Serum YKL-40 level is correlated with apnea hypopnea index in patients with obstructive sleep apnea sindrome.

OBJECTIVE: Obstructive sleep apnea syndrome (OSAS) has been associated with elevated biochemical markers of inflammation. Although the exact mechanism is unknown, both sleep deprivation and hypoxemia are believed to be important causative factors. YKL-40, also known as chitinase-like protein, has been shown to be related to various inflammatory conditions including atherosclerosis, diabetes, cancer, and asthma. The present study aimed to evaluate the relationship between YKL-40 levels and the Apnea Hypopnea Index (AHI) in patients with obstructive sleep apnea syndrome. PATIENTS AND METHODS: The study was conducted at the Sleep Unit of the Namik Kemal University Research Center. From January 2013 to December 2013, 120 patients diagnosed with OSAS by polysomnography and 40 subjects without OSAS were recruited. Patients in both groups were matched by age, sex, and body mass index (BMI). They were further divided into groups of mild, moderate and severe OSAS based on their AHI value. Serum YKL-40 concentrations were measured by the enzyme-linked immunosorbent assay (ELISA). RESULTS: OSAS patients showed significantly elevated YKL-40 levels compared to the control group; 102,05 (23.14) pg/ml in the control group vs. 144.81 (65.53) pg/ml in the OSAS group. A Spearman correlation analysis showed that serum YKL-40 levels were significantly and positively correlated with AHI (r = 0.434, p < 0.001) and oxygen desaturation index (r = 0.374, p < 0.001). CONCLUSIONS: The study demonstrated that high serum YKL-40 levels correlated with the severity of OSAS and might serve as a nonspecific biomarker for prediction and progression of the disease.

The serum copeptin levels in obstructive sleep apnea patients with prehypertensive.

OBJECTIVE: Copeptin is a precursor of AVP, an antidiuretic hormone, plays a pivotal role in the maintenance of cardiovascular homeostasis. Obstructive sleep apnea syndrome (OSAS) is related to cardiovascular disease. We sought to evaluate the serum copeptin levels in newly diagnosed prehypertensive patients with OSAS. PATIENTS AND METHODS: Eighty-four prehypertensive patients were evaluated using polysomnography and were divided into two groups, an OSAS (n = 41) group and a control (n = 43) group. Serum copeptin levels were measured using the ELISA method. RESULTS: Copeptin levels were significantly higher in the OSAS group compared to the control group (146 [93-739] pg/ml vs. 111 [33-253] pg/ml, respectively, p < 0.001). A regression analysis revealed that the apnea hypopnea index (AHI) and the lowest SpO2 were related to serum copeptin levels (unstandardized ß = 1.02 ± 0.40, p = 0.014 and unstandardized ß = -3.1 ± 0.9, p = 0.048 respectively). CONCLUSIONS: According to the results of our study, serum copeptin levels are higher in the prehypertensive patients with OSAS compared to those in the control group. Therefore, in assessing the severity of OSAS, serum copeptin levels can be a candidate for a biochemical marker in addition to polysomnographic findings.

Lipoprotein-associated phospholipase A2 levels are associated with erectile dysfunction in patients without known coronary artery disease.

Endothelial dysfunction and microvascular damage play a crucial role in the pathogenesis of erectile dysfunction (ED). Lp-PLA2 is a calcium-independent member of the phospholipase A2 family and hydrolyses oxidised phospholipids on low-density lipoprotein (LDL) particles that plays a pivotal role in ox-LDL-induced endothelial dysfunction. The purpose of the current study was to determine the association between Lp-PLA2 levels and ED in patients without known coronary artery disease (CAD). All patients were evaluated for ED and divided into two groups: 88 patients suffering from ED for >1 year were enrolled as an experimental group and 88 patients without ED were enrolled as a control group in this study. Diagnosis of ED was based on the International Index of Erectile Function Score-5. Levels of Lp-PLA2 were measured in serum by colorimetric assay. The relationship between Lp-PLA2 levels and ED in patients was evaluated statistically. The mean age of patients with ED group was 59.4 ± 11.32 and 55.8 ± 9.67 in the control group. Plasma Lp-PLA2 levels were significantly higher in ED than in the control group (220.3 ± 66.90 and 174.8 ± 58.83 pg ml(-1) , respectively, P < 0.001). The Lp-PLA2 levels were negatively correlated with score of ED (r = -0.482, P < 0.05). In logistic regression analysis, enhanced plasma Lp-PLA2 levels result in approximately 1.2-fold increase in ED [1.22 (1.25-2.76)]. In this study, serum Lp-PLA2 levels were found to be associated with endothelial dysfunction predictive of ED. Serum Lp-PLA2 level appears to be a specific predictor of ED, and it may be used in early prediction of ED in the male population.

Changes in expression of Slit1 and its receptor Robo2 in trigeminal ganglion and inferior alveolar nerve following inferior alveolar nerve axotomy in adult rats: a pilot study.

The objective of this study was to analyze changes in expression pattern of Slit1 and Robo2, and to clarify the relationship between these changes and functional recovery of the axotomized inferior alveolar nerve (IAN) without repair using a rat IAN axotomy model. Slit1 and Robo2 were weakly expressed in samples taken from trigeminal ganglion (TG) and IAN of sham surgery rats. In axotomized rats, expression levels increased significantly from day 2 to day 28 post-axotomy, with peaks on days 14 (Slit1) and 7 (Robo2) after axotomy (relative to sham: Slit1 in TG P<0.0005, Slit1 in IAN P = 0.003, Robo2 in TG P<0.0005, and Robo2 in IAN P<0.0005). Over-expressed Slit1 and Robo2 in both the TG and IANs of axotomized rats did not return to sham levels during the 28-day observation period of this study. The regeneration and functional recovery of axotomized IAN was evaluated by jaw opening reflex (JOR) recorded before and after axotomy. JOR occurrence (0% on day 7, 35% on day 14, and 85% on day 28) increased gradually, and the relative threshold of electrical stimulation eliciting JOR decreased gradually (1000.0 ± 0.0% on day 7, 854.3 ± 132.5% on day 14, and 302.6 ± 92.3% on day 28). On day 28 after axotomy, JOR occurrence and the relative JOR threshold had almost returned to those of sham rats. These findings suggest that Slit1 and Robo2 are involved in the regeneration and functional recovery of the axotomized IAN.

Protective effects of fish omega-3 fatty acids on doxorubicin-induced testicular apoptosis and oxidative damage in rats.

The aim of this study was to examine the protective effects of fish omega-3 (n-3) fatty acids on acute doxorubicin (DOX)-induced testicular apoptosis and oxidative damage. 24 male rats were divided into three groups: control, DOX-treated and DOX+fish n-3 fatty acids. Fish n-3 fatty acids (400 mg kg(-1) ) were given for 30 days by intragastric gavage. The rats received a single intraperitoneal injection of DOX (30 mg kg(-1) ) and were sacrificed after 48 h. The DOX+fish n-3 fatty acids group showed a decrease in malondialdehyde levels and increased activities of superoxide dismutase and glutathione peroxidase in comparison with the DOX-treated group. Acute DOX treatment caused severe damage such as disorganisation and separation of germ cells. The fish n-3 fatty acids-pretreated rats showed an improved histological appearance in the DOX-treated group. Our data indicate a reduction in the activity of terminal deoxynucleotidyl transferase mediated dUTP nick end labelling; there was a rise in the expression of proliferating cell nuclear antigen in testis tissues of the DOX+fish n-3 fatty acids group compared with DOX-treated group. These data suggested that fish n-3 fatty acids pre-treatment may be beneficial for spermatogenesis following acute DOX-induced testicular damage by decreasing germ cell apoptosis and oxidative stress.

Cardioprotective effects of fish omega-3 fatty acids on doxorubicin-induced cardiotoxicity in rats.

The aim of this study was to investigate the protective effects of fish omega-3 (n-3) fatty acids on doxorubicin (DOX)-induced acute cardiotoxicity. A total of 24 rats were divided into three groups: control, DOX-treated, and DOX treated with fish n-3 fatty acids. Control group received 0.4 ml/kg/day of saline intragastrically. The rats in the fish n-3 fatty acid-pretreated group were given 400 mg/kg/day fish n-3 fatty acids for 30 days by intragastric intubation. To induce acute cardiotoxicity, DOX (30 mg/kg) was injected intraperitoneally by a single dose and the rats were killed after 48 h. DOX treatment caused severe damage in heart tissues. Disorganization of myocardial muscle fibers, myofibrillar loss, and cardiotoxic myocardial fibers with cytoplasmic vacuoles were seen. Fish n-3 fatty acid-treated rats showed an improved histological appearance in the DOX-treated group. Our data indicate a significant reduction in the activity of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling in cardiomyocytes of the DOX-treated group with fish n-3 fatty acids therapy. The DOX-treated with fish n-3 fatty acids group showed a significant decrease in malondialdehyde levels, and an increase in superoxide dismutase and glutathione peroxidase activities in comparison with the DOX-treated group. This study showed that fish n-3 fatty acids may be a suitable cardioprotector against acute toxic effects of DOX.

Carotid intima-media thickness and serum paraoxonase-1 activity in patients with Helicobacter pylori.

AIM: To evaluate serum paraoxonase(PON)-1 activity and carotid intima-media thickness (CIMT) in patients with Cytotoxin-associated antigen(CagA)-positive and negative Helicobacter pylori strains. PATIENTS AND METHODS: The study group included a total of 134 individuals, of whom 103 were H. pylori positive, and 31 were H. pylori negative. Five biopsies were collected from each patient for histological examination: two from the antrum, two from the corpus, and one from the incisura angularis. The presence of H. pylori was determined using a modified Gram staining protocol. Peripheral blood was collected from each patient to determine levels of triglyceride, TC, HDL-cholesterol and LDL-cholesterol. IgG antibodies against CagA protein were analyzed by enzyme immunoassays. PON-1 activity was measured by colorimetric method. Carotid intima-media thickness and atherogenic plaques were measured using a grey scale color Doppler ultrasound. Data were analyzed by descriptive and inferential statistics. RESULTS: The right, the left and the mean CIMT were significantly higher in H. pylori (+) group versus H. pylori (-) group (p < 0.001 for all). However, the mean PON-1 concentration was significantly lower in H. pylori (+) group versus H. pylori (-) group (p < 0.001). The right, the left and the mean CIMT of CagA (+) group were significantly higher than that of CagA (-) group and controls, while PON-1 concentrations of CagA (+) group were significantly lower than that of CagA (-) group and controls (for all p = 0.0001). The right, the left and the mean CIMT of CagA (-) group were significantly higher than that of the control group, while the mean PON-1 concentration were significantly lower (for all p = 0.0001). CONCLUSIONS: Decreased PON-1 activity may be an etiopathogenetic factor in increased atherosclerosis in patients with H. pylori infection, especially in those infected with the CagA positive strain.