated with recurrence of endometriosis

The presence of gene polymorphisms of the estrogen receptors ERalpha (PvuII and XbaI) and ERbeta (AluI) in 61 women with endometriosis was investigated. A statistically significant correlation between PvuII ERalpha gene polymorphism (PvuII), both in homozygosity (PP) and in heterozygosity (Pp), and a recurrence of endometriosis was found. In conclusion, women affected by endometriosis with the ERalpha polymorphic allele, even if heterozygous, have a worse prognosis, and these results suggest that the ERalpha gene polymorphisms may be included among the genetic risk factors for endometriosi

Coxsackieviruses and Insulitis

Coxsackievirus infections are believed to be a relevant risk factor in the induction of pancreatic beta cell damage and autoimmune response in type 1 diabetes mellitus. Genomic RNA and proteins of coxsackieviruses have been detected in tissues of type 1 diabetes patients, supporting the involvement of enteroviruses in the pathogenesis of type 1 diabetes. Coxsackieviruses may infect beta cells, trigger the activation of innate immune systems, or accelerate the autoimmune process leading to the disease. Local inflammatory changes generated in pancreatic islets and the mechanisms leading to its generation and progression have been studied in animal models of type 1 diabetes and in humans. The role of coxsackieviruses in the insulitic process is discussed in this chapter, together with the ability of selected coxsackievirus serotypes to protect against type 1 diabetes

Increased expression of microRNA miR-326 in type 1 diabetic patients with ongoing islet autoimmunity.

The current paradigm that microRNAs represent a new layer of gene regulation has generated much interest in this field. MicroRNAs have emerged as important regulatory factors involved in the developmental processes and in the regulation of insulin secretion and signalling. Furthermore, recent studies revealed an altered microRNA profiling in lymphocytes of patients with autoimmune diseases like multiple sclerosis, in which a hyperexpression of miR-326 was reported. Here, we analysed the expression levels of miR-326 in peripheral blood lymphocytes from type 1 diabetic (T1D) patients in relationship with ongoing islet autoimmunity.FLWINinfo:eu-repo/semantics/publishe

Increased expression of microRNA miR-326 in type 1 diabetic patients with ongoing islet autoimmunity

info:eu-repo/semantics/nonPublishe

Coxsackie-Virus and Insulitis: Diabetes and Virus

info:eu-repo/semantics/published

MicroRNA profiling during expansion and differentiation of human islet-derived mesenchymal cells reveals differential expression of miR-375 and of a stemness-associated microRNA cluster

info:eu-repo/semantics/nonPublishe