Adoption of Consensus Guidelines for Safe Prevention of the Primary Cesarean Delivery by Freestanding Birth Centers.

INTRODUCTION: Slow or arrested progress in labor is the most frequent (64%) indication for nonemergent transfer of laboring people from freestanding birth centers to the hospital. After the 2014 publication of the Consensus Statement on Safe Prevention of Primary Cesarean Delivery (Consensus Statement), many freestanding birth centers changed their clinical practice guidelines to allow more time for active labor in the birth center prior to hospital transfer. The result of these changes has not been evaluated in birth centers. Evaluation of adoption of guidelines based on the Consensus Statement in hospitals has shown inconsistent results. METHODS: Birth centers were contacted to determine whether they changed clinical practice guidelines in response to the Consensus Statement. A before-after analysis compared outcomes for the 2 calendar years before and the 2 calendar years after adoption of new guidelines with a retrospective analysis of deidentified client-level data collected in the American Association of Birth Centers Perinatal Data Registry. RESULTS: A third of responding birth centers (11 of 33) changed their clinical practice guidelines, mostly redefining the onset of active labor as beginning at 6 cm cervical dilatation and allowing 4 hours of arrest of dilatation in active labor before transfer to the hospital. These changes were associated with fewer diagnoses of prolonged first stage of labor (13.8% vs 8.0%, P < .01) but not with fewer intrapartum transfers (14.0% vs 14.7%, P = .55) or cesarean births (5.0 vs 4.1%, P = .26.) DISCUSSION: We found no evidence that making these practice changes was associated with better outcomes. Two hours of a lack of documented cervical change in active labor is likely long enough to diagnose arrested progress in labor. Research on proportion of morbidity and mortality associated with prolonged labor could inform practice guidelines for transfers.

Associations between prolonged second stage of labor and maternal and neonatal outcomes in freestanding birth centers: a retrospective analysis.

BACKGROUND: Current guidelines for second stage management do not provide guidance for community birth providers about when best to transfer women to hospital care for prolonged second stage. Our goal was to increase the evidence base for these providers by: 1) describing the lengths of second stage labor in freestanding birth centers, and 2) determining whether proportions of postpartum women and newborns experiencing complications change as length of second stage labor increases. METHODS: This study is a retrospective analysis of de-identified client-level data collected in the American Association of Birth Centers Perinatal Data Registry, including women giving birth in freestanding birth centers January 1, 2007 to December 31, 2016. We plotted proportions of postpartum women and newborns transferred to hospital care against length of the second stage of labor, and assessed significance of these with the Cochran-Armitage test for trend or chi-square test. Secondary maternal and newborn outcomes were compared for dyads with normal and prolonged second stages of labor using Fisher's exact test. RESULTS: Second stage labor exceeded 3 hours for 2.3% of primiparous women and 2 hours for 6.6% of multiparous women. Newborn transfers increased as second stage increased from < 15 minutes to > 2 hours (0.6% to 6.33%, p for trend = 0.0008, for primiparous women, and 1.4% to 10.6%, p for trend < 0.0001, for multiparous women.) Postpartum transfers for multiparous women increased from 1.4% after second stage < 15 minutes to greater than 4% for women after second stage exceeding 2 hours (p for trend < 0.0001.) CONCLUSIONS: Complications requiring hospitalization of postpartum women and newborns become more common as the length of the second stage increases. Birth center guidelines should consider not just presence of progress but also absolute length of time as indications for transfer.

Strong Start in birth centers: Socio-demographic characteristics, care processes, and outcomes for mothers and newborns.

BACKGROUND: A recent Center for Medicare and Medicaid Innovation report evaluated the four-year Strong Start for Mothers and Newborns Initiative, which sought to improve maternal and newborn outcomes through exploration of three enhanced, evidence-based care models. This paper reports the socio-demographic characteristics, care processes, and outcomes for mothers and newborns engaged in care with American Association of Birth Centers (AABC) sites. METHODS: The authors examined data for 6424 Medicaid or Children's Health Insurance Program (CHIP) beneficiaries in birth center care who gave birth between 2013 and 2017. Using data from the AABC Perinatal Data Registry™, descriptive statistics were used to evaluate socio-behavioral and medical risks, and core perinatal quality outcomes. Comparisons are made between outcomes in the AABC sample and national data during the study period. RESULTS: Childbearing mothers enrolled at AABC sites had diverse socio-behavioral risk factors similar to the national profile. The AABC sites exceeded national quality benchmarks for low birthweight (3.28%), preterm birth (4.42%), and primary cesarean birth (8.56%). Racial disparities in perinatal indicators were present within the Strong Start sample; however, they were at narrower margins than in national data. The enhanced model of care was notable for use of midwifery-led prenatal, labor, and birth care and decreased hospital admission. CONCLUSIONS: Birth center care improves population health, patient experience, and value. The model demonstrates the potential to decrease racial disparity and improve population health. Reduction of regulatory barriers and implementation of sustainable reimbursement are warranted to move the model to scale for Medicaid beneficiaries nationwide.

Early sensing and gene expression profiling under a low dose of cadmium exposure.

Cadmium (Cd) has been shown to have various detrimental effects on health. In recent years progress has been made in dissecting apart the molecular mechanisms underlying the effects of exposure to this toxic metal. In this paper we investigated changes in gene expression using a global transcript profiling approach to better understand the early molecular events that occur in primary rat hepatocytes when exposed to Cd at a concentration (4 microM) and time (3 h) that is prior to any significant increase in cytotoxic parameters. Gene expression changes were most dramatically noticed for proteins involved in transcriptional regulation, zinc finger protein production, and heat shock protein expression. Other genes whose expression changed significantly were those associated with maintaining cellular redox homeostasis such as increasing glutathione synthesis and antioxidant capacity, facilitating the survival or death response, and repairing damage or stimulating degradation. Expression changes were confirmed for selected genes in various groups utilizing qRT-PCR. Various times of Cd incubation were also used to assess the extent of the impact. To define whether or not any of these changes were associated with cadmium's ability to disturb the redox balance, we also tested the effects of Cd in the presence of a blocker of glutathione synthesis, D,L-buthionine-(S,R)-sulfoximine (BSO), and an antioxidant, N-acetylcysteine (NAC). The results show that the Cd induction of some genes can be categorized as occurring primarily in response to changes in the redox state as measured by attenuation of the response by the addition of NAC or to the availability of reduced glutathione as measured by the increase in response in the presence of BSO.

Education resources for guiding discussions on ethics in science.

Faculty, staff, and students at all levels of educational institutions are becoming more aware about ethical issues in the classroom and in research. As educators, it is our responsibility to provide an opportunity to discuss these issues so that future scientists will be prepared to face the many ethical challenges they may encounter. Often, unfortunately, we are reticent to engage in this discussion due solely to the lack of our own repertoire of resources regarding ethics. Thus, this summary of educational resources was compiled to promote ethics discussions in science classrooms and research programs.

Characterization of Cd-induced molecular events prior to cellular damage in primary rat hepatocytes in culture: activation of the stress activated signal protein JNK and transcription factor AP-1.

The effect of Cadmium (Cd) on the expression of c-Jun N-terminal kinase (JNK), c-jun, and activator protein-1 (AP-1) has been investigated. We previously reported that Cd causes cell damage as indicated by increases in the cytotoxic parameters, lactate dehydrogenase and lipid peroxidation, and this damage was mediated by decreases in cellular concentration of glutathione. In the present study, we investigate the molecular events involved prior to the Cd-induced cellular toxicity and damage in primary rat hepatocytes. We propose that Cd, through the generation of reactive oxygen species (ROS) and prior to significant cellular damage, activates the stress activated signal protein JNK, regulates c-jun expression, and promotes the binding of a redox sensitive transcription factor AP-1. We show JNK activity and c-jun mRNA level significantly increased at 1 h and AP-1 DNA binding activity significantly enhanced at 3 h in the presence of 4 microM cadmium chloride. Blocking the Cd induction of JNK activity, c-jun mRNA level, and AP-1 binding activity using the antioxidants N-acetyl cysteine (10 mM) or carnosol (0.5 microg/mL) suggests a role for ROS. Blocking JNK activity and c-jun mRNA by SP600125 (20 microM), a JNK inhibitor, supports the role of JNK in transmission of signals induced by Cd.

Mediation of cadmium-induced oxidative damage and glucose-6-phosphate dehydrogenase expression through glutathione depletion.

The effect of cadmium (Cd), a significant environmental contaminant, on the expression of glucose-6-phosphate dehydrogenase (G6PDH), has been investigated. G6PDH is the key rate-limiting enzyme in the pentose pathway and the expression of its gene has been shown to be redox-sensitive. We show that incubation of primary rat hepatocytes with Cd induces oxidative stress in a time- and concentration-dependent manner as measured by increases in the cytotoxic parameters, lactate dehydrogenase (LDH) and lipid peroxidation (LPO). Significant increases in LDH leakage and LPO can be measured after 12 and 24 h, respectively, in the presence of 4 microM cadmium chloride. However, prior to significant increases in cytotoxic parameters, and within only 6 h of Cd treatment, significant decreases in reduced glutathione and increases in the expression of G6PDH as measured by mRNA levels and enzyme activity are observed. The signal protein MAP kinase (MAPK) is also induced by Cd within 6 h. Blocking the Cd induction of MAPK using the antioxidant N-acetyl cysteine (10 mM) or Trolox (0.5 mM) or the MEK specific inhibitor PD098059 (20 microM) also blocks the Cd induction of G6PDH suggesting that MAPK is a signal protein involved in the redox regulation of this gene.

Exogenous nitric oxide downregulates MIP-2 and MIP-1alpha chemokines and MAPK p44/42 after ischemia and reperfusion of the rat kidney.

The mechanisms by which nitric oxide (NO) exerts its protective effect in the ischemia/reperfusion (I/R) injury of the kidney have not been fully determined. The hypothesis of this study was based on the assumption that I/R upregulates some chemokines (MIP-2 and MIP-1alpha) as well as certain protein kinases (MAPK p44/42), and therefore we aimed in this work at recognizing if an exogenous NO donor would downregulate these effects in rat ischemic kidneys at the same time that it would offer functional protection as measured by serum creatinine. Sprague-Dawley rats were subjected to renal warm ischemia (75 min) and contralateral nephrectomy. Animals were divided into 3 groups (n = 8 per group): sham, ischemic control, and ischemic group treated with sodium nitroprusside (NaNP 5 mg/kg) given 15 min prior to reperfusion. Serum creatinine (SCr), serum chemokines (MIP-2 and MIP-1alpha), kidney tissue MAPK p44/42, kidney neutrophil infiltration determined by myeloperoxidase (MPO), and light histology were evaluated 4 h after reperfusion began. There were significant improvements in SCr and better histopathological features in the I/R-NaNP group compared with the I/R group. Similarly, the I/R-NaNP kidneys exhibited a downregulating effect of serum chemokines (MIP-2 and MIP-1alpha) and kidney tissue MAPK p44/42 that was not observed in the I/R group alone. The MPO levels were lower in the I/R-NaNP group compared with the I/R untreated group. We can conclude from these experiments that I/R of the rat kidney upregulated the production of MIP-2 and MIP-1alpha chemokines and the activation of MAPKp44/42. It also had a detrimental effect on the function and structure of the ischemic kidney. Exogenous NO had a temporal protective effect in organ function and histology and exerted a downregulating response in the production of MIP-2 and MIP-1alpha chemokines and the activation of MAPK p44/42 following I/R.