39 research outputs found

    PREVALÊNCIA DE ASMA EM ESCOLARES DA REDE PÚBLICA DE ENSINO NO MUNICÍPIO DE URUGUAIANA/RS

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    Este estudo objetiva estimar a prevalĂȘncia de sintomas de asma e de provĂĄvel asma em escolares de Uruguaiana, estado do Rio Grande do Sul, e relacionĂĄ-los com possĂ­veis fatores de risco. Para isso, participaram do estudo 391 crianças e adolescentes nas faixas etĂĄrias de 6-7 e 13-14 anos, tanto do gĂȘnero feminino quanto masculino, cujos responsĂĄveis preencheram corretamente o questionĂĄrio ISAAC fase I aplicado durante o perĂ­odo de janeiro a novembro de 2015. A prevalĂȘncia de asma relacionada aos sintomas e fatores de risco na população escolar de Uruguaiana foi de 15%, correspondendo 19% na faixa etĂĄria de 6-7 anos e 12% na faixa etĂĄria de 13-14 anos.  NĂŁo houve relação estabelecida entre prevalĂȘncia de sintomas asmĂĄticos e fatores ambientais. Conclui-se que a prevalĂȘncia de sintomas asmĂĄticos e de provĂĄvel asma Ă© similar as outras cidades do RS. Descritores: Asma; Escolares; QuestionĂĄrio ISAAC.

    Toxic effects of mercury, lead and gadolinium on vascular reactivity

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    Heavy metals have been used in a wide variety of human activities that have significantly increased both professional and environmental exposure. Unfortunately, disasters have highlighted the toxic effects of metals on different organs and systems. Over the last 50 years, the adverse effects of chronic lead, mercury and gadolinium exposure have been underscored. Mercury and lead induce hypertension in humans and animals, affecting endothelial function in addition to their other effects. Increased cardiovascular risk after exposure to metals has been reported, but the underlying mechanisms, mainly for short periods of time and at low concentrations, have not been well explored. The presence of other metals such as gadolinium has raised concerns about contrast-induced nephropathy and, interestingly, despite this negative action, gadolinium has not been defined as a toxic agent. The main actions of these metals, demonstrated in animal and human studies, are an increase of free radical production and oxidative stress and stimulation of angiotensin I-converting enzyme activity, among others. Increased vascular reactivity, highlighted in the present review, resulting from these actions might be an important mechanism underlying increased cardiovascular risk. Finally, the results described in this review suggest that mercury, lead and gadolinium, even at low doses or concentrations, affect vascular reactivity. Acting via the endothelium, by continuous exposure followed by their absorption, they can increase the production of free radicals and of angiotensin II, representing a hazard for cardiovascular function. In addition, the actual reference values, considered to pose no risk, need to be reducedResearch supported by CAPES and CNPq/FAPES/ FUNCITEC (#39767531/07), Brazil, and MCINN (#SAF 2009-07201) and ISCIII (Red RECAVA, #RD06/0014/0011), Spai

    Multi-functional egg white hydrolysate prevent hypertension and vascular dysfunction induced by cadmium in rats

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    We have investigated if EWH could counteract or prevent cardiovascular damage induced by high level of Cd exposure in rats. Male Wistar rats were treated for 14 days with: (A) Untreated - intraperitoneal (i.p.) injections of distilled water and tap water by gavage; (B) Cd − 1 mg/kg of bw/day of CdCl2 (i.p.) and tap water by gavage; (C) EWH – distilled water (i.p.) and 1 mg/kg/day of EWH by gavage; (D) CdEWH – both treatments. EWH prevented the increase on systolic blood pressure, vascular dysfunction, and inflammation after Cd exposure; prevent the activation of cyclooxygenase (COX)-2 and its derived contractile protanoids, inhibits angiotensin II by the reduction of ACE activity and prevents the increased oxidative stress mainly mediated by NADPH oxidase. Multifunctional EWH could be considered as a natural alternative therapy to counteract the deleterious effects caused by high level of Cd exposure.Supported by National Council for Scientific and Technological Development – CNPq [Edital Universal/CNPq No 44181/2014-9 and PQ/CNPq 311834/2020-5]; Coordenação de Aperfeiçoamento de Pessoal de NĂ­vel Superior - Brasil (CAPES); Fundação de Amparo Ă  Pesquisa do Rio Grande do Sul - FAPERGS/ Brazil [PQG:19/2551-0001810-0]; Programa Nacional de Cooperação AcadĂȘmica; PrĂł-reitoria de Pesquisa - Universidade Federal do Pampa [N. 20180615102630]; FAPES/CNPq/PRONEX [N. 80598773] and Spanish Goverment by the Agencia Estatal de InvestigaciĂłn (AEI) and Fondo Europeo de Desarrollo Regional (FEDER) [AGL2017-89213]; I-COOP+2020 (COOPA 20453). PZM and JEGPJr were supported by CAPES/Brazil, CSM by CNPq/Brazil; CRM and MDR by FAPERGS/ Brazil and GCS by PDA/Unipampa.Peer reviewe

    ROS suppression by egg white hydrolysate in DOCA-salt rats—An alternative tool against vascular dysfunction in severe hypertension

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    This article belongs to the Special Issue Antioxidant Properties and Potential Mechanisms of Protein Hydrolysates.This study aimed to evaluate the potential for lowering blood pressure and beneficial effects on mesenteric resistance arteries (MRA) and conductance vessels (aorta) produced by dietary supplementation of an egg white hydrolysate (EWH) in rats with severe hypertension induced by deoxycorticosterone plus salt treatment (DOCA-salt), as well as the underlying mechanisms involved. The DOCA-salt model presented higher blood pressure, which was significantly reduced by EWH. The impaired acetylcholine-induced relaxation and eNOS expression observed in MRA and aorta from DOCA-salt rats was ameliorated by EWH. This effect on vessels (MRA and aorta) was related to the antioxidant effect of EWH, since hydrolysate intake prevented the NF-ÎșB/TNFα inflammatory pathway and NADPH oxidase-induced reactive oxygen species (ROS) generation, as well as the mitochondrial source of ROS in MRA. At the plasma level, EWH blocked the higher ROS and MDA generation by DOCA-salt treatment, without altering the antioxidant marker. In conclusion, EWH demonstrated an antihypertensive effect in a model of severe hypertension. This effect could be related to its endothelium-dependent vasodilator properties mediated by an ameliorated vessel’s redox imbalance and inflammatory state.This work was supported by the National Council for Scientific and Technological Development—CNPq [Edital Universal/CNPq No 44181/2014-9 and PQ/CNPq 311834/2020-5]; Coordenação de Aperfeiçoamento de Pessoal de NĂ­vel Superior—Brasil (CAPES); Fundação de Amparo Ă  Pesquisa do Rio Grande do Sul—FAPERGS/Brazil [PQG:19/2551-0001810-0]; Programa Nacional de Cooperação AcadĂȘmica; PrĂł-reitoria de Pesquisa—Universidade Federal do Pampa [N. 20180615102630]; FAPES/CNPq/PRONEX [N. 80598773], Foundation for Research Support of the State of Sao Paulo (FAPESP 2019/08026-5), and Spanish Goverment by the Agencia Estatal de InvestigaciĂłn (AEI) and Fondo Europeo de Desarrollo Regional (FEDER) [AGL2017-89213]; I-COOP+2020 (COOPA 20453). ELA were supported by CAPES/Brazil, CRM by FAPERGS/Brazil and PHD, CTH by Unipampa. LVR are research fellows from CNPq (312237/2021-9).Peer reviewe

    Toxic Effects of Mercury on the Cardiovascular and Central Nervous Systems

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    Environmental contamination has exposed humans to various metal agents, including mercury. This exposure is more common than expected, and the health consequences of such exposure remain unclear. For many years, mercury was used in a wide variety of human activities, and now, exposure to this metal from both natural and artificial sources is significantly increasing. Many studies show that high exposure to mercury induces changes in the central nervous system, potentially resulting in irritability, fatigue, behavioral changes, tremors, headaches, hearing and cognitive loss, dysarthria, incoordination, hallucinations, and death. In the cardiovascular system, mercury induces hypertension in humans and animals that has wide-ranging consequences, including alterations in endothelial function. The results described in this paper indicate that mercury exposure, even at low doses, affects endothelial and cardiovascular function. As a result, the reference values defining the limits for the absence of danger should be reduced. History More than 2500 A.C., the prehistoric man used the cinabrio (mercury sulfide), due to its red-gold color, to draw on cave walls and perform face painting. Subsequently, mercury has been used in the amalgamation (direct burning of metallic mercury on the gravel, promoting the separation of gold), in photography and as an antiseptic in the treatment of syphilis Exposure to mercury brought harmful effects to health of humans, but changes resulting from human exposure to mercury only called the attention of the scientific society after the accidents in Japan and Iraq Mercury Characteristics Mercury is characterized as a highly malleable liquid at normal temperature and pressure Inorganic Mercury Compounds Elemental Mercury or Metalic Mercury Compounds. In its liquid form, the elemental mercury (Hg 0 ) is poorly absorbed and presents little health risk. However, in the vapor form, metallic mercury is readily absorbed through the lungs and can produce body damage Elemental mercury is used in thermometers and sphygmomanometers because of its uniform volumetric expansion, high surface tension, and lack of vitreous adherence to surfaces. Low electrical resistance and high thermal conductivity allow metallic mercury to be used in electrical and electronic materials. Because of its high oxidation power, metallic mercury is used in electrochemical operations in the chlorine and soda industries. Metallic mercury is also used in metallurgy, mining, and dentistry because of the easy amalgam formation with other metals. In addition, gold extraction with archaic and dangerous methods predispose miners to mercury poisoning. The burning of metallic mercury on the gravel promotes the separation of gold, a process called amalgamation, which causes emission of large amounts of mercury vapor that is inhaled immediately by the miner, since they do not use appropriate personal protective equipment Mercurous Mercury and Mercuric Mercury Compounds. The mercurous mercury in the form of mercurous chloride (Hg 2 Cl 2 ) is little absorbed in the body. It is believed that in the body the form of metallic mercury is changed to elemental mercury and mercuric mercury Mercuric mercury compounds, such as mercury salts, result from the combination of mercury with chlorine, sulfur, or oxygen. Mercuric mercury can be found in different states when combined with other chemical elements, including mercuric chloride (HgCl 2 ), which is highly toxic and corrosive; mercury sulfide (HgS), which is often used as a pigment in paints due to its red color; mercury fulminate (Hg(CNO) 2 ), which is used as an explosive detonator In the cardiovascular system, acute inorganic mercury exposition in vivo promotes reduction of myocardial force development Organic Mercury. Organic mercury compounds, also called organometallic, result from a covalent bond between mercury and the carbon [8] atom of an organic functional group such as a methyl, ethyl, or phenyl group. Methylmercury (CH 3 Hg + ) is by far the most common form of organic Hg to which humans and animals are exposed. CH 3 Hg + in the environment is predominantly formed by methylation of inorganic mercuric ions by microorganisms present in soil and water Journal of Biomedicine and Biotechnology 3 The organomercury antiseptics still used are Merthiolate, Bacteran, and Thimerosal [40]. Thimerosal is an organomercurial compound that since 1930 has been widely used as a preservative in biological material such as vaccines and serums used to prevent microbiological growth Forms of Mercury Exposure Mercury is now considered an environmental pollutant of high risk to public health because of its high toxicity and mobility in ecosystems More natural sources of mercury include volcanic activity, earthquakes, erosion, and the volatilization of mercury present in the marine environment and vegetation Mercury contaminates the environment through a cycle involving the initial emission, the subsequent atmospheric circulation of the vapor form, and the eventual return of mercury to the land and water via precipitation ( Mercury present in seas and rivers after methylation can contaminate fish Transport and Elimination of Mercury Inhaled elemental mercury vapor, for example, is readily absorbed through mucous membranes and the lung and is rapidly oxidized but not as quickly as to prevent the deposition of considerable amount in the brain Then, toxicity for man varies depending on the form of mercury, dose, and rate of exposure. The target organ for inhalted mercury vapor is primarily the brain Oxidized mercury binds strongly to SH groups; this reaction can inactivate enzymes, lead to tissue damage and interfere with various metabolic processes Doses of Mercury and Safety Legislation The chemical form of mercury in the air affects its time of permanence and its dispersion in the atmosphere. The elemental mercury form can persist for more than four years in the air, while its compounds are deposited in a short time at locations near their origin. In the northern hemisphere, their average concentration in the atmosphere is estimated at 2 ng/m 3 and in the southern hemisphere is less than 1 ng/m 3 . In urban areas, there is a great variability of these concentrations being found up to 67 ng/m 3 with a mean of 11 ng/m 3 in Japan In 2004, the Joint FAO (Food and Agriculture Organization of the United National)/WHO Expert Committee on Food Additives (JECFA) established that the safe concentration of methylmercury intake, without the appearance of neurological disorders, is 1.6 mg/kg of body weight. However, in 2006, JECFA stated that this concentration is not safe for intrauterine exposure, because fetuses are more sensitive to the onset of neurological disorders after exposure to methylmercury Currently, the general population is exposed to mercury by the following main sources: the consumption of contaminated fish, the use and manipulation of dental amalgam, thimerosal contained in vaccines, workers in industries of chlorine, caustic soda, miners, and workers in industries of fluorescent lamps In Brazil, the rules for vaccination of the Ministry of Health, published in June 2001, shows that thimerosal is used in many vaccines. These vaccines prevent flu (influenza vaccine), rabies (rabies vaccine), infection with meningococcus serogroup b, and hepatitis B The US Environmental Protection Agency's recommended a reference blood concentration of mercury to be 5.8 ng/mL; concentrations below this level are considered to be safe In the following sections, we will describe results obtained from animals with chronic and acute exposure to mercury. Some of these studies were performed with mercury exposure protocols that led to blood concentrations slightly above the reference values. Nevertheless, these concentrations could be easily found in exposed populations and may even be considered low when compared with concentrations in humans who consume large amounts of fish or who live in areas contaminated with mercury. Effect of Mercury on the Central Nervous System (CNS) Among the compounds of mercury, the methylmercury is primarily responsible for the neurological alterations present in humans and experimental animals. It is believed that the mechanisms are related to the toxic increase in reactive oxygen species (ROS). Oxidative stress is associated with the etiology of neurodegenerative diseases such as amyotrophic lateral sclerosis, Parkinson's disease, and Alzheimer's disease Reinforcing the hypothesis that the majority of injuries caused by methylmercury (MeHg) in the central nervous system are related to its ability to increase reactive oxygen species, Studies also demonstrate that mercury has the ability to reduce the number of neuron and cytoarchitecture in individuals with prenatal exposure to mercury In addition, because of its high affinity for sulfhydryl groups in tubulin, methylmercury inhibits the organization of microtubules that are important in CNS development Corroborating these findings, the study conducted by Halbach et al. [90] studied a correlation in Iraqi children between the level of maternal exposure to methylmercury during pregnancy and psychomotor retardation. SandborghEnglund et al. Effect of Mercury on the Cardiovascular System For decades, the toxic effects of mercury were associated mainly with the central nervous system; however, inorganic mercury also produces profound cardiotoxicity The mechanism by which mercury produces toxic effects on the cardiovascular system is not fully elucidated, but this mechanism is believed to involve an increase in oxidative stress. Exposure to mercury increases the production of free radicals, potentially because of the role of mercury in the Fenton reaction The reduction in glutathione peroxidase with seleniumdependent activity is the result of the decreased bioavailability of selenium, a molecule that is required for enzymatic activity Cardiovascular changes resulting from mercury poisoning are also described in animal models. However, the mechanism involved in the effects of mercury on the cardiovascular system is not fully understood but seems to be dependent on both the dose and time of exposure. Raymond and Ralston [123] studied the hemodynamic effects of an intravenous injection of HgCl 2 (5 mg/kg) in rats and observed that mercury produced cardiac diastolic failure and pulmonary hypertension. Moreover, Naganuma et al. Our group has found that chronic exposure to low doses of mercury (1st dose 4.6 ÎŒg/kg followed by 0.07 ÎŒg/kg/day for 30 days, im) attained a blood mercury concentration of approximately 8 ng/mL, a concentration similar to the levels found in exposed humans. This exposure produced a negative inotropic effect in perfused hearts, although increasing myosin ATPase activity. Invivo, arterial or ventricular pressures did not change The chronic exposure to low concentrations of mercury was also able to induce endothelial dysfunction in resistance and conductance vessels, most likely because of the decreased nitric oxide (NO) bioavailability due to the increased superoxide anion (O 2 ‱− ) production from NADPH oxidase Taken together, these data show that chronic low doses of mercury have an important and deleterious effect on vascular function by reducing NO bioavailability. The degree of severity of mercury exposure is comparable to traditional cardiovascular risk factors, such as hypertension diabetes or hypercholesterolemia. Therefore, mercury could be considered an important risk factor for cardiovascular disease that could play a role in the development of cardiovascular events. The association between mercury exposure and an increased risk of developing cardiovascular and neurological diseases is apparent. Thus, continuous exposure to mercury can be dangerous, and current reference values, once considered to be without risk, should be reevaluated and reduced

    Measurement of Upsilon production in collisions at root s=2.76 TeV

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    The production of ΄(1S)\Upsilon(1S), ΄(2S)\Upsilon(2S) and ΄(3S)\Upsilon(3S) mesons decaying into the dimuon final state is studied with the LHCb detector using a data sample corresponding to an integrated luminosity of 3.3 pb−1pb^{-1} collected in proton-proton collisions at a centre-of-mass energy of s=2.76\sqrt{s}=2.76 TeV. The differential production cross-sections times dimuon branching fractions are measured as functions of the ΄\Upsilon transverse momentum and rapidity, over the ranges $p_{\rm T} Upsilon(1S) X) x B(Upsilon(1S) -> mu+mu-) = 1.111 +/- 0.043 +/- 0.044 nb, sigma(pp -> Upsilon(2S) X) x B(Upsilon(2S) -> mu+mu-) = 0.264 +/- 0.023 +/- 0.011 nb, sigma(pp -> Upsilon(3S) X) x B(Upsilon(3S) -> mu+mu-) = 0.159 +/- 0.020 +/- 0.007 nb, where the first uncertainty is statistical and the second systematic

    Studies of beauty baryon decays to D0ph− and Λ+ch− final states

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    A study of CP violation in B-+/- -> DK +/- and B-+/- -> D pi(+/-) decays with D -> (KSK +/-)-K-0 pi(-/+) final states

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    A first study of CP violation in the decay modes B±→[KS0K±π∓]Dh±B^\pm\to [K^0_{\rm S} K^\pm \pi^\mp]_D h^\pm and B±→[KS0K∓π±]Dh±B^\pm\to [K^0_{\rm S} K^\mp \pi^\pm]_D h^\pm, where hh labels a KK or π\pi meson and DD labels a D0D^0 or D‟0\overline{D}^0 meson, is performed. The analysis uses the LHCb data set collected in pppp collisions, corresponding to an integrated luminosity of 3 fb−1^{-1}. The analysis is sensitive to the CP-violating CKM phase Îł\gamma through seven observables: one charge asymmetry in each of the four modes and three ratios of the charge-integrated yields. The results are consistent with measurements of Îł\gamma using other decay modes
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