Faculty Bibliography

BACKGROUND:Early initiation of prenatal care is widely accepted to improve the health outcomes of pregnancy for both mothers and their infants. Identification of the various barriers to entry into care that patients experience may inform and improve health care provision and, in turn, improve the patient's ability to receive necessary care. AIM/OBJECTIVE:This study implements a mixed-methods approach to establish methods and procedures for identifying barriers to early entry to prenatal care in a medically-vulnerable patient population and areas for future quality improvement initiatives. METHODS:An initial chart review was conducted on obstetrics patients that initiated prenatal care after their first trimester at a large federally qualified health center in Brooklyn, NY, to determine patient-specified reasons for delay. A thematic analysis of these data was implemented in combination with both parametric and non-parametric analyses to characterize the population of interest, and to identify the primary determinants of delayed entry. RESULTS:The age of patients in the population of interest (n = 169) was bimodal, with a range of 15 - 43 years and a mean of 28 years. The mean gestational age of entry into prenatal care was 19 weeks. The chart review revealed that 8% recently moved to Brooklyn from outside of NYC or the USA. Nine percent had difficulty scheduling an initial prenatal visit within their first trimester. Teenage pregnancy accounted for 7%. Provider challenges with documentation (21%) were noted. The most common themes identified (n = 155) were the patient being in transition (21%), the pregnancy being unplanned (17%), and issues with linkage to care (15%), including no shows or patient cancellations. Patients who were late to prenatal care also differed from their peers dramatically, as they were more likely to be Spanish-speaking, to be young, and to experience a relatively long delay between pregnancy confirmation and entry into care. Moreover, the greatest determinant of delayed entry into care was patient age. CONCLUSION/CONCLUSIONS:Our study provides a process for other like clinics to identify patients who are at risk for delayed entry to prenatal care and highlight common barriers to entry. Future initiatives include the introduction of a smart data element to document reasons for delay and use of community health workers for dedicated outreach after no show appointments or patient cancellations.

OBJECTIVE:To determine the use of end-tidal carbon dioxide (etco2) as an end point of sepsis resuscitation. METHODS:This was a prospective, observational, single-center cohort study of emergency department patients receiving treatment for severe sepsis with a quantitative resuscitation protocol. Three etco2 readings were taken during a 1-minute time frame at 0, 3, and 6 hours of treatment. Linear regression was used to characterize the association between etco2 and central venous oxygen saturation (SCVo2) and lactate and also to determine the relationship between their change. Analysis of variance was used to determine the relationship between etco2 and disposition. RESULTS:Sixty-nine patients were included in our final analysis. For baseline values, linear regression failed to show a relationship between etco2 and SCVo2 (β = -0.04, t(70) = -0.53, P = .60) but showed a nearly significant relationship (β = -0.51, t(70) = -1.90, P = .06) with lactate. There was no significant relationship between etco2 and SCVo2 at 3 hours (β = 0.12, t(70) = 1.43, P = .16) or 6 hours (β = 0.05, t(64) = 0.82, P = .67). There was also no significant relationship between 6-hour change in etco2 and change in SCVo2 (β = 0.04, t(64) = 0.43, P = .67) or lactate (β = 0.04, t(59) = 0.52, P = .60) or disposition (F(4) = 0.78, P = .54). CONCLUSION/CONCLUSIONS:End-tidal carbon dioxide is unlikely to be a useful clinical end point for sepsis resuscitation, although it may be useful as a triage tool in suspected sepsis because baseline values may reflect initial lactate.

Cyclin-dependent protein kinases (CDKs) are key regulators of the eukaryotic cell cycle and of the eukaryotic transcription machinery. Here we report the characterization of Pfcrk-3 (Plasmodium falciparum CDK-related kinase 3; PlasmoDB identifier PFD0740w), an unusually large CDK-related protein whose kinase domain displays maximal homology to those CDKs which, in other eukaryotes, are involved in the control of transcription. The closest enzyme in Saccharomyces cerevisiae is BUR1 (bypass upstream activating sequence requirement 1), known to control gene expression through interaction with chromatin modification enzymes. Consistent with this, immunofluorescence data show that Pfcrk-3 colocalizes with histones. We show that recombinant Pfcrk-3 associates with histone H1 kinase activity in parasite extracts and that this association is detectable even if the catalytic domain of Pfcrk-3 is rendered inactive by site-directed mutagenesis, indicating that Pfcrk-3 is part of a complex that includes other protein kinases. Immunoprecipitates obtained from extracts of transgenic parasites expressing hemagglutinin (HA)-tagged Pfcrk-3 by using an anti-HA antibody displayed both protein kinase and histone deacetylase activities. Reverse genetics data show that the pfcrk-3 locus can be targeted only if the genetic modification does not cause a loss of function. Taken together, our data strongly suggest that Pfcrk-3 fulfils a crucial role in the intraerythrocytic development of P. falciparum, presumably through chromatin modification-dependent regulation of gene expression.