Biomedical subjects
Publications and source records attributed to M S Shih.
Oral calcium tablets were given daily for 180 days to ovariectomized Beagle dams (n = 4). Total serum calcium, and bone mineral content of midshaft femur were measured and compared to that of the controls (ovariectomized alone, n = 4). The bone mineral density was significantly higher in the calcium supplemented dogs (p less than 0.01).
Prostaglandin E2 (PGE2) at a dose of 10 mg/kg was administered orally to beagles used in a study of rib fracture and drill hole defect healing. Double fluochrome labels were given prior to surgical manipulation and before necropsy at 30 days. Bone remodeling was evaluated in trabecular bone of the fourth lumbar vertebra. There was a decrease in the number and extent of posttreatment labels (P less than 0.05) in the controls, with decreased mineral apposition rate (P less than 0.05) and decreased active bone formation rate (P less than 0.01). In dogs given PGE2 for 30 days following surgery, the extent of posttreatment labels (P less than 0.05) and bone formation rate (P less than 0.01) were increased. There was no difference found, however, in static morphometric parameters, including osteoid and osteoblast-covered surface, indicating that the stimulation of bone formation may have been transitory and matrix synthesis had declined. In another group of dogs given PGE2 for 5 days prior to surgical manipulation and between the first and second pretreatment labels, the extent of the double-labeled surface was increased (P less than 0.05) indicating an acute PG effect to sustain formation at remodeling sites. These studies show that PGE2 given orally has a systemic effect on bone remodeling in vertebral trabeculae that involves the stimulation of formation activity.
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Bone remodeling activities were assayed on undecalcified sections of iliac crest biopsies obtained from patients with primary biliary cirrhosis (PBC) (n = 25), postmenopausal osteoporosis (n = 64), and age, sex-matched, nonosteoporotic peri- and postmenopausal subjects (n = 26). Thorough semiautomated static and dynamic bone histomorphometry was carried out. Statistical analysis was performed among the age-matched groups in 10-year intervals through the ages 45 to 74. No osteomalacia or osteoporotic condition was detected in the patients with PBC. Our data have shown they did not have a mineralization defect but rather high bone turnover rates. The discrepancy of our observations to other published studies is discussed. We suggest that the osteoporotic condition attributed by others to PBC may just be the result of the concomitant aging processes.
A histomorphometric study was carried out on healing defects in the ribs of beagles. A transverse fracture was made surgically in the midshaft of the left 9th and 10th ribs. Ten beagles received injections of either a buffer vehicle (n = 4) or prostaglandin E1 (PGE1) at a dose of 0.4 mg/day locally (n = 6) into the fracture sites for a 10-day period and were killed 30 days after the surgery. Double-pulsed fluorescent labels were given with each of two fluochrome markers, calcein before surgical treatment and oxytetracycline hydrochloride before killing. The objectives were to determine manifestations of the regional acceleratory phenomenon (RAP) as changes in regional remodeling in the haversian envelope induced by fracture, effects of PGE1 on modification of the RAP in the haversian envelope, and systemic effects of PGE1 on remodeling changes of the contralateral matching sites. The differences in haversian remodeling between the injured and uninjured ribs of the experimental dogs indicated an increase in activation frequency, that is, regional acceleratory phenomenon. The significant effect of PGE1 on enhancing fracture-induced acceleration of haversian remodeling was doubtful, because of the preexistent biologic differences found in the two experimental groups. Nevertheless, the two groups shared a similar pattern of remodeling activity. The posttraumatic mineralization that declined at the sampled sites need further investigation.
A histomorphometric study was done on healing defects in the ribs of Beagles. A transverse fracture was made in the left 9th and 10th ribs. Beagles were given either ethanol vehicle (n = 6) or prostaglandin E2 (PGE2) orally (n = 5) for the 30-day period after surgical manipulation to time of necropsy. Double fluorescent labels were given to measure bone matrix mineralization. Two fluorochrome markers were used: calcein before dogs were surgically manipulated and oxytetracycline HCl before they were killed. The two objectives of the present study were: (1) to determine the effects of fracture on regional cortico-endosteal remodeling 2 cm from a fracture site in the ribs of Beagles; and (2) to determine the effects of orally administered PGE2 on the above condition. The results suggested that the fractured and the non-fractured ribs in either group show a similar static and dynamic remodeling during the first 30 days of healing. The activation frequency in the PGE2 group was increased in both fractured and non-fractured ribs more than in the non-treated group. Therefore, the systemic administration of PGE2 can activate and synchronize remodeling cycles among BMUs.
Transverse fractures were made surgically in the midshaft of the left 9th and 10th ribs in adult Beagles. A buffer vehicle (n = 4) or 0.2 mg of prostaglandin (PG) E1/day (n = 6) was injected into the fracture sites twice a day for 10 days, and dogs were euthanatized on day 30. Double-pulsed fluorescent labels were given with each of 2 fluorochrome markers--calcein before surgical treatment and oxytetracycline HCl before euthanasia. Histomorphometric analysis was carried out on specimens collected in adjacent regions of the healing defects. The surface extent and width of the osteoid on fractured (P less than 0.01, P less than 0.05, respectively) and nonfractured (P less than 0.05) sites in the treated group were greater than those in the nontreated group. The net loss of mineralizing surfaces was noticed on both ribs of both groups. Of 11 samples on the fractured side in the treated group, 4 contained periosteal new bone proliferation. There was increased osteoid formation and decreased mineralizing surfaces in the PGE1-treated group. Seemingly, administration of PGE1 induced bone matrix formation on periosteal envelope adjacent to a fracture site and its contralateral matching site.
A histomorphometric study was carried out on bone samples in the region of healing defects in the tibias of beagles of various ages. A 5 mm diameter drill hole defect was made in the mid-shaft of the tibia. Eleven of the beagles received either vehicle (n = 6) or prostaglandin E2 orally (n = 5) for the 30-day period from surgery to time of necropsy. Ten dogs received local injections of vehicle (n = 4) or prostaglandin E1 directly into the defects for the first 10 days after surgery. Double labels were given with each of two fluochrome markers, calcein prior to surgical treatment, and oxytetracycline hydrochloride prior to 30-day sacrifice. The regional remodeling changes were evaluated in 40-50 micron thick cross-sections taken 2 cm proximal to the defect and matching samples from the contralateral side. In the controls, the changes were variable and reflected primarily increased formation on the surfaces of the cortex. Cortical endosteal bone formation, as indicated by oxytetracycline labeling, was increased in both control groups and there was an increase in labeling in the periosteal and haversian envelopes as well, in the local injection control group. In the dogs given prostaglandin E2 orally, there was increased periosteal bone formation in addition to increased cortical-endosteal formation. When healing sides were compared to controls, prostaglandin E2-treated dogs also had increased osteoid formation in all three envelopes and increased resorption surface in the cortical endosteal envelope, indicating accelerated remodeling.(ABSTRACT TRUNCATED AT 250 WORDS)
A histomorphometric study was done on healing defects in the ribs of Beagles. A transverse fracture was made in the left 9th and 10th ribs. Beagles were given either ethanol vehicle (n = 6) or prostaglandin (PG) E2 orally (n = 5) for the 30-day period after surgical manipulation to time of necropsy. Double fluorescent labels to measure bone matrix mineralization were given with each of 2 fluorochrome markers--calcein before dogs were surgically manipulated and oxytetracycline hydrochloride before they were euthanatized. The objectives were to determine the effects of fracture on regional remodeling in the periosteum, the effects of PGE2 on the regional remodeling changes in the periosteum induced by the fracture, and the systemic effect of PGE2 on remodeling changes of the contralateral matching sites. The fracture in the nontreated dogs (ethanol only) stimulated remodeling activity in the periosteum with increased resorption (P less than 0.01). However, after surgical manipulation (necropsy) was done, the extent of mineralization on the bone surface was decreased and was decreased more on the nonfractured ribs (right side) than on the fractured (healing) ribs (left side) (P less than 0.05). In the treated dogs, the administration of PGE2 increased the extent of mineralization on the bone surface on the healing ribs. However, as in the nontreated dogs, the administration of PGE2 did not alter the decreasing pattern of mineralization when comparing the bone surfaces at necropsy with the bone surfaces before surgical manipulation was done.(ABSTRACT TRUNCATED AT 250 WORDS)
A histomorphometric study was carried out in the region of healing defects in the ribs of Beagles. A transverse fracture was made in the left 9th and 10th ribs. Eleven Beagles received either ethanol vehicle (n = 6) or PGE2 orally (n = 5) for the 30 day period from surgery to time of necropsy. Double-pulsed labels were given with each of two fluochrome markers, calcein prior to surgical treatment and oxytetracycline hydrochloride prior to euthanasia. The objectives were to determine the effects of fracture on regional remodeling in the haversian envelope; to determine the effects of PGE2 on the regional remodeling changes in the haversian envelope; and to determine the systemic effects of PGE2 on remodeling changes of the contralateral matching sites. The remodeling changes after surgically induced fracture were relatively insignificant between the injured and uninjured sides in the non-treated dogs as well as in the PGE2 treated group. This may be attributable to the global effect of a fracture. However, there were significantly slower rates of mineral apposition (P less than 0.05) and a longer period for osteon formation time (P less than 0.05) on the injured side compared to the uninjured side of the PGE2 treated dogs. The remodeling activities were increased on both sides in the PGE2 treated dogs when compared to the non-treated ones with more remodeling sites per unit cortical area (P less than 0.01), and a higher turnover rate (shorter total remodeling period in days) with a faster resorption rate and a net increase in mineral apposition rates at the end of the experiment (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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Profiles of remodeling sites were evaluated in longitudinal sections of multiple ribs from 6 beagles with renal failure and parathyroid hyperplasia and compared with ribs from 20 controls. The dogs with renal failure had a marked increase in the number of cutting cones and closing cones. The length of the cutting cone was significantly greater than those found in controls, but there was no difference in the width of the base. There was no difference observed in the length or width or in the proportion of branching of closing cones in the two groups. In addition to cutting and closing cones, however, complex remodeling sites were also seen within the cortex. These were sites in which irregular tunnels that were wider than closing cones had intermittent segments of surface containing osteoid, osteoblasts, or osteoclasts or a mineralized surface with inactive lining cells. These complex remodeling sites were found infrequently in controls and occurred primarily near the cortical endosteal surface, where most contained hematopoietic cells and presumably represented endostealization of the cortex. In the dogs with renal failure, they were markedly increased in number, significantly greater in length, and found more frequently in the center cortex, often without hematopoietic cells.
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A tumor line (58-2T) was established from a slowly growing tumor in a BALB/c mouse inoculated with M58-2 cells. The latter clonal cell line was isolated after bromodeoxyuridine treatment as a flat variant from nonproducer BALB/3T3 cells transformed by the Kirsten sarcoma virus. The 58-2T cells produced type C virus with two discrete virus-specific RNA species. One of the species, which was probably an endogenous virus RNA subunit, had a sedimentation coefficient of 35S as the largest major subunit, and had sequences similar to Rauscher leukemia virus RNA based on nucleic acid hybridization. The other RNA species had 30S as the largest major subunit and corresponded to Kirsten sarcoma virus-specific RNA. These two RNA species formed heterogeneous, 60 to 70S, high-molecular-weight RNA in virions.DNA transcripts (58-2T DNA) from the activated virus contained base sequences complementary to Rauscher leukemia virus and Kirsten sarcoma virus. The Kirsten sarcoma virus-specific DNA sequences (58-2TS) were purified from 58-2T DNA by eliminating RLV-specific sequences.
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A 36-year-old Russian man presented with neck and low back pain in September 1990. He was of normal stature, and there were no stigmata of rickets. The family history was negative for bone disease. He was found to have hypophosphatemia (2.3 mg/dl), impaired phosphate reabsorption (TmP/GFR 2.08), hyperphosphatasemia (254 IU/l), normocalcemia, normal vitamin D metabolite levels, and secondary hyperparathyroidism. Clinically, his spinal movements were quite impaired and there was moderate proximal muscle weakness. On skeletal radiographs, there was generalized osteosclerosis and multiple ligamentous calcifications. Transiliac biopsy was diagnostic for severe osteomalacia. He was treated with oral phosphate (240 mEq daily) and calcitriol (4 micrograms daily) with resultant very slow clinical, biochemical, and histomorphologic improvement. The patient had hypophosphatemic osteomalacia with some features of X-linked hypophosphatemia, but sporadic and of relatively late onset. The osteopenia, height loss, incapacitating weakness, and glycinuria that are characteristics of sporadic adult onset nonfamilial hypophosphatemia, with or without an associated tumor, and the low serum calcitriol levels that may be an additional characteristic of tumor-induced osteomalacia were absent. Other known causes of acquired renal tubular dysfunction were ruled out. The etiology, pathogenesis, and nosology of the disorder remain obscure, but treatment based on experience with other forms of hypophosphatemic osteomalacia was ultimately effective.