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: Symmetric, progressive, necrotizing lesions in the brainstem are a defining feature of Leigh syndrome (LS). A mechanistic understanding of the pathogenesis of these lesions has been elusive. Here, we report that leukocyte proliferation is causally involved in the pathogenesis of LS. Depleting leukocytes with a colony-stimulating factor 1 receptor inhibitor disrupts disease progression, including suppression of CNS lesion formation and a substantial extension of survival. Leukocyte depletion rescues diverse symptoms including seizures, respiratory center function, hyperlactemia, and neurologic sequelae. These data reveal a mechanistic explanation for the beneficial effects of mTOR inhibition. More importantly, these findings dramatically alter our understanding of the pathogenesis of LS, demonstrating that immune involvement is causal in disease. This work has significant implications for the mechanisms of mitochondrial disease and may lead to novel therapeutic strategies. One-Sentence Summary: Leukocyte depletion prevents CNS lesions, neurological disease, and metabolic dysfunction in the Ndufs4(KO) model of Leigh syndrome.

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The study was done to examine hemodialysis unit nurses' knowledge on blood-borne infections, compliance and barriers to control and predictors of compliance. Methods: A descriptive correlational study was conducted with 122 nurses from hemodialysis units. Data were collected using a structured questionnaire. The data collection period was May to September, 2017. Data were analysed using descriptive statistics, t-test, ANOVA, Pearson correlation, and multiple linear regression. Results: The mean score for knowledge on blood-borne infections was 15.41±2.01 out of 19 and the compliance with blood-borne infection control was 4.08±0.49 out of 5. Barriers to the performance of blood-borne infections control were lack of time and personal protective devices. Knowledge on blood-borne infection did not correlate with compliance on blood-borne infection control (r=.13, p=.171). Predictors of compliance on blood-borne infections control were 1) infection control education on injuries caused by injection needles (β=.23, p=.010), 2) infection control room (β=.24, p=.006) and 3) blood exposure experience over the past week (β=-.24, p=.005) and explained 22.2% of the variance (F=10.81, p<.001). Conclusion: Findings suggest that to improve the performance of blood-borne infectious disease management, customized education for nurses on blood-borne infection and systematic support related to the infection control room should be given priority.

Volatile anesthetics (VAs) are widely used in medicine, but the mechanisms underlying their effects remain ill-defined. Though routine anesthesia is safe in healthy individuals, instances of sensitivity are well-documented, and there has been significant concern regarding the impact of VAs on neonatal brain development. Evidence indicates that VAs have multiple targets, with anesthetic and non-anesthetic effects mediated by neuroreceptors, ion channels, and the mitochondrial electron transport chain. Here, we characterize an unexpected metabolic effect of VAs in neonatal mice. Neonatal blood β-hydroxybutarate (β-HB) is rapidly depleted by VAs at concentrations well below those necessary for anesthesia. β-HB in adults, including animals in dietary ketosis, is unaffected. Depletion of β-HB is mediated by citrate accumulation, malonyl-CoA production by acetyl-CoA carboxylase, and inhibition of fatty acid oxidation. Adults show similar significant changes to citrate and malonyl-CoA, but are insensitive to malonyl-CoA, displaying reduced metabolic flexibility compared to younger animals.