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To evaluate the effectiveness of Sprinkles alongside infant and young child feeding (IYCF) education compared with IYCF education alone on anemia, deficiencies in iron, vitamin A, and zinc, and growth in Cambodian infants.Design: Cluster-randomized effectiveness study.Setting: Cambodian rural health district.Participants: Among 3112 infants aged 6 months, a random subsample (n = 1350) was surveyed at baseline and 6-month intervals to age 24 months.Intervention: Daily micronutrient Sprinkles alongside IYCF education vs IYCF education alone for 6 months from ages 6 to 11 months.Main Outcome Measures: Prevalence of anemia; iron, vitamin A, and zinc deficiencies; and growth via biomarkers and anthropometry.Results: Anemia prevalence (hemoglobin level Ͻ11.0 g/dL [to convert to grams per liter, multiply by 10.0]) was reduced in the intervention arm compared with the control arm by 20.6% at 12 months (95% CI, 9.4-30.2; P = .001), and the prevalence of moderate anemia (hemoglobin level Ͻ10.0 g/dL) was reduced by 27.1% (95% CI, 21.0-31.8; PϽ .001). At 12 and 18 months, iron deficiency prevalence was reduced by 23.5% (95% CI, 15.6-29.1; PϽ.001) and 11.6% (95% CI, 2.6-17.9; P=.02), respectively. The mean serum zinc concentration was increased at 12 months (2.88 µg/dL [to convert to micromoles per liter, multiply by 0.153]; 95% CI, 0.26-5.42; P =.03). There was no statistically significant difference in the prevalence of zinc and vitamin A deficiencies or in growth at any time.Conclusions: Sprinkles reduced anemia and iron deficiency and increased the mean serum zinc concentration in Cambodian infants. Anemia and zinc effects did not persist beyond the intervention period.

Despite their humble origins as anuclear fragments of megakaryocytes, platelets have emerged as versatile mediators of thrombosis and immunity. The diverse spectrum of platelet functions are on full display during the host response to severe infection and sepsis, with platelets taking center-stage in the intravascular immune response to blood-borne pathogens. Platelets are endowed with a comprehensive armamentarium of pathogen detection systems that enable them to function as sentinels in the bloodstream for rapid identification of microbial invasion. Through both autonomous anti-microbial effector functions and collaborations with other innate immune cells, platelets orchestrate a complex intravascular immune defense system that protects against bacterial dissemination. As with any powerful immune defense system, dysregulation of platelet-mediated intravascular immunity can lead to profound collateral damage to host cells and tissues, resulting in sepsis-associated organ dysfunction. In this article, the cellular and molecular contributions of platelets to intravascular immune defenses in sepsis will be reviewed, including the roles of platelets in surveillance of the microcirculation and elicitation of protective anti-bacterial responses. Mechanisms of platelet-mediated thromboinflammatory organ dysfunction will be explored, with linkages to clinical biomarkers of platelet homeostasis that aid in the diagnosis and prognostication of human sepsis. Lastly, we discuss novel therapeutic opportunities that take advantage of our evolving understanding of platelets and intravascular immunity in severe infection.

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BACKGROUND: Perinatal stroke encompasses multiple disease-specific cerebrovascular syndromes that cause lifelong neurodevelopmental morbidity for millions worldwide. Acute presentations include neonatal arterial ischemic stroke (NAIS), neonatal cerebral sinovenous thrombosis, and neonatal hemorrhagic stroke (NHS). Delayed presentations include arterial presumed perinatal ischemic stroke, periventricular venous infarction, and presumed perinatal hemorrhagic stroke. Our objective was to define the birth prevalence of all subtypes of perinatal stroke by using a population-based cohort. METHODS: The Alberta Perinatal Stroke Project is a research cohort established in 2008 in southern Alberta, Canada, with prospective (2008–2017) and retrospective (1990–2008) enrollment leveraging universal health care at a single tertiary care pediatric center. The primary outcome was the estimated birth prevalence of each perinatal stroke syndrome, secondary outcomes were birth prevalence over time, sex ratios, and change in age at diagnosis. Analysis included Poisson regression, Wilcoxon rank test, and Fisher exact test. RESULTS: The overall estimated birth prevalence of term-born perinatal stroke was 1:1100. The estimated birth prevalence was 1:3000 for NAIS, 1:7900 for arterial presumed perinatal ischemic stroke, 1:6000 for periventricular venous infarction, 1:9100 for cerebral sinovenous thrombosis, 1:6800 for NHS, and 1:65000 for presumed perinatal hemorrhagic stroke. The apparent birth prevalence of NAIS and NHS increased over time. There were more males affected than females. The age at diagnosis decreased for late-presenting stroke types. CONCLUSIONS: The estimated birth prevalence of term perinatal stroke is higher than previous estimates, which may be explained by population-based sampling of disease-specific states. This emphasizes the need for further studies to better understand the disease-specific pathophysiology to improve treatment and prevention strategies.

Serotonin (5-HT) can potently activate and modulate spinal locomotor circuits in a variety of species. Many of these findings have been obtained by applying serotonin exogenously to the isolated spinal cord of in vitro preparations, which has the drawback of indiscriminately activating extrasynaptic receptors and neurons. To investigate the role of endogenously released serotonin in modulating locomotor networks, the selective serotonin reuptake inhibitor citalopram was used. Fictive locomotion was elicited by either electrical stimulation of the brainstem or the sacral 4 (S4) dorsal root. The addition of 20 μm of citalopram caudal to thoracic segment 5 (T5) had an overall inhibitory effect on the lumbar central pattern generator (CPG). Left-right and flexor-extensor coupling were significantly decreased, and there was also a phase shift in the flexor-extensor relationship. In addition, there was a significant decrease in burst amplitude. These effects were observed during both afferent and brainstem evoked fictive locomotion. When citalopram was added in the presence of 5-HT 1A and 5-HT 1B antagonists, the inhibitory effects were largely reversed. The remaining excitatory effects were mediated by 5-HT 7 and 5-HT 2 receptors. These results suggest that endogenous 5-HT release can modulate locomotor-like activity early in neonatal development.

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