High-intensity exercise training induces morphological and biochemical changes in skeletal muscle

Skeletal muscle shows an elevated plasticity and can adapt its metabolic and contractile properties in response to a variety of stimuli such as physical exercise. This implies a series of biochemical and morphological changes in the recruited muscle, in order to produce the more appropriate functional response dependent on the specific stimulation. To determine the effective role of physical exercise in the muscle plasticity, in the present study we investigated the effect of two different exercise protocols on fiber composition and metabolism of two specific muscles of mice: the quadriceps -a fast-twitch muscle- and the gastrocnemius -a typical slow-twitch muscle. Mice were run daily on a motorized treadmill for 8 weeks, at a velocity corresponding to 60% (low-intensity exercise) or 90% (high-intensity exercise) of the maximal running velocity previously determined by an incremental exercise test. We found that at the end of training the body weight was significantly increased in highintensity exercise mice (18.2 ± 1.4 %) compared to low-intensity exercise (8.7 ± 0.6 %) and control (12.7 ± 0.5 %) groups, and it was lesser in low-intensity exercise mice compared to controls. In contrast, the food intake of both exercise training mice was greater compared to control group. Whereas low-intensity exercise mice, despite consumed significantly more food compared to control mice, increased the weight lesser, the weight increase of high-intensity exercise mice, that consumed significantly more food compared to other experimental groups, was significantly greater. These effects were accompanied by a progressive reduction in blood lactate levels at the end of training in both the exercised mice compared with controls; in particular, blood lactate levels after highintensity exercise were significantly lower than those measured in low-intensity exercise mice. Moreover, in the present study we demonstrated that high-intensity exercise training produced a significant increase in the expression of mitochondrial complex enzymes (significant for the enzymes corresponding to the Complex IV, II and I of mitochondrial chain) both in gastrocnemius and quadriceps muscle, compared with controls. These changes were associated with an increase in the amount of slow fibers in both these muscle of high-intensity exercise mice. No changing in the expression of mitochondrial enzymes and in the percentage of slow fibers were found in low-intensity exercise mice

Suramin inhibits bFGF-induced endothelial cell proliferation and angiogenesis in the chick chorioallantoic membrane

The effects of suramin, an inhibitor of growth factor mitogenic activity, were evaluated on basic fibroblast growth factor (bFGF)-induced proliferation of bovine aortic endothelial cells and on angiogenesis in the chorioallantoic membrane (CAM) of chick embryos. The role of bFGF gene expression in endothelial cell growth was also investigated by using an antisense oligodeoxynucleotide to bFGF. The 4-fold increase in [3H]-thymidine uptake in endothelial cells in vitro upon stimulation with 10 ng ml-1 of bFGF was inhibited by suramin 300 micrograms ml-1. bFGF antisense oligomer (10 microM) reduced [3H]-thymidine incorporation in exponentially growing cells by 76%; this effect was reversed by bFGF 10 ng ml-1. In the CAM of chick embryos suramin 50 micrograms was a more potent inhibitor of angiogenesis than the combination of heparin 60 micrograms/hydrocortisone 50 micrograms; the mean value of the area with reduced vascularity was significantly larger in suramin-treated CAMs (2.4 cm2) than in heparin/hydrocortisone (0.6 cm2), while the reduction of vascular density was similar (- 35 and - 29% compared to controls, respectively), In conclusion, the effects of treatments with bFGF and bFGF antisense oligomer demonstrate that bFGF plays a relevant role in endothelial cell proliferation and may be the target of suramin since the drug is able to suppress basal and bFGF-induced endothelial cell growth; in addition to this, suramin is a more potent angiogenesis inhibitor in the CAM than the combination of heparin/hydrocortisone

DNA damage associated with ultrastructural alterations in rat myocardium after loud noise exposure.

Noise exposure causes changes at different levels in human organs, particularly the cardiovascular system, where it is responsible for increasing heart rate, peripheral vascular resistance, and blood pressure. In this study, we evaluated the effect of noise exposure on DNA integrity and ultrastructure of rat cardiomyocytes. The exposure to loud noise (100 dBA) for 12 hr caused a significant increase of DNA damage, accompanied by swelling of mitochondrial membranes, dilution of the matrix, and cristolysis. These alterations were concomitant with increased in situ noradrenaline levels and utilization. Genetic and ultrastructural alterations did not decrease 24 hr after the cessation of the stimulus. An elevated oxyradical generation, possibly related to altered sympathetic innervation, is hypothesized as responsible for the induction and persistence of noise-induced cellular damage

Using instruments in the study of animate beings:Della Porta’s and Bacon’s experiments with plants

In this paper, I explain Francis Bacon's use of plants as philosophical instruments in the context of his Historia vitae et mortis. My main claim is that Bacon experimented with plants in order to obtain knowledge about the hidden processes of nature, knowledge that could be transferred to the human case and used for the prolongation of life. Bacon's experiments were based on Giambattista della Porta's reports from the Magia naturalis, but I show how a different metaphysics and research method made Bacon systematically rework, reconceptualise, and put to divergent uses the results of the same experimental reports

Interaction between cannabis consumption and childhood abuse in psychotic disorders:preliminary findings on the role of different patterns of cannabis use

Aim: Several studies have suggested that lifetime cannabis consumption and childhood abuse synergistically contribute to the risk for psychotic disorders. This study aimed to extend existing findings regarding an additive interaction between childhood abuse and lifetime cannabis use by investigating the moderating role of type and frequency of cannabis use. Methods: Up to 231 individuals presenting for the first time to mental health services with psychotic disorders and 214 unaffected population controls from South London, United Kingdom, were recruited as part of the Genetics and Psychosis study. Information about history of cannabis use was collected using the Cannabis Experiences Questionnaire. Childhood physical and sexual abuse was assessed using the Childhood Experience of Care and Abuse Questionnaire. Results: Neither lifetime cannabis use nor reported exposure to childhood abuse was associated with psychotic disorder when the other environmental variable was taken into account. Although the combination of the two risk factors raised the odds for psychosis by nearly three times (adjusted OR = 2.94, 95% CI: 1.44–6.02, P = 0.003), no evidence of interaction was found (adjusted OR = 1.46, 95% CI: −0.54 to 3.46, P = 0.152). Furthermore, the association of high-potency cannabis and daily consumption with psychosis was at least partially independent of the effect of childhood abuse. Conclusions: The heavy use of high-potency cannabis increases the risk of psychosis but, in addition, smoking of traditional resin (hash) and less than daily cannabis use may increase the risk for psychosis when combined with exposure to severe childhood abuse.</p