Vitamin D supplementation reduces serum lipids of children with hypertriacylglycerolemia: A randomized, triple-masked, placebo-controlled crossover trial.

OBJECTIVES: This study aimed to evaluate the effect of cholecalciferol supplementation on the body composition and metabolic profile of children with hypertriacylglycerolemia. METHODS: This is a randomized, triple-masked, placebo-controlled, crossover trial of 44 Brazilian children with hypertriacylglycerolemia, age 4 to 11 y. The sample included eutrophic and overweight/obese children according to body mass index for age, with sufficient and insufficient vitamin D basal levels. The intervention lasted 34 wk, with two periods of 12 wk each separated by a 10-wk washout. The two groups, supplemented and placebo, received five drops of cholecalciferol (equivalent to 1000 international unit/d) and five drops of sunflower oil, respectively, daily for 12 wk. Sociodemographic, economic, sunscreen use, percentage of body surface area daily exposed to sun, physical activity, anthropometry (body mass and height), body composition (waist circumference, body fat percentage, fat-free mass, triceps, and subscapular skinfolds), biochemical profile (25-hydroxyvitamin D, fasting glucose, and lipid fractions), blood pressure, and food intake data were collected. RESULTS: Of the 44 children who concluded the study, 56.80% were female, 54.50% were of brown race, 81.82% had sufficient serum 25-hydroxyvitamin D (≥75 nmol/L), and 50.00% were overweight/obese according to body mass index for age. There was a reduction in serum total cholesterol (P < 0.001), low-density lipoprotein cholesterol (P < 0.001), nonhigh-density lipoprotein cholesterol (P < 0.001), total cholesterol/high-density lipoprotein cholesterol (P = 0.001), and low/high-density lipoprotein cholesterol ratios (P < 0.001) in the supplemented group compared with the placebo group. CONCLUSIONS: Cholecalciferol supplementation improved the lipid profile of children with hypertriacylglycerolemia without altering body composition.

Vitamin D is not associated with body composition and metabolic profile among Brazilian children with 25-hydroxyvitamin D ≥ 75 nmol/L: A cross-sectional study.

BACKGROUND AND AIMS: The association of vitamin D with cardiovascular disease risk factors among children remains inconclusive, and there is a lack of studies that evaluate children with optimal serum 25-hydroxyvitamin D [25(OH)D]. Thus, this study aimed to analyze the relationship between serum 25(OH)D and body composition and metabolic profile among Brazilian children with sufficient serum 25(OH)D. METHODS AND RESULTS: A cross-sectional study was conducted with 88 Brazilian children aged 4-11 years. Self-reported race, physical activity, anthropometry (body mass and height), body composition (waist circumference, body fat percentage, fat free mass, triceps and subscapular skinfolds), biochemical profile [lipid fractions, fasting glucose and 25(OH)D] and blood pressure data were collected. No difference was found in sex, self-reported race, physical activity, age, anthropometry, body composition, biochemical parameters and blood pressure between children with 25(OH)D 75-99 and ≥ 100 nmol/L. In addition, there was no association between serum vitamin D and body composition and metabolic profile. CONCLUSIONS: Serum 25(OH)D was not associated with body composition and metabolic profile among Brazilian children with sufficient serum 25(OH)D. Further studies among children with serum levels ≥ 75 nmol/L are needed to confirm this finding.

Effects of Chemotherapy Treatment on Muscle Strength, Quality of Life, Fatigue, and Anxiety in Women with Breast Cancer.

The study aimed to evaluate the effects of chemotherapy treatment on muscle strength, quality of life, fatigue, and anxiety in women with breast cancer. Nineteen women who were undergoing a chemotherapy treatment (breast cancer treatment [BCT] group, 52.2 ± 13.1 years) and 18 women without cancer (control [CNT] group, 55.8 ± 8.4 years) answered questionnaires for evaluation of fatigue (Fatigue Scale), quality of life (Short-Form Healthy Survey [SF-36] questionnaire), and anxiety (State-Trait Anxiety Inventory [IDATE]) levels. Muscle strength was also assessed by an isometric grip test and an isokinetic knee extension test. Physical limitations, social and emotional domains of quality of life were lower in the BCT group in comparison to the CNT group (p = 0.002; p = 0.003; p = 0.0003, respectively). The other domains did not differ between groups (p > 0.05). There were no differences in fatigue and anxiety levels between both the BCT and CNT groups (p > 0.05). Additionally, isometric grip strength was higher in the CNT group when compared to the BCT group (p = 0.048). However, there were no differences between the BCT and CNT groups for peak torque and total work at both 60°.s-1 (p = 0.95 and p = 0.61, respectively) and 180°.s-1 (p = 0.94 and p = 0.72, respectively). These results suggest that three cycles of chemotherapy treatment may impair handgrip isometric strength and quality of life in women with breast cancer.

The new organic nitrate 2-nitrate-1,3-diocthanoxypropan (NDOP) induces nitric oxide production and vasorelaxation via activation of inward-rectifier potassium channels (KIR).

INTRODUCTION: Cardiovascular diseases are coupled to decreased nitric oxide (NO) bioavailability, and there is a constant search for novel and better NO-donors. Here we synthesized and characterized the cardiovascular effects of the new organic nitrate 2-nitrate-1,3-dioctanoxypropan (NDOP). METHODS: A combination of in vitro and in vivo experiments was performed in C57BL/6 mice and Wistar rats. Thus, the ability of NDOP in donating NO in a cell-free system and in vascular smooth muscles cells (VSMC) and its ability to induce vasorelaxation in aortic rings from mice were evaluated. In addition, changes in blood pressure and heart rate to different doses of NDOP were evaluated in conscious rats. Finally, acute pre-clinical toxicity to oral administration of NDOP was assessed in mice. RESULTS: In cell-free system, NDOP increased NO levels, which was dependent on xanthine oxidoreductase (XOR). NDOP also increased NO levels in VSMC, which was not influenced by endothelial NO synthase. Furthermore, incubation with the XOR inhibitor febuxostat blunted the vasorelaxation in aortic ring preparations. In conscious rats, NDOP elicited dose-dependent reduction in blood pressure accompanied with increased heart rate. In vessel preparations, NDOP (10-8-10-3 mol/L) induced endothelium-independent vasorelaxation, which was inhibited by the NO scavengers 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide and hydroxocobalamin or by inhibition of soluble guanylyl cyclase using H- [1,2,4] oxadiazolo [4,3-a]quinoxalin-1-one. To investigate if NDOP acts through potassium channels, selective blockers were used. Inhibition of BKCa, Kv or KATP subtypes of potassium channels had no effect, but inhibition of inward-rectifier potassium channels (KIR) significantly reduced NDOP-mediated vasorelaxation. Lastly, NDOP showed low toxicity (LD50 ~5000 mg/kg). CONCLUSION: Bioactivation of NDOP involves functional XOR, and this new organic nitrate elicits vasorelaxation via NO-cGMP-PKG signaling and activation of KIR channels. Future studies should further characterize the underlying mechanism and evaluate the therapeutic benefits of chronic NDOP treatment in relevant cardiovascular disease models.

Dysregulation of trophic factors contributes to diabetic retinopathy in the Ins2Akita mouse.

Diabetic retinopathy (DR) is considered as a diabetes-related complication that can lead to severe visual impairments. By 2030, it is expected that 1 in 5 adults will suffer from the disease. Suitable animal models for chronic DR are essential for a better understanding of the pathophysiology and to further develop new treatments. The Ins2Akita mouse is a type 1 diabetes model that shows signs of both early and late stages of DR, including pericyte loss, increased vascular permeability, increased acellular capillaries and neovascularization. To further characterize DR in the Ins2Akita mouse model, we have evaluated the protein levels of the angiogenesis inducers vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) and the angiogenesis inhibitor pigment epithelium-derived factor (PEDF). Additionally, we have analyzed the protein expression profile of the glial markers ionized calcium binding adaptor molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP) as well as of the chemokine monocyte chemoattractant protein 1 (MCP-1). In this study we demonstrate that, with disease progression, there is the development of an inflammatory response and an unbalanced expression of pro- and antiangiogenic factors in the neural retina and in the retinal pigment epithelium (RPE) of Ins2Akita mice. Therefore, our data provide support for the diabetic retinopathy features detected in the Ins2Akita retina, reflecting what is observed in the human pathology.

Electrochemical extraction of tin and copper from acid leachate of printed circuit boards using copper electrodes.

This paper presents new results for the recycling of electronic waste, specifically those from printed circuit boards (PCBs) of obsolete computers of the Federal University of Rio Grande do Norte. The main objective of this study is the comprehension of the extraction process of tin and cop per from PCBs by a hydrometallurgical route followed by electrodeposition using copper electrodes. PCBs powder were leached using 1N HNO3 and 3N HCl (aqua regia) aqueous solutions. The process permitted the extraction of all tin present on the PCBs. The electrodeposition processes were performed with currents from 0.5 to 1.5 A, at a constant time of 60 min, with and without mechanical stirring, and with different concentrations of leachate. The results showed that diluting the leachate favors the extraction of tin from the solution. At certain conditions we were able to extract approximately 100% of the tin, copper and lead present in the leachate.

Glial Cells Are Involved in ANG-II-Induced Vasopressin Release and Sodium Intake in Awake Rats.

It is known that circulating angiotensin II (ANG-II) acts on the circumventricular organs (CVOs), which partially lack a normal blood-brain barrier, to stimulate pressor responses, vasopressin (AVP), and oxytocin (OT) secretion, as well as sodium and water intake. Although ANG-II type 1 receptors (AT1R) are expressed in neurons and astrocytes, the involvement of CVOs glial cells in the neuroendocrine, cardiovascular and behavioral responses induced by central ANG II remains to be further elucidated. To address this question, we performed a set of experiments combining in vitro studies in primary hypothalamic astrocyte cells (HACc) and in vivo intracerebroventricular (icv) microinjections into the lateral ventricle of awake rats. Our results showed that ANG-II decreased glutamate uptake in HACc. In addition, in vivo studies showed that fluorocitrate (FCt), a reversible glial inhibitor, increased OT secretion and mean arterial pressure (MAP) and decreased breathing at rest. Furthermore, previous FCt decreased AVP secretion and sodium intake induced by central ANG-II. Together, our findings support that CVOs glial cells are important in mediating neuroendocrine and cardiorespiratory functions, as well as central ANG-II-induced AVP release and salt-intake behavior in awake rats. In the light of our in vitro studies, we propose that these mechanisms are, at least in part, by ANG-II-induced astrocyte mediate reduction in glutamate extracellular clearance.

Cardiac Autonomic Modulation and the Kinetics of Heart Rate Responses in the On- and Off-Transient during Exercise in Women with Metabolic Syndrome.

Objective: To test whether women with metabolic syndrome (MS) have impairments in the on- and off-transients during an incremental test and to study whether any of the MS components are independently associated with the observed responses. Research Design and Methods: Thirty-six women aged 35-55 years were divided into a group with MS (MSG, n = 19) and a control group (CG, n = 17). R-R intervals (RRi) and heart rate variability (HRV) were calculated on a beat-to-beat basis and the heart rate (HR) at the on- and off-transient were analyzed during an incremental cardiopulmonary exercise test (CPET). Results: MSG showed lower aerobic capacity and lower parasympathetic cardiac modulation at rest compared with CG. HR values in on-transient phase were significantly lower in MSG compared with CG. The exponential amplitudes "amp" and the parameters "τ" [speed of heart rate recovery (HRR)] were lower in MSG. MSG exhibited higher HR values in comparison to CG during the off-transient indicating a slower HRR. In MSG, there was an inverse and significant correlation between fasting plasma vs. ΔF and glucose vs. exponential "τ" of HRR dynamics. Conclusion: MS is associated with poor heart rate kinetics. The altered HR kinetics seems to be related to alterations in cardiac parasympathetic modulation, and glucose metabolism seems to be the major determinant.

A Disintegrin and Metalloprotease 17 in the Cardiovascular and Central Nervous Systems.

ADAM17 is a metalloprotease and disintegrin that lodges in the plasmatic membrane of several cell types and is able to cleave a wide variety of cell surface proteins. It is somatically expressed in mammalian organisms and its proteolytic action influences several physiological and pathological processes. This review focuses on the structure of ADAM17, its signaling in the cardiovascular system and its participation in certain disorders involving the heart, blood vessels, and neural regulation of autonomic and cardiovascular modulation.

Nitric oxide generation by the organic nitrate NDBP attenuates oxidative stress and angiotensin II-mediated hypertension.

BACKGROUND AND PURPOSE: NO deficiency and oxidative stress are crucially involved in the development or progression of cardiovascular disease, including hypertension and stroke. We have previously demonstrated that acute treatment with the newly discovered organic nitrate, 2-nitrate-1,3-dibuthoxypropan (NDBP), is associated with NO-like effects in the vasculature. This study aimed to further characterize the mechanism(s) and to elucidate the therapeutic potential in a model of hypertension and oxidative stress. EXPERIMENTAL APPROACH: A combination of ex vivo, in vitro and in vivo approaches was used to assess the effects of NDBP on vascular reactivity, NO release, NADPH oxidase activity and in a model of hypertension. KEY RESULTS: Ex vivo vascular studies demonstrated NDBP-mediated vasorelaxation in mesenteric resistance arteries, which was devoid of tolerance. In vitro studies using liver and kidney homogenates revealed dose-dependent and sustained NO generation by NDBP, which was attenuated by the xanthine oxidase inhibitor febuxostat. In addition, NDBP reduced NADPH oxidase activity in the liver and prevented angiotensin II-induced activation of NADPH oxidase in the kidney. In vivo studies showed that NDBP halted the progression of hypertension in mice with chronic angiotensin II infusion. This was associated with attenuated cardiac hypertrophy, and reduced NADPH oxidase-derived oxidative stress and fibrosis in the kidney and heart. CONCLUSION AND IMPLICATIONS: The novel organic nitrate NDBP halts the progression of angiotensin II-mediated hypertension. Mechanistically, our findings suggest that NDBP treatment is associated with sustained NO release and attenuated activity of NADPH oxidase, which to some extent requires functional xanthine oxidase.

Reactive Oxygen Species in the Paraventricular Nucleus of the Hypothalamus Alter Sympathetic Activity During Metabolic Syndrome.

The paraventricular nucleus of the hypothalamus (PVN) contains heterogeneous populations of neurons involved in autonomic and neuroendocrine regulation. The PVN plays an important role in the sympathoexcitatory response to increasing circulating levels of angiotensin II (Ang-II), which activates AT1 receptors in the circumventricular organs (OCVs), mainly in the subfornical organ (SFO). Circulating Ang-II induces a de novo synthesis of Ang-II in SFO neurons projecting to pre-autonomic PVN neurons. Activation of AT1 receptors induces intracellular increases in reactive oxygen species (ROS), leading to increases in sympathetic nerve activity (SNA). Chronic sympathetic nerve activation promotes a series of metabolic disorders that characterizes the metabolic syndrome (MetS): dyslipidemia, hyperinsulinemia, glucose intolerance, hyperleptinemia and elevated plasma hormone levels, such as noradrenaline, glucocorticoids, leptin, insulin, and Ang-II. This review will discuss the contribution of our laboratory and others regarding the sympathoexcitation caused by peripheral Ang-II-induced reactive oxygen species along the subfornical organ and paraventricular nucleus of the hypothalamus. We hypothesize that this mechanism could be involved in metabolic disorders underlying MetS.

Organic nitrates: past, present and future.

Nitric oxide (NO) is one of the most important vasodilator molecules produced by the endothelium. It has already been established that NO/cGMP signaling pathway deficiencies are involved in the pathophysiological mechanisms of many cardiovascular diseases. In this context, the development of NO-releasing drugs for therapeutic use appears to be an effective alternative to replace the deficient endogenous NO and mimic the role of this molecule in the body. Organic nitrates represent the oldest class of NO donors that have been clinically used. Considering that tolerance can occur when these drugs are applied chronically, the search for new compounds of this class with lower tolerance potential is increasing. Here, we briefly discuss the mechanisms involved in nitrate tolerance and highlight some achievements from our group in the development of new organic nitrates and their preclinical application in cardiovascular disorders.

Vasorelaxation induced by a new naphthoquinone-oxime is mediated by NO-sGC-cGMP pathway.

It has been established that oximes cause endothelium-independent relaxation in blood vessels. In the present study, the cardiovascular effects of the new oxime 3-hydroxy-4-(hydroxyimino)-2-(3-methylbut-2-enylnaphtalen-1(4H)-one (Oxime S1) derived from lapachol were evaluated. In normotensive rats, administration of Oxime S1 (10, 15, 20 and 30 mg/Kg, i.v.) produced dose-dependent reduction in blood pressure. In isolated aorta and superior mesenteric artery rings, Oxime S1 induced endothelium-independent and concentration-dependent relaxations (10(-8) M to 10(-4) M). In addition, Oxime S1-induced vasorelaxations were attenuated by hydroxocobalamin or methylene blue in aorta and by PTIO or ODQ in mesenteric artery rings, suggesting a role for the nitric oxide (NO) pathway. Additionally, Oxime S1 (30 and 100 µM) significantly increased NO concentrations (13.9 ± 1.6 nM and 17.9 ± 4.1 nM, respectively) measured by nitric oxide microsensors. Furthermore, pre-contraction with KCl (80 mM) prevented Oxime S1-derived vasorelaxation in endothelium-denuded aortic rings. Of note, combined treatment with potassium channel inhibitors also reduced Oxime S1-mediated vasorelaxation suggesting a role for potassium channels, more precisely Kir, Kv and KATP channels. We observed the involvement of BKCa channels in Oxime S1-induced relaxation in mesenteric artery rings. In conclusion, these data suggest that the Oxime S1 induces hypotension and vasorelaxation via NO pathway by activating soluble guanylate cyclase (sGC) and K+ channels.

Cardiorespiratory effects induced by 2-nitrate-1,3-dibuthoxypropan are reduced by nitric oxide scavenger in rats.

The search for new nitric oxide donors is warranted by the limitations of organic nitrates currently used in cardiology. The new organic nitrate 2-nitrate-1,3-dibuthoxypropan (NDBP) exhibited promising cardiovascular activities in previous studies. The aim of this study was to investigate the cardiorespiratory responses evoked by NDBP and to compare them to the clinically used organic nitrate nitroglycerine (NTG). Arterial pressure, heart rate and respiration were recorded in conscious adult male Wistar rats. Bolus i.v. injection of NDBP (1 to 15mg/kg; n=8) and NTG (0.1 to 5mg/kg; n=8) produced hypotension. NDBP induced bradycardia at all doses, while NTG induced tachycardia at three lower doses but bradycardia at higher doses. Hydroxocobalamin (20mg/kg; HDX), a NO scavenger, blunted hypotension induced by NDBP (15mg/kg), and its bradycardic effect (n=6). In addition, HDX blunted both hypotension and bradycardia induced by a single dose of NTG (2.5mg/kg; n=6). Both NDBP and NTG altered respiratory rate, inducing a biphasic effect with a bradypnea followed by a tachypnea; HDX attenuated these responses. Our data indicate that NDBP and NTG induce hypotension, bradycardia and bradypnea, which are mediated by nitric oxide release.

The new nitric oxide donor 2-nitrate-1,3-dibuthoxypropan alters autonomic function in spontaneously hypertensive rats.

Previously, we found that the nitrate synthesized from glycerin, 2-nitrate-1,3-dibuthoxypropan (NDBP), increased NO levels in rat aortic smooth muscle cells, inducing vasorelaxation in mesenteric artery. However, its effects on blood pressure and heart rate as well as on autonomic function were not investigated. This study evaluated the action of NDBP on these cardiovascular parameters in spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats. We found that NDBP causes a biphasic response: hypotension and bradycardia followed by hypertension and tachycardia in WKY and SHR rats. Atropine (2mg/kg) blunted the hypotension induced by NDBP (15 mg/kg) in WKY and SHR (-75 ± 9 vs -12 ± 3 mmHg, n=6; -101 ± 6 vs -7 ± 2 bpm, n=6; respectively, p<0.05) and the pressor response to the compound was potentiated. Furthermore, vagotomy reduced the bradycardia in WKY and SHR (-136 ± 8 vs -17 ± 2, n=4, p<0.05; -141 ± 9 vs -8 ± 2, n=6, p<0.05). Moreover, hexamethonium (30 mg/kg) reduced both bradycardia (-278 ± 23 vs -48 ± 3 in WKY; -285 ± 16 vs -27 ± 19 in SHR, n=4; p<0.05) and pressor response (28 ± 8 vs -9 ± 5-WKY, n=6; 42 ± 7 vs -19 ± 8-SHR, n=5; p<0.05). In addition, administration of methylene blue (4 mg/kg) attenuated the hypotensive and bradycardic responses to the NDBP in all groups. In conclusion, NDBP induces bradycardia by direct vagal stimulation and pressor response by increasing sympathetic outflow to the periphery.

Quercetin improves baroreflex sensitivity in spontaneously hypertensive rats.

Quercetin is a well-known antioxidant. Here, we investigated the effects of treatment with quercetin on mean arterial pressure (MAP), heart rate (HR) and baroreflex sensitivity (BRS) in spontaneously hypertensive rats (SHR). SHR and their controls (WKY) were orally treated with quercetin (2, 10 or 25 mg/kg/day) or saline for seven days. On the 8th day, MAP and HR were recorded. BRS was tested using phenylephrine (8 mg/kg, i.v.) and sodium nitroprusside (25 mg/kg, i.v.). Oxidative stress was measured by tiobarbituric acid reactive species assay. The doses of 10 (n = 8) and 25 mg/kg (n = 8) were able to decrease the MAP in SHR (n = 9) (163 ± 4 and 156 ± 5 vs. 173 ± 6, respectively, p < 0.05) but not in WKY (117 ± 1 and 118 ± 2 vs. 113 ± 1, respectively, p < 0.05). The dose of 25 mg/kg/day increased the sensitivity of parasympathetic component of the baroreflex (−2.47 ± 0.31 vs. −1.25 ± 0.8 bpm/mmHg) and decreased serum oxidative stress in SHR (2.04 ± 0.17 vs. 3.22 ± 0.37 nmol/mL, n = 6). Our data suggest that treatment with quercetin reduces hypertension and improves BRS in SHR via reduction in oxidative stress.

The 2-nitrate-1,3-dibuthoxypropan, a new nitric oxide donor, induces vasorelaxation in mesenteric arteries of the rat.

The reduced availability of nitric oxide (NO) is associated with cardiovascular diseases. Therefore, NO donors such as organic nitrates are useful for the treatment of these disorders. The 2-nitrate-1,3-dibuthoxypropan (NDBP) is an organic nitrate synthesized from glycerin, which the pharmacological effects have not been investigated. In this study we evaluated the vasorelaxant effect induced by NDBP in superior mesenteric artery from rats. In phenylephrine pre-contracted artery rings, NDBP (10(-8)-10(-4)M) elicited concentration-dependent and endothelium-independent relaxation, which were attenuated by hydroxocobalamin-HDX (30 µM), a NO extracellular scavenger, and 1-H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one-ODQ (10 µM), an inhibitor of soluble guanylyl cyclase (sGC). In addition, the NDBP-induced relaxation was reduced by non-selective K(+) channels blocker KCl (20 mM) or selective K(+) channels blockers such as tetraethylammonium-TEA (B(KCa), 1 mM), charybdotoxin-ChTX (B(KCa), 100 nM), glibenclamide (K(ATP), 1µM) and 4-aminopyridine-4-AP (K(V), 1mM). In preparations with ODQ (10 µM) plus TEA (1 mM), the response was virtually abolished. In rat smooth muscle cells culture, NDBP (10(-6)-10(-4)M) caused concentration-dependent increases in NO levels. These findings suggest that NDBP causes vasorelaxation through NO generation and activation of the sCG/cGMP/PKG pathway.

Factors associated with early weaning at a Child-Friendly Healthcare Initiative Hospitall / Fatores associados ao desmame precoce em Hospital Amigo da Criança

PURPOSE: Considering the benefits of breastfeeding on children's health, the aim of the present study was to determine factors associated with early weaning among children at a Child-Friendly Healthcare Initiative (CFHI) children's hospital in the city of Campina Grande, state of Paraíba, Brazil. METHODS: An analytical, cross-sectional study was carried out involving 800 mothers of children between 0 and 24 months of age at the Elpídio de Almeida Health Institute. A semi-structured questionnaire was administered and contained questions on socio-demographic characteristics, eating habits and nonnutritive sucking habits. The chi-square test and Fisher's exact test were employed for statistical analysis. A multivariate analysis was performed with variables that achieved a P-value < 0.25 in the bivariate analysis. RESULTS: The prevalence of early weaning was 13.5%. In the bivariate analysis, the factors associated with early weaning were income (P=0.001), child's birth weight (P=0.016), bottle feeding (P=0.003) and pacifier use (P<0.001). In the multivariate analysis, pacifier use remained significantly associated with early weaning (OR: 3.23; 95% CI: 1.871 to 5.591; P<0.001). CONCLUSION: Pacifier use was associated with early weaning, even when mothers were advised to avoid this habit.

OBJETIVO: Considerando os benefícios da amamentação para a saúde da criança, o objetivo do presente estudo foi determinar os fatores associados com o desmame precoce entre as crianças em um Hospital Amigo da Criança na cidade de Campina Grande, estado da Paraíba, Brasil. METODOLOGIA: Um estudo analítico e transversal foi realizado com 800 mães de crianças entre 0 e 24 meses de idade, no Elpídio de Almeida Instituto de Saúde. Um questionário semi-estruturado foi aplicado, contendo perguntas sobre características sócio-demográficas, hábitos alimentares e hábitos de sucção não nutritiva. O teste do qui-quadrado e teste exato de Fisher foram empregados na análise estatística. A análise multivariada foi realizada com as variáveis tendo atingido um valor de P<0,25 na análise bivariada. RESULTADOS: A prevalência de desmame precoce foi de 13,5%. Na análise bivariada, os fatores associados com o desmame precoce foram: renda (P=0,001), peso de nascimento da criança (P=0,016), uso de mamadeira (P=0,003) e uso de chupeta (P<0,001). Na análise multivariada, o uso de chupeta permaneceu significativamente associada com o desmame precoce (OR: 3,23 IC 95%: 1,871-5,591, P<0,001). CONCLUSÃO: O uso de chupeta foi associado com o desmame precoce, mesmo quando as mães foram aconselhadas a evitar esse hábito.

Uncovering the vasorelaxant effect induced by Vale do São Francisco red wine: a role for nitric oxide.

The aim of this study was to investigate the mechanisms underlying the vasorelaxant effect induced by the polyphenolic compounds found in red wine from Vale do São Francisco. In phenylephrine (10 µM) precontracted mesenteric artery rings, the red wine caused a concentration-dependent relaxation (maximum response to phenylephrine 10 µM = 87.5% ± 6.5%, n = 10). After endothelium removal, the vasorelaxant effect elicited by red wine was attenuated (28.4% ± 4.9%, n = 10). In addition, the vasorelaxant effect induced by red wine in rings pretreated with 100 µM of N(w)-nitro-l-arginine methyl ester and 10 µM of 1H-[1,2,4] oxadiazolo-[4,3-a]-quinoxalin-1-one was attenuated (23.4% ± 5.1%, n = 7 and 11.8% ± 2.7%, n = 6, respectively). Pretreatment with atropine did not affect the vasorelaxant effect induced by red wine (81% ± 3.9%, n = 6). Furthermore, in rabbit aortic endothelial cell line, red wine 100 and 300 µg/mL caused concentration-dependent increases in nitric oxide levels (58 ± 1; 82 ± 7.9; Δ% of fluorescence, n = 5, respectively). In conclusion, we suggest that the alcohol free-lyophilized red wine induces an endothelium-dependent vasorelaxant effect due, at least in part, to a secondary increase in the concentration of nitric oxide and that this effect might be associated with phenolic compounds found in the red wine.

Superoxide scavenging in the rostral ventrolateral medulla blunts the pressor response to peripheral chemoreflex activation.

Peripheral chemoreflex activation has been considered the key drive for the overactivity of the sympathetic nervous system observed in some pathological conditions such as sleep obstructive apnea. In addition, increases in angiotensin-II-derived reactive oxygen species found in some autonomic regulatory brain areas have been implicated in hypertension. However, a link between oxidative stress and peripheral chemoreflex integration within the RVLM has never been investigated. Here, we tested the hypothesis that the pressor response induced by peripheral chemoreflex activation involves the angiotensin-II/AT(1)R/superoxide pathway within the rostral ventrolateral medulla (RVLM). Seventeen male Wistar rats (260-300 g) were implanted with bilateral guide cannulae towards the RVLM and were fitted with catheters for blood pressure recordings and drug administration. Peripheral chemoreflex activation with potassium cyanide (80 microg/kg, i.v.) produced a transient increase in blood pressure, which was attenuated 2 minutes after bilateral microinjection of losartan (1 nmol), an AT(1) receptor antagonist, in the RVLM (+54+/-4 vs +19+/-3 Delta mmHg, P<0.05, n=6). Moreover, superoxide scavenging in the RVLM using a superoxide dismutase (SOD) mimetic, Tempol (5 nmol), significantly blunted the pressor response to peripheral chemoreflex activation (+50+/-3 vs +18+/-3 Delta mmHg, P<0.05, n=7). On the other hand, bilateral microinjection of saline (n=4) in the RVLM produced no change in the pressor response to chemoreflex activation. Taken together, these data suggest that the neurotransmission of the peripheral chemoreflex within the RVLM involves, at least in part, the activation of AT(1) receptors and downstream superoxide formation.