Investigation of diabetes-related molecular changes in embryo-endometrium crosstalk.

The primary aim of this study was to explore the impact of diabetes on matrix metalloproteases and tissue inhibitors, crucial factors for successful implantation, and to elucidate the molecular mechanisms that undergo changes in the endometrium and the embryo during diabetic pregnancies. In this investigation, we established a streptozotocin-induced diabetic pregnant rat model. Microarray analysis followed by RT-PCR was utilized to identify gene regions exhibiting expression alterations. Subsequently, we assessed the effects of MMPs and tissue inhibitors using ELISA and immunohistochemistry techniques, in addition to analyzing changes at the genetic level. Diabetes led to the upregulation of MMP3, MMP9, and MMP20 on the 6.5th day of pregnancy, while causing the downregulation of MMP3, MMP9, and MMP11 on the 8.5th day of pregnancy. TIMP1 expression was downregulated on the 8.5th day compared to the control group. No statistically significant differences were observed between the groups regarding other TIMP expressions. KEGG pathway analysis revealed that diabetes induced alterations in the expression of genes associated with certain microRNAs, as well as signaling pathways such as cAMP, calcium, BMP, p53, MAPK, PI3K-Akt, Jak-STAT, Hippo, Wnt, and TNF. Additionally, gene ontology analysis unveiled changes in membrane structures, extracellular matrix, signaling pathways, ion binding, protein binding, cell adhesion molecule binding, and receptor-ligand activity. This study serves as a valuable guide for investigating the mechanisms responsible for complications in diabetic pregnancies. By revealing the early-stage effects of diabetes, it offers insight into the development of new diagnostic and treatment approaches, ultimately contributing to improved patient care.

CD97 expression level and its effect on cell adhesion in Preeclampsia.

OBJECTIVES: Cellular interactions and cell adhesion underlie preeclampsia (PE). The aim of the current study is to investigate the role of cell adhesion molecules such as CD97, neural (N)-cadherin, epithelial (E) -cadherin and integrin beta-4 in PE. METHODS: This prospective study included 20 pregnant women with PE and a control group of 16 healthy pregnant women who were matched for age, gestational age, gravida and parity. Standard blood tests and placental cell adhesion molecule immunohistochemical staining were examined. RESULTS: The creatinine, uric acid and lactate dehydrogenase (LDH) levels from standard blood tests were found to be statistically higher in the PE group (p = 0.002, p = 0.000, p = 0.001; respectively). In the PE group, the CD97 maternal serum level was statistically significantly lower, as was its immunohistochemical expression in placental sections (p = 0.028, p = 0.000; respectively). The E-cadherin expression score was statistically higher in the PE group compared to the control group (3,65 ± 1,84 vs 2,06 ± 1,76 respectively; p = 0.003). The N-cadherin expression score was statistically lower in the PE group compared to the control group (1,50 ± 0,82 vs 2,43 ± 1,59 respectively; p = 0.049). Integrin beta-4 was not statistically different between groups. CONCLUSIONS: Cellular interaction may be responsible for PE as in cancer. A balance in intercellular communication, as researched in cancer therapy, may offer the solution in PE.

Suppression of Inflammatory Cytokines Expression with Bitter Melon (Momordica Charantia) in TNBS-instigated Ulcerative Colitis.

BACKGROUND AND OBJECTIVE: This study was aimed to elucidate the molecular mechanism of Momordica charantia (MCh), along with a standard drug prednisolone, in a rat model of colitis induced by trinitrobenzene sulfonic acid (TNBS). METHODS: After the induction of the experimental colitis, the animals were treated with MCh (4 g/kg/day) for 14 consecutive days by intragastric gavage. The colonic tissue expression levels of C-C motif chemokine ligand 17 (CCL-17), interleukin (IL)-1ß, IL-6, IL-23, interferon-γ (IFN-γ), nuclear factor kappa B (NF-kB), and tumor necrosis factor-α (TNF-α), were determined at both mRNA and protein levels to estimate the effect of MCh. Besides, colonic specimens were analyzed histopathologically after staining with hematoxylin and eosin. RESULTS: The body weights from TNBS-instigated colitis rats were found to be significantly lower than untreated animals. Also, the IFN-γ, IL-1ß, IL-6, Il-23, TNF-α, CCL-17, and NF-kB mRNA and protein levels were increased significantly from 1.86-4.91-fold and 1.46-5.50-fold, respectively, in the TNBS-instigated colitis group as compared to the control. Both the MCh and prednisolone treatment significantly reduced the bodyweight loss. It also restored the induced colonic tissue levels of IL-1ß, IL-6, IFN-γ, and TNF-α to normal levels seen in untreated animals. These results were also supported with the histochemical staining of the colonic tissues from both control and treated animals. CONCLUSION: The presented data strongly suggests that MCh has the anti-inflammatory effect that might be modulated through vitamin D metabolism. It is the right candidate for the treatment of UC as an alternative and complementary therapeutics.

Comparison of Vesikari and Clark scales regarding the definition of severe rotavirus gastroenteritis in children.

BACKGROUND: Two clinical severity scales, the Vesikari scale and the Clark scale, are commonly used to assess the efficacy of rotavirus vaccines. The results obtained using the two severity scales differ significantly and hamper comparisons. The aim of this study was to compare the Clark and Vesikari scales and to determine whether modified classifications would provide a better correlation between the two scales. METHODS: The severity of rotavirus gastroenteritis was assessed for each child using both the Vesikari and Clark scales. To make a statistical comparison between the two scales, the classifications were modified. RESULTS: In total, 200 children with rotavirus gastroenteritis were evaluated. Of these, 57% were classified as severe by the Vesikari scale, and only 1.5% by the Clark scale (p < 0.001). When the Clark three-category scale was transformed into a two-category scale by merging mild and moderate categories as non-severe, a good correlation with the Vesikari scale still could not be found. Using the median of the severity scores as the severity threshold did not provide a better correlation between the two scales. Transforming the Vesikari two-category scale into a three-category scale by further subdividing the severe category into two parts, as moderate and severe (≥ 16), provided a better correlation between the two severity scales, but still did not achieve a good level of agreement. CONCLUSIONS: The Clark and Vesikari scales differ significantly in the definition of severe gastroenteritis. Even the attempts at reclassifying the scales did not achieve a good correlation.