Hypoxic-preconditioning induces neuroprotection against hypoxia-ischemia in newborn piglet brain

Preconditioning-induced ischemic tolerance has been documented in the newborn brain, however, the signaling mechanisms of this preconditioning require further elucidation. The aims of this study were to develop a hypoxic-preconditioning (PC) model of ischemic tolerance in the newborn piglet, which emulates important clinical similarities to human situation of birth asphyxia, and to characterize some of the molecular mechanisms shown to be implicated in PC-induced neuroprotection in rodent models. One day old piglets were subjected to PC (8% O(2)/92% N(2)) for 3 h and 24 h later were exposed to hypoxia-ischemia (HI) produced by a combination of hypoxia (5% FiO(2)) for a period of 30 min and ischemia induced by a period of hypotension (10 min of reduced mean arterial blood pressure; 70% of baseline). Neuropathologic analysis and unbiased stereology, conducted at 24 h, 3 and 7 days of recovery following HI, indicated a substantial reduction in the severity of brain damage in PC piglets compared to non-PC piglets (P<0.05). PC significantly increased the mRNA expression of hypoxia-inducible factor-1 alpha (HIF-1 alpha) and its target gene, vascular endothelial growth factor (VEGF) at 0 h, 6 h, 24 h, 3 and 7 days of recovery. Immunoblot analysis demonstrated that PC resulted in HIF-1 alpha protein stabilization and accumulation in nuclear extracts of cerebral cortex of newborn piglet brain compared to normoxic controls. Protein levels of VEGF increased in a time-dependent manner in both cortex and hippocampus following PC. Double-immunolabeling indicated that VEGF is mainly expressed in neurons, endothelial cells and astroglia. Our study demonstrates for the first time the protective efficacy of PC against hypoxic-ischemic injury in newborn piglet model, which recapitulates many pathophysiological features of asphyxiated human neonates. Furthermore, as has been shown in rodent models of preconditioning, our results suggest that PC-induced protection in neonatal piglets may involve upregulation of VEGF. (C) 2011 Elsevier B.V. All rights reserved.

Hypoxia Enhances the Angiogenic Potential of Human Dental Pulp Cells

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Intermittent Therapy with 1,25 Vitamin D and Calcitonin Prevents Cyclosporin-Induced Alveolar Bone Loss in Rats

Bone loss associated with cyclosporin A (CsA) therapy can result in serious morbidity to patients. Intermittent administration of 1,25 Vitamin D and calcitonin reduces osteopenia in a murine model of postmenopausal osteoporosis. The purpose of this study was to evaluate the effects of this therapeutic approach on CsA-induced alveolar bone loss in rats. Forty male Wistar rats were allocated to four experimental groups according to the treatment received during 8 weeks: (1) CsA (10 mg/kg/day, s.c.); (2) 1,25 Vitamin D (2 mu g/kg, p.o.; in weeks 1, 3, 5, and 7) plus calcitonin (2 mu g/kg, i.p.; in weeks 2, 4, 6, and 8); (3) CsA concurrently with intermittent 1,25 Vitamin D and calcitonin administration; and (4) the control treatment group (vehicle). At the end of the 8-week treatment period, serum concentrations of bone-specific alkaline phosphatase, tartrate-resistant acid phosphatase (TRAP-5b), osteocalcin, interleukin (IL)-1 beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) were measured and an analysis of bone volume, bone surface, number of osteoblasts, and osteoclasts was performed. CsA administration resulted in significant alveolar bone resorption, as assessed by a lower bone volume and an increased number of osteoclasts, and increased serum bone-specific alkaline phosphatase, TRAP-5b, IL-1 beta, IL-6, and TNF-alpha concentrations. The intermittent administration of calcitriol and calcitonin prevented the CsA-induced osteopenic changes and the increased serum concentrations of TRAP-5b and inflammatory cytokines. Intermittent calcitriol/calcitonin therapy prevents CsA-induced alveolar bone loss in rats and normalizes the production of associated inflammatory mediators.

PHYSIOLOGICAL and PERCEIVED EXERTION RESPONSES AT INTERMITTENT CRITICAL POWER and INTERMITTENT MAXIMAL LACTATE STEADY STATE

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

The rating of perceived exertion predicts intermittent vertical jump demand and performance

The aims of this study were (a) to assess the ability of the rating of perceived exertion (RPE) to predict performance (i.e. number of vertical jumps performed to a fixed jump height) of an intermittent vertical jump exercise, and (b) to determine the ability of RPE to describe the physiological demand of such exercise. Eight healthy men performed intermittent vertical jumps with rest periods of 4, 5, and 6s until fatigue. Heart rate and RPE were recorded every five jumps throughout the sessions. The number of vertical jumps performed was also recorded. Random coefficient growth curve analysis identified relationships between the number of vertical jumps and both RPE and heart rate for which there were similar slopes. In addition, there were no differences between individual slopes and the mean slope for either RPE or heart rate. Moreover, RPE and number of jumps were highly correlated throughout all sessions (r=0.97-0.99; P0.001), as were RPE and heart rate (r=0.93-0.97; P0.001). The findings suggest that RPE can both predict the performance of intermittent vertical jump exercise and describe the physiological demands of such exercise.

Evaluation of an Innovative Critical Power Model in Intermittent Vertical Jump

The aim of this study was to test if the critical power model can be used to determine the critical rest interval (CRI) between vertical jumps. Ten males performed intermittent countermovement jumps on a force platform with different resting periods (4.1 +/- 0.3 s, 5.0 +/- 0.4 s, 5.9 +/- 0.6 s). Jump trials were interrupted when participants could no longer maintain 95% of their maximal jump height. After interruption, number of jumps, total exercise duration and total external work were computed. Time to exhaustion (s) and total external work (J) were used to solve the equation Work = a + b . time. The CRI (corresponding to the shortest resting interval that allowed jump height to be maintained for a long time without fatigue) was determined dividing the average external work needed to jump at a fixed height (J) by b parameter (J/s). in the final session, participants jumped at their calculated CRI. A high coefficient of determination (0.995 +/- 0.007) and the CRI (7.5 +/- 1.6 s) were obtained. In addition, the longer the resting period, the greater the number of jumps (44 13, 71 28, 105 30, 169 53 jumps; p<0.0001), time to exhaustion (179 +/- 50, 351 +/- 120, 610 +/- 141, 1,282 +/- 417 s; p<0.0001) and total external work (28.0 +/- 8.3, 45.0 +/- 16.6, 67.6 +/- 17.8, 111.9 +/- 34.6 kJ; p<0.0001). Therefore, the critical power model may be an alternative approach to determine the CRI during intermittent vertical jumps.

Does muscle imbalance affect fatigue after soccer specific intermittent protocol?

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Muscle protein metabolism in neonatal alloxan-administered rats: effects of continuous and intermittent swimming training

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cardiorespiratory responses to hypoxia in the African catfish, Clarias gariepinus (Burchell 1822), an air-breathing fish

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Role of central nitric oxide in behavioral thermoregulation of toads during hypoxia

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Fracture resistance of endodontically treated teeth with different heights of crown ferrule restored with prefabricated carbon fiber post and composite resin core by intermittent loading

This study evaluated the fracture resistance of endodontically treated teeth restored with prefabricated carbon fiber posts and varying quantities of coronal dentin. Sixty freshly extracted upper canines were randomly divided into groups of 10 teeth each. The specimens were exposed to 250,000 cycles in a controlled chewing simulator. All intact specimens were subjected to a static load (N) in a universal testing machine at 45 degrees to the long axis. Data were analyzed by 1-way analysis of variance and Tukey test (alpha = .05). Significant differences (P < .001) were found among the mean fracture forces of the test groups (positive control, 0 mm, 1 mm, 2 mm, 3 mm, and negative control groups: 1022.82 N, 1008.22 N, 1292.52 N, 1289.19 N, 1255.38 N, and 1582.11, respectively). These results suggested that the amount of coronal dentin did not significantly increase the fracture resistance of endodontically treated teeth restored with prefabricated carbon fiber post and composite resin core. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;106:e52-e57)

The role of branchial and orobranchial O-2 chemoreceptors in the control of aquatic surface respiration in the neotropical fish tambaqui (Colossoma macropomum): progressive responses to prolonged hypoxia

The present study examined the role of branchial and orobranchial O-2 chemoreceptors in the cardiorespiratory responses, aquatic surface respiration (ASR), and the development of inferior lip swelling in tambaqui during prolonged (6 h) exposure to hypoxia. Intact fish (control) and three groups of denervated fish (bilateral denervation of cranial nerves IX+X (to the gills), of cranial nerves V+VII (to the orobranchial cavity) or of cranial nerves V alone), were exposed to severe hypoxia (Pw(O2) = 10 mmHg) for 360 min. Respiratory frequency (fR) and heart rate (fH) were recorded simultaneously with ASR. Intact (control) fish increased fR, ventilation amplitude (V-AMP) and developed hypoxic bradycardia in the first 60 min of hypoxia. The bradycardia, however, abated progressively and had returned to normoxic levels by the last hour of exposure to hypoxia. The changes in respiratory frequency and the hypoxic bradycardia were eliminated by denervation of cranial nerves IX and X but were not affected by denervation of cranial nerves V or V+VII. The VAMP was not abolished by the various denervation protocols. The fH in fish with denervation of cranial nerves V or V+VII, however, did not recover to control values as in intact fish. After 360 min of exposure to hypoxia only the intact and IX+X denervated fish performed ASR. Denervation of cranial nerve V abolished the ASR behavior. However, all (control and denervated (IX+X, V and V+VII) fish developed inferior lip swelling. These results indicate that ASR is triggered by O-2 chemoreceptors innervated by cranial nerve V but that other mechanisms, such as a direct effect of hypoxia on the lip tissue, trigger lip swelling.