Catecholamines in amniotic fluid as indicators of intrapartum fetal stress.

Catecholamines were measured in the amniotic fluid and in the first voided newborn urine obtained from appropriate-for-date infants of term deliveries. Catecholamine values in the amniotic fluid and urine were nearly equal when expressed in terms of creatinine. Significant positive correlations were observed between the amniotic fluid and urine of norepinephrine and epinephrine. In normal cases (n = 32) that underwent uneventful vaginal delivery, the 95% confidence limits for norepinephrine and epinephrine in the amniotic fluid were 1.53 to 2.33 ng/ml and 0.16 to 0.30 ng/ml, respectively. In cases of moderate stress (n = 12), only norepinephrine showed significantly higher values than the normal cases, while in cases of severe stress (n = 12), norepinephrine became more significantly high, and epinephrine was found to be elevated significantly. A significant difference was noted in the incidence of fetal stress between the infants with more than and those with less than 2.30 ng/ml of norepinephrine, the upper limits of the normal 95% confidence limits. However, for epinephrine such a significant difference was not noted. It was concluded that amniotic fluid catecholamines are of fetal origin and reflect fetal sympathoadrenal activity directly, even during labor, and that their level may be a good indicator of fetal condition and stress.</p

Complete chemical structures of human mitochondrial tRNAs

Mitochondria generate most cellular energy via oxidative phosphorylation. Twenty-two species of mitochondrial (mt-)tRNAs encoded in mtDNA translate essential subunits of the respiratory chain complexes. mt-tRNAs contain post-transcriptional modifications introduced by nuclear-encoded tRNA-modifying enzymes. They are required for deciphering genetic code accurately, as well as stabilizing tRNA. Loss of tRNA modifications frequently results in severe pathological consequences. Here, we perform a comprehensive analysis of post-transcriptional modifications of all human mt-tRNAs, including 14 previously-uncharacterized species. In total, we find 18 kinds of RNA modifications at 137 positions (8.7% in 1575 nucleobases) in 22 species of human mt-tRNAs. An up-to-date list of 34 genes responsible for mt-tRNA modifications are provided. We identify two genes required for queuosine (Q) formation in mt-tRNAs. Our results provide insight into the molecular mechanisms underlying the decoding system and could help to elucidate the molecular pathogenesis of human mitochondrial diseases caused by aberrant tRNA modifications