Physical exercise recommendations improve postural changes found in children and adolescents with cystic fibrosis: a randomized controlled trial.

OBJECTIVE: To evaluate postural changes and the distribution of plantar pressures in patients with cystic fibrosis (CF). We also sought to evaluate the effects of an educational guideline for physical activity on body posture in children and adolescents with CF. STUDY DESIGN: This was a 2-phase study of individuals between age 7 and 20 years. Phase I was a cross-sectional study in which healthy subjects were selected for postural evaluation and baropodometry, aiming to perform a later comparison with patients with CF. In phase II, we performed a randomized controlled clinical trial to assess the influence of the exercise guideline on the postural changes. Patients were assigned to 2 groups: control and intervention. The intervention consisted of a handbook with instructions for aerobic exercise and stretching. Main outcomes were postural abnormalities, plantar pressure distribution, and lung function. RESULTS: In phase I, 34 patients with CF and 34 healthy matched individuals were included. No significant baseline differences were identified. Children with CF presented more postural deviations compared with healthy subjects (P < .05), as to alignment of the head, shoulder girdle, and pelvis, increased cervical lordosis, and lateral chest distance. In phase II (n = 34), there were no baseline differences between groups. The intervention caused (P < .05) a decrease in cervical lordosis, thoracic kyphosis, lumbar lordosis, lateral chest distance, and abdominal protrusion, as well as in the baropodometric mean pressure and contact area. CONCLUSIONS: Children and adolescents with CF present postural changes when compared with healthy individuals. The educational guideline for exercise practice helped to improve posture, preventing the progression of some postural disorders.

Therapeutic ultrasound stimulates MC3T3-E1 cell proliferation through the activation of NF-κB1, p38α, and mTOR.

BACKGROUND AND OBJECTIVES: As the population ages, osteometabolic diseases and osteoporotic fractures emerge, resulting in substantial healthcare resource utilization and impaired quality of life. Many types of mechanical stimulation have the potential of being recognized by bone cells after a mechanical sign is transformed into a biological one (a process called mechanotransduction). The therapeutic ultrasound (TU) is one of several resources capable of promoting bone cell mechanical stimulation. Therefore, the main purpose of present study was to evaluate the effect of TU on the proliferation of pre-osteoblasts using in vitro bioassays. STUDY DESIGN/MATERIALS AND METHODS: We used MC3T3-E1 pre-osteoblast lineage cells kept in Alpha medium. Cells were treated using pulsed mode therapeutic ultrasound, with frequency of 1 MHz, intensity of 0.2 W/cm(2) (SATA), duty cycle of 20%, for 30 minutes. Nifedipine and rapamycin were used to further investigate the role of L-type Ca(2+) channels and mTOR pathway. Intracellular calcium, TGF-ß1, magnesium, and the mRNA levels of osteopontin, osteonectin, NF-κB1, p38α were evaluated. RESULTS: The results show that TU stimulates the growth of MC3T3-E1 cells and decreases the supernatant calcium and magnesium content. Also, it increases intracellular calcium, activates NF-κB1 and mTOR complex via p38α. Moreover, TU promoted a decrease in the TGF-ß1 synthesis, which is a cell growth inhibitor. CONCLUSIONS: Therapeutic ultrasound, with frequency of 1 MHz, intensity of 0.2 W/cm(2) (SATA) and pulsed mode, for 30 minutes, was able to increase the proliferation of preosteoblast-like bone cells. This effect was mediated by a calcium influx, with a consequent activation of the mTOR pathway, through increased NF-κB1 and p38α.

Anti-Inflammatory effects of low-level laser therapy (660 nm) in the early phase in carrageenan-induced pleurisy in rat.

BACKGROUND AND OBJECTIVE: In the classic model of pleurisy there is little evidence about the anti-inflammatory effects of low-level laser therapy (LLLT) as well the dosage characteristics, such as wavelength, total energy, number and pattern of treatment. In this study we investigated the potential effects of LLLT on modulating the pro-inflammatory and anti-inflammatory mediators of acute inflammation in a rat pleurisy model. STUDY DESIGN/MATERIALS AND METHODS: A sample of 48 female Wistar rats were divided into control and experiential groups. An inflammation was induced by carrageenan (0.2 ml) injected into the pleural cavity. At 1, 2, and 3 hours after induction a continuous wave (20 mW) diode laser of the InGaAlP (660 nm) type was used in the four laser groups with different doses and treatment patterns. One group received a single dose of 2.1 J and the other three groups received a total energy of 0.9, 2.1, and 4.2 J. Four hours later the exudate volume, total and differential leukocytes, protein concentration, NO, IL-6, IL-10, TNF-alpha, and MCP-1 were measured from the aspirated liquid. RESULTS: All the treatment patterns and quantity of energy studied show significant reduction of the exudate volume (P<0.05). Using energy of 0.9 J only NO, IL-6, MCP-1 and IL-10 are significantly reduced (P<0.05). On the other hand, higher energies (2.1 and 4.2 J) significantly reduce all variables independently of the treatment pattern. The neutrophil migration has a straight correlation with the TNF-alpha (r = 0.551) and NO (r = 0.549) concentration. CONCLUSIONS: LLLT-660 nm induced an anti-inflammatory effect characterized by inhibition of either total or differential leukocyte influx, exudation, total protein, NO, IL-6, MCP-1, IL-10, and TNF-alpha, in a dose-dependent manner. Under these conditions, laser treatment with 2.1 J was more effective than 0.9 and 4.2 J.

Biochemical and inflammatory aspects in patients with severe sepsis and septic shock: The predictive role of IL-18 in mortality.

BACKGROUND: Sepsis is a major health care problem, with a significant mortality rate in intensive care units. We evaluated biochemical and inflammatory markers in patients with severe sepsis and septic shock and its association of with mortality rates. METHODS: Critically ill patients with diagnoses of sepsis - severe sepsis group (n=23) and septic shock group (n=25), and a control group (n=17) were recruited within 24h of entry into the ICU. Serum levels of inflammatory mediators were measured (IL-1ß, IL-6, IL-8, IL-10, TNF-α, IL-18 and nitric oxide). We have also collected clinical parameters and laboratorial tests to estimate severity and organ dysfunction (APACHE II, SOFA, lactate). These results were compared between survivors and no survivors. RESULTS: IL-18 was directly related to mortality independently of other inflammatory mediators, especially IL-1ß, although the inflammatory pathway is closely linked to inflammasome activation and both have simultaneous release in the infectious process. Mortality was directly proportional to IL-18 plasma levels, which did not occur with other inflammatory mediators. CONCLUSIONS: IL-18 is an important predictor of mortality in humans with both severe sepsis and septic shock, independent of IL-1ß.

Immediate effects of chest physiotherapy on hemodynamic, metabolic, and oxidative stress parameters in subjects with septic shock.

BACKGROUND: Septic shock presents as a continuum of infectious events, generating tissue hypoxia and hypovolemia, and increased oxidative stress. Chest physiotherapy helps reduce secretion, improving dynamic and static compliance, as well as improving secretion clearance and preventing pulmonary complications. The purpose of this study was to evaluate the immediate effect of chest physiotherapy on hemodynamic, metabolic, inflammatory, and oxidative stress parameters in subjects in septic shock. METHODS: We conducted a quasi-experimental study in 30 subjects in septic shock, who underwent chest physiotherapy, without associated heart diseases and with vasopressors < 0.5 µg/kg/min. Venous and arterial blood gases, clinical and hemodynamic data, inflammatory data, lactate, and oxidative stress were evaluated before and 15 min after physiotherapy. RESULTS: Thirty subjects with a mean age of 61.8 ± 15.9 y and Sequential Organ Failure Assessment of 8 (range 6-10) were included. Chest physiotherapy caused a normalization of pH (P = .046) and P(aCO2) (P = .008); reduction of lactate (P = .001); and an increase in P(aO2) (P = .03), arterial oxygen saturation (P = .02), and P(aO2)/F(IO2) (P = .034), 15 min after it was applied. CONCLUSIONS: The results indicate that chest physiotherapy has immediate effects, improving oxygenation and reducing lactate and oxidative damage in subjects in septic shock. However, it does not cause alterations in the inflammatory and hemodynamic parameters.