9 research outputs found
Effects of Smoking Cessation on Physical Exercise Capacity
Exercise has been recommended as an adjunct method for smoking cessation. From this point of view, performing exercise tests is becoming increasingly important for determining cardiopulmonary risk factors which individuals carry, for prescribing adequate exercise regimes, and for objectively measuring changes in physical capacity during abstinence period. In this study, we aimed to investigate short term changes in cardiopulmonary exercise capacity of individuals that stop smoking. Thirty-nine (25F/14M) asymptomatic volunteers were recruited from Stop Smoking Clinics, Department of Chest Diseases, Cerrahpasa Faculty of Medicine, Istanbul University. Participants underwent maximal cardiopulmonary exercise testing (CPET) on a cycle ergometer by 20 watt/2 min increases until reaching 85% of age-pre-dicted maximal heart rate. CPET was performed in the 1st and 10th weeks of abstinence period. Gas analyses (VO2 and VCO2) were made using expiration air. Prior to CPET, resting lung function tests were performed for each participant. In the whole group, body weight and body mass index increased (p< 0.01; p< 0.01). Maximal oxygen consumption (VO2max), exercise duration, and work performed by the participants also increased ( p< 0.01; p< 0.001; p< 0.001). In conclusion, smokers well-tolerated cardiopulmonary exercise test without any complications. Aerobic performance parameters of smokers improved significantly in an abstinence period of even as short as 10 weeks
Effects of Smoking Cessation on Physical Exercise Capacity
Exercise has been recommended as an adjunct method for smoking cessation. From this point of view, performing exercise tests is becoming increasingly important for determining cardiopulmonary risk factors which individuals carry, for prescribing adequate exercise regimes, and for objectively measuring changes in physical capacity during abstinence period. In this study, we aimed to investigate short term changes in cardiopulmonary exercise capacity of individuals that stop smoking. Thirty-nine (25F/14M) asymptomatic volunteers were recruited from Stop Smoking Clinics, Department of Chest Diseases, Cerrahpasa Faculty of Medicine, Istanbul University. Participants underwent maximal cardiopulmonary exercise testing (CPET) on a cycle ergometer by 20 watt/2 min increases until reaching 85% of age-pre-dicted maximal heart rate. CPET was performed in the 1st and 10th weeks of abstinence period. Gas analyses (VO2 and VCO2) were made using expiration air. Prior to CPET, resting lung function tests were performed for each participant. In the whole group, body weight and body mass index increased (p< 0.01; p< 0.01). Maximal oxygen consumption (VO2max), exercise duration, and work performed by the participants also increased ( p< 0.01; p< 0.001; p< 0.001). In conclusion, smokers well-tolerated cardiopulmonary exercise test without any complications. Aerobic performance parameters of smokers improved significantly in an abstinence period of even as short as 10 weeks
Cardiopulmonary responses to exercise in moderate-to-severe obstructive sleep apnea
Information regarding the safety of maximal cardiopulmonary exercise testing (CPET) or the mechanisms of exercise limitation in obstructive sleep apnea (OSA) patients is fairly limited. In the present study, we addressed the problem of exercise capacity in moderate-to-severe OSA patients. Nineteen non-consecutive patients (three female, 16 male) with moderate-to-severe OSA and 11 age and body mass index matched control subjects (four female, seven male) underwent respiratory function tests during pre-exercise resting period and volitionally limited cardiopulmonary exercise testing on an electronically braked cycle ergometer. All participants completed CPET without any complication. Control subjects were exercise limited due to deconditioning. None of the patients revealed mechanical ventilatory limitation to exercise or had evidence of cardiac ischaemia. Five patients had no limitation to exercise. Six patients had low VO2peak, low anaerobic treshold (AT), and low peak O-2 pulse, a pattern consistent with ventricular dysfunction. Six patients had low VO2peak, low AT, and peak heart rate less than 85% predicted. This pattern is consistent with exercise limitation due to peripheral vascular disease. Two patients had low VO2peak, low AT without peak oxygen pulse and peak heart rate abnormalities consistent with deconditioning. We concluded that moderate-to-severe OSA patients have impaired exercise capacity. Exercise limitation seems to originate from cardiovascular reasons namely left ventricular dysfunction and/or peripheral vascular impairment; and finally, maximal CPET can be tolerated by these patient group without serious complications
DNA repair gene XRCC1 polymorphisms and the risk of asthma in a Turkish population
Polymorphisms have been identified in several DNA damage repair genes. These polymorphisms may effect DNA repair capacity and modulate asthma susceptibility. In this study, we aimed to determine the two polymorphisms in DNA repair gene, x-ray repair cross-complementing group 1 (XRCC1), in a sample of Turkish patients with asthma, and evaluate their association with asthma development. We used polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) to analyze XRCC1 Arg194Trp and XRCC1 Arg399GIn polymorphisms in 116 patients with asthma and in 180 disease-free controls. Our data showed a positive association between the polymorphisms of codons 194 (odds ratio [OR] = 1.97, 95% confidence interval [CI] = 1.06-3.66, and p = 0.03 for Arg/Trp genotype) and 399 (OR = 1.87, 95% CI = 1.12-3.13, and p = 0.02 for Arg/Gln genotype, and OR = 2.59, 95% CI = 1.24-5.43, and p = 0.01 for Gln/Gln genotype) and asthma risk. No statistically significant difference was found for the allelic and genotypic distributions of the polymorphisms in XRCC1 gene between mild and moderate asthmatic patients. A combined analysis of the effect of XRCC1 codons 194 and 399 revealed the highest risk (OR = 4.17, 95% Cl = 1.77-9.83, and p = 0.001) for carriers of the polymorphic alleles in both of these codons. These results suggest that the risk of asthma may be associated with DNA repair mechanisms, and understanding these mechanisms will help identify individuals at increased risk of developing asthma and should lead to improved treatment of asthma. (Allergy Asthma Proc 31:349-354, 2010; doi: 10.2500/aap.2010.31.3332
The Ala Allele at Val762Ala Polymorphism in Poly(ADP-ribose) Polymerase-1 (PARP-1) Gene is Associated with a Decreased Risk of Asthma in a Turkish Population
Background and objective. It has been suggested that inhibition of poly (ADP-ribose) polymerase-1 (PARP-1), either pharmacologically or by a gene knockout provides significant protection against systemic or tissue inflammation in animal models. The aim of this study was to analyze the association of the PARP-1 Val762Ala polymorphism, which has beenreported to be associated with decreased enzymatic activity, in Turkish patients with adult asthma. Methods. A total of 112 subjects with stable asthma and 180 normal controls from the same geographic region were studied and polymerase chain reaction-based restriction analysis was used to identify Val762Ala polymorphism of the PARP-1. Results. In univariate analysis, PARP-1 762 AA genotype conferred a 3.4 fold reduction in risk (OR = 0.297, 95% CI = 0.105-0.813; P = 0.014), while heterozygous VA genotype conferred an even greater level of protection (OR = 0.06; 95%CI, 0.026-0.14; P 10-6). In addition, wild type PARP-1 762 V allele had 5 times the risk of developing asthma than those without the allele (OR 0.199, CI 0.118-0.334, P = 10-6). Conclusions. These findings suggest that PARP-1 V762A variants may be one of the factors participating in protection or susceptibility to asthma in our population
Antibacterial Resistance in Lower Respiratory Tract Bacterial Pathogens: A Multicenter Analysis from Turkey
Introduction: This study aimed to evaluate the etiology of lower respiratory tract infections (LRTIs) and their antibiotic resistance
Decreased multidrug resistance protein 1 and increased platelet activation in obstructive sleep apnea syndrome
Abstract Introduction Obstructive sleep apnea syndrome (OSAS) is an inflammatory disease characterized by recurrent apnea and hypopnea. Multidrug resistance protein 1 (MRP1) is an anti‐inflammatory protein that protects the cell from agents caused by oxidative stress. The aim of this study was to investigate the role of MRP1 in platelet function in OSAS. Methods According to the polysomnography results, 14 patients with simple snoring, 16 with mild OSAS, 14 with moderate OSAS, and 15 with severe OSAS were included in the study. Platelet aggregations were evaluated by an aggregometer. MRP1, CD62P (P‐selectin), CD41b, and CD42b expressions were measured by a flow cytometer. Results Platelet aggregation levels were higher in the severe OSAS group than in the simple, mild, and moderate OSAS groups (p = 0.041). On the other hand, CD42b+/MRP1+ expression was lower in the severe OSAS group than in the simple, mild, and moderate OSAS groups (p = 0.002). MRP1 and CD42b expressions were consistent with this result (p = 0.013, p = 0.009, respectively). A positive correlation was found between apnea/hypopnea index and platelet aggregation (r = 0.289 p = 0.028) and a negative correlation was found between CD42b, CD42b+/MRP1+ (r = −0.419 p = 0.001, r = −0.357 p = 0.006, respectively). Conclusion Our findings suggest that high platelet activity and low MRP1 expression contribute to inflammation in OSAS and thus may be biomarkers
Lack of association between increased mitochondrial DNA(4977) deletion and ATP levels of sputum cells from chronic obstructive pulmonary disease patients versus healthy smokers
WOS: 000397858400027PubMed ID: 26713688In this study we looked at smokers with and without chronic obstructive pulmonary disease (COPD) patients in order to evaluate the incidence of 4977 base pair (bp) mtDNA (mtDNA(4977)) deletion and mtDNA copy number in sputum cells and in peripheral blood leukocytes (PBLs) in relation to mitochondrial function and oxidative stress status. Twenty-five COPD patients who were current smokers, 22 smokers and 23 healthy nonsmokers (for only PBLs studies) participated in this study. The 4977-bp deletion was detected in all examined samples within 40 cyles of PCR amplification, using a quantitative real time PCR. The frequency of the mtDNA(4977) was significantly higher in the sputum cells of patients with COPD compared to smokers without COPD (p<0.0001). This difference was not observed in PBLs. Levels of cellular oxidative stress were significantly higher in the sputum cells of subjects with COPD than in the smoker group. However, mtDNA copy number, mitochondrial membrane potential (Delta Psi m) and cellular ATP levels in PBLs and sputum cells were not significantly different between the studied groups. The Pearson analysis revealed no correlations between the accumulation of mtDNA(4977), and intracellular ATP content and Delta Psi m values of the sputum cells, although there was a positive correlation between the increase in the percentage of deleted mtDNA(4977) and the levels of cellular oxidative stress in COPD patients (r = 0.80, p<0.0001). Our studies may suggest that the accumulation of mtDNA(4977) in the sputum cells of smokers with COPD does not seem to have an important impact on mitochondrial dysfunction in relation to ATP production and Delta Psi m when compared to those of healthy smokers.Research Fund of Istanbul University [T81/12122006]There is no conflict of interest among the author. This work was supported by the Research Fund of Istanbul University (project number: T81/12122006)
Can we predict patients that will not benefit from invasive mechanical ventilation? A novel scoring system in intensive care: the IMV Mortality Prediction Score (IMPRES)
Conclusion: The present study included a large number of patients from various geographical areas of the country who were admitted to various types of ICUs, had diverse diagnoses and comorbidities, were intubated with various indications in either urgent or elective settings, and were followed by physicians from various specialties. Therefore, our data are more general and can be applied to a broader population. This study devised a new scoring system for decision-making for critically ill patients as to whether they need to be intubated or not and presents a rapid and accurate prediction of mortality and prognosis prior to ICU admission using simple clinical data
