Prevalence of hepatitis C virus infection in patients with COPD.

Some studies have suggested that chronic hepatitis C virus (HCV) infection may induce an accelerated decline of forced expiratory volume in 1 second (FEV(1)). We performed a cross-sectional study to determine the prevalence of HCV infection in a sample of chronic obstructive pulmonary disease (COPD) patients and in a control group of blood donors. The clinical characteristics of HCV-positive and HCV-negative patients were compared. Anti-HCV antibody was determined and confirmed by HCV-RNA. The prevalence of HCV infection in COPD patients was 7.5% (95% CI 6.52-8.48) and in blood donors was 0.41% (95% CI 0.40-0.42). The HCV-positive patients had a lower FEV(1) (34.7 +/- 8.6%) and a higher BODE index (median = 6) than HCV-negative patients (42.7 +/- 16.5%, median = 4, respectively) (P = 0.011 and 0.027, respectively). Our results suggest a high prevalence of chronic HCV infection in patients with COPD in comparison with the blood donors. HCV-positive patients have a more severe disease.

Oxidative stress in chronic obstructive pulmonary disease patients submitted to a rehabilitation program.

Pulmonary rehabilitation (PR) improves physical capacity and health quality in patients with chronic obstructive pulmonary disease (COPD). However, the effect of exercise on oxidative stress markers in COPD patients is only partially known. This study was designed to evaluate the oxidative stress response to long-term exercise in patients with COPD enrolled in a PR program. Fifteen COPD patients (FEV1 < 60%), age between 50 and 60 years, ex-smokers, were separated in two groups: exercise-trained (n=8) and sedentary group (n=7). Exercise consisted of an 8-week conditioning program using a cycle ergometer (three times a week, 1h session). An endurance test (60% of maximal load in an incremental cycle test) was performed before and after PR. Blood samples were obtained at baseline and immediately after each endurance test. We measured the index of lipid peroxidation, thiobarbituric acid reactive species (TBARS), total radical-trapping antioxidant parameter (TRAP) and xanthine oxidase (XO) activity. TRAP was significantly different between the exercise-trained group and sedentary group of COPD patients. Baseline TBARS values were increased after the exercise training program but decreased after the endurance test. XO decrease after effort in the trained and untrained groups. The results suggest that patients with COPD are characterized by increased systemic and pulmonary oxidative stress markers both at rest as well as induced by cardiopulmonary exercise test and that PR program was associated with decreased systemic exercise-induced oxidative damage.

Instantaneous quantification of skeletal muscle activation, power production, and fatigue during cycle ergometry.

A rapid switch from hyperbolic to isokinetic cycling allows the velocity-specific decline in maximal power to be measured, i.e., fatigue. We reasoned that, should the baseline relationship between isokinetic power (Piso) and electromyography (EMG) be reproducible, then contributions to fatigue may be isolated from 1) the decline in muscle activation (muscle activation fatigue); and 2) the decline in Piso at a given activation (muscle fatigue). We hypothesized that the EMG-Piso relationship is linear, velocity dependent, and reliable for instantaneous fatigue assessment at intolerance during and following whole body exercise. Healthy participants (n = 13) completed short (5 s) variable-effort isokinetic bouts at 50, 70, and 100 rpm to characterize baseline EMG-Piso. Repeated ramp incremental exercise tests were terminated with maximal isokinetic cycling (5 s) at 70 rpm. Individual baseline EMG-Piso relationships were linear (r(2) = 0.95 ± 0.04) and velocity dependent (analysis of covariance). Piso at intolerance (two legs, 335 ± 88 W) was ∼45% less than baseline [630 ± 156 W, confidence interval of the difference (CIDifference) 211, 380 W, P < 0.05]. Following intolerance, Piso recovered rapidly (F = 44.1; P < 0.05; η(2) = 0.79): power was reduced (P < 0.05) vs. baseline only at 0-min (CIDifference 80, 201 W) and 1-min recovery (CIDifference 13, 80 W). Activation fatigue and muscle fatigue (one leg) were 97 ± 55 and 60 ± 50 W, respectively. Mean bias ± limits of agreement for reproducibility were as follows: baseline Piso 1 ± 30 W; Piso at 0-min recovery 3 ± 35 W; and EMG at Piso 3 ± 14%. EMG power is linear, velocity dependent, and reproducible. Deviation from this relationship at the limit of tolerance can quantify the "activation" and "muscle" related components of fatigue during cycling.

Effect of sulfur dioxide on cytokine production of human alveolar macrophages in vitro.

Tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and transforming growth factor-beta are cytokines synthesized by alveolar macrophages. We investigated the effect of sulfur dioxide, a major air pollutant, on the production of these cytokines by alveolar macrophages. The cells were layered on a polycarbonate membrane and exposed for 30 min to 0.0, 1.0, 2.5, and 5.0 ppm sulfur dioxide at 37 degrees C and 100% air humidity. The cells were incubated for 24 h after exposure, thus allowing cytokine release. Cytotoxic effects of sulfur dioxide were evaluated by trypan blue exclusion. Cytokines were measured with enzyme-linked immunosorbent assays (i.e., tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6) or by use of a specific bioassay (i.e., transforming growth factor-beta). The toxicity of sulfur dioxide for alveolar macrophages ranged from 3.1 % to 9.5 %. A 30-min exposure to sulfur dioxide induced a significant decrease in spontaneous and lipopolysaccharide-stimulated tumor necrosis factor-alpha (p < .001) and lipopolysaccharide-stimulated interleukin-1beta release (p < .05). The release of interleukin-6 and transforming growth factor-beta was not affected significantly by sulfur dioxide exposure. Our results demonstrated a functional impairment of alveolar macrophages after sulfur dioxide exposure (i.e., release of tumor necrosis factor-alpha and interleukin-1beta). Neither spontaneous nor stimulated release of interleukin-6 and transforming growth factors were influenced by exposure to sulfur dioxide.

[Narcolepsy, an epidemic?]. / Narcolepsia, uma epidemia?

Narcolepsy, was first described in 1880, is a chronic, disabling disease characterized by excessive daytime sleepiness and abnormal REM manifestations. It is estimated that, in Brazil, 15,000 to 150,000 cases may exist, but is was only since the first sleep laboratories were installed in the country that the disease began to be recognized. It created a sudden increase in the number of diagnosis which actually simulates an epidemics in the medical records. The existence of a sleep laboratory, however, is not necessary for the diagnosis of the disease. An informed clinician can identify it during the interview. The goal of this paper is to inform about the clinical, diagnostic, and therapeutic aspects of the disease through the report of four selected cases.

[In vitro studies of modification of mucociliary clearance by guinea pig tracheas by exposure to air pollutants of sulfur or nitrogen dioxide]. / In-vitro-Versuche zur Beeinflussung der mukoziliären Clearance von Meerschweinchentracheen durch Schadgasexpositionen mit Schwefel- oder Stickstoffdioxid.

We studied the effect of sulfur dioxide (SO2) and nitrogen dioxide (NO2) on mucociliary activity (MCA) and ciliary beat frequency (CBF) in 63 guinea pig tracheas. The tracheas were placed in a gas cylinder and exposed for 30 minutes to SO2 concentrations ranging from 2.5 to 12.5 ppm or to NO2 concentrations ranging from 3.0 to 15.0 ppm. Control experiments were performed with exposure of the tracheas to synthetic air. MCA was measured by recording the light reflected from ciliated mucous membranes using an infrared barcode reader and CBF using video-interference microscopy. The exposure to 2.5 ppm SO2 caused a reduction in mean MCA of 63% and no significant changes in CBF. Higher SO2 concentrations caused a further impairment of MCA as well as a dose-dependent decrease in CBF. 10.0 or 12.5 ppm SO2 induced a decrease from baseline values to approximately 20% in MCA and to roughly 30% in mean CBF. The exposure to NO2 at concentrations ranging from 3.0 to 15.0 ppm did not induce any changes in MCA or CBF of the guinea pig tracheas. Our results show that exposure to SO2 for 30 minutes is able to depress the mucociliary clearance of guinea pig tracheas, whereas the exposure to equivalent NO2 concentrations for the same time do not alter the mucociliary transport.

Effect of sulfur dioxide on mucociliary activity and ciliary beat frequency in guinea pig trachea.

The effects of 30 min exposure to sulfur dioxide on mucociliary activity (MCA) and ciliary beat frequency (CBF) were studied in 31 guinea pig tracheas. MCA was measured by recording the light reflected from ciliated mucous membranes using an infrared bar code reader. CBF of single ciliated cells obtained by brushing was measured with phase-contrast microscopy. Each tracheal sample was exposed to SO2 at concentrations ranging from 2.5 to 12.5 ppm, or to air for control purposes. MCA and CBF were measured before and immediately after gas exposure. A reduction in mean MCA of 63% (P = 0.0007) and statistically insignificant changes in CBF (P > 0.05) were recorded at concentrations of 2.5 ppm SO2. Higher SO2 concentrations caused a further impairment of MCA as well as a dose-dependent decrease in CBF (P = 0.002). A concentration of 12.5 ppm SO2 induced a decrease from baseline values of approximately 80% in mean MCA and of roughly 70% in mean CBF. This study demonstrates a dose-dependent SO2-induced decrease in MCA of guinea pig tracheas. The decrease in MCA was associated with an impairment of CBF only at SO2 concentrations higher than 5.0 ppm.

Chemotactic response of human alveolar macrophages and blood monocytes elicited by exposure to sulfur dioxide.

An experimental study was undertaken to investigate the in vitro effect of sulfur dioxide on the chemotactic activity of alveolar macrophages (AM) and blood monocytes (BM). The cells were placed on a polycarbonate membrane and exposed to SO2 0.5, 1.5 and 2.5 ppm for 15 min. Control experiments were performed with exposure of the cells to synthetic air with 5% CO2. After gas exposure the cells were incubated with the chemotactic active agent C5a in 5% carbon dioxide (CO2) at 37 degrees C for 60 min. The numbers of AM and BM passing actively through the membrane were quantified using light microscopy. Our results show a dose-dependent reduction in the migration rate of cells under SO2 exposure. SO2 0.5 ppm induced a 29% and SO2 2.5 ppm a 53% decrease in migration of AM compared with the control exposure to synthetic air (P < 0.01). Identical experiments with BM resulted in a decrease in migration of up to 57% (P < 0.01). At SO2 concentrations of up to 2.5 ppm no significant cytotoxic effects were observed for AM or BM. The data demonstrate that exposure to SO2 may reduce the chemotactic activity of AM and BM. Our results further suggest that the decrease in cell migration induced by SO2 is due to changes in chemotactic mechanisms and not to cell death.

[Alveolar macrophages and mononuclear cells of the peripheral blood in sulfur dioxide and chrysotile B exposure: a realistic in vitro test of oxygen free radical liberation]. / Alveolarmakrophagen und mononukleäre Zellen des peripheren Bluts unter Schwefeldioxid- und Chrysotil B-Exposition: Ein realitätsnaher In-vitro-Versuch zur Sauerstoffradikalfreisetzung.

Sulfur dioxide (SO2) and Asbest are frequently found at workplaces. They can induce airway and lung parenchymal injury. Alveolar macrophages (AM) play an important and decisive role in the damage of respiratory tissue. We evaluated the reactive oxygen intermediates (ROI) production of AM and peripheral blood mononuclear cells after exposure with SO2 and Chrysotile B. The cells were exposed in a special gas exposure chamber at 37 degrees C and 100% air humidity for 30 minutes to 1.5 or 2.5 ppm SO2. Afterwards they were incubated for one hour with 100 micrograms or 200 micrograms Chrysotile B. Control experiments were performed with cell exposure to synthetic air without SO2 and Chrysotile B. Spontaneous and phorbol myristate acetate (PMA) stimulated ROI-release were measured by chemiluminescence and the cell toxicity was evaluated with the trypan blue exclusion test. Our results show a dose-dependent increase of the spontaneous ROI-production of AM after SO2 and Chrysotile B exposure. Exposure to 100 micrograms Chrysotile B caused an 1.5 fold, exposure to 1.5 or 2.5 ppm SO2 plus 100 micrograms Chrysotile B resulted in an 2.4 respectively 3.3 fold increase in ROI-release compared to control experiments. Exposure of AM to 200 micrograms Chrysotile B yielded an 1.9 fold, exposure to 2.5 ppm SO2 plus 200 micrograms Chrysotile B a 3.9 fold elevation in the spontaneous ROI-production compared to control experiment with standard air. A similar reaction pattern was observed in PMA-stimulated AM and in peripheral blood mononuclear cells.(ABSTRACT TRUNCATED AT 250 WORDS)