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FIRSТ INTERNATIONAL STUDENT SYMPOSIUM-FASPERIJADA
Angelka VELKOSKA
Journal of Special Education and Rehabilitation , 2011,
Abstract:
VOCATIONAL MEETING: PROGRAMS FOR INTERNATIONALIZATION OF UNIVERSITY’S STUDIES AND ITS POSITIVE EFFECTS ON THE QUALITY OF THE EDUCATION
Angelka VELKOSKA
Journal of Special Education and Rehabilitation , 2010,
Abstract:
3RD OF DECEMBER – INTERNATIONAL DAY OF PERSONS WITH DISABILITIES
Angelka VELKOSKA
Journal of Special Education and Rehabilitation , 2011,
Abstract:
60 YEARS OF EDUCATION, REHABILITATION AND EMPLOYMENT OF PERSONS WITH DISABILITIES IN THE REPUBLIC OF MACEDONIA
Angelka VELKOSKA
Journal of Special Education and Rehabilitation , 2010,
Abstract:
80 YEARS OF BIRTH AND 65 YEARS OF HUMANITARIAN PEDAGOGICAL AND SCIENTIFIC ACTIVITY OF PROF. DR. LJUPCHO AJDINSKI
Angelka VELKOSKA
Journal of Special Education and Rehabilitation , 2010,
Abstract:
Mechanisms behind early life nutrition and adult disease outcome
Elena Velkoska,Margaret J Morris
World Journal of Diabetes , 2011, DOI: 10.4239/wjd.v2.i8.127
Abstract: Obesity is increasing around the globe. While adult lifestyle factors undoubtedly contribute to the incidence of obesity and its attendant disorders, mounting evidence suggests that programming of obesity may occur following under- and over-nutrition during development. As hypothalamic control of appetite and energy expenditure is set early in life and can be perturbed by certain exposures such as undernutrition and altered metabolic and hormonal signals, in utero exposure to altered maternal nutrition and inadequate nutrition during early postnatal life may contribute to programming of obesity in offspring. Data from animal studies indicate both intrauterine and postnatal environments are critical determinants of the development of pathways regulating energy homeostasis. This review summarizes recent evidence of the impact of maternal nutrition as well as postnatal nutrition of the offspring on subsequent obesity and disease risk of the offspring. While much of the experimental work reviewed here was conducted in the rodent, these observations provide useful insights into avenues for future research into developing preventive measures to curb the obesity epidemic.
Subclinical hypothyroidism and risk to carotid atherosclerosis
Valentina, Velkoska Nakova;Marijan, Bosevski;Chedo, Dimitrovski;Branka, Krstevska;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2011, DOI: 10.1590/S0004-27302011000700007
Abstract: objective: the aim of this study was to assess whether subclinical hypothyroidism (sch) is associated with carotid atherosclerosis, as well as dyslipidemia, and arterial hypertension. subjects and methods: the study included 69 consecutive patients with newly diagnosed sch, and 30 matched healthy controls. body mass index (bmi), tsh, ft4, antibodies to thyroid peroxidase (tpoabs), lipids, blood pressure, mean and maximum carotid intima-media thickness (cimt) were determined in all participants. results: mean values of cimt, triglycerides, and total cholesterol/hdl-c ratio were significantly different in sch patients versus matched controls. linear multiple regression analysis demonstrated that tsh, diastolic blood pressure and triglycerides were independent predictors of mean cimt, ft4 for maximum cimt; and that tsh, ft4, age, and total cholesterol/hdl-c ratio were independent predictors of the presence of carotid plaques. conclusion: our data revealed that sch is associated with increase in cimt and presence of carotid plaques, independent of classical risk factors for atherosclerosis.
Unaltered TNF-α production by macrophages and monocytes in diet-induced obesity in the rat
Sammy Bedoui, Elena Velkoska, Steve Bozinovski, Jessica E Jones, Gary P Anderson, Margaret J Morris
Journal of Inflammation , 2005, DOI: 10.1186/1476-9255-2-2
Abstract: Male Sprague-Dawley rats were fed a high-fat or a standard chow diet for either 2 or 10 weeks. At the end of the intervention period animals were anaesthetised, blood collected for determination of plasma mediator concentrations and lipopolysaccharide (LPS) stimulated production of TNF-α by monocytes. LPS stimulated production of TNF-α in alveolar macrophages was also determined.High-fat feeding for either 2 or 10 weeks resulted in significant increases in fat mass and serum leptin. Although increased serum leptin has previously been linked to modulation of innate immunity, we found no significant difference in the LPS stimulated production of TNF-α by either blood monocytes or alveolar macrophages between the dietary groups. Furthermore, we failed to find a significant increase in circulating TNF-α concentrations in obese animals, as reported for genetically obese animals.Our data suggest that defects in innate immune function observed in genetically obese animals are not mimicked by dietary obesity, and may more likely reflect the gross abnormality in leptin function of these models. Further work is required delineate the effects of dietary obesity on inflammatory state and immune function.Obesity is a very common chronic disease that poses significant health risks such as diabetes, cardiovascular diseases and hypertension. This pathological condition is characterized by complex neuroendocrine changes in the brain as well as in the periphery, involving mediators such as neuropeptide Y (NPY) and leptin [1]. Additionally, there have been several reports demonstrating that obesity is associated with altered immune function and a chronic low-grade inflammatory status [summarized by [2,3]]. Specifically it has been reported that obese individuals have a higher incidence and severity of infectious diseases [4]. These defects also include disturbances in macrophage mediated phagocytosis and pro-inflammatory cytokine production [5] as well as increased sensitivity to endo
The CTGF gene ?945?G/C polymorphism is not associated with cardiac or kidney complications in subjects with type 2 diabetes
Sheila K Patel, Bryan Wai, Richard J MacIsaac, Sharon Grant, Elena Velkoska, Michelle Ord, Sianna Panagiotopoulos, George Jerums, Piyush M Srivastava, Louise M Burrell
Cardiovascular Diabetology , 2012, DOI: 10.1186/1475-2840-11-42
Abstract: The CTGF ?945?G/C polymorphism (rs6918698) was examined in 495 Caucasian subjects with type 2 diabetes. Cardiac structure and function were assessed by transthoracic echocardiography. Kidney function was assessed using estimated glomerular filtration rate (eGFR) and albuminuria, and CKD defined as the presence of kidney damage (decreased kidney function (eGFR <60?ml/min/1.73?m2) or albuminuria).The mean age?±?SD of the cohort was 62?±?14?years, with a body mass index (BMI) of 31?±?6?kg/m2 and median diabetes duration of 11?years [25th, 75th interquartile range; 5, 18]. An abnormal echocardiogram was present in 73% of subjects; of these, 8% had LVH alone, 74% had diastolic dysfunction and 18% had systolic?±?diastolic dysfunction. CKD was present in 42% of subjects. There were no significant associations between the CTGF ?945?G/C polymorphism and echocardiographic parameters of LV mass or cardiac function, or kidney function both before and after adjustment for covariates of age, gender, BMI, blood pressure and hypertension. CTGF ?945 genotypes were not associated with the cardiac complications of LVH, diastolic or systolic dysfunction, nor with CKD.In Caucasians with type 2 diabetes, genetic variation in the CTGF ?945?G/C polymorphism is not associated with cardiac or kidney complications.Connective tissue growth factor (CTGF) also known as CCN-2, is a cysteine rich secreted protein that mediates tissue fibrosis in multiple organs including the heart and kidney [1-3]. In the heart, CTGF is expressed in myocytes and fibroblasts [4] and can induce hypertrophy [5], and extracellular matrix production [6]. In man, CTGF gene expression is increased in ischaemic cardiac tissue [4], and both CTGF gene and protein expression are up-regulated in experimental models of cardiac injury and diabetes, and associated with ongoing cardiac fibrosis [5,7-10]. Cardiac fibrosis increases the mechanical stiffness of the heart, which impairs myocardial contractility and contributes to lef
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