Use of birth weight threshold for macrosomia to identify fetuses at risk of shoulder dystocia among Chinese populations.

Objective: To assess the incidence of macrosomia and the influence of birth weight on shoulder dystocia risk among a cohort of Chinese women.

Methods: A retrospective analysis was conducted of 80953 singleton deliveries recorded at the Prince of Wales Hospital, Hong Kong, between 1995 and 2009. The incidences of macrosomia (birth weight ≥ 4000 g) and shoulder dystocia were assessed by birth weight; risk factors for shoulder dystocia were examined by multiple logistic regression analysis.

Solid-phase immunoglobulins IgG and IgM activate macrophages with solid-phase IgM acting via a novel scavenger receptor a pathway.

IgG may accelerate atherosclerosis via ligation of proinflammatory Fcγ receptors; however, IgM is unable to ligate FcγR and is often considered vasculoprotective. IgM aggravates ischemia-reperfusion injury, and solid-phase deposits of pure IgM, as seen with IgM-secreting neoplasms, are well known clinically to provoke vascular inflammation. We therefore examined the molecular mechanisms by which immunoglobulins can aggravate vascular inflammation, such as in atherosclerosis.

Intrapleural injection of OK-432 as the primary in-utero treatment for fetal chylothorax.

Chylothorax is a rare congenital condition associated with significant perinatal mortality and morbidity. Previous treatments with repeated thoracocentesis or thoracoamniotic shunting were technically demanding, and associated with significant procedure-related complications and neonatal complications. Here we report the first successful case in Hong Kong treated by a simple and effective intervention, namely pleurodesis with OK-432, in a fetus presenting at 20 weeks of gestation with bilateral pleural effusion.

Decay-accelerating factor suppresses complement C3 activation and retards atherosclerosis in low-density lipoprotein receptor-deficient mice.

Decay-accelerating factor (DAF; CD55) is a membrane protein that regulates complement pathway activity at the level of C3. To test the hypothesis that DAF plays an essential role in limiting complement activation in the arterial wall and protecting from atherosclerosis, we crossed DAF gene targeted mice (daf-1(-/-)) with low-density lipoprotein-receptor deficient mice (Ldlr(-/-)). Daf-1(-/-)Ldlr(-/-) mice had more extensive en face Sudan IV staining of the thoracoabdominal aorta than Ldlr(-/-) mice, both following a 12-week period of low-fat diet or a high-fat diet.

Determinants of hepatitis B vaccine uptake among pregnant Chinese women in Hong Kong.

Objective: To determine the prevalence of a history of hepatitis B vaccination among pregnant Chinese women in Hong Kong, and to identify factors associated with vaccine uptake at their own expense.

Methods: A prospective, cross-sectional survey was conducted in a university obstetric unit in Hong Kong. Pregnant Chinese women who attended the prenatal clinic were invited to complete a self-administered questionnaire, which requested details of their history of hepatitis B vaccination and sociodemographic characteristics.

Brief report: accelerated atherosclerosis in low-density lipoprotein receptor-deficient mice lacking the membrane-bound complement regulator CD59.

Objective: Whereas studies in humans and animal models have suggested a role for complement activation in atherosclerosis, there has been little analysis of the importance of complement regulators. We tested the hypothesis that the terminal pathway inhibitor CD59 plays an essential role in limiting the proinflammatory effects of complement activation.

Methods And Results: CD59 gene targeted mice (CD59a(-/-)) mice were crossed with low-density lipoprotein receptor-deficient (Ldlr(-/-)) mice.

KLF2-dependent, shear stress-induced expression of CD59: a novel cytoprotective mechanism against complement-mediated injury in the vasculature.

Complement activation may predispose to vascular injury and atherogenesis. The atheroprotective actions of unidirectional laminar shear stress led us to explore its influence on endothelial cell expression of complement inhibitory proteins CD59 and decay-accelerating factor. Human umbilical vein and aortic endothelial cells were exposed to laminar shear stress (12 dynes/cm(2)) or disturbed flow (+/- 5 dynes/cm(2) at 1Hz) in a parallel plate flow chamber.

Complement C1q reduces early atherosclerosis in low-density lipoprotein receptor-deficient mice.

We explored the role of the classic complement pathway in atherogenesis by intercrossing C1q-deficient mice (C1qa-/-) with low-density lipoprotein receptor knockout mice (Ldlr-/-). Mice were fed a normal rodent diet until 22 weeks of age. Aortic root lesions were threefold larger in C1qa-/-/Ldlr-/- mice compared with Ldlr-/- mice (3.