Trends of child undernutrition in rural Ecuadorian communities with differential access to roads, 2004-2013.

Road access can influence protective and risk factors associated with nutrition by affecting various social and biological processes. In northern coastal Ecuador, the construction of new roads created a remoteness gradient among villages, providing a unique opportunity to examine the impact of roads on child nutritional outcomes 10 years after the road was built. Anthropometric and haemoglobin measurements were collected from 2,350 children <5 years in Esmeraldas, Ecuador, from 2004 to 2013 across 28 villages with differing road access. Logistic generalized estimating equation models assessed the longitudinal association between village remoteness and prevalence of stunting, wasting, underweight, overweight, obesity, and anaemia. We examined the influence of socio-economic characteristics on the pathway between remoteness and nutrition by comparing model results with and without household-level socio-economic covariates. Remoteness was associated with stunting (OR = 0.43, 95% CI [0.30, 0.63]) and anaemia (OR = 0.56, 95% CI [0.44, 0.70]). Over time, the prevalence of stunting was generally decreasing but remained higher in villages closer to the road compared to those farther away. Obesity increased (0.5% to 3%) over time; wasting was high (6%) but stable during the study period. Wealth and education partially explained the better nutritional outcomes in remote vs. road villages more than a decade after some communities gained road access. Establishing the extent to which these patterns persist requires additional years of observation.

A Defective Meiotic Outcome of a Failure in Homologous Pairing and Synapsis Is Masked by Meiotic Quality Control.

Successful gamete production is ensured by meiotic quality control, a process in which germ cells that fail in bivalent chromosome formation are eliminated during meiotic prophase. To date, numerous meiotic mutants have been isolated in a variety of model organisms, using defects associated with a failure in bivalent formation as hallmarks of the mutant. Presumably, the meiotic quality control mechanism in those mutants is overwhelmed. In these mutants, all germ cells fail in bivalent formation, and a subset of cells seem to survive the elimination process and develop into gametes. It is possible that mutants that are partially defective in bivalent formation were missed in past genetic screens, because no evident meiotic defects associated with failure in bivalent formation would have been detectable. Meiotic quality control effectively eliminates most failed germ cells, leaving predominately successful ones. Here, we provide evidence supporting this possibility. The Caenorhabditis elegans mrg-1 loss-of-function mutant does not appear to be defective in bivalent formation in diakinesis oocytes. However, defects in homologous chromosome pairing and synapsis during the preceding meiotic prophase, prerequisites for successful bivalent formation, were observed in most, but not all, germ cells. Failed bivalent formation in the oocytes became evident once meiotic quality control was abrogated in the mrg-1 mutant. Both double-strand break repair and synapsis checkpoints are partly responsible for eliminating failed germ cells in the mrg-1 mutant. Interestingly, removal of both checkpoint activities from the mrg-1 mutant is not sufficient to completely suppress the increased germline apoptosis, suggesting the presence of a novel meiotic checkpoint mechanism.

Burden of Clostridium difficile infection on hospital readmissions and its potential impact under the Hospital Readmission Reduction Program.

BACKGROUND: Both Clostridium [corrected] difficile infection (CDI) rates in hospitals and interest in reducing 30-day readmission rates have increased dramatically in the United States. The objective of this study was to characterize the burden of CDI on 30-day hospital readmissions at a tertiary care health-system. METHODS: A patient discharge database was used to identify patients with a CDI diagnosis (ICD-9 code 008.45) during their stay in 2012. Patients were classified as index admissions (CDI discharges) or 30-day readmissions (CDI readmissions). Readmission rates, length of stay (LOS), and time to readmission were assessed among CDI readmissions. RESULTS: Among discharges from the health system (n = 51,353), 615 were diagnosed with CDI (1%). Thirty-day readmissions were more common among CDI discharges (30.1%) than non-CDI discharges (14.4%). Average LOS for CDI readmissions was 5-6 days longer than non-CDI readmissions. Time to readmission was shorter among CDI discharges diagnosed on admission than CDI discharges diagnosed later during their hospital stay (median, 7 days). CONCLUSION: Reductions in hospital-onset CDI and readmission of patients with an index CDI can provide tremendous cost savings to hospitals. This calls for better infection control and antibiotic stewardship measures toward CDI management in the hospital and as patients transition to the next level of care.

Assembly of the Synaptonemal Complex Is a Highly Temperature-Sensitive Process That Is Supported by PGL-1 During Caenorhabditis elegans Meiosis.

Successful chromosome segregation during meiosis depends on the synaptonemal complex (SC), a structure that stabilizes pairing between aligned homologous chromosomes. Here we show that SC assembly is a temperature-sensitive process during Caenorhabditis elegans meiosis. Temperature sensitivity of SC assembly initially was revealed through identification of the germline-specific P-granule component PGL-1 as a factor promoting stable homolog pairing. Using an assay system that monitors homolog pairing in vivo, we showed that depletion of PGL-1 at 25° disrupts homolog pairing. Analysis of homolog pairing at other chromosomal loci in a pgl-1-null mutant revealed a pairing defect similar to that observed in mutants lacking SC central region components. Furthermore, loss of pgl-1 function at temperatures ≥25° results in severe impairment in loading of SC central region component SYP-1 onto chromosomes, resulting in formation of SYP-1 aggregates. SC assembly is also temperature sensitive in wild-type worms, which exhibit similar SYP-1 loading defects and formation of SYP-1 aggregates at temperatures ≥26.5°. Temperature shift analyses suggest that assembly of the SC is temperature sensitive, but maintenance of the SC is not. We suggest that the temperature sensitive (ts) nature of SC assembly may contribute to fitness and adaptation capacity in C. elegans by enabling meiotic disruption in response to environmental change, thereby increasing the production of male progeny available for outcrossing.

The chromodomain protein MRG-1 facilitates SC-independent homologous pairing during meiosis in Caenorhabditis elegans.

Homologous chromosome pairing is a prerequisite to establish physical linkage between homologs, which is critical for faithful chromosome segregation during meiosis I. The establishment of pairing is genetically separable from subsequent synapsis, defined as stabilization of pairing by the synaptonemal complex (SC). The underlying mechanism of presynaptic pairing is poorly understood. In the nematode Caenorhabditis elegans, a unique cis-acting element, the pairing center (PC), is essential for presynaptic pairing; however, it is not known whether and how the remainder of the chromosome contributes to presynaptic pairing. Here we report direct evidence for presynaptic pairing activity intrinsic to non-PC regions, which is facilitated by a conserved chromodomain protein, MRG-1. In mrg-1 loss-of-function mutants, pairing is compromised specifically in non-PC regions, leading to nonhomologous SC assembly. Our data support a model in which presynaptic alignment in non-PC regions collaborates with initial PC pairing to ensure correct homologous synapsis.