Temporal changes in key maternal and fetal factors affecting birth outcomes: A 32-year population-based study in an industrial city

Background

In Australia and internationally, there is concern about the growing proportion of women giving birth by caesarean section. There is evidence of increased risk of placenta accreta and percreta in subsequent pregnancies as well as decreased fertility; and significant resource implications. Randomised controlled trials (RCTs) of continuity of midwifery care have reported reduced caesareans and other interventions in labour, as well as increased maternal satisfaction, with no statistically significant differences in perinatal morbidity or mortality. RCTs conducted in the UK and in Australia have largely measured the effect of teams of care providers (commonly 6–12 midwives) with very few testing caseload (one-to-one) midwifery care. This study aims to determine whether caseload (one-to-one) midwifery care for women at low risk of medical complications decreases the proportion of women delivering by caesarean section compared with women receiving 'standard' care. This paper presents the trial protocol in detail.

Methods/design

A two-arm RCT design will be used. Women who are identified at low medical risk will be recruited from the antenatal booking clinics of a tertiary women's hospital in Melbourne, Australia. Baseline data will be collected, then women randomised to caseload midwifery or standard low risk care. Women allocated to the caseload intervention will receive antenatal, intrapartum and postpartum care from a designated primary midwife with one or two antenatal visits conducted by a 'back-up' midwife. The midwives will collaborate with obstetricians and other health professionals as necessary. If the woman has an extended labour, or if the primary midwife is unavailable, care will be provided by the back-up midwife. For women allocated to standard care, options include midwifery-led care with varying levels of continuity, junior obstetric care and community based general medical practitioner care. Data will be collected at recruitment (self administered survey) and at 2 and 6 months postpartum by postal survey. Medical/obstetric outcomes will be abstracted from the medical record. The sample size of 2008 was calculated to identify a decrease in caesarean birth from 19 to 14% and detect a range of other significant clinical differences. Comprehensive process and economic evaluations will be conducted.

Trial registration

Australian New Zealand Clinical Trials Registry ACTRN012607000073404.     

Do pregnant women want to know the sex of the expected child at routine ultrasound and are they interested in sex selection?

Background: The aim of the study was to investigate if expecting parents wanted to know the sex of the fetus during ultrasound examination and if they had discussed it with the midwife. Another aim was to explore any interest in sex selection.

Methods: A longitudinal survey in early and late pregnancy among 2393 women in Sweden.

Results: Almost all (95.8%, n?=?2289) women had discussed sex determination with the partner before the ultrasound scan, and 57% (n?=?1356) of women and their partners wanted to find out the fetal sex. The expecting parents mostly initiated a discussion with the midwife (46%, n?=?1088), but 10% (n?=?229) stated that the midwives initiated the discussion. Few (5%, n?=?118) expressed a potential interest in selecting sex of a baby. Women who were interested in sex determination did not differ from those who were not, with respect to age, origin, education, parity, level of pregnancy planning, or importance of religion, but women who had chosen another fetal diagnostic method were more interested in sex determination and in potential sex selection.

Conclusions: Half of women and their partners wanted to know the fetal sex, and 5% were interested in sex selection. This high interest in sex determination is a challenge, since present national guidelines do not include sex determination as an option.     

Butyrate Induces Glutathione S-Transferase in Human Colon Cells and Protects From Genetic Damage by 4-Hydroxy-2-Nonenal

Butyrate, one of the major products of gut fermentation, is known to inhibit proliferation, induce apoptosis and differentiation, and increase phase II enzyme activities in tumor cells, whereas little information is available on protective effects in less-transformed colon cells. The aim of this study was to investigate whether the chemoprotective mechanism of glutathione S-transferase (GST) induction by butyrate could also play a role in earlier stages of colon carcinogenesis and whether chemoresistance of cells toward the endogenous genotoxic risk factor 4-hydroxy-2-nonenal (HNE) could be a consequence of butyrate treatment. As cell models, we used the human tumor cell lines HT29 and HT29 clone 19A, a differentiated subclone with properties resembling primary colon cells. We determined the expression of GSTP1 protein (enzyme-linked immunosorbent assay), the major GST in HT29, GSTP1 mRNA (Northern blotting), GST activity, intracellular glutathione, and total protein. The genotoxic impact of HNE (100-200 μM) was compared in butyrate-treated and nontreated cells using single-cell microgel electrophoresis. Our results show that GSTP1 mRNA, GSTP1 protein, GST activity, and total protein were increased (1.2- to 2.5-fold) and glutathione levels were maintained after 24- 72 h of incubation with 4 mM butyrate. Moreover, a marked reduction of HNE-induced genotoxicity was caused by preincubation with butyrate. Butyrate also induced the phosphorylation of extracellular signal-regulated kinases (ERK1/2, Western blotting) after 5-30 min, which indicates a regulation of GST expression by this signal pathway. Most effects were greater in HT29 parent cells than in clone cells. In conclusion, butyrate enhances expression of GST and other proteins in both cell lines, which leads to an enhanced chemoprotection, reducing the impact of HNE genotoxicity. Thus butyrate could play a role in early and later stages of cancer prevention by reducing exposure to relevant risk factors.     

Performance of cobas® 4800 and m2000 real-time™ assays for detection of Chlamydia trachomatis and Neisseria gonorrhoeae in rectal and self-collected vaginal specimen

A prospective, multicenter trial was designed to compare the performance characteristics of the cobas® 4800 (Roche Diagnostics, Indianapolis, IN, USA) and m2000 real-time™ (Abbott Molecular Inc., Des Plaines, IL, USA) assays for detection of Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG) in rectal and self-collected vaginal swabs. Rectal (n = 234) or self-collected vaginal swabs (n = 687) were obtained from consenting individuals visiting their general practitioners, dermatologists, gynecologists, sexually transmitted disease clinics, or family planning centers from May 2010 to February 2011. High concordance rates (≥96%) were observed between the cobas® 4800 and m2000 real-time™ assays for CT/NG detection in both rectal and self-collected vaginal swabs. The performance profiles confirm the usefulness of both kinds of swab types for CT and NG detection using described nucleic acid amplification tests assays. Based on this study, rectal and self-collected vaginal swabs offer a noninvasive alternative, which may improve screening for CT and NG infections.     

Genetics of inflammation and atopy

Multiple chromosomal regions and polymorphisms of several candidate genes have been linked to or associated with atopic diseases (hayfever, asthma, allergic eczema and rhinitis). In this mini-review, we present data demonstrating that the genetic regulation of the inflammatory response makes a major contribution to the risk of atopy. These data also suggest that the quantity (or quality) of the inflammation affects the priming phase of atopy, i.e., that induced by allergens or infectious agents in early childhood.     

The Rodent Tibia Fracture Model: A Critical Review and Comparison With the Complex Regional Pain Syndrome Literature

Distal limb fracture is the most common cause of complex regional pain syndrome (CRPS), thus the rodent tibia fracture model (TFM) was developed to study CRPS pathogenesis. This comprehensive review summarizes the published TFM research and compares these experimental results with the CRPS literature. The TFM generated spontaneous and evoked pain behaviors, inflammatory symptoms (edema, warmth), and trophic changes (skin thickening, osteoporosis) resembling symptoms in early CRPS. Neuropeptides, inflammatory cytokines, and nerve growth factor (NGF) have been linked to pain behaviors, inflammation, and trophic changes in the TFM model and proliferating keratinocytes were identified as the primary source of cutaneous cytokines and NGF. Tibia fracture also activated spinal glia and upregulated spinal neuropeptide, cytokine, and NGF expression, and in the brain it changed dendritic architecture. B cell-expressed immunoglobulin M antibodies also contributed to pain behavior, indicating a role for adaptive immunity. These results modeled many findings in early CRPS, but significant differences were also noted.