WITHDRAWN: Subsegmental Thrombus in COVID-19 Pneumonia: Immuno-Thrombosis or Pulmonary Embolism? Data Analysis of Hospitalized Patients with Coronavirus Disease.

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Impact of Continuous Positive Airway Pressure Treatment on Leptin Levels in Patients with Obstructive Sleep Apnea Syndrome.

BACKGROUND: There is growing evidence that leptin regulation is altered in obstructive sleep apnea syndrome (OSAS). Several potential mechanisms have been purported to explain how sleep apnea may alter leptin levels. We investigated whether repeated apneas, hypoxia, or excessive daytime sleepiness influenced the levels of leptin in OSAS patients. We also evaluated whether a 3-month continuous positive airway pressure (CPAP) treatment affected leptin levels in patients. METHODS: Randomly selected 31 untreated, otherwise healthy male, overweight [body mass index (BMI) >25 kg/m(2)] obstructive sleep apnea syndrome (OSAS) patients [apnea-hypopnea index (AHI) ≥15] and 25 control (AHI <5) were included in this study. To confirm the diagnosis, all subjects underwent standard polysomnography. Serum samples were taken at 07:00-08:00 a.m. after overnight fasting. The OSAS patients that had regular CPAP treatment (n=26) were re-evaulated 3 months later. RESULTS: Leptin levels (50.5±17.5 grams/L in OSAS and 56.3±25.5 grams/L in controls) and lipid profiles (TC, TGs, HDL-C, and LDL-C) between patient and control groups did not differ (P>0.05). Leptin levels were not correlated with the AHI, oxygen saturation, or excessive daytime sleepiness. CPAP treatment did not significantly change the (BMI), waist and neck circumference, or leptin levels in OSAS patients. Furthermore, we found no correlation between the decrease in serum leptin levels and parameters that were improved by CPAP treatment. CONCLUSION: Leptin levels and lipid profile of overweight subjects with and without OSAS were not different, and our results suggest that OSAS-related parameters and CPAP treatment do not play a significant role in the serum leptin levels.

Arginase activity and nitric oxide levels in patients with obstructive sleep apnea syndrome.

OBJECTIVE: Obstructive sleep apnea syndrome is characterized by repetitive obstruction of the upper airways, and it is a risk factor for cardiovascular diseases. There have been several studies demonstrating low levels of nitric oxide in patients with obstructive sleep apnea syndrome compared with healthy controls. In this study, we hypothesized that reduced nitric oxide levels would result in high arginase activity. Arginase reacts with L-arginine and produces urea and L-ornithine, whereas L-arginine is a substrate for nitric oxide synthase, which produces nitric oxide. METHODS: The study group consisted of 51 obstructive sleep apnea syndrome patients (M/F: 43/8; mean age 49±10 years of age) and 15 healthy control subjects (M/F: 13/3; mean age 46±14 years of age). Obstructive sleep apnea syndrome patients were divided into two subgroups based on the presence or absence of cardiovascular disease. Nitric oxide levels and arginase activity were measured via an enzyme-linked immunosorbent assay of serum samples. RESULTS: Serum nitric oxide levels in the control subjects were higher than in the obstructive sleep apnea patients with and without cardiovascular diseases (p<0.05). Arginase activity was significantly higher (p<0.01) in obstructive sleep apnea syndrome patients without cardiovascular diseases compared with the control group. Obstructive sleep apnea syndrome patients with cardiovascular diseases had higher arginase activity than the controls (p<0.001) and the obstructive sleep apnea syndrome patients without cardiovascular diseases (p<0.05). CONCLUSION: Low nitric oxide levels are associated with high arginase activity. The mechanism of nitric oxide depletion in sleep apnea patients suggests that increased arginase activity might reduce the substrate availability of nitric oxide synthase and thus could reduce nitric oxide levels.

Arginase activity and nitric oxide levels in patients with obstructive sleep apnea syndrome

OBJECTIVE: Obstructive sleep apnea syndrome is characterized by repetitive obstruction of the upper airways, and it is a risk factor for cardiovascular diseases. There have been several studies demonstrating low levels of nitric oxide in patients with obstructive sleep apnea syndrome compared with healthy controls. In this study, we hypothesized that reduced nitric oxide levels would result in high arginase activity. Arginase reacts with L-arginine and produces urea and L-ornithine, whereas L-arginine is a substrate for nitric oxide synthase, which produces nitric oxide. METHODS: The study group consisted of 51 obstructive sleep apnea syndrome patients (M/F: 43/8; mean age 49±10 years of age) and 15 healthy control subjects (M/F: 13/3; mean age 46±14 years of age). Obstructive sleep apnea syndrome patients were divided into two subgroups based on the presence or absence of cardiovascular disease. Nitric oxide levels and arginase activity were measured via an enzyme-linked immunosorbent assay of serum samples. RESULTS: Serum nitric oxide levels in the control subjects were higher than in the obstructive sleep apnea patients with and without cardiovascular diseases (p<0.05). Arginase activity was significantly higher (p<0.01) in obstructive sleep apnea syndrome patients without cardiovascular diseases compared with the control group. Obstructive sleep apnea syndrome patients with cardiovascular diseases had higher arginase activity than the controls (p<0.001) and the obstructive sleep apnea syndrome patients without cardiovascular diseases (p<0.05). CONCLUSION: Low nitric oxide levels are associated with high arginase activity. The mechanism of nitric oxide depletion in sleep apnea patients suggests that increased arginase activity might reduce the substrate availability of nitric oxide synthase and thus could reduce nitric oxide levels. .

Detection of reactive oxygen metabolites in malignant and adjacent normal tissues of patients with lung cancer.

BACKGROUND: Different types of reactive oxygen metabolites (ROMs) are known to be involved in carcinogenesis. Several studies have emphasized the formation of ROMs in ischemic tissues and in cases of inflammation. The increased amounts of ROMs in tumor tissues can either be because of their causative effects or because they are produced by the tumor itself. Our study aimed to investigate and compare the levels of ROMs in tumor tissue and adjacent lung parenchyma obtained from patients with lung cancer. METHODS: Fifteen patients (all male, mean age 63.6 ± 9 years) with non-small cell lung cancer were enrolled in the study. All patients were smokers. Of the patients with lung cancer, twelve had epidermoid carcinoma and three had adenocarcinoma. During anatomical resection of the lung, tumor tissue and macroscopically adjacent healthy lung parenchyma (control) that was 5 cm away from the tumor were obtained. The tissues were freshly frozen and stored at -20°C. The generation of ROMs was monitored using luminol- and lucigenin-enhanced chemiluminescence (CL) techniques. RESULTS: Both luminol (specific for (.)OH, H(2)O(2), and HOCl(-)) and lucigenin (selective for O(2)(.)(-)) CL measurements were significantly higher in tumor tissues than in control tissues (P <0.001). Luminol and lucigenin CL measurements were 1.93 ± 0.71 and 2.5 ± 0.84 times brighter, respectively, in tumor tissues than in the adjacent parenchyma (P = 0.07). CONCLUSION: In patients with lung cancer, all ROM levels were increased in tumor tissues when compared with the adjacent lung tissue. Because the increase in lucigenin concentration, which is due to tissue ischemia, is higher than the increase in luminol, which is directly related to the presence and severity of inflammation, ischemia may be more important than inflammation for tumor development in patients with lung cancer.

Lipid peroxidation and paraoxonase activity in nocturnal cyclic and sustained intermittent hypoxia.

PURPOSE: Obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD) have been known to be associated with atherosclerosis and hypoxia which was suggested to have an important role in this process by the way of increased oxidative stress. In the present study, we aimed to evaluate the effects of nocturnal hypoxia pattern (intermittent versus sustained) on serum lipid peroxidation and paraoxonase (PON) activity. METHODS: Blood collections were performed in 44 OSA, 11 non-apneic, nocturnal desaturated COPD, and 14 simple snorer patients after full-night polysomnographic recordings. Nocturnal sleep and respiratory parameters, oxygen desaturation indexes, serum malondialdehyde (MDA) levels by measuring with the help of the formation of thiobarbituric acid reactive substances (TBARS), and PON activity were assessed in all subjects. RESULTS: OSA and COPD patients showed nocturnal hypoxemia, with a minimum oxygen saturation (SaO(2)) in ranges of 53-92 % and 50-87 %, respectively. The mean levels of TBARS was 15.7 ± 3.6 nmol and 15.3 ± 3.4 nmol malondialdehyde (MDA)/ml in OSA and COPD patients, respectively, while the mean level of the control group was 4.1 ± 1.2 nmol MDA/ml. The mean PON activity was found to be 124.2 ± 35.5 U/l in OSA patients and 124.6 ± 28.4 U/l in COPD patients. The mean PON activity of the control group was 269.0 ± 135.8 U/l. The increase in TBARS levels and the decrease in PON1 levels were statistically significant in both OSA and COPD patients according to controls (p < 0.001 for TBARS as well as PON1). CONCLUSION: The results of this study revealed that both OSA and non-apneic, nocturnal desaturated COPD patients showed increased levels of lipid peroxidation and decreased PON activity despite the differences in nocturnal hypoxia pattern.

Streptokinase for malignant pleural effusions: a randomized controlled study.

Effective palliative treatment in malignant pleural effusion can only be carried out when the lung is fully expanded after drainage of effusion. We investigated the efficacy of intrapleural fibrinolytics for lysing fibrin deposits and improving lung reexpansion in patients with malignant pleural effusion. We randomly allocated 47 patients with malignant pleural effusion into 2 groups: a fibrinolytic group of 24 were given 3 cycles of 250,000 U intrapleural streptokinase; the control group of 23 received pleural drainage only. Pleurodesis with 5 mg of talc slurry was performed in all patients who had lung reexpansion after drainage. Patient characteristics, pleural drainage, lung expansion assessed by chest radiography, and pleurodesis outcomes were compared between the 2 groups. Patient characteristics were similar in both groups. Lung reexpansion was adequate for performing talc pleurodesis in 96% of patients in the fibrinolytic group and 74% in the control group. In the fibrinolytic group, the mean volume of daily pleural drainage before streptokinase administration was 425 mL, and it increased significantly to 737 mL after streptokinase infusion. Intrapleural administration of streptokinase is advisable for patients with malignant pleural effusion.