Preterm delivery in normoalbuminuric, diabetic women without preeclampsia: the role of metabolic control

OBJECTIVE: The aim of this study was to examine the importance of glycemic regulation on the risk of preterm delivery in women with normoalbuminuria and no preeclampsia later in pregnancy. STUDY DESIGN AND METHODS: A prospective study of 71 women with type 1 diabetes mellitus where complete data were collected on HbA1c, insulin dose, and albumin excretion rate from week 12 and every second week hereafter. Fundus photography was performed and diurnal blood pressure measured three times during pregnancy. RESULTS: The preterm rate was 23% and women delivering preterm showed higher HbA1c throughout pregnancy. At regression analysis HbA1c was the strongest predictor for preterm delivery from week 6 to 32, also when including insulin dose, BMI, age, duration of diabetes, and diurnal blood pressure. The risk of delivering preterm was more than 40% when HbA1c was above 7.7% in week 8. Diurnal blood pressure was not found associated with preterm delivery. CONCLUSION: The quality of glycemic regulation in the early and mid-pregnancy is a major, independent risk factor for preterm delivery in normoalbuminuric diabetic women without preeclampsia.     

Premature ovarian failure and pregnancy

Setting: A case study of a woman with presumed premature menopause is presented. Results: After more than 4 years of premature menopause judged by subjective symptoms, bleeding history, and postmenopausal levels of gonadotropins, a woman conceived spontaneously 2 months after the start of hormone replacement treatment (HRT). Previously, ovarian stimulation with clomifen citrate had failed. She delivered prematurely due to preeclampsia and intrauterine growth retardation. Conclusions: Reviewing the literature finds that pregnancy is reported in woman with premature ovarian failure after the use of birth-control pills, HRT, ovarian stimulation, and in spontaneous cycles. Lack of oocyte donors and prohibition of the donor technique in some countries make other options valuable when optimal infertility treatment cannot be offered.     

Expression and functional role of adenosine receptors in regulating inflammatory responses in human synoviocytes

Background and purpose:

Adenosine is an endogenous modulator, interacting with four G-protein coupled receptors (A₁, A_2A, A_2B and A₃) and acts as a potent inhibitor of inflammatory processes in several tissues. So far, the functional effects modulated by adenosine receptors on human synoviocytes have not been investigated in detail. We evaluated mRNA, the protein levels, the functional role of adenosine receptors and their pharmacological modulation in human synoviocytes.

Experimental approach:

mRNA, Western blotting, saturation and competition binding experiments, cyclic AMP, p38 mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB activation, tumour necrosis factor α (TNF-α) and interleukin-8 (IL-8) release were assessed in human synoviocytes isolated from patients with osteoarthritis.

Key results:

mRNA and protein for A₁, A_2A, A_2B and A₃ adenosine receptors are expressed in human synoviocytes. Standard adenosine agonists and antagonists showed affinity values in the nanomolar range and were coupled to stimulation or inhibition of adenylyl cyclase. Activation of A_2A and A₃ adenosine receptors inhibited p38 MAPK and NF-κB pathways, an effect abolished by selective adenosine antagonists. A_2A and A₃ receptor agonists decreased TNF-α and IL-8 production. The phosphoinositide 3-kinase or G_s pathways were involved in the functional responses of A₃ or A_2A adenosine receptors. Synoviocyte A₁ and A_2B adenosine receptors were not implicated in the inflammatory process whereas stimulation of A_2A and A₃ adenosine receptors was closely associated with a down-regulation of the inflammatory status.

Conclusions and implications:

These results indicate that A_2A and A₃ adenosine receptors may represent a potential target in therapeutic modulation of joint inflammation.     

江西省8所大学1348名大学生主观幸福感影响因素的调查

目的:对江西省8所大学部分学生主观幸福感进行调查分析,为进一步开展大学生心理健康教育工作提供依据。方法:于2005-10-20/11-30运用主观幸福感量表、青少年生活事件量表、领悟社会支持量表、内在-外在心理控制源量表对江西省8所大学的1348名大学生进行抽样调查。其中主观幸福感量表分数越高,幸福感越高。内在-外在心理控制源量表得分越低,越倾向内控,得分越高,越倾向外控。结果:共发放问卷1348份,收回有效问卷1231份,其中男生539名,女生692名,大一学生421名,大二学生390名,大三学生420名,城市452名,农村779名,平均年龄20.4岁。①男生主观幸福感的得分略低于女生的得分,但差异没有显著性(25.97±5.80,26.61±5.03,t=0.309,P>0.05)。②大一学生主观幸福感评分为26.97±4.61,大二学生为25.35±6.37,大三学生为25.92±5.75,3个年级之间的主观幸福感评分比较差异无显著性(F=2.769,P>0.05),两两比较发现,大一学生主观幸福感的得分显著高于大三学生(P<0.05)。③家庭经济收入低的大学生(家庭人均年收入≤2000元)主观幸福感评分显著低于普通大学生(21.58±3.97,26.30±5.43,t=3.015,P<0.01)。④生活事件与主观幸福感存在显著性负相关(r=-0.289,P<0.01),社会支持与主观幸福感存在显著性正相关(r=0.384,P<0.01)。生活事件、社会支持分别对主观幸福感的回归分析发现,生活事件、社会支持分别解释了主观幸福感变异的7.2%,11.7%。⑤按照控制感量表得分把分数由高到低进行排序,把分数处于最低点的30%的学生作为内控组的学生,分数处于最高点的30%的学生作为外控组的学生。内控组大学生的主观幸福感得分显著高于外控组(27.29±5.86,21.83±7.03,t=5.359,P<0.01)。结论:高年级学生、低收入家庭的学生幸福感水平低,负性生活事件能降低大学生的主观幸福感,而较多社会支持会产生较高的主观幸福感。     

Antibody-dependent Lymphocyte-mediated Cytotoxicity in Man: No Requirement for Lymphocytes with Membrane-bound Immunoglobulin

Normal human lymphocytes, depleted of B-lymphocytes by passage through nylon-wool columns, manifested intact antibody-dependent cell-mediated cytotoxicity. Similar findings were made with lymphocytes from four hypo-gammaglobulinaemic patients lacking B-lymphocytes. It is concluded that antibody-induced cell-mediated cytotoxicity in man is independent of B-lymphocytes, as identifiable by membrane-bound immunoglobulin.     

Association of polymorphism of methylene-tetrahydro-folate-reductase with urinary albumin excretion rate in type 1 diabetes mellitus but not with preeclampsia, retinopathy, and preterm delivery

AIM: The genetic setting is a potential risk factor for dysfunction of vascular endothelial cells. The prevalence of polymorphism in the methylene-tetrahydro-folate-reductase (MTHFR) gene (677C-->T) was evaluated in diabetic pregnancy complicated by preeclampsia, nephropathy, retinopathy, and preterm delivery. The role of hyperhomocysteinemia in microangiopathy in diabetes mellitus has been debated and is mainly seen with reduced activity of the MTHFR gene. A polymorphism in the gene for MTHFR is identified causing this phenomenon. DESIGN: Two hundred and sixty-eight pregnant women with type 1 diabetes mellitus were recruited. Two hundred and thirty-three women were successfully analyzed for MTHFR gene polymorphism 677C-->T and compared to the incidence of the polymorphism in the background population (n=1084). The pregnancy data charts were reviewed retrospectively. RESULTS: The frequency of the MTHFR polymorphism in the background population was 29% and the heterozygozity 42%. The women with type 1 diabetes mellitus had a higher frequency of the MTHFR polymorphism with 52% heterozygotes and 9% homozygotes than had the background population (heterozygotes, background vs. type 1 diabetes mellitus: chi(2)=14, df=1, p<0.0002). The odds ratio for heterozygozity of the MTHFR polymorphism was 1.8 (95% Cl: 1.3-2.4) in women with type 1 diabetes mellitus. Women with either micro- or macroalbuminuria had a higher frequency of MTHFR polymorphism with 61% heterozygotes and 3% homozygotes than had the background population (heterozygotes: chi(2)=8.9, df=1, p<0.01). The odds ratio for heterozygozity of the MTHFR polymorphism was 2.3 (95% CI: 1.4-4) in women with type 1 diabetes mellitus. CONCLUSION: An association was demonstrated between the MTHFR polymorphism and type 1 diabetes mellitus as well as increasing albumin excretion rate in pregnant women.     

Plasma growth hormone response to growth hormone-releasing hexapeptide (GH-RP-6) in children with short stature

Eighteen children with short stature were evaluated for growth hormone (GH) reserve after pharmacological tests and a single iv injection of GH-RP-6. These children were divided into two groups: 10 were diagnosed as having idiopathic GH deficiency by classical stimulation tests (group A) and the remaining 8 (group B) were considered growth-retarded children with normal GH secretion, following conventional stimulation, but reduced endogenous GH secretion. The results were compared with a group of 12 normal children. As a group, patients in group A showed a lower GH response to GH-RP-6, while patients in group B had a similar response as normal controls. However, on an individual basis, a considerable degree of overlapping in responses among the three groups was evident. These data indicate that, on an individual basis, GH-RP-6 testing is not of diagnostic value in children suspected of having idiopathic GH deficiency.GH deficiency, GH-RP-6, short stature C Dieguez, PO Box 563, 15705 Santiago de Compostela, Spain     

糖尿病大鼠卵巢组织中细胞色素C、线粒体Ca2+变化与灵芝孢子粉的干预

目的:以卵巢组织中细胞色素C、线粒体Ca2 和性激素水平为观察指标,观察灵芝孢子粉对2型糖尿病大鼠卵巢组织的保护作用。方法:实验于2006-06/08在佳木斯大学黑龙江省小儿神经康复重点实验室完成。①实验对象:Wistar雌性大鼠50只,随机分为对照组10只,2型糖尿病模型组20只,灵芝孢子粉组20只。②实验方法:大鼠禁食16～18h,自由饮水,模型组及灵芝孢子粉组大鼠经尾静脉一次性按25mg/kg注射2%链脲佐菌素,正常对照组尾静脉注射等量柠檬酸钠-柠檬酸缓冲液。正常饮食喂养2周后,进行糖耐量试验,模型组和灵芝组以糖耐量异常者保留,余去除,并改喂高脂高糖饮食,灵芝孢子粉组另加灵芝孢子粉[250mg/(kg·d)]持续10周,实验结束前一天再次做糖耐量试验。③实验评估:实验结束后,各组动物均禁食12h,乙醚吸入浅麻醉,内眦静脉取血待测血清胰岛素。解剖出卵巢,待测线粒体细胞色素C、线粒体Ca2 含量。结果:选用Wistar雌性大鼠50只,结果分析数量每组8只。①葡萄糖耐量试验:实验开始及实验12周时,模型组大鼠均表现出糖耐量异常的变化(P<0.05),1h血糖增高显著(P<0.05)达到高峰,2h血糖仍较高;对照组大鼠30min血糖达到峰值,2h血糖基本恢复正常。②血清胰岛素和卵巢性激素水平:模型组血清胰岛素明显升高(P<0.05)。而灵芝孢子粉组与对照组比较差异无显著性。模型组雌二醇含量明显降低(P<0.05),卵胞刺激素含量、睾酮含量明显升高(P<0.05),而灵芝孢子粉组与对照组比较差异无显著性。③胞浆细胞色素C、线粒体细胞色素C、线粒体钙变化:模型组卵巢组织胞浆细胞色素C含量明显升高(P<0.05),模型组卵巢组织线粒体细胞色素C含量明显降低(P<0.05),模型组卵巢组织线粒体钙含量明显降低(P<0.05);而灵芝孢子粉组与对照组比较差异均无显著性。结论:灵芝孢子粉可降低糖尿病大鼠血清胰岛素、卵巢组织卵胞刺激素、睾酮、胞浆细胞色素C含量,调节卵巢组织雌二醇、线粒体细胞色素C、钙含量,对糖尿病大鼠卵巢组织具有一定保护作用。