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The influence of physical activity in the progression of experimental lung cancer in mice
- PMID: 22683274
- DOI: 10.1016/j.prp.2012.04.006
GRUPO_AF1 – GROUP AFA1 – Aerobic Physical Activity – Atividade Física Aeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
GRUPO AFAN 1 – GROUP AFAN1 – Anaerobic Physical Activity – Atividade Física Anaeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
GRUPO_AF2 – GROUP AFA2 – Aerobic Physical Activity – Atividade Física Aeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
GRUPO AFAN 2 – GROUP AFAN 2 – Anaerobic Physical Activity – Atividade Física Anaeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
Slides – mestrado – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
DMBA CARCINOGEN IN EXPERIMENTAL MODELS
Avaliação da influência da atividade física aeróbia e anaeróbia na progressão do câncer de pulmão experimental – Summary – Resumo – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto
Lung cancer is one of the most incident neoplasms in the world, representing the main cause of mortality for cancer. Many epidemiologic studies have suggested that physical activity may reduce the risk of lung cancer, other works evaluate the effectiveness of the use of the physical activity in the suppression, remission and reduction of the recurrence of tumors. The aim of this study was to evaluate the effects of aerobic and anaerobic physical activity in the development and the progression of lung cancer. Lung tumors were induced with a dose of 3mg of urethane/kg, in 67 male Balb – C type mice, divided in three groups: group 1_24 mice treated with urethane and without physical activity; group 2_25 mice with urethane and subjected to aerobic swimming free exercise; group 3_18 mice with urethane, subjected to anaerobic swimming exercise with gradual loading 5-20% of body weight. All the animals were sacrificed after 20 weeks, and lung lesions were analyzed. The median number of lesions (nodules and hyperplasia) was 3.0 for group 1, 2.0 for group 2 and 1.5-3 (p=0.052). When comparing only the presence or absence of lesion, there was a decrease in the number of lesions in group 3 as compared with group 1 (p=0.03) but not in relation to group 2. There were no metastases or other changes in other organs. The anaerobic physical activity, but not aerobic, diminishes the incidence of experimental lung tumors.
Copyright © 2012 Elsevier GmbH. All rights reserved.
Moderate- and Low-Dose of Atorvastatin Alleviate Cognition Impairment Induced by High-Fat Diet via Sirt1 Activation.
- Department of Neurology, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China.
- Department of Neurology, East Hospital, Tongji University School of Medicine, Shanghai, 200120, China. firstname.lastname@example.org.
Mounting evidences have demonstrated that diet-induced obesity is associated with cognition impairment via increasing oxidative stress and inflammation in the brain. Atorvastatin (Ator, a HMG-CoA reductase inhibitor) is a cholesterol lowering drug. Studies have reported that Ator can ameliorate the development and progression of cognition impairment. Additionally, silent information regulator 1 (SIRT1) has been demonstrated to be beneficial in cognition impairment. However, the interaction between Ator and SIRT1 activation for cognition impairment remains unclear. This study aimed to identify a relationship between the use of Ator and cognition impairment induced by high-fat diet via Sirt1 activation. A total of 60 healthy male C57BL/6J mice were purchased and then divided into 6 groups, including normal diet group (control), a high-fat diet group (40%HFD, 40% energy from fat), a model group (60%HFD, 60% energy from fat), and model group treated with different doses of Ator (high-dose (80 mg), moderate-dose (40 mg), and low-dose (20 mg) groups). All interventions took place for 7 months. Metabolic phenotypes were characterized for body weight and analysis of serum lipid level. The level of cognition development was examined by Morris water maze (MWM) approach and novel object recognition test (NORT); besides, the expression of Creb1, Gap-43, BDNF, CaMKII, and ERKs of frontal cortex and hippocampus was determined by reverse transcription polymerase chain reaction (RT-PCR). Then, the levels of factors related to inflammation (TNF-a, IL-1β, HMGB1 and IL-6) and oxidation stress (SOD, MDA, CAT and GSH-Px) were assessed using commercially available kits. Finally, SIRT1 and its downstream molecules (Ac-FoxO1, Ac-p53, Ac-NF-κB, Bcl-2 and Bax) were evaluated by Western blot analysis. Compared with the 60% HFD group, body weight and serum lipid levels were significantly decreased in the Ator treated groups. The results of MWM and NORT, as well as the levels of Creb1, Gap-43, BDNF, CaMKII, and ERKs were markedly reversed in the moderate- and low-dose of Ator treated groups. Meanwhile, the expression of IL-1β, TNF-a, IL-6, HMGB1, and MDA was notably decreased, whereas the activity of SOD, CAT, and GSH-Px was increased. It was also revealed that the expression of SIRT1 was remarkably unregulated, the level of Bcl-2 was upregulated, and the content of Ac-FoxO1, Ac-p53, Ac-NF-κB, and Bax was downregulated in the moderate- and low-dose of Ator. Furthermore, results showed that the effect of moderate-dose of Ator was significantly greater than the low-dose of Ator. However, these effects were not observed in the high-dose of Ator. Our results showed that moderate- and low-dose of Ator can significantly attenuate cognition impairment induced by HFD through its antioxidant and anti-inflammatory functions related to SIRT1 activation.
Atorvastatin; Cognition impairment; Dosage; High-fat diet; SIRT1 activation