BackgroundSystemic inflammation in psoriasis causes insulin resistance and cardiovascular diseases. Adipokines are adipose-tissue-derived factors that are involved in metabolic processes. It is thought that these adipokines are associated with the development of psoriasis.ObjectiveThe purpose of this study was to determine the changes in adipokine levels, insulin resistance, hypertension, and dyslipidemia over a 12-week period.MethodsThe study comprised 35 psoriasis patients and 50 controls. Blood samples were obtained twice from the patients, one sample at the start and one at the end of a 12-week follow-up period. The following parameters were assessed in both groups: serum fasting glucose, fasting insulin, homeostasis model assessment-estimated insulin resistance (HOMA-IR) index, serum lipids, adiponectin, leptin, resistin, chemerin, omentin, vaspin, visfatin, retinol-binding protein 4, and high-sensitivity C-reactive protein (hs-CRP) levels; blood pressure; body mass index; and the psoriasis area severity index (PASI) scores.ResultsThe patients showed an improvement in the PASI score and a significant decrease in serum hs-CRP, omentin, and chemerin values. Moreover, at the start of the follow-up, the psoriasis patients had significantly lower levels of adiponectin and visfatin and significantly higher levels of vaspin and resistin than those of the control group. Visfatin levels correlated negatively with low-density lipoprotein (LDL) and cholesterol, while vaspin and omentin levels correlated positively with diastolic blood pressure. Decreased adiponectin levels correlated negatively with diastolic blood pressure and LDL.ConclusionPlasma levels of adipokines might be useful for evaluating the disease activity of psoriasis and its comorbidities.

High copper, cadmium and lead decreased iron absorption and negatively affected hematological parameters.

Our results suggest that IGF-I (CA) 19 polymorphism may contribute to a predisposition to acne in Turkish patients.

No abstract

Apelin, a novel multifunctional peptide implicated in the regulation of the cardiovascular system, including blood pressure and cardiac function control, has been postulated to be involved in the pathophysiology of hypertension and hypertensive heart disease. The aim of this study was to investigate, for the first time, whether the effects of apelin's chronic application might be involved in deoxycorticosterone acetate-salt-induced hypertensive rats (DOCA-salt rats). In this study, 8-10-week-old male Wistar rats were divided into four groups: control, control + apelin, DOCA-salt rats, DOCA-salt rats + apelin. Deoxycorticosterone Acetate (25 mg/kg of body weight) was injected subcutaneously, twice a week for 4 weeks. These rats received NaCl 1% instead of tap water for drinking during the experimental period. Later, rats were randomly treated with pyroglutamylated apelin-13 (200 μg. kg(-1). day(-1) intraperitonealy) for 17 days. The concentrations of apelin, endothelin-1, angiotensin-converting enzyme, angiotensinogen, and angiotensin II were analyzed in the plasma. The mRNA level of apelin and apelin receptor were determined in the heart and aorta tissue by real-time polymerase chain reaction, respectively. It was found that apelin reduces blood pressure in DOCA-salt rats. Apelin can be used as a therapeutic agent in the treatment of hypertension in the future.

he vascular endothelium plays an important role in the regulation of vascular tone and the maintenance of cardiovascular homeostasis. 1 Importantly, endothelial dysfunction, particularly impaired endotheliumdependent vasodilation, has been linked to the pathogenesis of atherosclerotic vascular disease and acute cardiovascular events. 2 Indeed, reduced endothelial vasodilatory function occurs early in atherogenesis before histological and angiographic evidence. 3,4 Epidemiologic studies have shown that high levels of physical activity and cardiorespiratory fitness reduce cardiovascular morbidity and mortality in the general population, including healthy subjects. 5,6 It is clinically important to select the appropriate kind of exercise. Regular aerobic exercise is associated with beneficial changes in blood pressure, lipid metabolism, glucose metabolism, neurohormonal factors, body weight, and shear stress. 7,8 Although the mechanism of improvement in endothelial function during exercise has not been fully clarified, it is thought that nitric oxide (NO) production is increased by up-regulation of endothelial NO synthase gene expression and vascular endothelial growth factor-induced angiogenesis, as well as decreased NO inactivation with augmented antioxidants, Circulation Journal Vol. 69, September 2005 such as superoxide dismutase and glutathione peroxidase, and attenuation of nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide phosphate (NADH/NADPH) oxidase activity, all leading to an increase in NO bioavailability. 9 Polymorphisms of the angiotensin converting enzyme (ACE) gene, located on chromosome 17, have been found and the polymorphism is characterized by the presence (insertion (I)) or absence (deletion (D)) of a 287-base-pair alu repeat within intron 16. The presence of the D allele has been associated with higher concentrations of circulating and tissue ACE. Increased ACE activity might lead to high Angiotensin II (Ang II) concentrations. 10 Of the several candidate genes for endothelial dysfunction, the ACE gene appears to be a likely one because (1) it is anchored via its carboxyl terminus to the endoluminal side of the endothelial cell plasma membrane, from where it can be released in the bloodstream, 11,12 and (2) the increased plasma ACE activity found in subjects with the D allele could decrease bradykinin bioactivity with ensuing blunting of receptormediated release of NO. 13 Furthermore, even though the literature is variable on whether Ang II effects are increased in subjects with the D allele, 14,15 enhanced Ang II production can increase the concentrations of superoxide through increased activity of NADH/NADPH oxidase activity 16 and thus lower the bioactivity of NO. 17 The balance of vasodilators and vasoconstrictors also plays an important role in the physiologic regulation of vascular tone; 18 However, it is not clear whether the ACE genotype can modify the endothelial response to exercise in athletes.The aim of this study was to investigate the relationship between the...

Aluminum (Al) is a nonessential element and humans are constantly exposed to Al as a result of an increase in industrialization and improving technology practices. Al toxicity can induce several clinical disorders such as neurotoxicity, gastrointestinal toxicity, hepatotoxicity, bone diseases, and anemia. This study aimed at evaluating the possible effects of short term and low dose Al exposure on hemorheological and hematological parameters in rats. Fourteen young, male Wistar albino rats were divided into two groups: 1 mg/200 g body weight of aluminum sulfate (Al(2)(SO(4))(3) was injected intraperitoneally to the first group for two weeks, three times a week. The animals of the control group received only physiological saline solution during this period. At the end of the experimental period, anticoagulated blood samples were collected and hematological parameters were determined using an electronic hematology analyzer. Red blood cell (RBC) deformability and aggregation were measured using an ektacytometer (LORCA) and plasma and whole blood viscosities were determined with a Wells-Brookfield cone-plate rotational viscometer. Significant decreases in mean corpuscular volume (MCV), red blood cell (RBC) deformability at low shear stress levels, the aggregation half time (t1/2) and the amplitude (AMP) of aggregation and significant increments in whole blood viscosity (WBV) at native and 40% hematocrit (Hct) of Al-treated rats have been observed. In conclusion, low dose Al(2)(SO(4))(3) exposure for a short-time may be responsible for alterations in either rheological properties of blood or hemorheological properties through a remarkable effect on RBC membrane mechanical properties . These alterations may also play an important role in the development of anemia in the Al-treated animals.

The ACE gene polymorphism was not associated with PCOS. However, the presence of D allele was associated with higher rate of insulin resistance in patients with PCOS.