Context:Polycystic ovary syndrome (PCOS) is an important cause of infertility. In women with PCOS have increased rate of spontaneous abortion and reduced rate of conception. HOXA–10 and HOXA–11 are proteinous products of homeobox gene group and play an important role during implantation.Aims:The aim of this study was to evaluate endometrial receptivity by measuring HOXA–10, HOXA–11, and leukemia inhibitory factor (LIF) gene expressions in women with PCOS.Settings and Design:A tertiary referral center.Materials and Methods:This study was conducted on reproductive age women with abnormal uterine bleeding without sonographically proven anatomical reason. Endometrial sampling procedures were done in proliferative phase using low-pressure endometrial suction device to exclude endometrial pathology. HOXA–10, HOXA–11, and LIF gene expressions were measured from endometrial sampling material. Blood sample was taken to measure serum estradiol level on the day of endometrial sampling.Statistical Analysis Used:Statistical analysis was performed using SPSS software version 17 (SPSS Inc., Chicago, IL, USA). Mann–Whitney U-test was used to compare the variables.Results:A total of 53 patients were included in this study. Study group consisted of 33 patients with PCOS. Gene expressions of HOXA–10, HOXA–11, and LIF were significantly lower in patients with PCOS (P < 0.05).Conclusions:This study results showed that in patients with PCOS have decreased gene expression of HOXA-10, HOXA-11, and LIF which might contribute PCOS-related infertility.
Psoriasis is a chronic autoimmune disease in which peripheral blood mononuclear cells (PBMCs) are involved in the pathological process. Transient receptor potential (TRP) channels expressed in immune cells have been shown to be associated with inflammatory diseases. We aimed to evaluate mRNA expression levels of TRP channels in PBMCs of patients with psoriasis. 30 patients with plaque psoriasis and 30 healthy age- and gender-matched control subjects were included in this study. mRNA expression levels of TRP channels in psoriasis patients were determined by Real-time polymerase chain reaction. A decreased TRPM4, TRPM7, TRPV3, TRPV4, and TRPC6 genes expression levels were found in the patient group compared to controls, respectively ( p = 0.045, p = 0.000, p = 0.000, p = 0.045, p = 0.009), whereas, an increased expression level was found in TRPM2 and TRPV1 genes in the patient group compared to controls ( p = 0.001 and p = 0.028). This is the first study showing the TRP channel mRNA expressions in PBMCs of psoriasis patients. Different expression patterns of TRP channels may have a role in pathogenesis of psoriasis.
The aim of the current study was to identify whether serum pentraxin 3 (PTX3) level could be a marker of increased inflammation in rheumatoid arthritis (RA) patients. Material and methods: The study included 41 patients diagnosed with RA according to the American College of Rheumatology (ACR) 1990 diagnostic criteria. We compared the serum PTX3 levels between RA patients and a healthy control group, the relationship between PTX3 level and disease activity was also examined. Results: A statistically significant difference was determined between the RA patients and controls as regards PTX3, platelets, C-reactive protein, and mean platelet volume results (p = 0.042, p = 0.007, p = 0.017, p < 0.001, respectively). There was no statistically significant difference in terms of PTX3 level between anti-CCP-positive and-negative patients (p = 0.368). No statistically significant difference was determined in respect of PTX3 levels between RA patients with different disease activity scores (p = 0.346). Conclusions: No relationship was determined between PTX3 and disease activity in RA patients, nor with traditional clinical and biochemical measurements of disease activity. However, the PTX3 levels of the RA patients were found to be high in comparison with the control group. Because, from these results, the role of PTX3 in the pathogenesis of RA cannot be ignored, there is a need for further studies to determine the potential role of PTX3 in RA pathogenesis.
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