Subclinical hypothyroidism is common in pregnant women and often related to adverse pregnancy outcomes, but its relationship with gestational diabetes remains controversial. In particular, the impact of thyroperoxidase antibodies status on the relationship between subclinical hypothyroidism and gestational diabetes is not clear. We investigated the association between combined thyroid stimulating hormone (TSH) level and thyroperoxidase antibodies status in early pregnancy (<20 weeks of gestation) and gestational diabetes mellitus. A total of 7084 pregnant women met the inclusion criteria, which included thyroperoxidase antibodies-positive subclinical hypothyroidism [TSH(H)TPOAb(+)] (n = 78), thyroperoxidase antibodies-negative subclinical hypothyroidism [TSH(H)TPOAb(-)] (n = 281), thyroperoxidase antibodies-positive euthyroidism [TSH(N)TPOAb(+)] (n = 648), and thyroperoxidase antibodies-negative euthyroidism [TSH(N)TPOAb(-)] (n = 6077). Of the 7084 cases included in our study, 1141 cases were diagnosed with gestational diabetes mellitus at 24-28 weeks of pregnancy. The prevalence of gestational diabetes mellitus in TSH(N)TPOAb(-), TSH(H)TPOAb(-), TSH(N)TPOAb(+), and TSH(H)TPOAb(+) was 14.65, 19.57, 24.85, and 46.15 %, respectively. Compared with TSH(N)TPOAb(-) women, the risk of gestational diabetes mellitus was increased in all other groups of women in early pregnancy. After dividing early pregnancy into first and second trimesters, we found that TSH(H)TPOAb(-) women in the first trimester do not show this increase. Our study suggests that subclinical hypothyroidism and thyroperoxidase antibodies-positive euthyroidism in early pregnancy are associated with an increased risk of gestational diabetes mellitus.
Familial isolated GH deficiency type 1A (IGHD1A) results from deletion of both GH alleles. To facilitate detection of cases of IGHD1A, we have developed a rapid method that uses polymerase chain reaction amplification of small amounts of genomic DNA, digestion with a single restriction endonuclease, and visualization of DNA fragments after gel electrophoresis. Employing this method we have identified two subjects with IGHD1A among a cohort of seven Chinese subjects with severe growth retardation due to GHD.
Both 6.6""-dimethyl-(dmqpy) and 6,6""-dimethyl-4',4'"-diphenyl-2,2' : 6',2" : 6",2"' : 6"',2""-quinquepyridine (dmpqpy) have been found to form dinuclear double helical silver(1) complexes [Ag,(dmqpy),][ClO,], 1 and [Ag2(dmpqpy)2][C10,]2~2H20 2. The introduced terminal methyl groups play a crucial role in the assembly processes. According to their crystal structures, the ligand adopts the usual [2 + 31 co-ordination mode in 1 and the silver(1) is five-co-ordinated with a flattened and distorted trigonal-bipyramidal geometry. In 2 the ligand dmpqpy adopts a [2 + 1 + 21 mode and is unexpectedly tetradentate with the central pyridyl nitrogen atom having no direct co-ordination and acting as a rigid spacer. The silver(1) atoms are four-co-ordinated. It is supposed that the increased conjugation and rigidity caused by the phenyl groups at the 4',4"' positions makes it difficult for the central pyridine nitrogen to co-ordinate to Ag'. Strong intramolecular n-n stacking interactions exist in complex 1, but the stacking effects in 2 are much weaker. The NMR results indicate that both complexes adopt more symmetric configurations in solution than in the solid state.
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