AKT1 and MAPK8: New Targets for Gestational Diabetes Mellitus?

Objective: Gestational diabetes mellitus (GDM) disrupts placental function and increases risks for pregnancy. This study investigates the potential involvement of AKT1 and MAPK8 genes, known for their roles in insulin resistance and cell signaling, in GDM pathophysiology. Methods: Placental tissues from GDM patients and healthy controls were analyzed using real-time PCR to quantify gene expression levels. In silico analysis further explored the functional implications of expression changes. Results: AKT1 and MAPK8 displayed significantly altered expression in GDM placentas compared to controls (p = 0.047 and p = 0.007, respectively). In silico analysis suggests potential functional consequences related to diabetes-associated pathways. Conclusion: This study identifies differential expression of AKT1 and MAPK8 in GDM placentas, suggesting their potential roles in the disease process. Further investigation into their functional contributions could provide valuable insights into GDM pathophysiology and potential therapeutic targets.

Unveiling the placental secrets: Exploring histopathological changes and TROP2 expression in intrahepatic cholestasis of pregnancy.

INTRODUCTION: Gestational cholestasis, also known as intrahepatic cholestasis of pregnancy (ICP) or obstetric cholestasis, is a liver disease that can manifest in late pregnancy. Trophoblast cell surface antigen (TROP2) is a type I transmembrane glycoprotein identified in placental trophoblast cells that plays a critical role in trophoblast invasion of the decidua upon implantation into the placenta. Our study aims to investigate the role of TROP2 in pregnancy cholestasis. MATERIALS AND METHODS: Study groups: Group 1 (control group) (n = 10): consists of healthy normal pregnant women without any disease, Group 2 (cholestasis group) (n = 10): consists of pregnant women diagnosed with cholestasis. After routine histological follow-up, hematoxylin and eosin staining and TROP2 immunostaining were performed and scored. RESULTS: In the cholestasis group, in contrast to the control group, thrombus structures were observed in the intervillous space. In the cholestasis group compared to the control group, villus mesenchymal connective tissue cells, capillary endothelium and trophoblasts around the villus showed significantly stronger anti-TROP2 staining (p < 0.05). DISCUSSION: Cholestasis, a condition that may manifest during pregnancy, may be associated not only with observable pathological changes in placental tissues at the light microscopic level, but also with an increase in TROP2 expression. Given the critical role of TROP2 in trophoblast invasion during placental implantation, we hypothesize that TROP2 may serve as a key marker of the cholestatic processes occurring during pregnancy.

Changes of miR-139-5p, TGFB1, and COL1A1 in the placental tissue of cases with gestational diabetes mellitus.

There are structural changes in the placenta of cases with Gestational Diabetes Mellitus (GDM). TGF-ß and collagen pathways have crucial roles in tissue remodeling and TGF-ß1 and COL1A1 are important genes in these signalling respectively. Also, lncRNA NEAT1, and miRNA hsa-miR-139-5p and hsa-miR-129-5p have regulatory effects on TGF-ß1 and COL1A1. Here we aimed to assess their expressions in the placenta tissue of GDM cases. 30 patients with GDM and 30 healthy pregnant women participated in the study. Placental tissues taken during normal or cesarean delivery were used and total RNA was isolated from the tissues. mRNA levels were determined by qPCR and protein levels were determined by ELISA methods. An in silico analysis was done to elucidate the possible relation of TGF-ß1 and COL1A1 gene networks with GDM. We determined that NEAT1 and miR-129-5p expression levels did not differ between GDM and healthy control groups (p = 0.697 and 0.412, respectively). But, miR-139-5p mRNA level, TGFB1 and COL1A1 protein levels significantly differ between the GDM and control groups (p = 0.000, p = 0.000 and p = 0.001, respectively). The in silico analysis revealed that TGFB1 and COL1A1 genes network may have important role in the GDM with their variety of members and regulatory molecules NEAT1, hsa-miR-139-5p, and hsa-miR-129-5p can control their functions. The expression of TGFB1, COL1A1 and miR-139-5p is changed in placenta tissue of GDM cases and many genes in the interacting networks of TGFB1 and COL1A1 could contribute to the pathogenicity of GDM.

SMAD2, SMAD3 and TGF-ß GENE expressions in women suffering from urge urinary incontinence and pelvic organ prolapse.

We evaluated the changes in the levels of TGF-ß and SMAD gene and protein expression in the uterosacral ligament (USL) of patients with concomitant pelvic organ prolapse (POP) and urgency urinary incontinence (UUI) to illuminate the pathophysiology of UUI. The TGF-ß pathway is involved in collagen synthesis and degradation. The Transforming Growth Family-ß (TGF-ß) superfamily has essential intracellular signaling components, such as newly identified SMAD family members. We evaluated the changes in the levels of TGF-ß and SMAD gene and protein expression in the USL of patients with concomitant pelvic organ prolapse (POP) and UUI. This study included 10 patients who had been diagnosed with POP and UUI in the study group and 14 asymptomatic women without complaints of POP and UUI in the control group. Biopsy samples were collected from bilateral USL tissues during vaginal or abdominal hysterectomy. Total RNA was extracted from USL tissue and analyzed by qPCR. The protein expression levels were also analyzed with ELISA. In UUI patients, SMAD3 and TGF-ß1 gene expression levels significantly decreased compared to the control patients (p = 0.008 and p = 0.006, respectively). SMAD2 mRNA levels did not differ between the study and control groups (p = 0.139). No differences was found in the levels of SMAD2, SMAD3, and TGF-ß1 protein expression between the two groups. The reduction in the gene and protein expression levels of SMAD3 and TGF-ß1 in women with UUI and lax uterosacral ligaments may indicate a causal link.Clinical trial registration: NCT04525105.

Subtype Distribution of Blastocystis in Pregnant Women and Analysis of Possible Risk Factors.

OBJECTIVE: Since the identification of Blastocystis subtypes (ST) in the last decade, much has been learned about the genetic diversity of Blastocystis isolates in different populations, except pregnant women. The objective of this study is to investigate the genetic diversity of Blastocystis in pregnant women and analyse some demographic factors. METHODS: The faecal samples from 100 pregnant women were collected at an Obstetrics and Gynecology Department in Mugla, Turkey. Thereafter, Blastocystis positivity was detected by direct microscopy and culture. The positive cultures were subjected to DNA isolation, and the Blastocystis barcode region was amplified with polymerase chain reaction. Next, the sequences were queried against GenBank nucleotide and Blastocystis STs (18S) databases. RESULTS: Blastocystis was detected in 14% (14 out of 100) of the faecal samples by culture and 10% (10 out of 100) of the samples by direct microscopy. Nine of Blastocystis isolates (64.4%) were ST3, three (21.4%) were ST1 and two (14.2%) were ST2. Neither the demographic features nor the gastrointestinal symptoms were statistically related to Blastocystis infection. CONCLUSION: The findings in this study agreed with the most of the previous human studies that found ST3 as the most abundant genotype. This study reported the frequency of Blastocystis in pregnant women and highlighted the importance of comprehensive studies with more cases of Blastocystis during pregnancy.

Effects of adipose and bone marrow-derived mesenchymal stem cells on vaginal atrophy in a rat menopause model.

BACKGROUND & OBJECTIVES: Vaginal atrophy is characterized by thinning of vaginal epithelial layers and decreased local blood flow. We aimed to evaluate the regenerative effects of Adipose derived mesenchymal stem cells (ADMSC) and Bone marrow derived mesenchymal stem cells (BMDSC) on vaginal atrophy in rat menopause model. MATERIALS AND METHODS: Rats were randomly divided into 4 (four) groups: sham, control, ADMSC, BMDSC. Vaginal epithelial thickness, structure of the lamina propria, blood vessels in the lamina propria, collagen deposition, and muscle structure were evaluated. Anti ER α, VEGF, VEGFR 1, Bax and bcl-2 antibodies were analyzed. Beta actin gene was used as endogenous control. Genetical differences among the groups were compared by using Kruskal Wallis and Mann Whitney U test. p < 0.05 was regarded as statistically significant. RESULTS: Epithelial thickness of ADMSC group was higher than control group, but less than sham group Epithelial thickness of BMDSC group was less than sham group. Lamina propria and muscle tissue of ADMSC and BMDSC groups were found to be similar to sham group. VEGFR-1, VEGF, Bax and ER-α staining levels were higher in ADMSC and BMDSC groups than control group. ADMSC group stained stronger with VEGFR-1 and VEGF than BMDSC group. Bcl-2 staining level was increased in ADMSC applied group. No statistically significant difference was detected in Bax and Bcl-2 genes and Bax-/Bcl-2 ratio. CONCLUSIONS: Although genetic expression might have ended and could not be significantly demonstrated, histological and immunohistochemical results favor ADMSC application in vaginal atrophy rather than BMDSC.

Is There Any Impact of Copper Intrauterine Device on Female Sexual Functioning?

INTRODUCTION: Intrauterine Device (IUD) is the most preferred modern contraceptive method in Turkey. Female Sexual Dysfunction (FSD) is defined as lack of one or more of the components in the sexual response cycle which includes sexual desire, impaired arousal and inability achieving an orgasm or pain with intercourse. FSD has multi-factorial aetiology. Advanced age and menopause, fatigue and stress, psychiatric and neurologic disease, childbirth, pelvic floor or bladder dysfunction, endometriosis, uterine fibroids, hypertension obesity, medication and substances, hormonal contraceptives, relationship factors are known risk factors for FSD. AIM: To investigate if IUD has any impact on female sexual functioning. MATERIALS AND METHODS: In this cross-sectional study subjects were divided into two groups. Study group consisted of 92 IUD-users (mean 5.1±1.2 years) and the control group consisted of 83 women with no contraception. Female Sexual Function Index (FSFI) questionnaire was performed to both two groups. Women with a total score lower than 26.5 were considered as having sexual dysfunction. RESULTS: The prevalence of FSD was 57.1% among participants. IUD users had a lower total FSFI score comparing to control group but the difference was not statistically different (p=0.983). A positive correlation was found between total FSFI score and duration of IUD (p=0.003). CONCLUSION: No difference was found in terms of sexual dysfunction between IUD users and women with no contraception. The prevalence of FSD was very high in both groups which may be attributed to the socio-cultural factors such as embarrassment of women due to conservatism.

Mesonephric adenocarcinoma of the uterine cervix: A case report and review of the literature.

Mesonephric adenocarcinoma is a rare neoplasm of uterine cervix. It originates from the mesonephric ductus remnant or mesonephric hyperplasia area. There have been few such cases reported. Our case was 64 years of age and her tumour held the whole endocervical wall. It was around 5cm in diameter, and had exophytic component as well. Bilateral pelvic and paraaortic lymph nodes were negative for metastasis.

Serum vitamin D and C-reactive protein levels are independently associated with diastolic dysfunction.

BACKGROUND AND AIM: Vitamin D deficiency is common and may contribute to cardiovascular diseases. We hypothesized that serum 25-hydroxyvitamin D [25(OH)D] levels would be inversely associated with inflammation and with diastolic dysfunction. We therefore investigated the link between serum vitamin D levels (i) echocardiographic measures and (ii) inflammatory parameters. METHODS: The cross-sectional study included 281 patients who were referred to coronary angiography for stable angina pectoris. Patients were recruited between December 2010 and November 2011. Patients with established congestive heart failure, gout, chronic kidney disease (estimated glomeruler filtration rate <60 mL/min per 1.73 m), and acute infection were not included. We measured serum 25(OH)D levels, C-reactive protein and fibrinogen levels. A radioimmunoassay procedure was used to measure 25(OH)D (DiaSorin, Stillwater, MN). We also performed standardized left ventricular (LV) echocardiograms, and echocardiographic data were used for classification of systolic and diastolic dysfunction. We analyzed the relation between serum levels of 25(OH)D and inflammatory markers and echocardiographic measures of LV mass and diastolic dysfunction. RESULTS: At baseline, subjects had a mean age of 59.5 ± 10 years, and 43.4% were women. Left ventricular mass index, left atrial diameter, isovolumic relaxation time, and E/E' ratio were significantly higher in patients with lower 25(OH)D levels. In ordinal logistic regression analysis, higher 25(OH)D was negatively associated only with LV mass index (odds ratio [OR], 0.965; 95% confidence interval [95% CI], 0.939-0.992; P = 0.015), isovolumic relaxation time (OR, 0.962; 95% CI, 0.939-0.985; P = 0.001), E/E' ratio (OR, 0.874; 95% CI, 0.811-0.942; P = 0.008), and C-reactive protein (OR, 0.802; 95% CI, 0.668-0.962; P = 0.021). CONCLUSIONS: Serum levels of 25(OH)D are significantly associated with LV diastolic dysfunction and LV mass index, although the effect size is rather small. Longitudinal studies in larger populations are needed to establish firmly or refute a causal relationship between vitamin D levels and diastolic dysfunction and LV mass index.

Effect of atorvastatin on hematologic parameters in patients with hypercholesterolemia.

Hematologic parameters such as mean platelet volume (MPV), red cell distribution width (RDW), and neutrophil to lymphocyte (N/L) ratio are associated with increased cardiovascular risk. We investigated the effect of atorvastatin on hematologic parameters in patients with hypercholesterolemia. A total of 79 patients with hypercholesterolemia and 47 normocholesterolemic healthy participants were included. Patients with hypercholesterolemia received 10 to 80 mg/d atorvastatin during a 24-week period. Hematologic parameters were measured at baseline and after 6 months. Atorvastatin treatment produced a significant decrease in MPV levels (9.3 ± 1.3 vs 9.1 ± 1.2 fL, P = .008) and platelet count (259 ± 61 vs 248 ± 51 10(9)/L, P = .005). The N/L ratio decreased significantly after atorvastatin treatment from 2.9 ± 1.2 to 2.6 ± 1.1, (P = .014). The RDW and platelet distribution width levels were not different among the study groups, before and after treatment. Atorvastatin may beneficially reduce MPV levels and N/L ratio. This antiplatelet and anti-inflammatory effect of atorvastatin treatment could play a role in reducing cardiovascular risk.