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R I Price

Publications and source records attributed to R I Price.

43 records · Page 3Linked to original sources

Forearm bone loss in hemiplegia: a model for the study of immobilization osteoporosis.

Hemiplegia is associated with excessive bone loss in the paralyzed arm. The forearm bone mineral content was measured at a proximal cortical site and a distal trabecular site of both the normal and hemiplegic arms in 74 patients with hemiplegia. By comparing the ratios of bone mineral content in the two arms, the effect of immobilization could be quantitated independently of the large population variance in bone mineral content. Bone loss, estimated from this single comparison of bone mineral content in the normal and hemiplegic arms, at the trabecular and cortical sites was positively correlated with the duration of stroke and negatively correlated with reduction in forearm function. At the trabecular site females had a proportionately greater bone loss than males, indicating an interaction between gender and immobilization associated bone loss at this site. The regression line of excess bone loss in the hemiplegic limb against time had a negative slope of 1.3% and 1.5% a year of the starting value for the trabecular and cortical sites, respectively, over the 15 years studied. This study indicates that a reduction in function is associated with significant bone loss occurring over prolonged periods that may account, at least in part, for the significant osteoporosis seen in elderly people and in subjects with conditions resulting in reduced mobility such as arthritis, obstructive airways disease, and neurological disease.

Aged↗

Fasting calcium excretion and parathyroid hormone together distinguish familial hypocalciuric hypercalcaemia from primary hyperparathyroidism.

Routine estimation of plasma calcium has made the finding of asymptomatic hypercalcaemia a frequent occurrence. A high index of suspicion for familial hypocalciuric hypercalcaemia (FHH) will lead to accurate diagnosis and avoidance of unnecessary parathyroid surgery. Four FHH kindreds with 16 hypercalcaemic members were found in an unselected referral population over 3 years. Differentiation from primary hyperparathyroidism (42 patients in the same period) was facilitated by analysis of fasting blood and urine for renal handling of calcium, phosphate and cyclic AMP. We found that a plot of serum PTH against fasting calcium excretion separated all cases of each disorder. The discriminatory power of these two variables was confirmed by multivariate discriminant function analysis. An elevated plasma chloride was found to be common to both diseases and of no value in differentiation.

Adult↗

Effect of blood flow reversal in liver autotransplants upon the site of hepatocyte regeneration.

We studied the role of the direction of intrahepatic blood flow upon the location of hepatocyte formation in regenerating liver. Single liver lobes in the dog were autotransplanted to the region of the neck with the blood supply reestablished in a manner to perfuse the hepatic lobule from portal tract to central vein or, in a reverse direction, from central vein to portal tract. Partial resection of the nontransplanted liver was later performed to induce regeneration in the grafts by humoral means. Tritiated thymidine was administered, and radioautographs were prepared from excised graft and nontransplanted liver. In the "straight" blood flow grafts, as well as in all nontransplanted livers, labeled hepatocytes indicating DNA synthesis were found predominantly in the vicinity of the portal tracts. In the "reverse" blood flow grafts, labeled hepatocytes were more prevalent about the central veins. Thus, the localization of hepatocyte formation in the lobule during active liver regeneration cannot be attributed to an inherently greater capacity of periportal liver cells to divide but is probably related to their preferential exposure to blood constituent changes (humoral mechanisms). Hepatocyte regeneration in the presence of abnormal directional circulation might lead to lobular disorganization resulting in consequent biochemical aberrations despite the formation of new cells.

Animals↗