Concentration of vaginal and systemic cytokines obtained early in pregnancy and their impact on preterm birth.

OBJECTIVE: A number of factors can lead to a maternal pro-inflammatory response resulting in a spontaneous preterm birth. However, it remains unknown if an upregulation in the maternal immune system early in pregnancy leads to an increase in pro-inflammatory cytokines and ultimately preterm birth. Therefore, we hypothesize an increase in vaginal and systemic pro-inflammatory cytokines early pregnancy is associated with an increased risk of preterm birth. STUDY DESIGN: Patients initiating prenatal care prior to 14 weeks gestation were recruited for eligibility. A vaginal swab and serum sample was obtained at the first prenatal visit and these were then stored at -80 C. Patients were then followed for their gestational age at delivery. Five patients delivering preterm (cases) were matched with ten patients delivering at term (controls) based on age, BMI, smoking status and ethnicity. The serum and vaginal swabs from the cases and controls were then analyzed for the following cytokines using a multiplex cytokine assay: GM-CSF, IL-1b, IL-6, TNFα, and Rantes. RESULTS: A total of 116 patients were screened for eligibility and 96 of these patients had samples obtained prior to 14 weeks gestation. Of these 96, 5 had a spontaneous preterm birth and these were matched to 10 controls. There was no difference detected in the cytokine concentrations of GM-CSF, IL-1b, IL-6, TNFα, and Rantes in the serum or cervicovaginal fluid between cases and controls. CONCLUSION: This study demonstrates there is no difference in cytokine concentrations of several pro-inflammatory cytokines in the vagina or in the serum prior to 14 weeks gestation in patients delivering preterm. Therefore, the concentration of the cytokines analyzed in this study from the vagina and serum have little predictive value on the risk of preterm birth. Further research is needed to deepen our understanding of the mechanisms leading to preterm birth.

A comparison of carbon monoxide exposures after snowstorms and power outages.

BACKGROUND: Unintentional carbon monoxide poisoning occurs frequently after natural disasters. Although the epidemiology of carbon monoxide exposures that occur after power loss storms has been reported, few publications detail the characteristics of carbon monoxide exposures after massive snowstorms. PURPOSE: To compare the differences in patient characteristics of carbon monoxide exposures after a snowstorm and power loss storm. METHODS: In 2013, a retrospective review was conducted of patient characteristics and exposure data from all carbon monoxide cases reported to the Connecticut Poison Control Center in the days following both a major snowstorm in 2013 and a winter storm that caused extensive power outages in 2011. RESULTS: Portable generators were the most common source of carbon monoxide exposure after a storm that resulted in power losses; car exhaust was the most frequent source of exposure after an extensive snowstorm. Most exposures occurred within the first day after the snowstorm, and on the second and third days after the power outage storm. There were no significant differences between the two storms in terms of patient age, gender, or median carboxyhemoglobin concentration. CONCLUSIONS: Future public health and medical education regarding the dangers of carbon monoxide in the aftermath of storms should include attention to the differences in the typical exposure sources and timing.

Uncovering buffered pleiotropy: a genome-scale screen for mel-28 genetic interactors in Caenorhabditis elegans.

mel-28 (maternal-effect-lethal-28) encodes a conserved protein required for nuclear envelope function and chromosome segregation in Caenorhabditis elegans. Because mel-28 is a strict maternal-effect lethal gene, its function is required in the early embryo but appears to be dispensable for larval development. We wanted to test the idea that mel-28 has postembryonic roles that are buffered by the contributions of other genes. To find genes that act coordinately with mel-28, we did an RNA interference-based genetic interaction screen using mel-28 and wild-type larvae. We screened 18,364 clones and identified 65 genes that cause sterility in mel-28 but not wild-type worms. Some of these genes encode components of the nuclear pore. In addition we identified genes involved in dynein and dynactin function, vesicle transport, and cell-matrix attachments. By screening mel-28 larvae we have bypassed the requirement for mel-28 in the embryo, uncovering pleiotropic functions for mel-28 later in development that are normally provided by other genes. This work contributes toward revealing the gene networks that underlie cellular processes and reveals roles for a maternal-effect lethal gene later in development.