Birth outcomes following self-inflicted poisoning during pregnancy, California, 2000 to 2004.

OBJECTIVE: To describe birth outcomes following intentional acute poisoning during pregnancy. SETTING: California Linked Vital Statistics-Patient Discharge Database, 2000 to 2004. PARTICIPANTS: Pregnant women age 15 to 44, who had a singleton live birth or fetal death that occurred between gestational ages 20 and 42 weeks who were discharged from the hospital for an intentional poisoning were compared to pregnant women discharged from the hospital for any nonpoisoning diagnosis. Intentional acute poisoning hospital discharges were identifed by the presence of an ICD-9-CM E-Codes E950-E952 (suicide, attempted suicide and self-inflicted injuries specified as intentional.) METHODS: Through a retrospective cohort design, birth outcomes including low birth weight; preterm birth; fetal, neonatal, and infant death; and congenital anomalies were identified by the presence of ICD-9-CM diagnosis codes or by notation in the dataset. RESULTS: There were 430 hospital discharges for an intentional poisoning during pregnancy documented in the dataset (rate=25.87/100,000 person years). The rate of intentional poisoning was greatest in the first weeks of gestation and declined with increasing gestational age. Analgesics, antipyretics, and antirheumatics were most commonly implicated. Adverse birth outcomes associated with intentional poisoning included preterm birth (odds ratio [OR]=1.34; 95% Confidence Interval [CI] [1.01, 1.77]), low birth weight (OR=1.49; 95% CI [1.04, 2.12]), and circulatory system congenital anomalies (OR=2.17; 95% CI [1.02, 4.59]). CONCLUSION: Intentional acute poisoning during pregnancy was associated with several adverse birth outcomes; however, these relationships may be confounded by concomitant maternal substance abuse

Aging and the Environment: A Research Framework

The rapid growth in the number of older Americans has many implications for public health, including the need to better understand the risks posed to older adults by environmental exposures. Biologic capacity declines with normal aging; this may be exacerbated in individuals with pre-existing health conditions. This decline can result in compromised pharmacokinetic and pharmacodynamic responses to environmental exposures encountered in daily activities. In recognition of this issue, the U.S. Environmental Protection Agency (EPA) is developing a research agenda on the environment and older adults. The U.S. EPA proposes to apply an environmental public health paradigm to better understand the relationships between external pollution sources → human exposures → internal dose → early biologic effect → adverse health effects for older adults. The initial challenge will be using information about aging-related changes in exposure, pharmacokinetic, and pharmacodynamic factors to identify susceptible subgroups within the diverse population of older adults. These changes may interact with specific diseases of aging or medications used to treat these conditions. Constructs such as “frailty” may help to capture some of the diversity in the older adult population. Data are needed regarding a) behavior/activity patterns and exposure to the pollutants in the microenvironments of older adults; b) changes in absorption, distribution, metabolism, and excretion with aging; c) alterations in reserve capacity that alter the body’s ability to compensate for the effects of environmental exposures; and d) strategies for effective communication of risk and risk reduction methods to older individuals and communities. This article summarizes the U.S. EPA’s development of a framework to address and prioritize the exposure, health effects, and risk communications concerns for the U.S. EPA’s evolving research program on older adults as a susceptible subpopulation

Pregnant driver-associated motor vehicle crashes in North Carolina, 2001–2008

Motor vehicle crashes are the leading cause of maternal injury-related mortality during pregnancy in the United States, yet pregnant women remain an understudied population in motor vehicle safety research

Adverse Pregnancy Outcomes Following Motor Vehicle Crashes

Motor vehicle crashes are a leading cause of serious trauma during pregnancy, but little is known about their relationships with pregnancy outcomes

How Phase-Breaking Affects Quantum Transport Through Chaotic Cavities

We investigate the effects of phase-breaking events on electronic transport through ballistic chaotic cavities. We simulate phase-breaking by a fictitious lead connecting the cavity to a phase-randomizing reservoir and introduce a statistical description for the total scattering matrix, including the additional lead. For strong phase-breaking, the average and variance of the conductance are calculated analytically. Combining these results with those in the absence of phase-breaking, we propose an interpolation formula, show that it is an excellent description of random-matrix numerical calculations, and obtain good agreement with several recent experiments.Comment: 4 pages, revtex, 3 figures: uuencoded tar-compressed postscrip

Chaos in Quantum Dots: Dynamical Modulation of Coulomb Blockade Peak Heights

The electrostatic energy of an additional electron on a conducting grain blocks the flow of current through the grain, an effect known as the Coulomb blockade. Current can flow only if two charge states of the grain have the same energy; in this case the conductance has a peak. In a small grain with quantized electron states, referred to as a quantum dot, the magnitude of the conductance peak is directly related to the magnitude of the wavefunction near the contacts to the dot. Since dots are generally irregular in shape, the dynamics of the electrons is chaotic, and the characteristics of Coulomb blockade peaks reflects those of wavefunctions in chaotic systems. Previously, a statistical theory for the peaks was derived by assuming these wavefunctions to be completely random. Here we show that the specific internal dynamics of the dot, even though it is chaotic, modulates the peaks: because all systems have short-time features, chaos is not equivalent to randomness. Semiclassical results are derived for both chaotic and integrable dots, which are surprisingly similar, and compared to numerical calculations. We argue that this modulation, though unappreciated, has already been seen in experiments.Comment: 4 pages, 3 postscript figs included (2 color), uses epsf.st

Meta-analysis of genome-wide association studies of asthma in ethnically diverse North American populations.

Asthma is a common disease with a complex risk architecture including both genetic and environmental factors. We performed a meta-analysis of North American genome-wide association studies of asthma in 5,416 individuals with asthma (cases) including individuals of European American, African American or African Caribbean, and Latino ancestry, with replication in an additional 12,649 individuals from the same ethnic groups. We identified five susceptibility loci. Four were at previously reported loci on 17q21, near IL1RL1, TSLP and IL33, but we report for the first time, to our knowledge, that these loci are associated with asthma risk in three ethnic groups. In addition, we identified a new asthma susceptibility locus at PYHIN1, with the association being specific to individuals of African descent (P = 3.9 × 10(-9)). These results suggest that some asthma susceptibility loci are robust to differences in ancestry when sufficiently large samples sizes are investigated, and that ancestry-specific associations also contribute to the complex genetic architecture of asthma

Mass Spectrometry Analysis of Hepcidin Peptides in Experimental Mouse Models

The mouse is a valuable model for unravelling the role of hepcidin in iron homeostasis, however, such studies still report hepcidin mRNA levels as a surrogate marker for bioactive hepcidin in its pivotal function to block ferroportin-mediated iron transport. Here, we aimed to assess bioactive mouse Hepcidin-1 (Hep-1) and its paralogue Hepcidin-2 (Hep-2) at the peptide level. To this purpose, fourier transform ion cyclotron resonance (FTICR) and tandem-MS was used for hepcidin identification, after which a time-of-flight (TOF) MS-based methodology was exploited to routinely determine Hep-1 and -2 levels in mouse serum and urine. This method was biologically validated by hepcidin assessment in: i) 3 mouse strains (C57Bl/6; DBA/2 and BABL/c) upon stimulation with intravenous iron and LPS, ii) homozygous Hfe knock out, homozygous transferrin receptor 2 (Y245X) mutated mice and double affected mice, and iii) mice treated with a sublethal hepatotoxic dose of paracetamol. The results showed that detection of Hep-1 was restricted to serum, whereas Hep-2 and its presumed isoforms were predominantly present in urine. Elevations in serum Hep-1 and urine Hep-2 upon intravenous iron or LPS were only moderate and varied considerably between mouse strains. Serum Hep-1 was decreased in all three hemochromatosis models, being lowest in the double affected mice. Serum Hep-1 levels correlated with liver hepcidin-1 gene expression, while acute liver damage by paracetamol depleted Hep-1 from serum. Furthermore, serum Hep-1 appeared to be an excellent indicator of splenic iron accumulation. In conclusion, Hep-1 and Hep-2 peptide responses in experimental mouse agree with the known biology of hepcidin mRNA regulators, and their measurement can now be implemented in experimental mouse models to provide novel insights in post-transcriptional regulation, hepcidin function, and kinetics