fawn/heilablóðfall

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GreinarKlínískar rannsóknirEinkaleyfi

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Renal disease susceptibility and hypertension are under independent genetic control in the fawn-hooded rat.

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Hypertension, diabetes and hyperlipidemia are risk factors for life-threatening complications such as end-stage renal disease, coronary artery disease and stroke. Why some patients develop complications is unclear, but only susceptibility genes may be involved. To test this notion, we studied

Kidney angiotensin receptors and their role in renal pathophysiology.

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A considerable amount of data have implicated angiotensin receptors (AT receptors) in the development and maintenance of essential hypertension and renovascular hypertension as well as in progressive renal pathologies. Inhibition of angiotensin II (Ang II) action by blocking Ang II formation through

Mapping genetic determinants of kidney damage in rat models.

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During the last two decades, significant progress in our understanding of the development of kidney diseases has been achieved by unravelling the mechanisms underlying rare familial forms of human kidney diseases. Due to the genetic heterogeneity in human populations and the complex multifactorial

Rat models of cardiometabolic diseases: baseline clinical chemistries, and rationale for their use in examining air pollution health effects.

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Individuals with cardiovascular and metabolic diseases (CVD) are shown to be more susceptible to adverse health effects of pollutants. Rodent models of CVD are used for examining susceptibility variations. CVD models developed by selective inbreeding are shown to represent the etiology of human

Clinical and pathological manifestations of cardiovascular disease in rat models: the influence of acute ozone exposure.

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Rodent models of cardiovascular diseases (CVD) and metabolic disorders are used for examining susceptibility variations to environmental exposures. However, cross-model organ pathologies and clinical manifestations are often not compared. We hypothesized that genetic CVD rat models will exhibit

Strain differences in antioxidants in rat models of cardiovascular disease exposed to ozone.

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We examined the hypothesis that antioxidant substances and enzymes in lung, heart and in bronchoalveolar lavage fluid (BALF) are altered in response to O3 in cardiovascular disease and/or metabolic syndrome (CVD)-prone rat models. CVD strains [spontaneously hypertensive (SH), SH stroke-prone (SHSP),

Variability in ozone-induced pulmonary injury and inflammation in healthy and cardiovascular-compromised rat models.

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The molecular bases for variability in air pollutant-induced pulmonary injury due to underlying cardiovascular (CVD) and/or metabolic diseases are unknown. We hypothesized that healthy and genetic CVD-prone rat models will exhibit exacerbated response to acute ozone exposure dependent on the type

Whole body plethysmography reveals differential ventilatory responses to ozone in rat models of cardiovascular disease.

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To elucidate key factors of host susceptibility to air pollution, healthy and cardiovascular (CV)-compromised rats were exposed to air or ozone (O3) at 0.25, 0.5, or 1.0 ppm for 4 h. We hypothesized that rat strains with the least cardiac reserve would be most prone to develop significant health

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Herbal & Natural Medicine

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