By Michael Alan Singer
This e-book describes a singular and new angle to the therapy of human ailments in accordance with the examine of normal animal types. A normal animal version is outlined as an animal team or species that possesses a suite of biochemical/physiological features that are usual and adaptive for that animal, yet are rather irregular for people. for instance, how is it that birds can tolerate blood glucose concentrations which in people are linked to diabetes. The ordinary animal version resides evidence organic resolution to this question is out there. by means of learning usual animal types, we will be able to achieve important insights into the therapy of varied human scientific problems. overlaying a variety of issues, this publication describes intimately how scientific scientists can benefit from all of the "research" that nature has already played over billions of years in organic challenge fixing via wide animal layout trying out and choice.
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Extra info for Comparative Physiology, Natural Animal Models and Clinical Medicine: Insights into Clinical Medicine from Animal Adaptations
Sci. USA 88, 5779–5783. , 2004. Application of the diabetes control and complications trial. M. ), Diabetes Mellitus: A Fundamental and Clinical Text, 3rd Edn. Lippincott Williams and Wilkins, Philadelphia, PA, pp. 645–657. , 1996. The pecten oculi of the chicken as a new in vivo model of the blood-brain barrier. Cell Tissue Res. 285, 91–100. , 2000. Renal and extrarenal regulation of body ﬂuid composition. C. ), Sturkie’s Avian Physiology, 5th Edn. Academic Press, San Diego California, pp. 265–297.
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2002). However the intrarenal location, abundance and activity proﬁle of these kidney transporters are unknown. Once avian renal glucose transporters have been deﬁned, their properties should be compared to those of mammals exposed to both normal and high glucose concentrations? (2) Is a glomerulotubular feedback mechanism present in the avian kidney? If so, does this glomerulotubular feedback mechanism have different “settings” from that of mammals? Is the rate of proximal tubular glucose reabsorption in the bird low enough after feeding (see in “Renal Glucose Transporters section” “Diabetic Nephropathy”) that proximal electrolyte reabsorption is not increased above that of the fasting state and suppression of the glomerulotubular feedback signal does not occur in contrast to the situation in the diabetic mammal?