32 research outputs found

    The Role of Oxidative Stress and Lipid Peroxidation in Ventricular Remodeling Induced by Tobacco Smoke Exposure after Myocardial Infarction

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    OBJECTIVE: To evaluate the roles of oxidative stress and lipid peroxidation in the ventricular remodeling that is induced by tobacco smoke exposure after myocardial infarction.METHODS: After induced myocardial infarction, rats were allocated into two groups: C (control, n=25) and ETS (exposed to tobacco smoke, n=24). After 6 months, survivors were submitted to echocardiogram and biochemical analyses.RESULTS: Rats in the ETS group showed higher diastolic (C = 1.52 +/- 0.4 mm(2), ETS = 1.95 +/- 0.4 mm(2); p=0.032) and systolic (C = 1.03 +/- 0.3, ETS = 1.36 +/- 0.4 mm(2)/g; p=0.049) ventricular areas, adjusted for body weight. The fractional area change was smaller in the ETS group (C = 30.3 +/- 10.1 %, ETS = 19.2 +/- 11.1 %; p=0.024) and E/A ratios were higher in ETS animals (C = 2.3 +/- 2.2, ETS = 5.1 +/- 2.5; p=0.037). ETS was also associated with a higher water percentage in the lung (C = 4.8 (4.3-4.8), ETS = 5.5 (5.3-5.6); p=0.013) as well as higher cardiac levels of reduced glutathione (C = 20.7 +/- 7.6 nmol/mg of protein, ETS = 40.7 +/- 12.7 nmol/mg of protein; p=0.037) and oxidized glutathione (C = 0.3 +/- 0.1 nmol/g of protein, ETS = 0.9 +/- 0.3 nmol/g of protein; p=0.008). No differences were observed in lipid hydroperoxide levels (C = 0.4 +/- 0.2 nmol/mg of tissue, ETS = 0.1 +/- 0.1 nmol/mg of tissue; p=0.08).CONCLUSION: In animals exposed to tobacco smoke, oxidative stress is associated with the intensification of ventricular re-remodeling after myocardial infarction

    Effect of pruning strategy on 'Syrah' bud necrosis and fruitfulness in Brazilian subtropical Southeast

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    The change of wine grape harvest from wet season (summer) to dry season (winter) by changing the pruning management has improved quality of wines produced in the Brazilian Southeast. However, the vines need to be spur pruned twice a year, i.e. with a 1st pruning in August (winter pruning) for a vegetative cycle during the hot and wet summer, and a 2nd pruning in January (summer pruning) for a productive cycle during the cold and dry season. This double pruning strategy is made necessary by the fact that latent buds developed during the dry season cycle are not fruitful to support a productive cycle in the following year. This histological study, performed in the South of Minas Gerais State (Brazil), showed that annual single pruning done in the wet season (in January) displayed a high rate of necrosis on primary and secondary buds (bud necrosis – BN). In April, 99 days after summer pruning (DASP), the rates of BN were 40 % and 50 % at basal and apical node positions, respectively, reaching 80 % of BN in December (322 DASP). As a consequence of BN, bud potential fertility was drastically reduced from 0.5 inflorescence primordial (IP) per bud (in July) to 0.06 (in December) and bud burst in the next cycle from secondary and tertiary bud axes. Vines managed by double pruning system (submitted to summer and winter pruning) displayed a much higher fruitfulness potential, i.e. 1.46 IP per bud in December (112 days after winter pruning) and limited BN occurrence (20 %). On single pruned vines, we also observed a significant decrease of starch content in canes, trunks and roots. Internal bud anatomy showed that a random cell breakdown started 70 days DASP. At 211 DASP, all buds showed a large starch granule concentration, raphides and crystals of calcium oxalate inside idioblasts of leaf primordia and also in cortical parenchyma of the vegetative axis. The bud starch content was increased and a positive correlation between necrosis and starch accumulation was observed. The impact of carbohydrate availability on bud necrosis development was discussed. This study showed that the necrosis development towards secondary and tertiary axis of the dry season buds is the main reason of unfruitfulness in the vineyards managed by single pruning in the wet season, making the double pruning compulsory

    A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

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    Low Dose Rate Radiosensitization of Hepatocellular Carcinoma In Vitro and in Patients

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    Transarterial radioembolization (TARE) with 90Y microspheres delivers low dose rate radiation (LDR) to intrahepatic tumors. In the current study, we examined clonogenic survival, DNA damage, and cell cycle distribution in hepatocellular carcinoma (HCC) cell lines treated with LDR in combination with varying doses and schedules of 5-fluorouracil (5-FU), gemcitabine, and sorafenib. Radiosensitization was seen with 1 to 3 μM 5-FU (enhancement ratio 2.2–13.9) and 30 to 100 nM gemcitabine (enhancement ratio 1.9–2.9) administered 24 hours before LDR (0.26 Gy/h to 4.2 Gy). Sorafenib radiosensitized only at high concentrations (3–10 μM) when administered after LDR. For a given radiation dose, greater enhancement was seen with LDR compared to standard dose rate therapy. Summarizing our clinical experience with low dose rate radiosensitization, 13 patients (5 with HCC, 8 with liver metastases) were treated a total of 16 times with TARE and concurrent gemcitabine. Six partial responses and one complete response were observed with a median time to local failure of 7.1 months for all patients and 9.9 months for patients with HCC. In summary, HCC is sensitized to LDR with clinically achievable concentrations of gemcitabine and 5-FU in vitro. Encouraging responses were seen in a small cohort of patients treated with TARE and concurrent gemcitabine. Future studies are needed to validate the safety and efficacy of this approach

    Fractionated ionizing radiation exposure induces apoptosis through caspase-3 activation and reactive oxygen species generation

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    Background: Radiation therapy (RT) is a well established therapeutic modality for the treatment of solid tumors. In particular, post-operative RT is considered the standard treatment adjuvant to surgery since its ability to prolong median survival of patients with malignant astrocytoma has been shown; nevertheless the ionizing radiation (IR) treatment fails in a considerable number of astrocytoma patients. Materials and Methods: Using an ADF human astrocytoma cell line the molecular mechanisms involved in the DNA damage induced by fractionated irradiation (FIR) and single IR treatment have been investigated. Results: FIR and single IR treatment inhibited the growth of the ADF human astrocytoma cell line. FACS analysis revealed that FIR treatment, but not single IR treatment, induced growth inhibition associated with the induction of apoptosis. Apoptosis was related to caspase-3 activation and reactive oxygen species (ROS) generation. ROS formation depends on the up-regulation of the cytochrome P450 enzyme gene. On the contrary, 12.5 Gy induced necrotic cell death up-regulating the HSPD1, HSPCB, HSPCA and HSPB1 genes. Conclusion: FIR treatment induced cell death through caspase-3 and ROS-mediated apoptosis
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