Morphine modulates inducible nitric oxide synthase expression and reduces pulmonary oedema induced by alpha-naphthylthiourea

This study was designed to investigate the possible participation of morphine in pulmonary oedema induced by alpha-naphthylthiourea (ANTU), which is a well-known noxious chemical agent in the lung. Injection of ANTU (15 mg/kg i.p.) produced pulmonary oedema as indicated by an increase in lung weight/body weight ratio and pleural effusion reaching a maximum within 4 h in rat. Administration of morphine prior to ANTU significantly inhibited to pulmonary oedema with a dose-dependent manner. The protective effect of morphine is prevented by peripheral opioid receptor antagonist, naloxone methiodide. ANTU-treated rats were shown positive by inducible nitric oxide synthase immunohistochemical staining. There was no staining in the control group. On the other hand, the degree of staining was markedly reduced in tissue sections by morphine. These results suggest that previous administration of subcutaneous morphine has preventive effect on ANTU-induced pulmonary inflammatory reaction and its effect mediated via peripheral opioid receptors. Application of naloxone with ANTU has no effect on the lung parameters indicating that endogenous opioids do not modulate ANTU-induced damage.     

Increasing dietary palmitic acid decreases fat oxidation and daily energy expenditure

BACKGROUND: Oleic acid (OA) is oxidized more rapidly than is palmitic acid (PA). OBJECTIVE: We hypothesized that changing the dietary intakes of PA and OA would affect fatty acid oxidation and energy expenditure. DESIGN: A double-masked trial was conducted in 43 healthy young adults, who, after a 28-d, baseline, solid-food diet (41% of energy as fat, 8.4% as PA, and 13.1% as OA), were randomly assigned to one of two 28-d formula diets: high PA (40% of energy as fat, 16.8% as PA, and 16.4% as OA; n = 21) or high OA (40% of energy as fat, 1.7% as PA, and 31.4% as OA; n = 22). Differences in the change from baseline were evaluated by analysis of covariance. RESULTS: In the fed state, the respiratory quotient was lower (P = 0.01) with the high OA (0.86 +/- 0.01) than with the high-PA (0.89 +/- 0.01) diet, and the rate of fat oxidation was higher (P = 0.03) with the high-OA (0.0008 +/- 0.0001) than with the high-PA (0.0005 +/- 0.0001 mg . kg fat-free mass(-1) . min(-1)) diet. Resting energy expenditure in the fed and fasting states was not significantly different between groups. Change in daily energy expenditure in the high-OA group (9 +/- 60 kcal/d) was significantly different from that in the high-PA group (-214 +/- 69 kcal/d; P = 0.02 or 0.04 when expressed per fat-free mass). CONCLUSIONS: Increases in dietary PA decrease fat oxidation and daily energy expenditure, whereas decreases in PA and increases in OA had the opposite effect. Increases in dietary PA may increase the risk of obesity and insulin resistance.     

Periapical health related to the type of coronal restorations and quality of root canal fillings in a Turkish subpopulation.

OBJECTIVE: The purpose of this study was to evaluate the relationship between the quality of root canal fillings and type of permanent coronal restorations and their association with the periapical status in a Turkish subpopulation. STUDY DESIGN: There were 1268 endodontically treated teeth from 280 panoramic radiographs that were evaluated. Two observers assessed the radiographs using an x-ray viewer with 2 times magnification. Teeth were classified according to the type of restorations. The quality of root canal fillings were evaluated according to the criteria determined by Tronstad et al. Apical status was assessed by the Periapical Index scores (PAI) proposed by ?rstavik et al. Chi-square test was used for statistical analysis. RESULTS: There were 59.5% of endodontically treated teeth that showed healthy periapex. Teeth with good endodontic treatment showed statistically significant high healthy periapex rates regardless of the type of the restoration. In addition, the evaluation of the entire material also showed that the roots with posts had significantly more periapical pathosis than roots without posts (P = .001). CONCLUSIONS: It can be concluded that, although the quality of the root canal filling plays a key role in the outcome of endodontic therapy, the type of restoration can also be a contributing factor in the treatment outcome.     

Withdrawal of inhaled steroids in children with non‐cystic fibrosis bronchiectasis

Background: To study the effects of inhaled steroid withdrawal on bronchial hyperreactivity, sputum inflammatory markers and neutrophilic apoptosis in children with non‐cystic fibrosis (non‐CF) bronchiectasis. Objectives: To evaluate the role of inhaled steroids in the treatment of children with non‐CF bronchiectasis with specific emphasis on the bronchial hyperreactivity and neutrophilic apoptosis. Methods: Twenty‐seven children with steady‐state non‐CF bronchiectasis were evaluated primarily with metacholine challenge tests and apoptotic neutrophil ratios in induced sputum and secondarily with symptom scores, pulmonary function tests and tumour necrosis factor‐alpha (TNF‐α), interleukin‐8 (IL‐8) levels and neutrophil ratios in induced sputum before and after 12‐week withdrawal of inhaled steroids. Results: There were 16 girls and 11 boys. Median (interquartile range) age was 11·4 (9·5–13·6) years, follow‐up duration was 3·5 (2–6·5) years. Symptom scores (4 vs. 3; P = 0·27), oxygen saturation (95% vs. 97%; P = 0·06), pulmonary function tests (FEV1: 82% predicted vs. 83% predicted; P = 0·73), sputum neutrophil ratios (29·9% vs. 46·8%; P = 0·20), TNF‐α (58 pg/mL vs. 44·5 pg/mL; P = 0·55) and IL‐8 (2·7 ng/mL vs. 2·4 ng/mL; P = 0·82) levels in induced sputum were similar before and after 12‐week withdrawal of inhaled steroids. However, the number of patients with bronchial hyperreactivity increased (37% vs. 63% of patients; P = 0·016) and neutrophilic apoptosis in induced sputum decreased (42·8% vs. 20·2%; P = 0·03) after withdrawal. Conclusion: In this study, 12 week‐withdrawal of inhaled steroid treatment resulted in a significant increase in bronchial hyperreactivity and decrease in neutrophil apoptosis, but no change in sputum inflammatory markers in children with non‐CF bronchiectasis was observed.     

Psychological distress in chronic obstructive pulmonary disease patients

Stress is defined as the exposure of an individual to a threatening stimulus or overwhelming event. Increased rates of psychological distress have been established in patients with chronic diseases compared to healthy individuals. The objective of the present study is to assess the indicators and correlates of psychological distress in chronic obstructive pulmonary disease (COPD) patients. We evaluated the stress exposure (stressful events that COPD patients and control subjects had been exposed) by a life events checklist and psychological distress by General Health Questionnaire in 74 COPD patients and 30 control subjects. Serum adrenocorticotropic hormone (ACTH) and cortisol levels were measured as biochemical indicators of stress. Distress score was higher in COPD group compared to age‐matched controls, although the stress exposure score were not statistically different; indicating that COPD itself is a source of distress. 92% of COPD patients and 87% of control subjects had varying degrees of distress. Severe distress was more frequent in COPD group. Distress score was further increased in patients with severe COPD and severe hypoxemia.There was no significant difference in serum ACTH and cortisol levels of COPD patients and control subjects and distress scores were not correlated to serum ACTH and cortisol levels. However, serum cortisol was higher in patients with severe hypoxemia. These findings support the importance of screening for psychological distress symptoms in COPD outpatients. Since high degree of distress contributes to impaired quality of life and added morbidity, patients with COPD need a comprehensive care including a psychological evaluation. Copyright © 2008 John Wiley & Sons, Ltd.     

Circulating leptin and body composition in chronic obstructive pulmonary disease

Nutritional depletion and weight loss are two features of chronic obstructive pulmonary disease (COPD), and the association between low body mass index (BMI) and poor prognosis in patients with COPD is a common clinical observation. Mechanisms of weight loss are still unclear in COPD. Excessive energy expenditure partly due to increased work of breathing was shown, but other mechanisms have been searched for. Leptin is a hormone secreted by adipocytes that plays an important role in energy homeostasis and regulates body weight through control of appetite and energy expenditure. The aim of this study was to evaluate the association of circulating leptin levels and measures of body composition in COPD patients. Thirty male COPD outpatients (mean age 66.3 +/- 8.4) and 20 controls (mean age 65.9 +/- 10.8) were included in the study. After standard spirometry and body composition measurements, serum leptin concentration was measured by ELISA assay. COPD patients were grouped according to BMI. Mean BMI was 19.01 +/- 2.26 kg/m2 in group 1 (COPD patients with low BMI), 26.85 +/- 4.51 in group 2 COPD (COPD patients with normal/high BMI) and 27.64 +/- 2.75 kg/m2 in healthy controls (group 3). Mean serum leptin concentration was 1.41 +/- 1.86 ng/ml in group 1, 2.60 +/- 1.38 ng/ml in group 2 and 2.82 +/- 1.46 ng/ml in group 3 (p = 0.002). Leptin correlated to not only BMI but also body weight, waist circumference, triceps and biceps skinfold thickness and body fat percent (p < 0.05 for all). Results of this study suggest that the cause of weight loss is not increased circulating leptin in COPD. Instead, leptin remains regulated in COPD and further decreased in patients with low BMI, probably as a compensatory mechanism to preserve body fat content, which should be evaluated in further studies.     

Anti-Saccharomyces cerevisiae Antibodies in Acute Myocardial Infarction.

BACKGROUND: Elevated anti-Saccharomyces cerevisiae antibody (ASCA) immunoglobulin (IgG) and IgA levels were first described in the serum of Crohn disease patients and have increasingly been reported in other inflammatory diseases. The role of in situ and remote inflammation in atherosclerosis is a major area of interest. In this study, we compared ASCA IgG and IgA levels in acute myocardial infarction (AMI) and controls to investigate the possible role of ASCA in AMI. METHODS: Serum samples were obtained from 140 consecutive patients who presented to the emergency department with acute chest pain. AMI was diagnosed by electrocardiography and serial enzymes. Patients ruled out for acute coronary event were grouped as controls. ASCA IgA and IgG levels were determined using enzyme-linked immunosorbent assay. Groups were compared for statistically significant difference. RESULTS: ASCA IgG titers ranged between 0.1 and 31.0 RIU/mL (mean 4.92) in the AMI group and 0.1 and 6.0 (mean 0.84) in the controls. The groups were found to differ very significantly (p = .001). ASCA IgA titers ranged between 2.0 and 200.0 RIU/mL (mean 13.73) in the AMI group and 2.0 and 11.5 RIU/mL, (mean 4.25) in controls. The groups differed significantly (p = .32). AMI and controls were also analyzed for ASCA IgA and IgG positivity. Both groups differed significantly from controls (p = .013). CONCLUSION: Elevated ASCA IgA and IgG levels as well as ASCA positivity in the AMI might suggest use of ASCA as a marker for atherosclerotic plaque instability. It might also provide a link between inflammatory processes and increased cardiovascular risk. Further studies are needed on a Saccharomyces cerevisiae-based diet, related intestinal colonization, and associated inflammation, autoimmune disorders, and cardiovascular events.