Evaluation of Serum Fetuin-A and Osteoprotegerin Levels in Patients with Psoriasis.

Psoriasis patients are determined to have a high ratio of coronary artery calcification. Fetuin-A and osteoprotegerin are systemic calcification inhibitors and related to vascular calcification and cardiovascular mortality. In this study we investigated the relationship between fetuin-A and osteoprotegerin levels in psoriasis patients. The study included 40 healthy volunteers and 40 psoriasis patients. Venous blood were collected from healthy volunteers and psoriasis patients in order to search the fetuin-A and osteoprotegerin levels. Disease severity were grouped as mild, moderate and severe according to psoriasis area and severity index (PASI). The relationship between fetuin-A and osteoprotegerin levels and clinical features as sex, PASI and presence of psoriatic arthritis were analyzed. Fetuin-A levels in psoriasis patients were statistically lower than the control group (p < 0.001). In serum osteoprotegerin levels, no statistically significant difference was found in two groups (p > 0.05). Serum fetuin-A and osteoprotegerin level differences were not statistically significant between patients with psoriatic arthritis history and those without. When we grouped patients in respect of their sexes fetuin-A and osteoprotegerin levels of males and females were not significantly different (p > 0.05). No correlation was detected between the ages and PASI scores and the fetuin-A and osteoprotegerin levels of patients. As a result fetuin-A levels in psoriasis patients are found to be low but not related to disease severity. In the light of our results we concluded that fetuin-A may have a role in psoriasis pathogenesis and may contribute to the calcification process developed in psoriasis.

Leptin levels in children with obstructive sleep apnea syndrome.

INTRODUCTION: The aim of this study is to assess the effect of obstructive sleep apnea syndrome (OSAS) severity on leptin levels in children. PATIENTS AND METHODS: Children with habitual snoring underwent overnight polysomnography. Fasting venous blood samples were obtained between 8 AM and 9 AM, following the night of the sleep study. Children with an apnea-hypopnea index of ≥ 5/h were included in the moderate-to-severe OSAS group while those with an apnea-hypopnea index of < 5/h formed the mild OSAS/primary snoring group. RESULT: 47 children (51% male and 49% female; mean age 7.8 ± 2.6 years) were recruited. Twenty seven participants were diagnosed with moderate-to-severe OSAS, and twenty children who had AHI < 5 were included in the mild OSAS/primary snoring. The two groups did not differ regarding age, gender and body mass index z score (p> 0.05). Furthermore there were no differences in log serum leptin levels (p= 0.749). Log serum leptin levels correlated with the BMI z score in the whole study group (p= 0.001; r= 0.499) but they were not associated with apnea-hypopnea index, mean and lowest oxygen saturation during sleep. CONCLUSIONS: Serum leptin levels are affected by adiposity but not by OSAS severity among children with habitual snoring.

Ischemia modified albumin increase indicating cardiac damage after experimental subarachnoid hemorrhage.

BACKGROUND: Cardiac complications are often developed after subarachnoid hemorrhage (SAH) and may cause sudden death of the patient. There are reports in the literature addressing ischemia modified albumin (IMA) as an early and useful marker in the diagnosis of ischemic heart events. The aim of this study is to evaluate serum IMA by using the albumin cobalt binding (ACB) test in the first, second, and seventh days of experimental SAH in rats.Twenty-eight Wistar albino rats were divided into four groups each consisting of seven animals. These were classified as control group, 1st, 2nd and 7th day SAH groups. SAH was done by transclival basilar artery puncture. Blood samples were collected under anesthesia from the left ventricles of the heart using the cardiac puncture method for IMA measurement. Histopathological examinations were performed on the heart and lung tissues. Albumin with by colorimetric, creatine kinase (CK), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) were determined on an automatic analyser using the enzymatic method. IMA using by ACB test was detected with spectrophotometer. RESULTS: Serum IMA (p = 0.044) in seventh day of SAH were higher compared to the control group. Total injury scores of heart and lung tissue, also myocytolysis at day 7 were significantly higher than control group (p = 0.001, p = 0.001, p = 0.001), day 1 (p = 0.001, p = 0.001, p = 0.001) and day 2 (p = 0.001, p = 0.007, p = 0.001). A positive correlation between IMA - myocytolysis (r = 0.48, p = 0.008), and between IMA - heart tissue total injury score (r = 0.41, p = 0.029) was found. CONCLUSION: The results revealed that increased serum IMA may be related to myocardial stress after SAH.

Levels of oxidized LDL, estrogens, and progesterone in placenta tissues and serum paraoxonase activity in preeclampsia.

In vitro literature studies have suggested that atherosclerotic oxidized low density lipoprotein (OxLDL) inhibits trophoblast invasion. The objective of this study was to determine the levels of OxLDL and to examine the relationship between antioxidative estradiol, estriol, and prooxidative progestin in normal and preeclamptic placental tissues and measure the serum activity of antioxidative paraoxonase (PON1). The study included 30 preeclamptic and 32 normal pregnant women. OxLDL was determined with ELISA, estradiol, unconjugated estriol, and progesterone that were determined with chemiluminescence method in placental tissues. Serum PON1 activity was determined with spectrophotometric method. Levels of OxLDL (P = 0.027), estriol (P < 0.001), estradiol (P = 0.008), and progesterone (P = 0.009) were lower in the placental tissues of preeclamptic group compared to the normal pregnant women. Serum PON1 activity was higher in preeclamptic group (P = 0.040) and preeclamptic group without intrauterine growth restriction (P = 0.008) compared to normal pregnant women. Tissue estriol of preeclamptic group without/with IUGR (P < 0.001, P = 0.002) was lower than the normal group. Results of our study suggest that the events leading to fetoplacental insufficiency lead to a reduction in the levels of estriol limit deposition of OxLDL in placental tissues. The serum PON1 activity is probably important in the inhibition of OxLDL in preeclampsia.

Evaluation of serum lipid levels in children.

This study aimed to establish reference values for serum levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) in children. The study included samples from 4,102 healthy children (2,003 boys and 2,099 girls) ages 1-18 years. The serum levels of total cholesterol, triglycerides, and HDL-C were determined using the Advia 2400 autoanalyzer. The LDL-C levels were calculated using the Friedewald equation. The mean, standard deviation, and 5th, 10th, 25th, 50th, 75th, 90th, and 95th percentile values of the biochemical parameters for boys and girls were detected. The total cholesterol and HDL-C levels were higher among the girls than among the boys in 15- to 18-year-old group. No significant difference was found for the other serum lipid levels among any of the age groups. This study provided pediatric reference intervals for the lipid parameters for children.

Effect of coenzyme Q10 on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats.

BACKGROUND: Head trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ10 in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ10 administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out. RESULTS: In the biochemical tests, tissue malondialdehyde (MDA) levels were significantly higher in the traumatic brain-injury group compared to the sham group (p < 0.05). Administration of CoQ10 after trauma was shown to be protective because it significantly lowered the increased MDA levels (p < 0.05). Comparing the superoxide dismutase (SOD) levels of the four groups, trauma + CoQ10 group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ10 and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema (p < 0.05). CONCLUSION: Neuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ10 use in rats with traumatic brain injury.

Inflammatory markers in preeclamptic patients.

BACKGROUND: Preeclampsia is characterized by hypertension and proteinuria that begins in the second half of pregnancy. Endothelial dysfunction and trophoblastic hypoperfusion seen in preeclampsia suggested to be part of an increased maternal inflammatory response to pregnancy. In this study, we aimed to evaluate some inflammatory markers in pre-eclamptic and normotensive pregnants. METHODS: The study included 36 cases with mild preeclamp-sia, 36 cases with severe preeclampsia and 33 cases of normotensive pregnant. High sensitive C-reactive protein (hsCRP) and serum amyloid A (SAA) were measured by enzyme-linked immunosorbent assays, serum procalcitonin was measured by enzyme-linked fluorescent immunassay. Mean arterial pressure (MAP) was used as an indicator of the severity of the disease. RESULTS: In severe preeclampsia group hsCRP, serum amyloid A and procalcitonin levels were significantly higher than mild preeclamptic and normotensive groups. SAA and hsCRP levels were higher in mild preeclamptic group when compared with normotensive pregnant but no significant difference was found in procalcitonin between these groups. There were significant correlations betweeen hsCRP, SAA, procalcitonin and MAP. CONCLUSIONS: The results confirm that inflammatory reactions are closely associated with preeclampsia.

Low-density lipoproteins oxidized after intestinal ischemia/reperfusion in rats.

BACKGROUND: Intestinal ischemia/reperfusion (I/R) is a complex phenomenon causing destruction of both local and remote tissues, as well as multiple-organ failure. We investigated the role of lipid peroxidation in damage to intestinal, liver, and lung tissues in this pathology. MATERIALS AND METHODS: The superior mesenteric artery was blocked for 30 min followed by 24 h of reperfusion. Tissues were removed and the presence of oxidized LDL, the activities of the superoxide dismutase enzyme, malondialdehyde levels, and inducible nitric oxide synthase expression were each evaluated in the intestinal, liver, and lung tissues. RESULTS: While there was no staining in the control group tissues, ischemia/reperfusion resulted in positive oxidized LDL staining in all of the I/R test group tissue samples. Inducible nitric oxide synthase expression was significantly increased in the ischemia/reperfusion group tissues. Compared with those of the control group rats, the ischemia/reperfusion group tissues showed significantly higher malondialdehyde levels and lower superoxide dismutase activities. CONCLUSIONS: This study demonstrated for the first time that oxidized LDL accumulated in the terminal ileum, liver, and lung tissues after intestinal ischemia/reperfusion. This occurrence (or the presence of oxidized LDL) may be an indicator of ongoing oxidative stress and enhanced lipid peroxidation. Augmentation of inducible nitric oxide synthase expression may play a role in progression of inflammation and LDL oxidation. These data support the hypothesis that cellular oxidative stress is a critical step in reperfusion-mediated injury in both the intestine and end organs, and that antioxidant strategies may provide organ protection in patients with reperfusion injury, at least through affecting interaction with free radicals, nitric oxide, and oxidized LDL.

Erythropoietin: a possible cytoprotective cytokine in acute necrotizing pancreatitis.

BACKGROUND/PURPOSE: Despite decades of research and clinical trials, a specific therapeutic treatment for acute pancreatitis (AP) has yet to be developed. The aim of the present study was to investigate the effects of erythropoietin on the severity of taurocolic acid-induced acute necrotizing pancreatitis. METHODS: Forty-seven male Wistar albino rats were randomized into seven experimental groups. In group I, animals were sham-operated (n = 5). In groups II, III, IV, IIepo, IIIepo, and IVepo, AP was induced by sodium taurodeoxycholate treatment (n = 7). In groups II, III, and IV, 1 ml normal saline and in groups IIepo, IIIepo, and IVepo, 1000 U/kg body weight erythropoietin (EPO) was administered intramuscularly immediately after the induction of AP. Animals were killed at 24, 48, and 72 h postoperatively. Histopathological and biochemical evaluations were performed. RESULTS: The serum levels of interleukin-6 (IL-6) and tissue levels of malondialdehyde were found to be significantly lower in EPO-administered groups when compared with the levels in groups without EPO treatment. The severity of pancreatic edema, acinar necrosis, inflammation, and perivascular infiltrate were reduced in all the EPO groups compared with the no-treatment groups. CONCLUSIONS: Our findings may reflect the possible cytoprotective effect of EPO in acute necrotizing pancreatitis.

Comparison of the calculated and measured osmolality in intracranial bleeding and head injury patients.

Not all clinical laboratories have an osmometer, and calculations for osmolality are a frequently used method for determining osmolality. The purpose of this study was to evaluate the performance of four formulas for the estimation of osmolality, with cryoscopic measurement as the reference standard in intracranial hemorrhage (ICH) and head injury (HI) patients who were not treated with mannitol. Forty HI and 31 ICH patients treated in the Neurosurgery Department were included in the study. Every 6 h over a period of 24 h, serum samples were collected from patients and osmolality was measured. In conclusion, our study shows that only formulas F1 [Osmolality = 1.86(Na) + 1.86(K) + Glucose + Urea] and F4 [Osmolality = 1.86(Na) + Glucose + Urea + Ethanol + 9] can be used to evaluate osmolality in ICH patients who were not treated with mannitol. In HI patients, none of the formulas should be used to calculate osmolality.

Oxidized low-density-lipoprotein accumulation is associated with liver fibrosis in experimental cholestasis.

OBJECTIVE: The aim of the present study was to examine the probable relationship between the accumulation of oxLDL and hepatic fibrogenesis in cholestatic rats. INTRODUCTION: There is growing evidence to support the current theories on how oxidative stress that results in lipid peroxidation is involved in the pathogenesis of cholestatic liver injury and fibrogenesis. One of the major and early lipid peroxidation products, OxLDL, is thought to play complex roles in various immuno-inflammatory mechanisms. METHODS: A prolonged (21-day) experimental bile duct ligation was performed on Wistar-albino rats. Biochemical analysis of blood, histopathologic evaluation of liver, measurement of the concentration of malondialdehyde (MDA) and superoxide-dismutase (SOD) in liver tissue homogenates, and immunofluorescent staining for oxLDL in liver tissue was conducted in bile-duct ligated (n=8) and sham-operated rats (n=8). RESULTS: Significantly higher levels of MDA and lower concentrations of SOD were detected in jaundiced rats than in the sham-operated rats. Positive oxLDL staining was also observed in liver tissue sections of jaundiced rats. Histopathological examination demonstrated that neither fibrosis nor other indications of hepatocellular injury were found in the sham-operated group, while features of severe hepatocellular injury, particularly fibrosis, were found in jaundiced rats. CONCLUSION: Our results support the finding that either oxLDLs are produced as an intermediate agent during exacerbated oxidative stress or they otherwise contribute to the various pathomechanisms underlying the process of liver fibrosis. Whatever the mechanism, it is clear that an association exists between elevated oxLDL levels and hepatocellular injury, particularly with fibrosis. Further studies are needed to evaluate the potential effects of oxLDLs on the progression of secondary biliary cirrhosis.

Predictors of atrial fibrillation after coronary artery bypass surgery.

OBJECTIVE: Atrial fibrillation is one of the most common arrhythmias associated with not only increased morbidity after coronary artery bypass grafting but also increased healthcare costs. Many factors are associated with atrial fibrillation onset after coronary artery bypass grafting. We prospectively examined which factors could predict atrial fibrillation after coronary artery bypass grafting. METHODS: Fifty-seven consecutive patients (37 men, mean age=60.2+/-12 years) with sinus rhythm before coronary artery bypass grafting are included the study. Clinical, demographic, laboratory and echocardiographic characteristics are all evaluated prospectively. The maximum and minimum P-wave duration (P(max) and P(min)) were measured from the 12-lead surface electrocardiogram. The difference between the P(max) and the P(min) was calculated and defined as P-wave dispersion. Preoperative venous blood samples were taken for N-terminal proBrain natriuretic peptide level analysis. RESULTS: Ten (17%) patients had postoperative atrial fibrillation. Patients with postoperative atrial fibrillation were older (69.4+/-6 versus 58.2+/-12 years, P=0.01), had lower ejection fraction (44.1+/-8.9% versus 54.3+/-9; P=0.002), higher proBrain natriuretic peptide levels (538+/-136 pg/ml versus 293+/-359 pg/ml; P=0.03), longer P(max) (142.2+/-13.7 ms versus 120.8+/-21.2 ms; P=0.006) and longer P-wave dispersion (55.0+/-8.2 ms versus 41.3+/-14.3 ms; P=0.008) compared with the patients without atrial fibrillation. Univariate analysis showed that increased age (P=0.01), lower ejection fraction (P=0.02), enlargement of left atrium (P=0.02), increased P(max) (P=0.006) and increased P-wave dispersion (P=0.008) and increased level of preoperative proBrain natriuretic peptide (P=0.03) were associated with postoperative atrial fibrillation. Positive correlation was seen between the age and level of proBrain natriuretic peptide (r=0.322 and P=0.015). In multivariate analysis, age (P=0.05), lower ejection fraction (P=0.03), left atrial enlargement (P=0.05), longer P(max) (P=0.01) and P-wave dispersion (P=0.01) were found to be independent predictors of postoperative atrial fibrillation. CONCLUSION: Age, poor left ventricular functions, P(max) and P-wave dispersion are found to be independent predictors of atrial fibrillation after coronary artery bypass grafting.

Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis.

AIM: To investigate the effect of exogenous erythro-poietin (EPO) administration on acute lung injury (ALI) in an experimental model of sodium taurodeoxycholate- induced acute necrotizing pancreatitis (ANP). METHODS: Forty-seven male Wistar albino rats were randomly divided into 7 groups: sham group (n = 5), 3 ANP groups (n = 7 each) and 3 EPO groups (n = 7 each). ANP was induced by retrograde infusion of 5% sodium taurodeoxycholate into the common bile duct. Rats in EPO groups received 1000 U/kg intramuscular EPO immediately after induction of ANP. Rats in ANP groups were given 1 mL normal saline instead. All animals were sacrificed at postoperative 24 h, 48 h and 72 h. Serum amilase, IL-2, IL-6 and lung tissue malondialdehyde (MDA) were measured. Pleural effusion volume and lung/body weight (LW/BW) ratios were calculated. Tissue levels of TNF-alpha, IL-2 and IL-6 were screened immunohistochemically. Additionally, ox-LDL accumulation was assessed with immune-fluorescent staining. Histopathological alterations in the lungs were also scored. RESULTS: The mean pleural effusion volume, calculated LW/BW ratio, serum IL-6 and lung tissue MDA levels were significantly lower in EPO groups than in ANP groups. No statistically significant difference was observed in either serum or tissue values of IL-2 among the groups. The level of tumor necrosis factor-alpha (TNF-alpha) and IL-6 and accumulation of ox-LDL were evident in the lung tissues of ANP groups when compared to EPO groups, particularly at 72 h. Histopathological evaluation confirmed the improvement in lung injury parameters after exogenous EPO administration, particularly at 48 h and 72 h. CONCLUSION: EPO administration leads to a significant decrease in ALI parameters by inhibiting polymorphonuclear leukocyte (PMNL) accumulation, decreasing the levels of proinflammatory cytokines in circulation, preserving microvascular endothelial cell integrity and reducing oxidative stress-associated lipid peroxidation and therefore, can be regarded as a cytoprotective agent in ANP-induced ALI.

Effects of angiotensin-converting enzyme gene polymorphism and serum vitamin D levels on ambulatory blood pressure measurement and left ventricular mass in Turkish hypertensive population.

INTRODUCTION: Regulation of angiotensin converting enzyme (ACE) and angiotensin II (ang-II) levels is under genetic control. 1,25(OH)2 vitamin D3 treatment has been shown to reduce the ang-II level, reduce myocardial hypertrophy and to decrease blood pressure. This study was designed to examine the effect of ACE gene polymorphisms on 24-h ambulatory blood pressure measurement (24 h) values, vitamin D levels and target organ damage in hypertensive patients. METHODS: This study was carried on 118 patients with essential hypertension (female/male: 70/48, mean age: 49.1+/-7.6 years, hypertension duration: 56+/-40.5 months). All patients were assessed for target organ damage; the eye by retinal examination, the heart with echocardiography and the kidney with blood and 24-h urine analysis. 24-h ambulatory blood pressure measurement was performed in all patients. PCR amplification was employed to detect ACE genotypes. RESULTS: ACE genotypes were as follows: DD (n=49) 41.5%; ID (n=37) 31.4% and II (n=32) 27.1%. No difference was present between groups of ACE polymorphism when 24-h ambulatory blood pressure measurement values, retinal vascular changes and microalbuminuria were taken into account. Statistically significant left ventricular mass index levels were obtained in the DD group when compared with the non-DD (ID+II) group (P : 0.009). Positive correlations have been noted between left ventricular mass index and day/night and early morning systolic pressures. A negative correlation exists between serum 25 (OH) vitamin D levels and 24-h ambulatory blood pressure measurement values (P<0.05). CONCLUSIONS: The presence of the D allele is linked with a higher risk for left ventricular mass index in the Turkish hypertensive population.

Sclerostin and bone metabolism markers in hyperthyroidism before treatment and interrelations between them.

Sclerostin, which is a glycoprotein produced by osteocytes, reduces the formation of bones by inhibiting the Wnt signal pathway. Thyroid hormones are related with Wnt signal pathway and it has been reported that increased thyroid hormones in hyperthyroidism fasten epiphysis maturation in childhood, and increase the risk of bone fractures by stimulating the bone loss in adults. The aim of this study was to examine the sclerostin serum levels, the relation between sclerostin and thyroid hormones as well as the biochemical markers of the bone metabolism in patients with hyperthyroidism (including multinodular goiter and Graves' disease), whose treatments have not started yet. No difference was found in the serum sclerostin levels between the hyperthyroidism group (n=24) and the control group (n=24) (p=0.452). The serum osteocalcin levels and 24-hour urinary phosphorus excretion were found to be higher in the hyperthyroid group than in the control group (p<0.001, p=0.009). A positive correlation was determined between the sclerostin and bone alkaline phosphatase levels (p<0.001); a negative correlation between the osteocalcin and thyroid stimulating hormone (TSH) (p<0.05); a positive correlation between the osteocalcin and thyroid hormones (FT3,FT4) (p<0.001); and a positive correlation between the deoxypyridinoline and hydroxyproline (p<0.001). No correlation was determined between sclerostin and TSH,FT3,FT4 (p>0.05). Therefore, we consider that a long-term study that covers the pre-post treatment stages of hyperthyroidism, including both the destruction and construction of the skeleton would be more enlightening. Moreover, the assessment of the synthesis of sclerostin in the bone tissue and in the serum level might show differences.

Serum cardiovascular risk factors in obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) patients have increased cardiovascular morbidity and mortality. The cardiovascular markers associated with OSA are currently not defined. OBJECTIVES: The aims of this study were to determine whether OSA is associated with serum cardiac risk markers and to investigate the relationship between them. METHODS: Sixty-two male patients were classified into two groups with respect to apnea-hypopnea index (AHI): group 1, sleep apnea (n = 30), with AHI > 5; and group 2 (n = 32), with AHI < 5. We compared cardiovascular risk factors in both groups with control subjects (n = 30) without OSA (AHI < 1). Serum cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A-I, apolipoprotein B, lipoprotein (a), C-reactive protein (CRP), and homocysteine were measured. Statistical significance was assessed with analysis of variance at p < 0.05. In correlation analysis, Pearson correlation was used. RESULTS: There was no significant difference between group 1 and group 2 in total cholesterol, LDL-C, HDL-C, triglyceride, apolipoprotein A-I, apolipoprotein B, and lipoprotein (a). All of the M-mode echocardiographic parameters were in the normal reference range. Serum homocysteine and CRP levels were significantly increased in group 1 compared to group 2 (p < 0.05). Serum CRP values were increased in both group 1 and group 2 when compared with control subjects (p < 0.05). Serum homocysteine values were higher in group 1 than in control subjects (p < 0.05). CONCLUSIONS: Our results show that OSA syndrome is associated not only with slight hyperhomocysteinemia but also with increased CRP concentrations. Increased plasma concentrations of homocysteine and CRP can be useful in clinical practice to be predictor of long-term prognosis for cardiovascular disease and the treatment of OSA.

Comparison of angiotensin-converting enzyme, malonaldehyde, zinc, and copper levels in preeclampsia.

Preeclampsia is a syndrome of unknown etiopathogenesis. Recent studies carried out on preeclampsia have focused on the increase in free radicals in the feto-placental unit with poor perfusion. It is believed that the renin-angiotensin system (RAS) has a role in the poor perfusion of the placenta. It is uncertain whether there is a pre-existing impairment in RAS in pre-eclamptic pregnant women or not. In the present study, we measured angiotensin-converting enzyme (ACE), malonaldehyde (MDA), zinc, and copper levels in the placental tissue of 16 pre-eclamptic pregnant women and compared them with those in 20 healthy pregnant women. Whereas ACE activity and MDA were found to be high in the placentas of pre-eclamptic patients, zinc and copper levels were low and there was a negative correlation between ACE activity and zinc concentration. These findings suggest that high ACE activity might play a role in the increase in tissue hypoxia and consequent lipid peroxidation through vasoconstriction; zinc deficiency in the placental tissue might cause insufficiency of superoxide dismutase, an antioxidant enzyme. Furthermore, deficiency in placental zinc also plays a role in the biosynthesis of connective tissue, maintaining its integrity, which might have an impact on the structure of the spiral arteries.

Apoptosis and necrosis in the circumventricular organs after experimental subarachnoid hemorrhage as detected with annexin V and caspase 3 immunostaining.

OBJECTIVES: The circumventricular organs (CVOs) are essential for most autonomic and endocrine functions. Trauma and bleeding can affect their function. The aim of this study was to investigate apoptosis and necrosis in CVOs in the early period after experimental subarachnoid hemorrhage (SAH) in rats, using annexin V affinity and caspase 3 immunostaining. METHODS: Three experimental groups were used: Days 1 and 2 after SAH, and a control group, seven Wistar albino rats each. Subarachnoid hemorrhage was accomplished by transclival basilar artery puncture. Rats were perfused with 0.9% NaCl and 0·1M phosphate buffer pH 7.4 until heart stoppage. Apoptosis and necrosis in CVOs were measured by flow cytometry with annexin V staining, and by caspase 3 immunostaining. RESULTS: Apoptosis in the organum vasculosum lamina terminalis (OVLT), median eminence (ME), and area postrema (AP) was significantly higher in the Day 1 group than in the control group. Apoptosis in the subfornicial organ (SFO), OVLT, ME, and AP was significantly higher in the Day 2 group than in the control group. There were significant differences between the Day 1 and Day 2 groups, except for AP. Necrosis in SFO and OVLT was significantly higher in the Day 2 group than in the Day 1 or control groups, whereas necrosis in the ME and AP did not differ between the three groups. Caspase 3-positive cell density was more intense in the Day 2 group than in the Day 1 and control groups. DISCUSSION: Prevention of apoptosis may potentially improve impaired functions of CVOs after SAH.

Cystain C and neuropeptid Y levels in brain tissues after experimental subarachnoid hemorrhage.

The aim of this study was to investigate the changes in the levels of cystatin C, which protects neurodegeneration in the central nervous system with the inhibition of cysteine protease and by inducing autophagy in the pathogenesis of cerebral vasospasm and levels of vasoconstrictive neuropeptid Y (NPY) in the brain tissue homogenates of rat model of subarachnoid hemorrhage (SAH). Three experimental groups were used: Day 2 and Day 7 groups after SAH, and also a control group. There were seven Wistar albino rats in each group. SAH was accomplished by transclival basilar artery puncture. Rat cystatin C, rat NPY were determined with ELISA in brain tissue homogenates. Day 2 group showed significantly enhanced cystatin C values in comparision with the control group (P=0.048). NPY levels between the Day 2 and Day 7 groups and the control groups were not significantly different (P=0.315). In histopathological examination, there was less neuronal loss in the Day 2 group than in the Day 7 group. Regarding our results, it would be more valuable to measure NPY levels in specific brain areas. The increased cystatin C levels on the second day after SAH is probably a pathophysiologic mechanism to organize protease activity.

Determinants of plasma homocysteine in coal miners.

AIM: Several studies suggest that coal miners are under risk of severe health problems such as cardiovascular, pulmonary, neurological, renal, hematological and musculoskeletal disorders. However, there are limited data on biochemical changes in underground workers. In our study we aimed to evaluate the association between serum homocysteine (Hcy), vitamin B12, cystatin C and folate levels in the blood of underground coal miners. MATERIALS AND METHODS: Eighty one coal miners who work as underground or surface workers were recruited into our study. The study population was divided into two groups: the surface worker group (control group, n=33) and the underground worker group (n=48). The folate, vitamin B12, Hcy, cystatin C levels and body mass indexes (BMI) of both groups were measured and compared. Serum folate, Hcy and vitamin B12 levels were measured with a competitive chemiluminescence immunassay. Serum levels of cystatin C were determined by the latex particle-enhanced turbidimetric method using a cystatin C kit. Urea values were measured with a kinetic method on an automated analyzer. RESULTS: There were no statistically significant differences between the underground workers and surface workers in the urea, cystatin C and vitamin B12 levels. High serum Hcy levels and low folate levels were found in underground workers compared with those in surface workers. The correlation between Hcy and folate levels was also statistically significant. Similarly, there was also a significant correlation between Hcy and vitamin B12, and between Hcy and cystatin C levels. CONCLUSIONS: Elevated Hcy levels may be associated with underground working but further research is necessary to understand the relation between elevated Hcy and increased prevalence of health problems in coal miners.