Gravgaardroman7012

Background Maternal obesity is a risk factor for multiple obstetrics complications and adverse outcomes. The objective of the study was to investigate the association between obesity (IMC >30) and fetal acidosis at birth.Methods and findings This hospital-based cohort study was based on 24,307 live-born infants in which maternal body mass index (BMI) information was available and delivered in the Granada north region during 2007-2018 from data of the Hospital Medical Birth Registry. Multivariate using logistic regression was performed to assess the association between fetal acidosis and BMI, crude, and adjusted odds ratio of fetal acidosis were calculated. p  less then  .05 was considered statistically significant. We adjusted by maternal age, parity, hypertension, diabetes, and smoking habits. In the study population of 17,167 term live births, 518 infants (3.02%) had an umbilical cord blood pH  less then  7.10. The obesity rate in mothers with acidosis at delivery was 12.7%, but morbid obesity rate was 2.51% (adjusted OR 1.82).Conclusion This study strengthens the evidence that demonstrates that morbid obesity is an independent risk factor for fetal acidosis at birth.Background The methylene tetrahydrofolate reductase (MTHFR) is a folate-dependent enzyme which catalyzes the conversion of homocysteine to methionine. Two single nucleotide polymorphisms (SNPs) within this gene namely rs1801133 (C677T) and rs1801131 (A1298C) have been associated with elevated risk of ischemic stroke and total serum homocysteine in some populations.Aim To assess associations between MTHFR SNPs and risk of ischemic stroke in Iranian population.Methods In the current case-control study, we genotyped rs1801133 and rs1801131 SNPs in 318 Iranian patients with history of ischemic stroke and 400 age- and sex-matched controls using tetra-primer amplification refractory mutation system-polymerase chain reaction method.Results The rs1801133 was significantly associated with risk of stroke in recessive model (OR (95% CI) = 1.89 (1.12-3.20), p = 0.03). The CT haplotype (rs1801131 and rs1801133, respectively) was significantly over-represented in patients compared with controls (OR (95% CI) = 1.71 (0.25-2.32), p = 0.002).Conclusion Consequently, our data demonstrate contribution of MTHFR variants in risk of ischemic stroke in Iranian population.Introduction Mitogen-activated protein kinases (MAPKs) are a large family of evolutionary conserved intracellular enzymes that play a pivotal role in signaling pathways mediating the biologic actions of a wide array of extracellular stimuli.Areas covered MAPKs are implicated in most pathogenic events involved in asthma, including both inflammatory and structural changes occurring in the airways. Indeed, MAPKs are located at the level of crucial convergence points within the signal transduction networks activated by many cytokines, chemokines, growth factors, and other inducers of bronchial inflammation and remodeling such as immunoglobulin E (IgE) and oxidative stress.Expert opinion Therefore, given the growing importance of MAPKs in asthma pathobiology, these signaling enzymes are emerging as key intracellular pathways whose upstream activation can be inhibited by biological drugs such as anti-cytokines and anti-IgE.Objectives The aim of this study is to investigate the correlations between the changes of body weight and metabolic parameters during canagliflozin treatment.Methods Drug naïve subjects with T2DM (n = 84) received canagliflozin monotherapy for 3 months. The subjects were divided into three groups with equal numbers of subjects (n = 28 each) according to the reductions of BMI levels; highest (group A), intermediate (group B), and lowest (group C) reductions. Changes of the metabolic parameters were compared between group A and group C. These two groups acted as a control of each other.Results Significant reductions of BMI levels (-4.1%, p less then  0.00001) were observed in group A, while, surprisingly, significant increases (+1.5%, p less then  0.00001) were seen in group C. In these two groups, similar reductions of HbA1c, FBG, or HOMA-R, and increases of HOMA-B levels were observed. Significant reductions of TG levels (-18.6%) were seen only in group A. At baseline, HbA1c levels were significantly lower in group A versus group C (p  less then  0.03). In group A, significant correlations between the changes of BMI and those of HbA1c (R = 0.496) were seen. By contrast, in group C, significant negative correlations were observed between these parameters (R = -0.463).Conclusions These results suggest that certain populations treated with canagliflozin gained weight, though similar glycemic and beta-cell/insulin sensitivity enhancing properties were observed in comparison to those with efficient weight reductions. Those who lost more weight had better glycemic efficacy in group A. By contrast, those who gained more weight had better glycemic efficacy in group C. Distinct glucose-lowering mechanisms might be operating between these two groups. Involvement of some factors including glucagons and free fatty acids is hypothesized.Purpose/Aim of the study To report on the successful treatment of idiopathic intracranial hypertension (IIH) in a patient with venous sinus stenosis secondary to a persistent occipital-marginal sinus (POMS) utilizing venous sinus stenting.Materials/Methods A 55-year-old female presented with headaches and blurry vision. Ophthalmologic examination demonstrated papilledema. Deruxtecan purchase Two lumbar punctures demonstrated opening pressures of 31 and 38 cmH2O and provided temporary symptom relief. Cerebral venography demonstrated hypoplastic bilateral transverse-sigmoid sinuses with dominant drainage through a persistent occipital-marginal sinus (POMS). Multiple enlarged arachnoid granulations resulted in stenosis in the marginal sinus with an 18 mmHg mean pressure gradient across the stenosis.Results The decision was made for venous sinus stenting of the POMS. Immediate post-stenting venography demonstrated resolution of the POMS stenosis with flow only into the POMS and a mean pressure gradient across the stenosis normalized to 2 mmHg.