11-beta-Hydroxysteroid Dehydrogenase Type 2/genetics* ; Humans ; Mineralocorticoid Excess Syndrome, Apparent/genetics* ; Pedigree

OBJECTIVETo explore the relationship between HSD11B2 polymorphisms and fetal growth during normal pregnancy.

METHODSThe HSD11B2 promoter/G-209A, G-194C, G-151A and G-126A genotypes were examined in 33 samples from Chinese Han subjects by gene sequencing. HSD11B2 (CA)n microsatellite polymorphism in the first intron was detected in blood samples from 187 maternal and newborn pairs by PCR-capillary electrophoresis.

RESULTSAll the HSD11B2 promoter/G-209A, G-194C, G-151A and G-126A genotypes were wild-type GG. The offspring birth weight and any ultrasound parameters describing late gestational fetal body shape were not significantly different between maternal or fetal SS, SL and LL groups or combined SS+SL and LL groups. When considering the relevant confounding factors (gestational age at delivery, newborn's gender, maternal body mass index before pregnancy, maternal weight at delivery and maternal age), the offspring birth weight and late pregnancy ultrasound parameters were still not associated with the maternal or fetal HSD11B2 (CA) n microsatellite polymorphisms.

CONCLUSIONSFetal and maternal HSD11B2 polymorphism is not related to fetal growth during normal pregnancy.

11-beta-Hydroxysteroid Dehydrogenase Type 2 ; genetics ; Birth Weight ; Body Mass Index ; Female ; Fetal Development ; genetics ; Genotype ; Gestational Age ; Humans ; Infant, Newborn ; Polymorphism, Genetic ; Pregnancy ; Promoter Regions, Genetic

OBJECTIVETo investigate the mRNA and protein expressions of 11beta-Hydroxysteroid dehydrogenase type 2 (11betaHSD2) in patients with atrial fibrillation.

METHODSRight and left atrial lateral wall tissue samples were obtained during mitral/aortic valve replacement operation from 25 patients with rheumatic heart valve disease (12 in sinus rhythm and 13 in chronic atrial fibrillation). Realtime quantitative PCR and Western blot were used to determine the mRNA and protein expressions of 11betaHSD2 in atria specimens. The distribution of 11betaHSD2 in human atrial tissue was analyzed by specific immunohistochemical staining. Echocardiography examination was performed before operation.

RESULTSThe left atrial diameters were significantly higher in the atrial fibrillation group as compared to sinus rhythm group (P < 0.01). Similarly, mRNA expression of 11betaHSD2 (0.86 +/- 0.14 vs 0.33 +/- 0.12 in right atria, 0.95 +/- 0.15 vs 0.37 +/- 0.10 in left atria, all P < 0.01) and protein expression of 11betaHSD2 (1.18 +/- 0.64 vs 0.71 +/- 0.21 in right atria, P < 0.01; and 1.36 +/- 0.58 vs 0.85 +/- 0.15 in left atria, P < 0.05) were also significantly upregulated in atrial fibrillation groups than those in sinus rhythm groups. The mRNA and protein expressions of 11betaHSD2 were similar between left atria and right atria both in fibrillation and sinus groups (all P > 0.05). The special immunohistochemical staining demonstrated that 11betaHSD2 was abundant in the human atrial myocardium and located mainly in the cytoplasm.

CONCLUSIONThese findings suggested that upregulated 11betaHSD2 might be associated to the development and persistence of atrial fibrillation.

11-beta-Hydroxysteroid Dehydrogenase Type 2 ; metabolism ; Adult ; Atrial Fibrillation ; metabolism ; physiopathology ; Female ; Heart Atria ; metabolism ; physiopathology ; Humans ; Male ; Middle Aged ; Myocardium ; metabolism ; RNA, Messenger ; genetics ; Rheumatic Heart Disease ; metabolism ; physiopathology