The risk of complications in second pregnancy by maternal BMI: The role of first-pregnancy complications, pregestational diabetes and chronic hypertension.
- 作者列表："Sormunen-Harju H","Koivusalo S","Gissler M","Metsälä J
INTRODUCTION:Maternal obesity is associated with an increased risk of several pregnancy complications. In the second pregnancy, previous pregnancy and other medical history provide additional information about individual morbidity risk. In this study, we assess the risk of pregnancy complications in the second pregnancy by maternal body mass index (BMI) and evaluate how first-pregnancy complications and preexisting conditions modify these associations. MATERIAL AND METHODS:We have used nationwide data on all women (n = 48 963) experiencing their first and second pregnancy between 2006 and 2013 in Finland. The associations between the full scale of maternal BMI and pregnancy complications (gestational diabetes, gestational hypertension and preeclampsia) were analyzed using logistic regression and restricted cubic spline regression models and interactions between BMI and first-pregnancy complications, pregestational diabetes or chronic hypertension were tested. RESULTS:The risk of pregnancy complications increased with adiposity. Unadjusted probability of second-pregnancy gestational diabetes with BMI of 25 kg/m2 was 56% and 8.4% among women with and without first-pregnancy gestational diabetes, respectively. The corresponding figures with BMI of 30 kg/m2 were 64% and 17%. Adjusted odds ratio (OR) (95% CI) for second-pregnancy gestational diabetes with BMI of 25 kg/m2 was 45 (34-59) and 3.3 (2.6-4.0) among women with and without first-pregnancy gestational diabetes, respectively, when compared with women with BMI of 20 kg/m2 and no first-pregnancy gestational diabetes. Adjusted OR (95% CI) for second-pregnancy gestational hypertension among women with BMI of 25 kg/m2 was 42 (26-66) and 2.3 (1.4-3.8) among women with and without first-pregnancy hypertensive disorder, respectively, when compared with women with BMI of 20 kg/m2 and no first-pregnancy hypertensive disorder. The risk of preeclampsia increased with adiposity independent of first-pregnancy complications. Pregestational diabetes or chronic hypertension did not modify the association between adiposity and any of the second-pregnancy complications. CONCLUSIONS:As maternal BMI increases, the risk of complications increases in the second pregnancy. The risk of gestational diabetes and hypertension is, however, highest among women with complications in the first pregnancy.
简介: 母亲肥胖与几种妊娠并发症的风险增加有关。在第二次怀孕中，以前的怀孕和其他病史提供了关于个体发病风险的额外信息。在这项研究中，我们通过母体体重指数 (BMI) 评估第二次妊娠中妊娠并发症的风险，并评估第一次妊娠并发症和先前存在的情况如何改变这些关联。 材料和方法: 我们使用了芬兰所有妇女 (n = 48 963) 在2006年至2013年间第一次和第二次怀孕的全国数据。使用logistic回归和限制性三次样条回归模型分析孕妇BMI与妊娠并发症 (妊娠期糖尿病、妊娠期高血压和子痫前期) 之间的关联，并测试BMI与首次妊娠并发症、孕前糖尿病或慢性高血压之间的相互作用。 结果: 妊娠并发症的风险随着肥胖的增加而增加。在具有和不具有首次妊娠糖尿病的妇女中，BMI为25千克kg/m2的第二次妊娠糖尿病的未校正概率分别为56% 和8.4%。BMI为30千克kg/m2的相应数字为64% 和17%。BMI为95% kg/m2的第二次妊娠糖尿病患者的校正比值比 (OR) (25千克CI) 分别为45 (34-59) 和3.3 (2.6-4.0)。与BMI为20千克kg/m2且无首次妊娠妊娠糖尿病的女性相比。BMI为95% kg/m2的女性中，第二次妊娠妊娠高血压的校正OR (25千克CI) 分别为42 (26-66) 和2.3 (1.4-3.8)。与BMI为20千克kg/m2且无首次妊娠高血压疾病的女性相比。先兆子痫的风险增加与肥胖无关的首次妊娠并发症。孕前糖尿病或慢性高血压并未改变肥胖与任何第二次妊娠并发症之间的关联。 结论: 随着产妇BMI的增加，再次妊娠并发症的风险增加。然而，妊娠糖尿病和高血压的风险在第一次怀孕时出现并发症的女性中最高。
METHODS::The ATP binding-cassette superfamily corresponds the mostly transmembrane transporters family found in humans. These proteins actively transport endogenous and exogenous substrates through biological membranes in body tissues, so they have an important role in the regulation of many physiological functions necessary for human homeostasis, as well as in response regulation to several pharmacological substrates. The development of multidrug resistance has become one of the main troubles in conventional chemotherapy in different illnesses including cancer, being the increased efflux of antineoplastic drugs the main reason for this multidrug resistance, with a key role of the ABC superfamily. Likely, the interindividual variability in the pharmacological response among patients is well known, and may be due to intrinsically factors of the disease, genetic and environmental ones. Thus, the understanding of this variability, especially the genetic variability associated with the efficacy and toxicity of drugs, can provide a safer and more effective pharmacological treatment, so ABC genes are considered as important regulators due to their relationship with the reduction in pharmacological response. In this review, updated information about transporters belonging to this superfamily was collected, the possible role of these transporters in cancer, the role of genetic variability in their genes, as well as some therapeutic tools that have been tried to raise against main transporters associated with chemoresistance in cancer.
METHODS:BACKGROUND:Cholinergic neurotransmission regulates neuroinflammation in Parkinson disease (PD). RESEARCH DESIGN AND METHODS:The authors conducted a delayed-start study of donepezil for cognitive decline in non-demented PD patients. The study consisted of a 96-week randomized placebo-controlled double-blind phase 1, followed by a 24-week donepezil extension phase 2. The primary outcome measure was a change in the Mini-Mental State Examination (MMSE) at week 120. RESULTS:A total of 98 patients were randomly allocated to the early-start (donepezil-to-donepezil) and delayed-start (placebo-to-donepezil) groups. Mean (SD) of the baseline MMSE was 27.6 (2.0) and 28.0 (2.1), respectively. MMSE change at week 120 was better in the early-start group than in the delayed-start group, but the difference was not significant. The MMSE declined in apolipoprotein ε4 carriers, but not in non-carriers, and the factor interaction (intervention × ε4 genotype) was highly significant (P < 0.001). Analyzed with the interaction, the difference was significant (group difference 1.95 [0.33 to 3.57], P = 0.018). The MMSE decline slope in phase 1 was significantly better in the early-start group than in the delayed-start group (P = 0.048). CONCLUSIONS:Cognitive function deteriorated in ε4 carriers, but not in non-carriers, and early-start donepezil may postpone cognitive decline in the former.
METHODS::Since the discovery of dental pulp stem cells, a lot of teams have expressed an interest in dental pulp regeneration. Many approaches, experimental models and biological explorations have been developed, each including the use of stem cells and scaffolds with the final goal being clinical application in humans. In this review, the authors' objective was to compare the experimental models and strategies used for the development of biomaterials for tissue engineering of dental pulp with stem cells. Electronic queries were conducted on PubMed using the following terms: pulp regeneration, scaffold, stem cells, tissue engineering and biomaterial. The extracted data included the following information: the strategy envisaged, the type of stem cells, the experimental models, the exploration or analysis methods, the cytotoxicity or viability or proliferation cellular tests, the tests of scaffold antibacterial properties and take into account the vascularization of the regenerated dental pulp. From the 71 selected articles, 59% focused on the "cell-transplantation" strategy, 82% used in vitro experimentation, 58% in vivo animal models and only one described an in vivo in situ human clinical study. 87% used dental pulp stem cells. A majority of the studies reported histology (75%) and immunohistochemistry explorations (66%). 73% mentioned the use of cytotoxicity, proliferation or viability tests. 48% took vascularization into account but only 6% studied the antibacterial properties of the scaffolds. This article gives an overview of the methods used to regenerate dental pulp from stem cells and should help researchers create the best development strategies for research in this field.