Abstract. The aim of this study was to explore the relationship between serum profiles of adiponectin, leptin, resistin and visfatin and traditional and non-traditional cardiovascular risk factors in patients with type 2 diabetes mellitus (T2DM). A total of 85 patients with T2DM and 30 non-diabetic controls were enrolled in the study. Levels of adipocytokines (adiponectin, leptin, resistin and visfatin), lipids (total cholesterol, triglycerides), lipoproteins [HDL-cholesterol, LDL-cholesterol, lipoprotein (a)], apolipoproteins (Apo-A1 and Apo-B), non-traditional cardiovascular risk markers [asymmetric dimethylarginine (ADMA), homocysteine] and the inflammatory marker hs-CRP were measured, and anthropometric variables were determined. Serum adiponectin levels were decreased and leptin, resistin and visfatin levels were increased in T2DM patients compared to controls. They were associated with obesity (BMI), insulin resistance (HOMA-IR) and various markers of glucose/lipid profile, inflammation and endothelial dysfunction markers. These results suggest that decreased serum adiponectin and increased leptin, resistin and visfatin levels in T2DM may be novel biochemical risk factors for cardiovascular complications.
Amyloid β42 (Aβ42) and proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) have been suggested to contribute to the pathogenesis of Alzheimer's disease (AD) and vascular dementia (VaD). Our aim was to examine whether the changes in these parameters would be able to discriminate the patients with AD from those with VaD and from healthy individuals. We have analyzed the levels of Aβ42, IL-6 and TNF-α in the serum of newly diagnosed 28 AD patients, 16 VaD patients and 26 healthy non-demented controls. We also investigated whether there is an association between Aβ42, IL-6 and TNF-α levels and mini-mental state examination (MMSE) scores and body mass indexes (BMI) of patients. Our data showed a significant decrease in serum Aβ-42 levels in AD patients compared to VaD patients and controls. Levels of IL-6 and TNF-α were not different between AD patients, VaD patients and controls. We observed a correlation between Aβ-42 levels and MMSE scores and BMI levels in both AD and VaD patients. However, Aβ-42 levels were not correlated with IL-6 and TNF-α levels. Significantly lower levels of Aβ42 found in the serum of AD patients than that of VaD patients and controls suggests that it can be a specific biochemical marker for AD.
Melatonin (MEL) and coenzyme Q10 (CoQ10) both display antioxidant and free radical scavenger properties. In the present study, the effect of MEL and CoQ10 on the oxidative stress and fibrosis induced by ochratoxin A (OTA) administration in rats was investigated. Rats were divided into five equal groups, each consisting of seven rats: (1) controls; (2) OTA-treated rats (289 microg/kg/day); (3) OTA+MEL-treated rats (289 microg/kg/day OTA + 10 mg/kg/day MEL); and (4) OTA+CoQ10-treated rats (289 microg/kg/day OTA + 1 mg/100 g/day body weight (bw) CoQ10). After 4 weeks of treatment, the level of malondialdehyde (MDA), glutathione peroxidase (GPx), and hydroxyproline (Hyp) were measured in the homogenates of liver and kidney. In the OTA-treated group, the levels of MDA and Hyp in both liver and kidney were significantly increased when compared with the levels of control, whereas GPx activities decreased. In OTA+MEL-treated rats, the levels of MDA and Hyp in both liver and kidney were significantly decreased when compared with the levels of OTA-treated rats; however; GPX activities increased. In the OTA+CoQ10-treated group, the levels of MDA and Hyp were decreased when compared with the levels of OTA-treated rats, whereas GPx activities increased. In the OTA+CoQ10-treated group, the levels of MDA, Hyp, and GPx were not significantly changed in kidney when compared with OTA-treated group. MEL has a protective effect against OTA toxicity through an inhibition of the oxidative damage and fibrosis both liver and kidney. Although CoQ10 has protective effect against OTA toxicity in liver tissue, it has no effect in kidney tissue.
RESUMENEl objetivo de este estudio fue evaluar la distribución de mastocitos en el ovario y el útero durante el ciclo estral de ratas. Se utilizaron cuarenta ratas Albino de Wistar hembras, de 10 a 12 semanas de edad. Se tomaron muestras de los tejidos del ovario y útero para luego ser fijadas en Mota por 48 horas y parafina, luego se cortaron secciones de 6 μm de espesor las cuales fueron teñidas con Azul de Toluidina (1% de solución acuosa) y Alcian safranina-azul (pH: 1,0, utilizando 0,1 HCl N como tampón). En el ovario, los mastocitos se presentaron principalmente en la túnica albugínea, en las áreas intersticiales entre folículos o cuerpos lúteos y en la proximidad de vasos sanguíneos en la médula. El número de mastocitos en la médula y la corteza ovárica y en el endometrio y miometrio uterino fueron mayores durante el estro, metaestro, las fases de estro y metaestro, respectivamente. Se encontró que el número de mastocitos fue mayor en la médula (7,4 ± 0,52) y la corteza ovárica (2,1 ± 0,30) de hembras en estro, en comparación a otras fases del ciclo estral (P<0,05), con un mayor número en el endometrio de hembras en estro y metaestro (6,8 ± 0,45 para el estro, 6,2 ± 0,56 para el metaestro) y en el miometrio (7,1 ± 0,63 para el estro, 7,5 ± 0,33 para el metaestro) comparado a otras fases del ciclo (P < 0,05). Durante todas las etapas del ciclo estral, excepto el proestro, los mastocitos teñidos con safranina se mostraron numerosos en todos los tejidos. Los mastocitos resultaron safranina positivos en el miometrio sólo en el proestro. Se concluyó que algunos cambios fisiológicos podrían ser responsables de la variación en la distribución de mastocitos en los tejidos ováricos y uterinos de la rata durante el ciclo estral.Palabras clave: mastocitos, ciclo estral, rata.
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