Risk factors for early childhood growth faltering in rural Cambodia: a cross-sectional study.

OBJECTIVE: This study aimed to determine risk factors of growth faltering by assessing childhood nutrition and household water, sanitation, and hygiene (WASH) variables and their association with nutritional status of children under 24 months in rural Cambodia. DESIGN: We conducted surveys in 491 villages (clusters) randomised across 55 rural communes in Cambodia in September 2016 to measure associations between child, household and community-level risk factors for stunting and length-for-age z-score (LAZ). We measured 4036 children under 24 months of age from 3877 households (491 clusters). We analysed associations between nutrition/WASH practices and child growth (LAZ, stunting) using generalised estimating equations (GEEs) to fit linear regression models with robust SEs in a pooled analysis and in age-stratified analyses; child-level and household-level variables were modelled separately from community-level variables. RESULTS: After adjustment for potential confounding, we found household-level and community-level water, sanitation and hygiene factors to be associated with child growth among children under 24 months: presence of water and soap at a household's handwashing station was positively associated with child growth (adjusted mean difference in LAZ +0.10, 95% CI 0.03 to 0.16); household-level use of an improved drinking water source and adequate child stool disposal practices were protective against stunting (adjusted prevalence ratio (aPR) 0.80, 95% CI 0.67 to 0.97; aPR 0.82, 95% CI 0.64 to 1.03). In our age-stratified analysis, we found associations between child growth and community-level factors among children 1-6 months of age: shared sanitation was negatively associated with growth (-0.47 LAZ, 95% CI -0.90 to -0.05 compared with children in communities with no shared facilities); improved sanitation facilities were protective against stunting (aPR 0.43, 95% CI 0.21 to 0.88 compared with children in communities with no improved sanitation facilities); and open defecation was associated with more stunting (aPR 2.13, 95% CI 1.10 to 4.11 compared with children in communities with no open defecation). These sanitation risk factors were only measured in the youngest age strata (1-6 months). Presence of water and soap at the household level were associated with taller children in the 1-6 month and 6-12 month age strata (+0.10 LAZ, 95% CI -0.02 to 0.22 among children 1-6 months of age; +0.11 LAZ, 95% CI -0.02 to 0.25 among children 6-12 months of age compared with children in households with no water and soap). Household use of improved drinking water source was positively associated with growth among older children (+0.13 LAZ, 95% CI -0.01 to 0.28 among children 12-24 months of age). CONCLUSION: In rural Cambodia, water, sanitation and hygiene behaviours were associated with growth faltering among children under 24 months of age. Community-level sanitation factors were positively associated with growth, particularly for infants under 6 months of age. We should continue to make effort to: investigate the relationships between water, sanitation, hygiene and human health and expand WASH access for young children.

Cell Specific Changes of Autophagy in a Mouse Model of Contusive Spinal Cord Injury.

Autophagy is an essential process of cellular waist clearance that becomes altered following spinal cord injury (SCI). Details on these changes, including timing after injury, underlying mechanisms, and affected cells, remain controversial. Here we present a characterization of autophagy in the mice spinal cord before and after a contusive SCI. In the undamaged spinal cord, analysis of LC3 and Beclin 1 autophagic markers reveals important differences in basal autophagy between neurons, oligodendrocytes, and astrocytes and even within cell populations. Following moderate contusion, western blot analyses of LC3 indicates that autophagy increases to a maximum at 7 days post injury (dpi), whereas unaltered Beclin 1 expression and increase of p62 suggests a possible blockage of autophagosome clearance. Immunofluorescence analyses of LC3 and Beclin 1 provide additional details that reveal a complex, cell-specific scenario. Autophagy is first activated (1 dpi) in the severed axons, followed by a later (7 dpi) accumulation of phagophores and/or autophagosomes in the neuronal soma without signs of increased initiation. Oligodendrocytes and reactive astrocytes also accumulate phagophores and autophagosomes at 7 dpi, but whereas the accumulation in astrocytes is associated with an increased autophagy initiation, it seems to result from a blockage of the autophagic flux in oligodendrocytes. Comparison with previous studies highlights the complex and heterogeneous autophagic responses induced by the SCI, leading in many cases to contradictory results and interpretations. Future studies should consider this complexity in the design of therapeutic interventions based on the modulation of autophagy to treat SCI.