Framingham risk score and severity of coronary artery disease.

OBJECTIVES: Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Easy-to-perform and reliable parameters are needed to predict the presence and severity of CAD and to implement efficient diagnostic and therapeutic modalities. We aimed to examine whether the Framingham risk scoring system can be used for this purpose. METHODS: A total of 222 patients (96 women, 126 men; mean age, 59.1 ± 11.9 years) who underwent coronary angiography were enrolled in the study. Presence of > %50 stenosis in a coronary artery was assessed as critical CAD. The Framingham risk score (FRS) was calculated for each patient. CAD severity was assessed by the Gensini score. The relationship between the FRS and the Gensini score was analyzed by correlation and regression analyses. RESULTS: The mean Gensini score was 18.9 ± 25.8, the median Gensini score was 7.5 (0-172), the mean FRS was 7.7 ± 4.2, and the median FRS was 7 (0-21). Correlation analysis revealed a significant relationship between FRS and Gensini score (r = 0.432, p < 0.0001). This relationship was confirmed by linear regression analysis (ß = 0.341, p < 0.0001). A cut-off level of 7.5 for FRS predicted severe CAD with a sensitivity of 68 % and a specificity of 73.6 % (ROC area under curve: 0.776, 95 % CI: 0.706-0.845, PPV: 78.1 %, NPV: 62.3 %, p < 0.0001). CONCLUSION: Our work suggests that the FRS system is a simple and feasible method that can be used for prediction of CAD severity. As the sample size was small in our study, further large-scale studies are needed on this subject to draw solid conclusions.

Aortic elastic properties : effects of carvedilol versus nebivolol.

OBJECTIVES: The aim of this study was to compare the effects of the new generation ß-blocker anti-hypertensive drugs carvedilol and nebivolol on aortic elastic properties which are important indicators of hypertension-related morbidity and mortality. METHODS: A total of 50 patients who had been diagnosed with stage 1 hypertension according to the Joint National Committee (JNC) VII criteria and who had not received any anti-hypertensive treatment were enrolled in this study. Patients were randomized to receive either 25 mg/day carvedilol (n=25) or 5 mg/day nebivolol (n=25) for 3 months at the beginning of the study. Three patients (1 in the carvedilol group, 2 in the nebivolol group) who did not attend 3 month follow-up measurements were excluded from the study. The study was completed with 47 patients (25 women; mean age: 49 ± 9 years). The aortic elastic parameters such as aortic strain (AS), aortic distensibility (AD), and aortic stiffness index (ASI) were measured by echocardiography. RESULTS: Carvedilol and nebivolol provided a similar decline in both systolic and diastolic blood pressures (-12/-7 mmHg, p<0.0001 and -12/-7 mmHg, p=0.002, respectively). Both carvedilol and nebivolol induced a significant decrease in heart rate (-15 bpm, p<0.0001, -17 bpm, p<0.0001, respectively). Even though the heart rate at the end of the treatment was lower for the nebivolol group, the rate of decrease of heart rates between carvedilol and nebivolol groups was not statistically significant (p=0.074). Both groups demonstrated improvements in the diastolic functions of the left ventricle where certain values showed more improvement for the nebivolol group. Both groups showed improvements in AS and AD rates compared to basal rates; however, these improvements were not statistically significant. Although the improvement rates in AS, AD, and ASI were higher in the nebivolol group compared to the carvedilol group, the differences were not statistically significant (p=0.091, p=0.095, p=0.259, respectively). CONCLUSION: Both carvedilol and nebivolol induced a decrease in blood pressure and heart rate and showed an improvement in left ventricular diastolic functions. It was observed that both drugs did not cause deterioration in the aortic elastic properties but a slight improvement was seen. However, this improvement was not statistically significant. The improvement was more explicit in the nebivolol group. It may be concluded that nebivolol is slightly superior to carvedilol in reducing heart rate and improving left ventricular diastolic functions. However, further long-term studies with larger sample sizes should be performed in order to better define the effects of both drugs.

Natural radiation monitoring and control treatment in the Hantepe beach.

This work has been carried out to monitor and decrease the natural radiation exposure at the Hantepe beach (Çanakkale, Turkey). A 0.25- to 0.30-m-thick layer of sand was scraped, removed and deposited in a safe place in order to decrease people's exposure to radiation and to relieve relevant radiophobia. The original mean value of dose rate on the beach was 1.38 µGy h(-1) at the contact and 1.0 µGy h(-1) at 1 m above the ground. After the scraping process, the mean value of dose rate decreased to 0.98 µGy h(-1) at the contact and to 0.78 µGy h(-1) at 1 m above the ground. One year later, these values decreased to 0.70 µGy h(-1) at the contact and to 0.56 µGy h(-1) at 1 m above the ground. The effective original dose rate of 1.2 mSv y(-1) decreased to 0.95 mSv y(-1) after the surface treatment and to 0.69 mSv y(-1) one year later.

L-Carnitine ameliorates methotrexate-induced oxidative organ injury and inhibits leukocyte death.

Methotrexate (MTX), a folic acid antagonist widely used for the treatment of a variety of tumors and inflammatory diseases, affects normal tissues that have a high rate of proliferation, including the hematopoietic cells of the bone marrow and the gastrointestinal mucosal cells. To elucidate the role of free radicals and leukocytes in MTX-induced oxidative organ damage and the putative protective effect of L-carnitine (L-Car), Wistar albino rats were administered a single dose of MTX (20 mg/kg) followed by either saline or L-Car (500 mg/kg) for 5 days. After decapitation of the rats, trunk blood was obtained, and the ileum, liver, and kidney were removed for histological examination and for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen content. Our results showed that MTX administration increased the MDA and MPO activities and collagen content and decreased GSH levels in all tissues, while these alterations were reversed in L-Car-treated group. The elevated serum TNF-alpha level observed following MTX treatment was depressed with L-Car. The oxidative burst of neutrophils stimulated by Annexin V was reduced in the saline-treated MTX group, while L-Car abolished this inhibition. Similarly, flow cytometric measurements revealed that leukocyte apoptosis was increased in MTX-treated animals, while L-Car reversed these effects. Severe degeneration of the intestinal mucosa, liver parenchyma, and glomerular and tubular epithelium observed in the saline-treated MTX group was improved by L-Car treatment. These results suggest that L-Car, possibly via its free radical scavenging and antioxidant properties, ameliorates MTX-induced oxidative organ injury and inhibits leukocyte apoptosis. Thus, supplementation with L-Carnitine as an adjuvant therapy may be promising in alleviating the systemic side-effects of chemotherapeutics.

Effect of interferon-alpha(2a) on neutrophil adhesion and phagocytosis in chronic myeloid leukemia and Behçet's disease.

Alpha-interferon (alpha-IFN) is implicated in a Behçet's disease (BD)-like syndrome observed in a small number of chronic myeloid leukemia (CML) patients. The effect of alpha-IFN on neutrophil adhesion and phagocytosis in CML patients, BD patients and healthy volunteers was investigated to clarify the reason for this observation. Ten subjects were studied for each group by incubating neutrophils with various doses of alpha-IFN. Basal neutrophil adhesions for CML patients, BD patients and healthy volunteers were similar. However, BD patients had greater basal phagocytosis than CML patients, and both groups had greater basal phagocytosis than healthy volunteers. Neutrophil adhesion and phagocytosis of CML patients increased following incubation with higher doses of alpha-IFN, and phagocytosis approached the high levels observed with BD neutrophils. This study provides evidence that alpha-IFN activates neutrophils in CML patients in a dose-dependent manner, and leads to a neutrophil function profile that resembles BD.

Effect of omeprazole on gallbladder contraction in humans.

BACKGROUND/AIMS: Omeprazole causes hypergastrinemia because of the effects of prolonged complete suppression of acid secretion and also gastrin has an excitatory effect on gallbladder contraction. Therefore, we investigated the meal-induced gallbladder emptying in healthy subjects receiving omeprazole and compared them to controls. METHODOLOGY: Twenty healthy volunteers participated in this study. Gallbladder volume was measured by ultrasonography. After basal measurement, the volunteers received saline intravenously (i.v.) 2 cc (no:10) or omeprazole 20 mg i.v. (no:10). After 15 min the gallbladder volume was scanned at 15 min intervals for 60 min for each of the subjects. At the end of the period, all the subjects received a standard test meal (ensure 250 cal/250 mL), after 1 hour the gallbladder volumes were rescanned at 15 min periods for 60 min. RESULTS: Mean gallbladder volume in the omeprazole group was not significantly different during a 45 min period as compared to the baseline value. The residual gallbladder volume at the end of the 15th minute (43.9 +/- 5.6 mL), 30th minute (45.4 +/- 5.9 mL), 45th minute (40.5 +/- 6.1 mL) and 60th minute (40.5 +/- 6.1 mL) showed no significant differences in both the omeprazole group and the controls. Mean gallbladder volumes of both groups after meal intake were significantly lower during the 1-hour period as compared to the baseline value (P < 0.05). The mean volumes did not show any significant differences between the omeprazole group and the control subjects. CONCLUSIONS: Omeprazole did not change the gallbladder volume during fasting and the postprandial period as compared to the control group.

Role of hepatocyte growth factor in the development of dendritic cells from CD34+ bone marrow cells.

BACKGROUND AND OBJECTIVE: Hepatocyte growth factor (HGF) is known to augment the effects of stem cell factor, interleukin-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), erythropoetin, and granulocyte colony-stimulating factor, all of which are involved in hematopoiesis. HGF is also known to have a role in immune responses. The aim of this study was to investigate whether HGF is involved in the development of dendritic cells (DC) from CD34+ bone marrow cells. DESIGN AND METHODS: CD34+ cells obtained from three healthy donors were incubated in various combinations of HGF, GM-CSF, and tumor necrosis factor (TNF) for 12 days. Developing cell populations were analyzed for surface markers, morphology and functional capacities by flow cytometry, light microscopy and mixed lymphocyte reaction, respectively. RESULTS: Incubation with HGF alone generated greater number of dendritic cells from CD34+ bone marrow cells than incubation with GM-CSF, or a combination of GM-CSF with TNF. HGF was also found to potentiate the effect of GM-CSF on DC and monocyte development. The effects of HGF were inhibited by the concurrent use of TNF. INTERPRETATION AND CONCLUSIONS: HGF appears to be a significant factor in the development of dendritic cells from CD34+ bone marrow cells.

Normal Pressure Hydrocephalus Associated with Chronic Alpha Interferon Treatment: A Case Report.

Chronic a-interferon use has been reported to cause a variety of neurotoxic side effects. This case summary suggests the possibility of a new neurotoxic side effect of normal pressure hydrocephalus following chronic a-interferon use.

Nitric oxide modulation of calcium-activated potassium channels in postganglionic neurones of avian cultured ciliary ganglia.

1. A study has been made of the modulation of calcium-activated potassium channels in cultured neurones of avian ciliary ganglia by sodium nitroprusside and L-arginine. 2. Sodium nitroprusside (100 microM) reduced the net outward current by 22 +/- 1% at 4.8 ms (mean +/- s.e. mean) and 25 +/- 1% at 350 ms during a test depolarization to +40 mV from a holding potential of -40 mV. The outward current remained reduced for the duration of the recording following a single application of sodium nitroprusside. These effects did not occur if the influx of calcium ions was first blocked with Cd2+ (500 microM). Application of ferrocyanide (100 microM) reduced the net outward current by only 6 +/- 3% at 350 ms during a test depolarization to +40 mV. 3. L-Arginine (270 microM) reduced the net outward current on average by 19 +/- 2% at 4.8 ms and 22 +/- 2% at 350 ms during a test depolarization to +40 mV. The current remained in this reduced state for the duration of the recording following a single application of L-arginine. These effects were reduced to 11 +/- 1% at 4.8 ms and 11 +/- 2% at 350 ms in the presence of N omega-nitro-L-arginine methyl ester (L-NAME, 100 microM). 4. In order to alleviate the dependence of calcium-activated potassium channels (Ik(Ca)) on the inward flux of calcium ions, the patch-clamp pipettes were filled with a solution containing 100 microM CaCl2, and the Ca2+ in the bathing solution was replaced with EGTA. Under these conditions sodium nitroprusside reduced the total outward current during a depolarizing pulse of + 40 mV by 9 +/_ 1% at 4.8 ms and by 36 +/- 3% at 350 ms. L-Arginine (270 microM) reduced this current under the same conditions by 9 +/- 1% at 4.8 ms and by 35 +/- 2% at 350 ms.5. Calcium-activated potassium currents were sensitive to apamin (50 nM), as this reduced the outward current by 23 +/- 3% at 350 ms when a high calcium-containing pipette was used during a depolarizing command to + 40 mV. L-Arginine still decreased the outward current in the presence of apamin(50 nM), by 5 +/- 1% at 4.8 ms and by 19 +/- 2% at 350 ms, indicating that L-arginine could reduce an apamin-insensitive Ik(Ca)6. Calcium-activated potassium currents were also sensitive to charybdotoxin (10 nM), as this reduced the outward current by 34 +/- 4% at 350 ms when a high calcium-containing pipette was used during a depolarizing command to + 40 mV. L-Arginine still decreased the outward current in the presence of charybdotoxin, by 6 +/- 1% at 4.8 ms and 12 +/- 4% at 350 ms, showing that L-arginine could reduce a charybdotoxin-insensitive Ik(Ca).7. The present results indicate that NO-synthase in ciliary ganglia can modulate Ik(Ca) by a method which is independent of the action of NO on the calcium channels. The Ik(ca) is decreased significantly at 4.8 ms into a depolarizing pulse, at a time that would decrease the rate of repolarization of the action potential. Ik(Ca) is also reduced at longer times (350 ms), indicating an affect on the inactivating process.