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Richard A. Galosy

Researcher at University of Texas Southwestern Medical Center

Publications -  15
Citations -  344

Richard A. Galosy is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Hypercalciuria & Heart rate. The author has an hindex of 7, co-authored 15 publications receiving 339 citations. Previous affiliations of Richard A. Galosy include University of Texas System & Oregon Research Institute.

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Neurophysiology and neuropharmacology of cardiovascular regulation and stress

TL;DR: The conclusion is reached that further multidisciplinary research will reveal underlying neurophysiological and neuropharmacological mechanisms responsible for stress induced cardiovascular disease and lead to new methods of treatment.
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Fasting urinary calcium and adenosine 3',5'-monophosphate: a discriminant analysis for the identification of renal and absorptive hypercalciurias.

TL;DR: Values in absorptive hypercalciuria were within 2 SES of estimate for the control group, though they were higher in calcium and lower in cAMP than in other groups, and the individual values for fasting urinary cAMP overlapped widely into the ranges found in the control and absorptiveHyperCalciuria groups.
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Propensity for spontaneous nucleation of calcium oxalate: Quantitative assessment by urinary FPR-APR discriminant score

TL;DR: It is concluded that FPR-APR discriminant scores are useful in the identification of stone-forming potential in urine, and in the assessment of response to therapy.
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Renal Oxalate Excretion in Calcium Urolithiasis

TL;DR: The results indicate that renal oxalate excretion in an ambulatory setting is not critically dependent on the state of calcium absorption and intake, and that the imposition of a low calcium dietary regimen in patients with an increased calcium absorbing rate and in whom stones form does not necessarily augment oxalates excretion.
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Cardiac changes during behavioral stress in dogs

TL;DR: It was concluded that controlled behavioral stress produces increased cardiac performance without increased bodily activity.