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Purpose: To investigate the effect of obesity on fetal cortical development. Methods: This prospective cross-sectional study was conducted with 91 pregnant women. Fetal neurosonography scans were performed in the third trimester, and according to body mass index (BMI) values, the patients were evaluated in two groups: obese (BMI ≥ 30 kg/m2) and normal weight (BMI < 30 kg/m2). During neurosonography, fetal insular depth and Sylvian fissures, parieo-occipital and cingulate fissure depth, frontal lobe length, and the sizes of the corpus callosum and cavum septum pellucidum were measured using a transvaginal approach. Fetal cortical development and Sylvian fissure operculization were graded. Results: The number of patients with grade 2 fetal cortical development was significantly higher among the pregnant women in the obese group compared to the normal weight group (n = 17, 41.5% and n = 8, 16.0%, respectively; p = 0.007). In the obese group, the number of pregnant women with grade 4 or below fetal Sylvian fissure operculization was significantly higher (n = 13, 31.7%), and the number of those with grade 9 or above operculization was significantly lower (n = 1, 2.5%) (p = 0.003). The fetal insular depth, frontal lobe anterior–posterior diameter, cingulate fissure depth, and corpus callosum thickness were lower in the obese group, albeit with no significant difference. Parieto-occipital depth significantly decreased in the obese group [6.8 (6) mm)] compared to the control group [10.5 (7.2) mm)] (p = 0.008). The fetal Sylvian fissure ratio and the cavum septum pellucidum ratio were found to be similar between the groups. Conclusion: The data obtained from this study showed that obesity caused fetal cortical changes in pregnant women. [ABSTRACT FROM AUTHOR]

Objectives: The aim of the present study was to investigate the effects of different degrees of obstruction, and the roles of inflammation, oxidative stress, and hypoxia parameters on bladder function. Methods: Thirty male Sprague–Dawley rats were divided into 3 groups (n = 10 in each group): (i) sham‐operated control; (ii) severe partial bladder outlet obstruction (PBOO); and (iii) moderate PBOO. Severe and moderate PBOO were induced by urethral ligation using 3‐Fr and 4‐Fr catheters, respectively, for 6 weeks. After 6 weeks, the in vitro contractile responses to carbachol, electrical field stimulation, ATP and KCl were measured in bladder strips. In addition, mRNA and protein expression of nuclear factor kappa B (NF‐κB) hypoxia‐inducible factor (HIF) and nuclear factor, erythroid 2‐like 2 (Nrf2) in bladder were determined by real‐time polymerase chain reaction and western blotting. Malondialdehyde (MDA) levels in bladder tissues were also determined. Results: Rats in the severe PBOO group had the highest bladder weight. Detrusor strips from rats in the severe PBOO group exhibited 61%–82% smaller contractile responses to all four stimuli than those from the sham‐operated group. Activity of NF‐κB as an inflammatory marker was increased in the severe PBOO group, whereas HIF‐1α and HIF‐2β protein levels were increased significantly in the moderate PBOO group. A master regulator of oxidative stress, Nrf2 expression was increased in all obstructed rats. MDA levels were higher in the severe PBOO group than in sham‐operated group. Conclusion: The results of the present study reveal the importance of oxidative stress‐induced NF‐κB signaling in bladder dysfunction with severe obstruction. Altered HIF signaling may contribute to the functional impairment after PBOO. Novel and evolving therapies targeting oxidative and/or inflammatory pathways may be a reasonable strategy for the management of lower urinary tract symptoms or benign prostatic hyperplasia. [ABSTRACT FROM AUTHOR]

Objectives: Theobromine, a naturally occurring alkaloid, is now recognized as a viable option due to its potential therapeutic benefit in many types of cancers. This preliminary study was undertaken to clarify how theobromine affects the viability, apoptosis, and migration of human non-small cell lung cancer (NSCLC) A549 cells. Methods: Water-soluble tetrazolium-1 (WST-1) assay was utilized to measure the cytotoxicity of theobromine (5-200 μM) in A549 cells for 24 and 48 hours. Flow cytometry analysis was used to detect apoptosis. A wound healing assay was carried out to evaluate the migration of A549 cells. Cells incubated with the IC50 concentration of cisplatin for 24 hours served as the reference group. Results: A time- and dose-dependent effect of theobromine on the inhibition of A549 cell viability was dramatically observed. Theobromine treatment led to an increased apoptotic cell population and caspase 3/7 activity (p<0.0001). Furthermore, the migratory capacity of A549 cells was reduced in the cells treated with theobromine. Conclusion: The results suggested that theobromine potently reduced the cell growth and migration capacity of NSCLC A549 cells by inducing caspase 3/7-mediated apoptosis. Additional studies are necessary to comprehend the antitumor mechanisms of theobromine against NSCLC and to provide helpful perspectives for more research. [ABSTRACT FROM AUTHOR]