Does a large infant head or a short perineal body increase the risk of obstetrical perineal trauma?

BACKGROUND: Perineal trauma after vaginal delivery can have significant long-term consequences. It is unknown if a larger infant head circumference or smaller maternal perineal anatomy are risk factors for perineal trauma after vaginal delivery. METHODS: We conducted a prospective cohort study of low-risk nulliparous women. Data collected included maternal characteristics, antepartum Pelvic Organ Prolapse Quantification measurements of the perineal body and genital hiatus, labor characteristics, perineal trauma, and infant head circumference. Perineal trauma was defined as trauma that extended into the muscles of the perineum (second-degree or deeper). Univariate and multivariate logistic models were created to calculate odds ratios (OR) and 95 percent confidence intervals (CI). RESULTS: We observed 448 vaginal births. Multivariate analysis demonstrated a significant association between infant head circumference at birth and perineal trauma: OR 1.22 for each increase of 1 cm in head circumference (95% CI 1.05-1.43). There was no association between perineal body or genital hiatus length and perineal trauma. CONCLUSIONS: In nulliparous low-risk women a larger infant head circumference at birth increases the likelihood of perineal trauma, although the effect is modest. Antenatal perineal body and genital hiatus measurements do not predict perineal trauma. These results do not support alteration in mode of delivery or other obstetric practices.

Evolution of gnathostome prodynorphin and proenkephalin: characterization of a shark proenkephalin and prodynorphin cDNAs.

Analyses of prodynorphin and proenkephalin cDNAs cloned from the central nervous system of the shark, Heterodontus portusjacksoni, provided additional evidence that these two opioid precursor-coding genes were most likely directly derived from a common ancestral gene. The two cDNAs could be aligned by inserting only seven gaps. The prodynorphin cDNA encodes five opioid sequences which could be aligned to opioid positions B through F in the proenkephalin cDNA. The sequence identity within the opioid positions was 59% at the amino acid level. Shark α-neo-endorphin, dynorphin A, and dynorphin B have amino acid motifs in common with shark met-enkephalin-8, and shark proenkephalin opioid positions E and F, respectively, which have not been observed in other gnathostome prodynorphin and proenkephalin precursor sequences. Shark prodynorphin encodes both kappa (α-neo-endorphin, dynorphin A, and dynorphin B) and delta (met-enkephalin and leu-enkephalin) opioid sequences. Mixed function prodynorphin precursors (encoding both enkephalins and dynorphins) are also found in representatives of the teleost fishes, lungfishes, and amphibians. It appears that only mammals evolved a prodynorphin precursor that exclusively encodes kappa opioid agonists (dynorphins).

Analysis of maternal-offspring HLA compatibility, parent-of-origin effects, and noninherited maternal antigen effects for HLA-DRB1 in systemic lupus erythematosus.

OBJECTIVE: Genetic susceptibility to systemic lupus erythematosus (SLE) is well established, with the HLA class II DRB1 and DQB1 loci demonstrating the strongest association. However, HLA may also influence SLE through novel biologic mechanisms in addition to genetic transmission of risk alleles. Evidence for increased maternal-offspring HLA class II compatibility in SLE and differences in maternal versus paternal transmission rates (parent-of-origin effects) and nontransmission rates (noninherited maternal antigen [NIMA] effects) in other autoimmune diseases have been reported. Thus, we investigated maternal-offspring HLA compatibility, parent-of-origin effects, and NIMA effects at DRB1 in SLE. METHODS: The cohort comprised 707 SLE families and 188 independent healthy maternal-offspring pairs (total of 2,497 individuals). Family-based association tests were conducted to compare transmitted versus nontransmitted alleles (transmission disequilibrium test) and both maternally versus paternally transmitted (parent-of-origin) and nontransmitted alleles (using the chi-square test of heterogeneity). Analyses were stratified according to the sex of the offspring. Maternally affected offspring DRB1 compatibility in SLE families was compared with paternally affected offspring compatibility and with independent control maternal-offspring pairs (using Fisher's test) and was restricted to male and nulligravid female offspring with SLE. RESULTS: As expected, DRB1 was associated with SLE (P < 1 x 10(-4)). However, mothers of children with SLE had similar transmission and nontransmission frequencies for DRB1 alleles when compared with fathers, including those for the known SLE risk alleles HLA-DRB1*0301, *1501, and *0801. No association between maternal-offspring compatibility and SLE was observed. CONCLUSION: Maternal-offspring HLA compatibility, parent-of-origin effects, and NIMA effects at DRB1 are unlikely to play a role in SLE.