Effect of Maternal Smoking on Breast Milk Interleukin-1α, β-Endorphin, and Leptin Concentrations

Tobacco smoke is immunotoxic, but the effect of smoking on the immunologic function of the mammary gland of mothers who smoke cigarettes (“smoker mothers”) has not been studied. Our objective was to test, in smoker mothers, the colostral and transitional milk concentrations of interleukin-(IL)1α. The immunomodulators β-endorphin and leptin were also tested. Pregnant women who self-identified as smokers (≥ 5 cigarettes per day through pregnancy) or nonsmokers were recruited for study participation. The study population included 42 smoker and 40 non-smoker nursing mothers, with otherwise uncomplicated gestation, delivery, and puerperium, who were breast-feeding ad libitum their healthy neonates. Colostrum was obtained on the third postpartum day at 0900 hr and transitional milk on the 10th postpartum day at 0900 hr. IL-1α concentrations were significantly reduced in the colostrum of smoker mothers compared with nonsmoker mothers (p < 0.01). Colostral β-endorphin and leptin concentrations were comparable. No significant differences were found between smoker and nonsmoker lactating mothers in transitional milk concentrations of IL-1α, β-endorphin, and leptin. Moreover, β-endorphin and leptin concentrations were significantly reduced in transitional milk samples compared with colostrum of both smoker and nonsmoker mothers (p < 0.05); also, IL-1α transitional milk concentrations were reduced compared with colostrum, but without any significance. This analysis shows that maternal smoking alters the colostral milk levels of the proinflammatory cytokine IL-1α. The altered postnatal provision of alternative source of the proinflammatory cytokine IL-1α adds understanding to how breast-feeding could be nonprotective against infections among the neonates nursed by smoker mothers

The T-786C and Glu298Asp polymorphisms of the endothelial nitric oxide gene affect the forearm blood flow responses of Caucasian hypertensive patients

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Relationship between the neonatal white blood cell count and histologic chorioamnionitis in preterm newborns.

Objective: The aim was to examine the relationship between neonatal white blood cell (WBC) count and the diagnosis of histologic chorioamnionitis (HCA). Design: We measured WBC, a widely used marker of inflammation, to evaluate whether the values at birth were associated with HCA. Setting: NICU, Department of Pediatrics of Padua University, Padua, Italy. Subjects: WBC count was evaluated in 71 preterm neonates (< 32 weeks of gestation) with HCA and in a control group without HCA on day 1, 3, and 6 after delivery. Logistic regression analysis and diagnostic accuracy analysis were used to assess the association between WBC counts and HCA. Main results: WBC levels were significantly higher in infants with HCA than in those without HCA (Median IQR, WBC (x10(9)/l): day 1, 13.2 (6.2-21.8) vs 8.1 (6-11.4), p < 0.001; day 3, 17.4 (11.4-26.9) vs 6.3 (5.2-8.3), p < 0.001; day 6, 18.4 (11.1-31) vs 6.5 (4.4-9), p < 0.0001). The neonatal WBC count on the third day of life was the most sensitive parameter associated with HCA (sensitivity: 0.80; specificity: 0.88). The cut-off value based on the ROC curve was 10 (x10(9)/l). Conclusions: WBC count in the third day of life is strongly associated with HCA

A boy with sudden headache

Headache is a common presenting complaint in pediatric emergency departments. The goal of emergent evaluation is to identify those children with potentially life-threatening conditions. We present the case of an adolescent boy presenting with headache and hypertension who was diagnosed with a catecholamine-secreting abdominal paraganglioma. Genetic testing eventually led to the diagnosis of SDHB-related hereditary paraganglioma-pheochromocytoma syndrome. Alarm features ("red flags") in children presenting with headache are reviewed, as well as the main features of paragangliomas and the indications for genetic testing

Neonatal tactile stimulation at birth in a low-resource setting

Abstract Background Stimulation is the most common intervention during neonatal resuscitation at birth, but scarce information is available on the actual methods, timing and efficacy of this basic step. To evaluate the occurrence, patterns and response to tactile stimulation at birth in a low-resource setting. Methods We reviewed 150 video recordings of neonatal resuscitation at Beira Central Hospital (Beira, Mozambique). Timing, method, duration and response to tactile stimulation were evaluated. Results One hundred two out of 150 neonates (68.0%) received stimulation, while the remaining 48 (32.0%) received positive pressure ventilation and/or chest compressions directly. Overall, 546 stimulation episodes (median 4 episodes per subject, IQR 2–7) were performed. Median time to the first stimulation episode was 134 s (IQR 53–251); 29 neonates (28.4%) received stimulation within the first minute after birth. Multiple techniques of stimulation were administered in 66 neonates (64.7%), while recommended techniques (rubbing the back or flicking the soles of the feet) only in 9 (8.8%). Median duration of stimulation was 17 s (IQR 9–33). Only 9 neonates (8.8%) responded to stimulation. Conclusions In a low-resource setting, stimulation of newly born infants at birth is underperformed. Adherence to international guidelines is low, resulting in delayed initiation, inadequate technique, prolonged duration and low response to stimulation. Back rubs may provide some benefits, but large prospective studies comparing different methods of stimulation are required

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Tobacco smoke is immunotoxic, but the effect of smoking on the immunologic function of the mammary gland of mothers who smoke cigarettes (&quot;smoker mothers&quot;) has not been studied. Our objective was to test, in smoker mothers, the colostral and transitional milk concentrations of interleukin-(IL)1α. The immunomodulators β-endorphin and leptin were also tested. Pregnant women who self-identified as smokers (≥ 5 cigarettes per day through pregnancy) or nonsmokers were recruited for study participation. The study population included 42 smoker and 40 nonsmoker nursing mothers, with otherwise uncomplicated gestation, delivery, and puerperium, who were breast-feeding ad libitum their healthy neonates. Colostrum was obtained on the third postpartum day at 0900 hr and transitional milk on the 10th postpartum day at 0900 hr. IL-1α concentrations were significantly reduced in the colostrum of smoker mothers compared with nonsmoker mothers (p &lt; 0.01). Colostral β-endorphin and leptin concentrations were comparable. No significant differences were found between smoker and nonsmoker lactating mothers in transitional milk concentrations of IL-1α, β-endorphin, and leptin. Moreover, β-endorphin and leptin concentrations were significantly reduced in transitional milk samples compared with colostrum of both smoker and nonsmoker mothers (p &lt; 0.05); also, IL-1α transitional milk concentrations were reduced compared with colostrum, but without any significance. This analysis shows that maternal smoking alters the colostral milk levels of the proinflammatory cytokine IL-1α . The altered postnatal provision of alternative source of the proinflammatory cytokine IL-1α adds understanding to how breast-feeding could be nonprotective against infections among the neonates nursed by smoker mothers

The T-786 C endothelial nitric oxide synthase genotype is a novel risk factor for coronary artery disease in caucasian patients of the GENICA study

IF 2004: 9.13

The T-786C and Glu298Asp polymorphisms of the endothelial nitric oxide gene affect the forearm blood flow responses of Caucasian hypertensive patients

OBJECTIVES: We sought to investigate whether two polymorphisms located in the promoter (T(-786)C) and exon 7 (Glu298Asp) of the endothelial nitric oxide (NO) synthase (eNOS) gene affected agonists-mediated NO release. BACKGROUND: Endothelial dysfunction can be genetically determined. Therefore, we investigated whether two polymorphisms located in the eNOS gene affected agonists-mediated NO release. METHODS: We compared endothelial-dependent and -independent vasodilation of the different eNOS genotypes in a cross-sectional study on 187 subjects, of whom 137 were uncomplicated essential hypertensive patients (PH) (49 +/- 9 years, 151 +/- 11/99 +/- 5 mm Hg) and 50 healthy normotensive subjects (NT) (43 +/- 16 years, 123 +/- 10/78 +/- 7 mm Hg). Endothelial-dependent and -independent vasodilation was assessed as the forearm blood flow response to incrementally increasing doses of acetylcholine (0.15, 0.45, 1.5, 4.5, 15 microg/100 ml/min) and sodium nitroprusside (1, 2, 4 microg/100 ml/min), respectively. Genotyping was performed with melting curve analysis (Lightcycler) of polymerase chain reaction products from acceptor (5' end-labeled with LCRed 640) and donor probes (3' end-labeled with fluorescein) specific for each polymorphism. The genotype distribution of T(-786)C (CC = 21.9%, CT = 48.7%, TT = 29.4%) and Glu298Asp (GG = 39.0%, GT =51.9%, TT = 9.1%) was similar in PH and NT. A repeated measure analysis of variance showed a blunting of endothelium-dependent vasodilation in PH compared with NT (p < 0.001). A significant effect of the T(-786)C (p = 0.002) but not of the Glu298Asp (p = NS) eNOS polymorphism on endothelial-dependent vasodilation was found. However, we also detected a significant interaction between the T(-786)C and Glu298Asp polymorphism (p < 0.001). No effect on either polymorphism on endothelial-independent vasodilation was seen. CONCLUSIONS: The T(-786)C promoter polymorphism and its interaction with exon 7 Glu298Asp affect endothelium-dependent vasodilation in mild-to-moderate PH patients and NT Caucasian subjects