Self-esteem and psychiatric features of Turkish adolescents with psychogenic non-epileptic seizures: a comparative study with epilepsy and healthy control groups.

OBJECTIVE: Children and adolescents with psychogenic non-epileptic seizures (PNES) and epilepsy are known to have psychosocial problems. The aim of the present study was to compare the psychosocial difficulties, history of stressful life events/abuse, psychiatric diagnosis, and self-esteem of adolescents with PNES to the ones with epilepsy and healthy controls at a tertiary care center in Turkey. METHOD: Thirty-four adolescents with PNES diagnosed by video-EEG were compared with 23 adolescents that have epilepsy and 35 healthy volunteers. Comorbid psychiatric diagnoses of participants were examined by semi-structured interviews using Schedule for Affective Disorders and Schizophrenia for School Age Children-Present and Lifetime Version (KSADS-PL). Self-esteem of adolescents was evaluated by Rosenberg Self Esteem Scale (RSES). RESULTS: No differences in sociodemographic features were observed between the groups. The PNES group showed significantly higher rates of parental conflicts, difficulties in relationship with siblings/peers, school under-achievement, and history of stressful events/abuse. The rates of comorbid psychiatric disorders were 64.7% in PNES and 47.8% in epilepsy group. The most common disorders in both groups were attention deficit hyperactivity disorder (ADHD) and depressive disorder. The rate of posttraumatic stress disorder (PTSD) was significantly increased in the PNES group. Additionally, adolescents with PNES displayed significantly lower levels of self-esteem than the other groups. CONCLUSION: It could be concluded that both disorders involved a high risk for developing psychiatric disorders; additionally, adolescents with PNES have higher rates of stressors and lower levels of self-esteem. Findings from this investigation point to the importance of psychiatric interventions in pediatric PNES and also epilepsy.

Relation of depot-specific adipose inflammation to insulin resistance in human obesity.

BACKGROUND: A low-grade state of adipose tissue inflammation associated with obesity has been linked to mechanisms of systemic metabolic dysfunction. However, the relation of clinical phenotypes to depot-specific inflammation has not been well examined in human obesity. OBJECTIVE: To characterize the inflammatory status of subcutaneous and visceral fat depots, as assessed by tissue presence of macrophage crown-like structures (CLS) as a hallmark of chronic inflammation, and determine the relation of systemic insulin resistance to inflammatory abnormalities in subcutaneous and visceral fat. METHODS: We collected adipose tissue simultaneously from subcutaneous and visceral (omental and mesenteric) depots in 92 obese participants (age 42±11 years; BMI30 kg m(-2)) during planned bariatric surgery. Using immunohistochemistry, we categorized individuals as CLS(+) or CLS(-) based on the presence or absence, respectively, of macrophage CLS in subcutaneous (CLSs), omental (CLSo) and mesenteric (CLSm) adipose depots. RESULTS: The majority of participants exhibited adipose tissue inflammation manifest by the presence of CLS (CLS(+)) in both subcutaneous and intra-abdominal visceral depots. CLS status in subcutaneous fat was highly sensitive and modestly specific for inflammation of visceral fat. In multivariable models, plasma insulin and homeostatis model assessment levels were positively associated with CLS(+) status in all depots independent of age, waist circumference, BMI and type 2 diabetes, and worsened with the increasing number of adipose regions involved. CONCLUSIONS: In severely obese participants, systemic insulin resistance is linked to adipose inflammation in both subcutaneous and visceral depots. The findings suggest that examination of subcutaneous regions that are more easily accessible by transcutaneous biopsy may prove useful in clinical studies designed to investigate adipose phenotypes in relation to human disease.

Mechanisms of oxidative stress and vascular dysfunction.

The endothelium regulates vascular homoeostasis through local elaboration of mediators that modulate vascular tone, platelet adhesion, inflammation, fibrinolysis, and vascular growth. Impaired vascular function contributes to the pathogenesis of atherosclerosis and acute coronary syndromes. There is growing pathophysiological evidence that increased generation of reactive oxygen species and oxidative stress participates in proatherogenic mechanisms of vascular dysfunction and atherothrombosis. In this review, the role of oxidative stress in mechanisms of vascular dysfunction is discussed, and potential antioxidant strategies are reviewed.

[The anatomists who started anthropology in Turkey and their contributions]. / Türkiyede antropoloji bilimini kuran anatomistler ve katkilari.

The Turkish Institute of Antropology was estabilished in 1925 as a unit of the Medical School of Istanbul University (Darülfünun), named the Antropology Research Center (Antropoloji Tetkikat Merkezi). It was a part of the medical faculty until 1932. After the university reform it was connected to the School of Science and in late 1935 it was transfered to the School of Languages History and Geography (Dil Tarih Cografya Fakültesi) in Ankara. The center started to publish "The Journal of Turkish Anthropology" with Dr. Nuretttin Ali Berkols researches in 1925. It was published in two languages, Turkish and French. The faculty members of the institute, Dr. Mouchet, Dr. Süreyya Ali and Dr. Ismail Hakki formed the editorial board of the journal. We see that from the first issue of the journal in 1925 until the special issue prepared for the XVIII. Anthropology and Prehistorical Archealogy Congress in 1939, Dr. Nurettin Ali Berkol and Dr. Mouchet were members of the administrative committee of the journal. In this article; we studied the contributions of the anatomists to the development of anthropology in Turkey.

Effects of race and hypertension on flow-mediated and nitroglycerin-mediated dilation of the brachial artery.

Black Americans have increased morbidity and mortality rates from cardiovascular disease, greater prevalence of hypertension, and altered responses to vasodilator medications compared with those of white Americans. Hypertension and black race have been linked to impaired vascular function in the microcirculation. To examine these effects and their interaction in the conduit vasculature, we examined vasomotor responses of the brachial artery by using high-resolution vascular ultrasound in 228 subjects (48% hypertensive, 54% black). Subjects had no history of diabetes mellitus and were matched for age and gender. Flow-mediated dilation (8.5+/-5.3% versus 11.7+/-6.3%, P<0.001) and nitroglycerin-mediated vasodilation (14.9+/-6.0 versus 18.5+/-7.8, P=0.003) were both impaired in hypertensive compared with normotensive individuals. Multivariate analysis identified higher systolic blood pressure (P=0.003) and larger baseline vessel (P<0.001) size as independent predictors of lower flow-mediated dilation. Race did not significantly influence flow-mediated dilation. In contrast, blacks had a greater vasodilator response to nitroglycerin compared with whites (17.7+/-7.5% versus 15.0+/-6.2%, respectively; P=0.02). By multivariate analysis, black race (P=0.004), smaller vessel size (P=0.001), lower serum glucose (P=0.02), lower systolic blood pressure (P=0.02), and lower serum total cholesterol (P=0.04) were independent predictors of higher nitroglycerin-mediated dilation. Thus, hypertension is associated with impaired NO-mediated vasodilation in the conduit brachial artery. Overall, race did not influence flow-mediated dilation, but black race was associated with an enhanced response to sublingual nitroglycerin. This later observation provides further evidence of racial differences in the responses to medical therapy that may be relevant to the treatment of patients with cardiovascular disease.

Acute hypertriglyceridemia is associated with peripheral vasodilation and increased basal flow in healthy young adults.

Prior studies suggest that acute elevations in plasma triglycerides alter vascular tone and impair endothelial function. To investigate the relation between acute hypertriglyceridemia and vascular function, we examined the effects of high- and low-fat meals on brachial artery reactivity in 14 healthy volunteers. Flow-mediated dilation declined from 14.7 +/- 8.3% to 10.6 +/- 6.2% after the high-fat meal only (p <0.001), and this decline was associated with a 6% increase in baseline brachial artery diameter (3.50 +/- 0.74 mm to 3.70 +/- 0.81 mm, p <0.001), but not a decrease in the arterial diameter during hyperemia. The high-fat meal increased serum triglycerides and insulin by 94% and 438%, respectively. To investigate the effects of triglyceride elevation in isolation from hyperinsulinemia, we examined vascular responses to an intravenous infusion of a triglyceride emulsion in 28 subjects. Triglyceride emulsion increased serum triglycerides 197% but had no effect on serum insulin. Brachial artery diameter increased 4%, from 3.68 +/- 0.51 mm to 3.81 +/- 0.56 mm (p <0.05), and forearm flow increased 36%, reflecting vasodilation of forearm resistance vessels. Flow-mediated dilation and nitroglycerin-mediated dilation were unaffected. The triglyceride emulsion had no direct dilator effect on rabbit aortic tissue in vitro. In conclusion, acute hypertriglyceridemia is associated with vasodilation of conduit and resistance vessels in the arm and does not impair endothelial vasodilator function per se. The dilator effect is not insulin-dependent and does not appear to be a direct effect of triglycerides on vascular tissue.

Short- and long-term black tea consumption reverses endothelial dysfunction in patients with coronary artery disease.

BACKGROUND: Epidemiological studies suggest that tea consumption decreases cardiovascular risk, but the mechanisms of benefit remain undefined. Endothelial dysfunction has been associated with coronary artery disease and increased oxidative stress. Some antioxidants have been shown to reverse endothelial dysfunction, and tea contains antioxidant flavonoids. Methods and Results-- To test the hypothesis that tea consumption will reverse endothelial dysfunction, we randomized 66 patients with proven coronary artery disease to consume black tea and water in a crossover design. Short-term effects were examined 2 hours after consumption of 450 mL tea or water. Long-term effects were examined after consumption of 900 mL tea or water daily for 4 weeks. Vasomotor function of the brachial artery was examined at baseline and after each intervention with vascular ultrasound. Fifty patients completed the protocol and had technically suitable ultrasound measurements. Both short- and long-term tea consumption improved endothelium- dependent flow-mediated dilation of the brachial artery, whereas consumption of water had no effect (P<0.001 by repeated-measures ANOVA). Tea consumption had no effect on endothelium-independent nitroglycerin-induced dilation. An equivalent oral dose of caffeine (200 mg) had no short-term effect on flow-mediated dilation. Plasma flavonoids increased after short- and long-term tea consumption. CONCLUSIONS: Short- and long-term black tea consumption reverses endothelial vasomotor dysfunction in patients with coronary artery disease. This finding may partly explain the association between tea intake and decreased cardiovascular disease events.

Iron chelation improves endothelial function in patients with coronary artery disease.

BACKGROUND: Some epidemiological studies have shown that increased iron stores are associated with increased cardiovascular events. Redox-active iron may contribute to lipid peroxidation, endothelial cell activation, and generation of reactive oxygen species (especially hydroxyl radical, via Fenton chemistry). Increased oxidative stress is associated with impaired action of endothelium-derived nitric oxide in patients with atherosclerosis. METHODS AND RESULTS: To test the hypothesis that reducing vascular iron stores would reverse endothelial dysfunction, we examined the effects of the iron chelator deferoxamine (500 mg intra-arterially over 1 hour) on vasomotor function in forearm resistance vessels of patients with coronary artery disease by venous occlusion plethysmography. Patients with coronary artery disease had impaired endothelium-dependent vasodilation in response to methacholine compared with healthy control subjects (P<0.001). Deferoxamine infusion decreased serum iron levels (P<0.001). Deferoxamine improved the blood flow response to methacholine in patients with coronary artery disease (P<0.01 by 2-way repeated-measures ANOVA) but had no effect on the response to sodium nitroprusside. In normal volunteers, deferoxamine had no effect on the response to methacholine. The nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine abolished augmentation of the methacholine response associated with deferoxamine. The hydroxyl radical scavenger mannitol had no effect on the methacholine response. CONCLUSIONS: Deferoxamine improved nitric oxide-mediated, endothelium-dependent vasodilation in patients with coronary artery disease. These results suggest that iron availability contributes to impaired nitric oxide action in atherosclerosis.

Effect of ascorbic acid treatment on conduit vessel endothelial dysfunction in patients with hypertension.

Hypertension is associated with low plasma ascorbic acid levels and impaired endothelial function. Recent evidence suggests that increased vascular oxidative stress contributes to the pathophysiology of endothelial dysfunction and hypertension. We recently showed that chronic oral ascorbic acid therapy lowers blood pressure in hypertensive patients. We hypothesized that it would also improve endothelial vasomotor function. In a randomized, double-blind, placebo-controlled study, we examined the effect of acute (2 g po) and chronic (500 mg/day for 1 mo) ascorbic acid treatment on brachial artery flow-mediated dilation in 39 patients with hypertension. Compared with 82 age- and gender-matched normotensive controls, these patients had impaired endothelium-dependent, flow-mediated dilation of the brachial artery [8.9 +/- 6.1 vs. 11.2 +/- 5.7% (SD), P < 0.04]. After therapy, plasma ascorbic acid concentrations increased acutely from 50 +/- 12 to 149 +/- 51 micromol/l and were maintained at 99 +/- 33 micromol/l with chronic treatment (both P < 0.001). As previously reported, chronic ascorbic acid therapy reduced systolic and mean blood pressure in these patients. However, acute or chronic ascorbic acid treatment had no effect on brachial artery endothelium-dependent, flow-mediated dilation or on endothelium-independent, nitroglycerin-mediated dilation. These results demonstrate that conduit vessel endothelial dysfunction secondary to hypertension is not reversed by acute or chronic treatment with oral ascorbic acid. The effects of this treatment on resistance vessel vasomotor function warrant further investigation.

[Preventive measures taken in Adrianople during the 1893-1894 cholera epidemic, as reflected in a local newspaper]. / 1893-1894 kolera salginlari karsisinda edirne'de alinan koruyucu saglik.

Cholera is derived from the Latin words colos (large intestine) and reo (to flow) and means flowing of the liquids through the stomach and the intestines. The first cholera epidemic was experienced in India and spread out to other countries. Although it had been known for ages, it was not recognized until the 16th century. Seven serious cholera epidemics have broken out in the world since the 19th century. In spite of all precautions taken by the Ottoman government, the sixth world cholera epidemic that started in Asia in 1891 and caused the loss of 40 thousand people, reached Istanbul in 1893. Later, it spread to Iznik, Salonika and Anatolia. Just as it appeared in Europe, precautions started to be taken in Adrianople. At first, special care was taken for city hygiene and a commission was formed to inspect the cleanliness of the city. Many brochures and articles were published on the protection against the illness, in order to inform the citizens of the cholera epidemic. Preachers spoke of cholera in their sermons. To protect Adrianople against the epidemic, entrance into and exit out of the city were patrolled and passengers coming from Europe or Istanbul to Adrianople were kept waiting for three days at the quarantines built in Cisri Mustafa Pasha and Catalca.

[The comparison of the two Ottoman books of anatomy (17-19th centuries) with regard to the circulatory system]. / 17. ve 19. yüzyil Osmanli dönemine ait iki anatomi kitabindaki dolasim sistemi bilgisinin karsilastirilmasi.

17th and 19th centuries were particularly important for the development of te Ottoman medicine. Westernization which had already started in the 17th century continued along the 19th and the early 20th centuries. Turkish physicians began to contact with their European colleagues and in this period Latin medical terminology began to appear in the Ottoman medical literature. Sirvanli Semseddin Itaki's work of the 17th century, the Tesrihü'l Ebdan ve Tercüman-i Kibale-i Feylesufan, is the first illustrated Turkish manuscript of anatomy. The illustrations are qualified as developed examples, compared with the medical literature and knowledge of the period. In the 19th century, Sanizade Mehmet Ataullah Efendi (1771-1826) wrote a modern book of anatomy for the Ottoman medical doctors. Miyarü'l Etibba was one of the earliest printed medical books in Turkish. The second volume of Sanizade's Hamse, Miratü'l Ebdan fi Tesrih-i-Azai'l Insan is the first printed Ottoman book on anatomy. In Usulü't-Tabia, the third volume of Hamse, the circulatory system is discussed. In this article, we studied the circulatory system described in Semseddin Itaki's Tesrih-ül Ebdan ve Tercüman-i-Kibale-i Feylesufan and in Sanizade's Usulü't-Tabia and compared them.

[The comparison of the two Ottoman books of anatomy (17-19th centuries) with regard to the circulatory system]. / 17. ve 19. yüzyil Osmanli dönemine ait iki anatomi kitabindaki dolasim sistemi bilgisinin karsilastirilmasi.

17th and 19th centuries were particularly important for the development of the Ottoman medicine. Westernization which had already started in the 17th century continued along the 19th and the early 20th centuries. Turkish physicians began to contact with their European colleagues and in this period Latin medical terminology began to appear in the Ottoman medical literature. Sirvanli Semseddin Itaki's work of the 17th century, the Tesrihü'l Ebdan ve Tercüman-i Kibale-i Feylesufan, is the first illustrated Turkish manuscript of anatomy. The illustrations are qualified as developed examples, compared with the medical literature and knowledge of the period. In the 19th century, Sanizade Mehmet Ataullah Efendi (1771-1826) wrote a modern book of anatomy for the Ottoman medical doctors. Miyarü'l Etibba was one of the earliest printed medical books in Turkish. The second volume of Sanizade's Hamse, Miratü'l Ebdan fi Tesrih-i Azai'l Insan is the first printed Ottoman book on anatomy. In Usulü't-Tabia, the third volume of Hamse, the circulatory system is discussed. In this article, we studied the circulatory system described in Semseddin Itaki's Tesrih-ül Ebdan ve Tercüman-i Kibale-i Feylesufan and in Sanizade's Usulü't-Tabia and compared them.

Acute effects of a high-fat meal with and without red wine on endothelial function in healthy subjects.

It has been suggested that a high-fat meal may acutely impair endothelium-dependent vasodilation and that this impairment may be prevented by concomitant intake of antioxidants. Because red wine contains antioxidant polyphenols and may reduce cardiovascular disease, we examined the effect of red wine on postprandial endothelial function. Using a crossover design, 13 healthy volunteers consumed a high-fat meal (0.8 g fat/kg body weight) with red wine (3 ml/kg) or an isocaloric control beverage on 2 separate days, 1 week apart. Flow-mediated dilation of the brachial artery was examined by vascular ultrasound at baseline and at 2, 4, and 6 hours after the meal. At these times, flow-mediated dilation with the high-fat meal and control beverage was 9.5 +/- 5.0%, 7.9 +/- 5.1%, 6.8 +/- 3.6%, and 7.3 +/- 4.6%, respectively (nonsignificant trend). There was also a nonsignificant trend for flow-mediated dilation after the high-fat meal with wine: 8.0 +/- 4.1%, 5.7 +/- 4.7%, 6.4 +/- 3.1%, and 6.9 +/- 3.8%, respectively. There was no difference in the effects between wine and the control beverage (p = 0.77). Triglycerides increased 2- to 2.7-fold over baseline (p = 0.0001) with a peak occurring 5 hours after the high-fat meals. In contrast to previous studies, the present study did not demonstrate a significant effect of a high-fat meal on endothelial vasomotor function in healthy subjects. Under these conditions, we did not demonstrate a beneficial acute effect of red wine on endothelial function.

Long-term ascorbic acid administration reverses endothelial vasomotor dysfunction in patients with coronary artery disease.

BACKGROUND: Loss of endothelium-derived nitric oxide (EDNO) contributes to the clinical expression of coronary artery disease (CAD). Increased oxidative stress has been linked to impaired endothelial vasomotor function in atherosclerosis, and recent studies demonstrated that short-term ascorbic acid treatment improves endothelial function. METHODS AND RESULTS: In a randomized, double-blind, placebo-controlled study, we examined the effects of single-dose (2 g PO) and long-term (500 mg/d) ascorbic acid treatment on EDNO-dependent flow-mediated dilation of the brachial artery in patients with angiographically established CAD. Flow-mediated dilation was examined by high-resolution vascular ultrasound at baseline, 2 hours after the single dose, and 30 days after long-term treatment in 46 patients with CAD. Flow-mediated dilation improved from 6.6+/-3.5% to 10.1+/-5.2% after single-dose treatment, and the effect was sustained after long-term treatment (9. 0+/-3.7%), whereas flow-mediated dilation was 8.6+/-4.7% at baseline and remained unchanged after single-dose (7.8+/-4.4%) and long-term (7.9+/-4.5%) treatment with placebo (P=0.005 by repeated-measures ANOVA). Plasma ascorbic acid concentrations increased from 41.4+/-12. 9 to 115.9+/-34.2 micromol/L after single-dose treatment and to 95. 0+/-36.1 micromol/L after long-term treatment (P<0.001). CONCLUSIONS: In patients with CAD, long-term ascorbic acid treatment has a sustained beneficial effect on EDNO action. Because endothelial dysfunction may contribute to the pathogenesis of cardiovascular events, this study indicates that ascorbic acid treatment may benefit patients with CAD.

Treatment of hypertension with ascorbic acid.

In a randomised, double-blind, placebo-controlled study we showed that treatment of hypertensive patients with ascorbic acid lowers blood pressure. Further studies of ascorbic acid to treat hypertension, with clinical endpoints, are warranted.

L-2-Oxothiazolidine-4-carboxylic acid reverses endothelial dysfunction in patients with coronary artery disease.

The effective action of endothelium-derived nitric oxide (EDNO) is impaired in patients with atherosclerosis. This impairment has been attributed in part to increased vascular oxidative stress. EDNO action is improved by administration of ascorbic acid, a water-soluble antioxidant. Ascorbic acid is a potent free-radical scavenger in plasma, and also regulates intracellular redox state in part by sparing cellular glutathione. We specifically investigated the role of intracellular redox state in EDNO action by examining the effect of L-2-oxo-4-thiazolidine carboxylate (OTC) on EDNO-dependent, flow-mediated dilation in a randomized double-blind placebo-controlled study of patients with angiographically proven coronary artery disease. OTC augments intracellular glutathione by providing substrate cysteine for glutathione synthesis. Brachial artery flow-mediated dilation was examined with high-resolution ultrasound before and after oral administration of 4.5 g of OTC or placebo in 48 subjects with angiographically documented coronary artery disease. Placebo treatment produced no change in flow-mediated dilation (7.0+/-3.9% vs. 7.2+/-3.7%), whereas OTC treatment was associated with a significant improvement in flow-mediated dilation (6.6+/-4.4% vs. 11.0+/-6.3%; P = 0.005). OTC had no effect on arterial dilation to nitroglycerin, systemic blood pressure, heart rate, or reactive hyperemia. These data suggest that augmenting cellular glutathione levels improves EDNO action in human atherosclerosis. Cellular redox state may be an important regulator of EDNO action, and is a potential target for therapy in patients with coronary artery disease.

Endothelial dysfunction and coronary risk reduction.

There is growing evidence that improvement of endothelial function has the potential to reduce cardiovascular ris. This article reviews the impact of coronary risk factors on endothelial function and the benefits of risk factor reduction. Recent studies indicate that chronic exercise may directly improve endothelial function, thus providing an additional explanation for the benefits of increased physical activity.

Basic research in antioxidant inhibition of steps in atherogenesis.

Oxidised low-density lipoprotein (LDL) contributes to atherogenesis by a number of mechanisms, and antioxidants may act as anti-atherogens. LDL oxidation is inhibited by LDL-associated antioxidants, particularly alpha-tocopherol (vitamin E), and water-soluble antioxidants present in LDL's biologic milieu, especially ascorbate (vitamin C). In addition to protecting LDL against oxidation, antioxidants may act at the level of the vascular cell by limiting cellular production of reactive oxygen species, and, thus, cell-mediated LDL oxidation. Cellular antioxidants can also protect against vascular cell dysfunction that would otherwise promote atherogenesis, such as increased adhesion molecule expression and monocyte recruitment, impaired production or release of nitric oxide, or both, and the proliferation of smooth muscle cells. Some of these processes are regulated by nuclear factor-kappa B or related transcription factors, which are redox-sensitive and inhibited by antioxidants. Furthermore, cellular antioxidants can limit cytotoxic effects of oxidised LDL and other oxidant insults, inhibiting vascular cell necrosis and lesion progression. Finally, some antioxidants, in particular alpha-tocopherol, may affect atherogenesis by inhibiting platelet function and mural thrombosis, although this effect appears to be explained by the inhibition of protein kinase C independent of alpha-tocopherol's antioxidant activity.

Thermophilic Bacillus sp. that shows the denitrification phenotype of Pseudomonas aeruginosa.

A thermophilic Bacillus sp. of marine origin was observed to grow anaerobically on nitrite, nitrous oxide (N2O) in the presence of nitrite, and N2O alone for a few hours after exhaustion of nitrite. This represents the second example of a denitrification phenotype originally observed to occur with Pseudomonas aeruginosa.