5 resultados para volume I

em Biblioteca Digital da Produção Intelectual da Universidade de São Paulo


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Barroso, R, Tricoli, V, dos Santos Gil, S, Ugrinowitsch, C, and Roschel, H. Maximal strength, number of repetitions, and total volume are differently affected by static-, ballistic-, and proprioceptive neuromuscular facilitation stretching. J Strength Cond Res 26(9): 2432-2437, 2012-Stretching exercises have been traditionally incorporated into warm-up routines before training sessions and sport events. However, the effects of stretching on maximal strength and strength endurance performance seem to depend on the type of stretching employed. The objective of this study was to compare the effects of static stretching (SS), ballistic stretching (BS), and proprioceptive neuromuscular facilitation (PNF) stretching on maximal strength, number of repetitions at a submaximal load, and total volume (i.e., number of repetitions 3 external load) in a multiple-set resistance training bout. Twelve strength-trained men (20.4 +/- 4.5 years, 67.9 +/- 6.3 kg, 173.3 +/- 8.5 cm) volunteered to participate in this study. All of the subjects completed 8 experimental sessions. Four experimental sessions were designed to test maximal strength in the leg press (i.e., 1 repetition maximum [1RM]) after each stretching condition (SS, BS, PNF, or no-stretching [NS]). During the other 4 sessions, the number of repetitions performed at 80% 1RM was assessed after each stretching condition. All of the stretching protocols significantly improved the range of motion in the sit-and-reach test when compared with NS. Further, PNF induced greater changes in the sit-and-reach test than BS did (4.7 +/- 1.6, 2.9 +/- 1.5, and 1.9 +/- 1.4 cm for PNF, SS, and BS, respectively). Leg press 1RM values were decreased only after the PNF condition (5.5%, p < 0.001). All the stretching protocols significantly reduced the number of repetitions (SS: 20.8%, p < 0.001; BS: 17.8%, p = 0.01; PNF: 22.7%, p < 0.001) and total volume (SS: 20.4%, p < 0.001; BS: 17.9%, p = 0.01; PNF: 22.4%, p < 0.001) when compared with NS. The results from this study suggest that, to avoid a decrease in both the number of repetitions and total volume, stretching exercises should not be performed before a resistance training session. Additionally, strength-trained individuals may experience reduced maximal dynamic strength after PNF stretching.

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Purpose: The aim of this study was to evaluate the accuracy of cone-beam computed tomography (CBCT) for measuring the buccal bone volume around dental implants. Materials and methods: Three to six implants were inserted into the anterior maxilla of eight skulls, depending on the availability of bone, and after this, the CBCT was performed. By means of CBCT image, measurements of the bone wall at three points of the implant were obtained, analyzed and compared with those obtained in the plaster skull casting. Results: The results showed that for the three points of the implants, no statistically significant difference in the measurements was obtained from the plaster model and CBCT images. Conclusions: CBCT can be a useful tool for assessing buccal bone volume along the implant. To cite this article:?Shiratori LN, Marotti J, Yamanouchi J, Chilvarquer I, Contin I, Tortamano-Neto P. Measurement of buccal bone volume of dental implants by means of cone-beam computed tomography.?Clin. Oral Impl. Res. 23, 2012; 797804.?doi: 10.1111/j.1600-0501.2011.02207.x

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Objectives. The C-Factor has been used widely to rationalize the changes in shrinkage stress occurring at the tooth/resin-composite interfaces. Experimentally, such stresses have been measured in a uniaxial direction between opposed parallel walls. The situation of adjoining cavity walls has been neglected. The aim was to investigate the hypothesis that: within stylized model rectangular cavities of constant volume and wall thickness, the interfacial shrinkage-stress at the adjoining cavity walls increases steadily as the C-Factor increases. Methods. Eight 3D-FEM restored Class I 'rectangular cavity' models were created by MSC.PATRAN/MSC.Marc, r2-2005 and subjected to 1% of shrinkage, while maintaining constant both the volume (20 mm(3)) and the wall thickness (2 mm), but varying the C-Factor (1.9-13.5). An adhesive contact between the composite and the teeth was incorporated. Polymerization shrinkage was simulated by analogy with thermal contraction. Principal stresses and strains were calculated. Peak values of maximum principal (MP) and maximum shear (MS) stresses from the different walls were displayed graphically as a function of C-Factor. The stress-peak association with C-Factor was evaluated by the Pearson correlation between the stress peak and the C-Factor. Results. The hypothesis was rejected: there was no clear increase of stress-peaks with C-Factor. The stress-peaks particularly expressed as MP and MS varied only slightly with increasing C-Factor. Lower stress-peaks were present at the pulpal floor in comparison to the stress at the axial walls. In general, MP and MS were similar when the axial wall dimensions were similar. The Pearson coefficient only expressed associations for the maximum principal stress at the ZX wall and the Z axis. Significance. Increase of the C-Factor did not lead to increase of the calculated stress-peaks in model rectangular Class I cavity walls. (C) 2011 Academy of Dental Materials. Published by Elsevier Ltd. All rights reserved.

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1. The present study provides the first in vivo evidence that the cannabinoid CB1 receptor mediates the effects of dexamethasone on hormone release induced by changes in circulating volume and osmolality. Male adult rats were administered with the CB1 receptor antagonist rimonabant (10 mg/Kg, p.o.), followed or not in 1 hour by dexamethasone (1 mg/Kg, i.p.). Extracellular volume expansion (EVE, 2 mL/100 g of body weight, i.v.) was performed 2 hours after dexamethasone or vehicle treatment using either isotonic (I-EVE, 0.15 mol/L) or hypertonic (H-EVE, 0.30 mol/L) NaCl solution. Five minutes after EVE, animals were decapitated and trunk blood was collected for all plasma measurements. 2. Rimonabant potentiated oxytocin (OT) secretion induced by H-EVE and completely reversed the inhibitory effects of dexamethasone in response to the same stimulus. These data suggest that glucocorticoid modulation of OT release is mediated by the CB1 receptor. 3. Although dexamethasone did not affect vasopressin (AVP) secretion induced by H-EVE, the administration of rimonabant potentiated AVP release in response to the same stimulus, supporting the hypothesis that the CB1 receptor regulates AVP secretion independently of glucocorticoid-mediated signalling. 4. Dexamethasone alone did not affect atrial natriuretic peptide (ANP) release stimulated by I-EVE or H-EVE. However, pretreatment with rimonabant potentiated ANP secretion induced by H-EVE, suggesting a possible role for the CB1 receptor in the control of peripheral factors that modulate cardiovascular function. 5. Rimonabant also reversed the inhibitory effects of dexamethasone on H-EVE-induced corticosterone secretion, reinforcing the hypothesis that the CB1 receptor may be involved in the negative feedback exerted by glucocorticoids on the activity of the hypothalamicpituitaryadrenal axis. 6. Collectively, the results of the present study indicate that the CB1 receptor modulates neurohypophyseal hormone secretion and systemic factors, such as corticosterone and ANP, thus participating in homeostatic responses to altered extracellular volume and plasma tonicity.

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The acute direct action of angiotensin-(1-7) [ANG-(1-7)] on bicarbonate reabsorption (JHCO(3)(-)) was evaluated by stationary microperfusions on in vivo middle proximal tubules in rats using H ion-sensitive microelectrodes. The control JHCO(3)(-) is 2.82 ± 0.078 nmol·cm(-2)·s(-1) (50). ANG-(1-7) (10(-12) or 10(-9) M) in luminally perfused tubules decreases JHCO(3)(-) (36 or 60%, respectively), but ANG-(1-7) (10(-6) M) increases it (80%). A779 increases JHCO(3)(-) (30%) and prevents both the inhibitory and the stimulatory effects of ANG-(1-7) on it. S3226 decreases JHCO(3)(-) (45%) and changes the stimulatory effect of ANG-(1-7) to an inhibitory effect (30%) but does not affect the inhibitory effect of ANG-(1-7). Our results indicate that in the basal condition endogenous ANG-(1-7) inhibits JHCO(3)(-) and that the biphasic dose-dependent effect of ANG-(1-7) on JHCO(3)(-) is mediated by the Mas receptors via the Na(+)/H(+) exchanger 3 (NHE3). The control value of intracellular Ca(2+) concentration ([Ca(2+)](i)), as monitored using fura-2 AM, is 101 ± 2 nM (6), and ANG-(1-7) (10(-12), 10(-9), or 10(-6)M) transiently (3 min) increases it (by 151, 102, or 52%, respectively). A779 increases the [Ca(2+)](i) (25%) but impairs the stimulatory effect of all doses of ANG-(1-7) on it. The use of BAPTA or thapsigargin suggests a correlation between the ANG-(1-7) dose-dependent effects on [Ca(2+)](i) and JHCO(3)(-). Therefore, the interaction of the opposing dose-dependent effects of ANG II and ANG-(1-7) on [Ca(2+)](i) and JHCO(3)(-) may represent an physiological regulatory mechanism of extracellular volume and/or pH changes. However, whether [Ca(2+)](i) modification is an important direct mechanism for NHE3 activation by these peptides or is a side effect of other signaling pathways will require additional studies.