116 research outputs found

    Cycling training effects on fat metabolism blood parameters

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    BACKGROUND: Study the acute and middle term (4 weeks training) effect of cycling training on fat blood hematological parameters, urine, fatigue, and general health in recreational well-trained cyclists. METHODS: Nineteen cyclists underwent five blood sample collections: before and after an incremental maximal ramp test 7 days before day 0 (D-0); before and after 1 hour exhaustion trial test at baseline (D-0); and after 28 days of training (D-28). Age 34.5 years (\ub19.5); weight 74.87 kg (\ub16.6); height 177.3 cm (\ub15.2); BMI 26.3 (\ub14.9); VO2max 53.75 mL/kg/ min (\ub16.01); distance cycled 314.7 km/week (\ub1137.1). RESULTS: Acute effect was strong elevating WBC from 6.27\ub12.34 to 9.01\ub13.63 7103/\ub5L, an increase in LDL and total CHOL, in this respect, existing literature is controversial. No changes in body weight or blood pressure was observed after 1 month of regular training albeit lipid profile significantly improved, as well as GOT. CONCLUSIONS: Effect of a short incremental bout of exercise was to temporary elevated all the blood parameters except MCH and MCHC. A month of intensive training (distance cycled: 314.7\ub1137.1 km/week) significantly improved blood lipids profile with no permanent effect on WBC, blood pressure or body weight, but improved post effort lactate concentration and fatigue perception. Hematuria is confirmed to be a rare occurrence in recreational cyclists. Data can be useful for training monitoring and comparisons with similar groups of athletes, where there is a lack of information in literature and for comparing exercise effects

    Toxicological Aspects Associated with Consumption from Electronic Nicotine Delivery System (ENDS): Focus on Heavy Metals Exposure and Cancer Risk

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    Tobacco smoking remains one of the leading causes of premature death worldwide. Electronic Nicotine Delivery Systems (ENDSs) are proposed as a tool for smoking cessation. In the last few years, a growing number of different types of ENDSs were launched onto the market. Despite the manufacturing differences, ENDSs can be classified as “liquid e-cigarettes” (e-cigs) equipped with an atomizer that vaporizes a liquid composed of vegetable glycerin (VG), polypropylene glycol (PG), and nicotine, with the possible addition of flavorings; otherwise, the “heated tobacco products” (HTPs) heat tobacco sticks through contact with an electronic heating metal element. The presence of some metals in the heating systems, as well as in solder joints, involves the possibility that heavy metal ions can move from these components to the liquid, or they can be adsorbed into the tobacco stick from the heating blade in the case of HTPs. Recent evidence has indicated the presence of heavy metals in the refill liquids and in the mainstream such as arsenic (As), cadmium (Cd), chromium (Cr), nickel (Ni), copper (Cu), and lead (Pb). The present review discusses the toxicological aspects associated with the exposition of heavy metals by consumption from ENDSs, focusing on metal carcinogenesis risk

    Ultrasonic evidence of an uncorrelated cluster formation temperature in manganites with first-order magnetic transition at T_C

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    Ultrasonic attenuation and phase velocity measurements have been carried out in the ferromagnetic perovskites La_{2/3}Ca_{1/3}MnO_3 and La_{2/3}Sr_{1/3}MnO_3. Data show that the transition at the Curie temperature, T_C, changes from first- to second-order as Sr replaces Ca in the perovskite. The compound with first-order transition shows also another transition at a temperature T* > T_C. We interpret the temperature window T_C < T < T* as a region of coexistence of a phase separated regime of metallic and insulating regions, in the line of recent theoretical proposals.Comment: 4 pages, 2 figure

    Potential Harm of IQOS Smoke to Rat Liver

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    The Food and Drug Administration has recently classified the IQOS electronic cigarette as a modified-risk tobacco product. However, IQOS cigarettes still release various harmful constituents typical of conventional cigarettes (CCs), although the concentrations are markedly lower. Here, we investigated the damaging effects of IQOS smoking on the liver. Male Sprague Dawley rats were exposed, whole body, 5 days/week for 4 weeks to IQOS smoke (4 sticks/day), and hepatic xenobiotic metabolism, redox homeostasis and lipidomic profile were investigated. IQOS boosted reactive radicals and generated oxidative stress. Exposure decreased cellular reserves of total glutathione (GSH) but not GSH-dependent antioxidant enzymes. Catalase and xanthine oxidase were greater in the exposed group, as were various hepatic CYP-dependent monooxygenases (CYP2B1/2, CYP1A1, CYP2A1, CYP2E1-linked). Respiratory chain activity was unaltered, while the number of liver mitochondria was increased. IQOS exposure had an impact on the hepatic lipid profile. With regard to the expression of some MAP kinases commonly activated by CC smoking, IQOS increased the p-p38/p38 ratio, while erythroid nuclear transcription factor 2 (Nrf2) was negatively affected. Our data suggest that IQOS significantly impairs liver function, supporting the precautionary stance taken by the WHO toward the use of these devices, especially by young people and pregnant women

    Results of the engineering run of the coherent neutrino nucleus interaction experiment (CONNIE)

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    The CONNIE detector prototype is operating at a distance of 30 m from the core of a 3.8 GWth nuclear reactor with the goal of establishing Charge-Coupled Devices (CCD) as a new technology for the detection of coherent elastic neutrino-nucleus scattering. We report on the results of the engineering run with an active mass of 4 g of silicon. The CCD array is described, and the performance observed during the first year is discussed. A compact passive shield was deployed around the detector, producing an order of magnitude reduction in the background rate. The remaining background observed during the run was stable, and dominated by internal contamination in the detector packaging materials. The in-situ calibration of the detector using X-ray lines from fluorescence demonstrates good stability of the readout system. The event rates with the reactor ON and OFF are compared, and no excess is observed coming from nuclear fission at the power plant. The upper limit for the neutrino event rate is set two orders of magnitude above the expectations for the standard model. The results demonstrate the cryogenic CCD-based detector can be remotely operated at the reactor site with stable noise below2 e RMS and stable background rates. The success of the engineering test provides a clear path for the upgraded 100 g detector to be deployed during 2016.Fil: Aguilar Arevalo, A.. Universidad Nacional Autónoma de México; MéxicoFil: Bertou, Xavier Pierre Louis. Comisión Nacional de Energía Atómica; Argentina. Comisión Nacional de Energía Atómica. Fundación José A. Balseiro; ArgentinaFil: Bonifazi, C.. Universidade Federal do Rio de Janeiro; BrasilFil: Butner, M.. Fermi National Accelerator Laboratory; Estados UnidosFil: Cancelo, G.. Fermi National Accelerator Laboratory; Estados UnidosFil: Castañeda Vazquez, A.. Universidad Nacional Autónoma de México; MéxicoFil: Cervantes Vergara, B.. Universidad Nacional Autónoma de México; MéxicoFil: Chavez, C. R.. Universidad Nacional de Asunción; ParaguayFil: Da Motta, H.. Centro Brasileiro de Pesquisas Físicas; BrasilFil: D'Olivo, J. C.. Universidad Nacional Autónoma de México; MéxicoFil: Dos Anjos, J.. Centro Brasileiro de Pesquisas Físicas; BrasilFil: Estrada, J.. Fermi National Accelerator Laboratory; Estados UnidosFil: Fernández Moroni, Guillermo. Universidad Nacional del Sur. Departamento de Ingeniería Eléctrica y de Computadoras. Instituto ; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Ford, R.. Fermi National Accelerator Laboratory; Estados UnidosFil: Foguel, A.. Centro Brasileiro de Pesquisas Físicas; Brasil. Universidade Federal do Rio de Janeiro; BrasilFil: Hernandez Torres, K. P.. Universidad Nacional Autónoma de México; MéxicoFil: Izraelevitch, F.. Fermi National Accelerator Laboratory; Estados UnidosFil: Kavner, A.. University of Michigan; Estados UnidosFil: Kilminster, B.. Universitat Zurich; SuizaFil: Kuk, K.. Fermi National Accelerator Laboratory; Estados UnidosFil: Lima Jr, H. P.. Centro Brasileiro de Pesquisas Físicas; BrasilFil: Makler, M.. Centro Brasileiro de Pesquisas Físicas; BrasilFil: Molina, J.. Universidad Nacional de Asunción; ParaguayFil: Moreno Granados, G.. Universidad Nacional Autónoma de México; MéxicoFil: Moro, Juan Manuel. Universidad Nacional del Sur. Departamento de Ingeniería; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Paolini, Eduardo Emilio. Universidad Nacional del Sur. Departamento de Ingeniería Eléctrica y de Computadoras. Instituto ; ArgentinaFil: Sofo Haro, Miguel Francisco. Comision Nacional de Energia Atomica. Gerencia D/area de Energia Nuclear; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Tiffenberg, Javier Sebastian. Fermi National Accelerator Laboratory; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Trillaud, F.. Universidad Nacional Autónoma de México; MéxicoFil: Wagner, S.. Centro Brasileiro de Pesquisas Físicas; Brasil. Pontificia Universidade Católica do Rio Grande do Sul; Brasi

    On the toxicity of e-cigarettes consumption: Focus on pathological cellular mechanisms

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    Tobacco smoking remains without a doubt one of the leading causes of premature death worldwide. In combination with conventional protocols for smoking cessation, e-cigarettes have been proposed as a useful tool to quit smoking. Advertised as almost free of toxic effects, e-cigarettes have rapidly increased their popularity, becoming a sought-after device, especially among young people. Recently some health concerns about e-cigarette consumption are being raised. It is well known that they can release several toxic compounds, some of which are carcinogenic to humans, and emerging results are now outlining the risks related to the onset of respiratory and cardiovascular diseases and even cancer. The present review shows the emerging evidence about the role of technical components of the devices, the e-liquid composition as well as customization by consumers. The primary topics we discuss are the main toxicological aspects associated with e-cigarette consumption, focusing on the molecular pathways involved. Here it will be shown how exposure to e-cigarette aerosol induces stress/mitochondrial toxicity, DNA breaks/fragmentation following the same pathological pathways triggered by tobacco smoke, including the deregulation of molecular signalling axis associated with cancer progression and cell migration. Risk to fertility and pregnancy, as well as cardiovascular risk associated with e-cigarette use, have also been reported.This work was supported by a grant from the Italian Ministry of Education, University and Research. S.G., PhD fellowship grants were awarded from the Italian Ministry of Education, University and Research. L.R. and F.V. postdoctoral fellowship grant was cofounded by D.C., M.P., S.C., and P.R.; I.C-C. was supported by a postdoctoral fellowship from the Andalusian Government Ministry of Economy, Knowledge, Business, and University (DOC_00587/2020).Peer reviewe

    Measurement of RyR permeability reveals a role of calsequestrin in termination of SR Ca2+ release in skeletal muscle

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    The mechanisms that terminate Ca2+ release from the sarcoplasmic reticulum are not fully understood. D4cpv-Casq1 (Sztretye et al. 2011. J. Gen. Physiol. doi:10.1085/jgp.201010591) was used in mouse skeletal muscle cells under voltage clamp to measure free Ca2+ concentration inside the sarcoplasmic reticulum (SR), [Ca2+]SR, simultaneously with that in the cytosol, [Ca2+]c, during the response to long-lasting depolarization of the plasma membrane. The ratio of Ca2+ release flux (derived from [Ca2+]c(t)) over the gradient that drives it (essentially equal to [Ca2+]SR) provided directly, for the first time, a dynamic measure of the permeability to Ca2+ of the releasing SR membrane. During maximal depolarization, flux rapidly rises to a peak and then decays. Before 0.5 s, [Ca2+]SR stabilized at ∼35% of its resting level; depletion was therefore incomplete. By 0.4 s of depolarization, the measured permeability decayed to ∼10% of maximum, indicating ryanodine receptor channel closure. Inactivation of the t tubule voltage sensor was immeasurably small by this time and thus not a significant factor in channel closure. In cells of mice null for Casq1, permeability did not decrease in the same way, indicating that calsequestrin (Casq) is essential in the mechanism of channel closure and termination of Ca2+ release. The absence of this mechanism explains why the total amount of calcium releasable by depolarization is not greatly reduced in Casq-null muscle (Royer et al. 2010. J. Gen. Physiol. doi:10.1085/jgp.201010454). When the fast buffer BAPTA was introduced in the cytosol, release flux became more intense, and the SR emptied earlier. The consequent reduction in permeability accelerated as well, reaching comparable decay at earlier times but comparable levels of depletion. This observation indicates that [Ca2+]SR, sensed by Casq and transmitted to the channels presumably via connecting proteins, is determinant to cause the closure that terminates Ca2+ release

    Paradoxical buffering of calcium by calsequestrin demonstrated for the calcium store of skeletal muscle

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    Contractile activation in striated muscles requires a Ca2+ reservoir of large capacity inside the sarcoplasmic reticulum (SR), presumably the protein calsequestrin. The buffering power of calsequestrin in vitro has a paradoxical dependence on [Ca2+] that should be valuable for function. Here, we demonstrate that this dependence is present in living cells. Ca2+ signals elicited by membrane depolarization under voltage clamp were compared in single skeletal fibers of wild-type (WT) and double (d) Casq-null mice, which lack both calsequestrin isoforms. In nulls, Ca2+ release started normally, but the store depleted much more rapidly than in the WT. This deficit was reflected in the evolution of SR evacuability, E, which is directly proportional to SR Ca2+ permeability and inversely to its Ca2+ buffering power, B. In WT mice E starts low and increases progressively as the SR is depleted. In dCasq-nulls, E started high and decreased upon Ca2+ depletion. An elevated E in nulls is consistent with the decrease in B expected upon deletion of calsequestrin. The different value and time course of E in cells without calsequestrin indicate that the normal evolution of E reflects loss of B upon SR Ca2+ depletion. Decrement of B upon SR depletion was supported further. When SR calcium was reduced by exposure to low extracellular [Ca2+], release kinetics in the WT became similar to that in the dCasq-null. E became much higher, similar to that of null cells. These results indicate that calsequestrin not only stores Ca2+, but also varies its affinity in ways that progressively increase the ability of the store to deliver Ca2+ as it becomes depleted, a novel feedback mechanism of potentially valuable functional implications. The study revealed a surprisingly modest loss of Ca2+ storage capacity in null cells, which may reflect concurrent changes, rather than detract from the physiological importance of calsequestrin
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