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Biomedical subjects

L Krook

Publications and source records attributed to L Krook.

At least 37 records · Page 2Linked to original sources
PubMed1987

Annual skeletal changes in the little brown bat, Myotis lucifugus lucifugus, with particular reference to pregnancy and lactation.

Studies of bone from summer-active little brown bats, Myotis lucifugus lucifugus, have demonstrated sex differences in the renewal of skeletal mineral reserves following spring-arousal from hibernation. Patterns of bone remodeling in both sexes of bats indicate that new bone formation does not occur during hibernation: All new bone formation occurs during the summer-active season. Results show that a short period of time elapses after hibernation before the initial demands of a large fetus and rapidly growing neonate are expressed on maternal skeletal reserves. Bone loss in summer-active females was associated with pregnancy and lactation, whereas summer-active males did not show evidence of bone loss but, instead, uninterrupted bone accretion throughout the summer-active season. Osteoclasts and bone-forming osteoblasts, absent during the hibernation period, reappeared on bone surfaces following spring-arousal from hibernation. There was no apparent increase in osteoclast numbers or activity during lactation but resorption cavities were found in deep cortical lamellae distant from bone surfaces. The increase in bone resorption in lactating bats appeared to be by osteocytic osteolysis, suggesting that it might be a significant mechanism of bone/calcium regulation in this hibernating mammal throughout the year.

Animals↗
PubMed1987

Morphology of thyroid C-cells and parathyroid glands in summer-active little brown bats, Myotis lucifugus lucifugus, with particular reference to pregnancy and lactation.

Morphological studies of thyroid C-cells and morphometric analyses of parathyroid glands in summer-active little brown bats indicated concomitant regulatory endocrine functions correlating with bone remodeling. C-cells apparently maintain maximal activity throughout the summer-active period in all bats. However, the hyperactivity of the parathyroid glands in summer-active female bats can be correlated with the maintenance of plasma calcium concentrations during lactation, when the female skeleton undergoes a period of bone demineralization. In summer-active male bats, which did not lose bone, the parathyroid glands did not show morphological evidence of hyperactivity; instead they were found to exhibit moderate parathyroid activity.

Animals↗
PubMed1987

Fluoride intoxication in dairy calves.

Chronic fluoride intoxication in dairy cattle, caused by feeding fluoride contaminated commercial feed, was previously described in a dairy herd. Dental fluorosis and a catastrophic decrease in milk yield were the foremost findings. In calves born to the fluoride intoxicated cows, congenital fluorosis was manifested by brown discoloration of enamel, enamel hypoplasia, brown mottling of bone, severe retardation of cartilage cell differentiation, atrophy of osteoblasts, osteopenia, atrophy of bone marrow cells, serous atrophy of bone marrow fat and severely stunted growth.

Animal Feed↗
PubMed1986

Teratogenic effect of calcium edetate (CaEDTA) in rats and the protective effect of zinc.

The calcium chelate of EDTA (CaEDTA) currently is the drug of choice in the treatment of lead intoxication. This study investigated the teratogenic potential of CaEDTA, administered parenterally during periods of organogenesis and determined if incorporating zinc into EDTA would protect against teratogenic effects. Four doses (2, 4, 6, and 8 mmol/m2/day) of CaEDTA, two concentrations (8 and 20 mmol/m2/day) of ZnEDTA and ZnCaEDTA (molar ratio 0.5:0.5:1) were used, and a saline control (0.9% NaCl). Timed-pregnant Long-Evans rats were assigned at random to the treatment groups, 20 per dose for each chelate and 30 to the saline control. Rats were injected with the chelate or saline solution sc, twice daily during the 11th through 15th days of gestation. Pups removed by cesarean section on the 21st day were processed for osseous and visceral examination. Additional animals per treatment group were used for maternal plasma and liver and fetal zinc determinations. Results showed increases in several abnormalities (submucous cleft, cleft palate, adactyly-syndactyly, curly tail, abnormal rib and vertebrae) with increasing amounts of CaEDTA. No malformations were seen with ZnEDTA at either dose or with ZnCaEDTA at 8 mmol/m2/day. However, submucous cleft was seen in 6 of 20 litters from the dams receiving the higher dose of ZnCaEDTA. It was concluded that CaEDTA is teratogenic in rats at concentrations which, except for decreased weight gain, produce no discernible toxicity to the dam, and which are comparable to the recommended therapeutic dosage in humans (1500 mg/m2/day corresponding to 4 mmol/m2/day). Protection is afforded by incorporating zinc in the chelate.

Abnormalities, Drug-Induced↗
PubMed1986

Track condition and racing injuries in thoroughbred horses.

The incidences of fractures and soft tissue injuries during 68397 starts of thoroughbred horses at New York Racing Association tracks were analyzed concerning track condition, dirt and turf tracks, environmental conditions, length of races, location of fractures on the track, and age of horses. It was concluded that the conditions evaluated are of no importance in the occurrence of racing injuries to thoroughbred horses.

Animals↗
PubMed1986

Toxic effects of food-borne fluoride in silver foxes.

Chronic ingestion of excessive amounts of fluoride from commercial fox food is associated with agalactia in vixens resulting in the starvation deaths of large numbers of kits in three fox herds. Evidence of infectious disease or poor management could not be found and a causal relationship between fluoride and high kit mortality is suggested.

Animal Feed↗
PubMed1986

Milk production of cows fed fluoride contaminated commercial feed.

A commercial feed concentrate and a mineral mix with excessive amounts of fluoride were introduced into a Holstein dairy herd with an average milk production well above national standards. Milk production decreased drastically, and during the following 6 years the deficit in milk production in the herd ranging from 52 to 120 milking cows was 1.5 million Kg (3 1/4 million lbs.). The tolerance levels set by the National Academy of Sciences for fluoride ingestion by lactating cow were found to be inadequate.

Animal Feed↗
PubMed1985

Bilateral degenerative coxofemoral joint disease in a foal.

Bilateral degenerative coxofemoral joint disease and noninflammatory osteonecrosis in the femoral heads were diagnosed in a 5-month-old Standardbred colt. Cytologic evaluation and bacterial cultures of coxofemoral synovial fluid, and radiographic and pathologic examination of the coxofemoral joints were conducted. The cause was not determined; however, a thrombus found in association with 1 focus of osteonecrosis was suspected as an etiologic factor.

Animals↗
PubMed1984

Skeletal disease in a hypothyroid foal.

Hypothyroidism was diagnosed in a 5-month-old Thorough-bred colt by clinical and clinico-pathology examinations, thyroid stimulating hormone response test and by microscopic evaluation of the thyroid gland. Skeletal lesions included delayed appearance of ossification centers and delayed development of bone in cartilage models, delayed closure of epiphyseal plates, transverse trabeculation in metaphyses, osteochondrosis dissecans and subchondral cysts.

Animals↗
PubMed1984

Vascular pathology in phenylbutazone intoxicated horses.

Three mature Thoroughbred geldings were given 13.63 mg phenylbutazone/Kg bodyweight intravenously for 3 days and repeated in one horse 4 days later. After 4, 7 and 10 days (double treatment), degeneration of the wall of small veins occurred in all horses. The veins were dilated and/or showed hyalin degeneration. The phlebopathy was interpreted to be paramount in phenylbutazone intoxication. All other manifestations, including erythro- and leukodiapedesis, submucosal edema and ulceration of the gastrointestinal mucosa, phlebothrombosis and significant changes in the hemogram and serum chemistry, were considered secondary to the vein lesions.

Animals↗
PubMed1983

Defects in collagen fibrillogenesis causing hyperextensible, fragile skin in dogs.

Two unrelated mixed-breed dogs were donated for studies of their fragile, hyperextensible skin. Breeding of these dogs to bitches with normal skin showed that half of their male and female offspring also had fragile, hyperextensible skin, indicating that the defect was transmitted as an autosomal dominant trait in both dogs. Electron microscopy showed distinct abnormalities in the packing of collagen into fibrils and fibers in affected skin. These packing defects in dermal collagen were identical in related dogs, but were slightly different in unrelated animals. A clinical test, the skin extensibility index, was used to quantitate the extensibility of affected and unaffected skin. This index ranged from 8% to 15% in normal dogs and from 17% to 25% in newborn pups and adult dogs with collagen packing defects. The tensile strength of dorsolateral thoracic skin of affected pups was only 5% to 10% of that of matched specimens of paired littermates. The hyperextensibility and fragility of skin were the only clinical signs, but radiographic and microradiographic studies revealed subclinical involvement of bone.

Animals↗
PubMed1983

Dental fluorosis in cattle.

Five expressions of dental fluorosis are described in cattle exposed to industrial fluoride pollution: 1. Hypercementosis with tooth ankylosis, cementum necrosis and cyst formation; 2. Delayed eruption of permanent incisor teeth; 3 Necrosis of alveolar bone with recession of bone and gingiva; 4. Oblique eruption of permanent teeth, hypoplasia of teeth with diastemata; and 5. Rapid progression of dental lesions. The five entities are not recognized in the "standard for the classification of dental fluorosis" by the National Academy of Sciences. Since this classification it too limited and superficial, adherence to this standard has left severe cases of fluoride intoxication in cattle undetected in field surveys.

Alveolar Process↗
PubMed1983

Morphologic and biochemical changes in cartilage of foals treated with dexamethasone.

Epiphyseal and articular cartilages were examined in pony foals treated with intramuscular injections of either 0.5 mg dexamethasone per 100 kg bodyweight daily for 3, 8 or 11 months, or 5.0 mg per 100 kg for 11 months, and in horse foals treated with 5.0 mg per 100 kg for 20 weeks. The proximal femoral growth plates exhibited increased spatial separation between chondrocyte columns, narrowed zones of disorganized columnar and hypertrophic cartilage, abnormal penetration of hypertrophic cartilage by metaphyseal capillaries, retained cartilage in the spongiosa, distal terminal plate formation, transverse trabeculation, chondronecrosis and metaphyseal osteochondrosis dissecans. Destructive articular lesions were observed after 3 months of treatment with 0.5 mg per 100 kg bodyweight. Joint damage originated either at the joint surface or deep within the cartilage. Signs of surface deterioration included edema, fibrillation, enlargement of lacunae, pitting, shredding and erosions of cartilage. Inactivity of articular cartilage growth centers was common, with failure of epiphyseal capillaries to penetrate the lacunae in the calcified cartilage. Chondronecrosis adjacent to the calcification front was accompanied by cartilage ulceration and fracture. Intracartilaginous cysts and subchondral chondroid cysts were also observed. Healing responses included reparative chondrogenesis (focal cartilage hyperplasia), formation of fibrous or fibrocartilaginous "scars," subchondral osteopetrosis and epiphyseal marrow petrosis. Lactate dehydrogenase specific activities per chondrocyte, 35S uptake per cell and glycosaminoglycan contents of articular cartilages were all reduced 55% by 3 months of treatment. This inhibition of articular chondrocyte metabolism initiated cartilage degeneration. Surface destruction and osteochondrosis dissecans followed continued mechanical stress of compromised cartilage.

Animals↗
PubMed1982

Milk production of cows exposed to industrial fluoride pollution.

Milk sales records for a dairy herd showed that milk production did not decrease during the first 4 yr of exposure of cows to fluoride pollution from an aluminum plant. During the next 3 yr milk production decreased, but not significantly. From yr 8 of exposure there was a significant decrease, which persisted through yr 19, when the dairy operation was terminated. From yr 15 through yr 19, the milk yield averaged less than 60% of the expected value.

Aluminum↗
PubMed1982

Calcium metabolism in glucocorticoid-treated pony foals.

Pony foals were injected intramuscularly with 0, 0.5, or 5.0 mg dexamethasone per 100 kg body weight daily for up to 11 months. True absorption of dietary calcium was inhibited by treatment at 18 days (57% versus 14% of intake; P less than .01) and 10 months (72% versus 55% versus 43%: P less than .01), but not at 2 or 7 months, and was independent of age and treatment related decreases in intestinal calcium binding protein activities. Uninary excretion of calcium was increased by treatment through 7 months but decreased at 10 months. Treatment for 18 days resulted in total calcium excretions equivalent to 127% of dietary intake. All animals were in positive calcium balance thereafter. Endogenous fecal calcium excretion was not affected by treatment, age, or sex, averaging 18.0 mg per kg body weight per day. At 2 months, rates of calcium deposition into bone were 13.02, 7.01 and 6.83 g per 100 kg per day in ponies treated with 0, 0.5 and 5.0 mg per 100 kg, respectively. Corresponding rates of calcium removal from bone were 5.41, 1.88, and 2.69 g per 100 kg per day. These rates remained significantly inhibited in the treated ponies at 7 and 10 months. The net effect of dexamethasone treatment was an inhibition of bone turnover: calcium removal was suppressed more than inhibition of bone turnover: calcium removal was suppressed more than calcium deposition.

Absorption↗
PubMed1982

Bone lesions in growing swine fed 3% cement kiln dust as a source of calcium.

Cement kiln dust (CKD) samples of which have been reported to stimulate growth in cattle and sheep, was fed to weanling pigs in a 42-d experiment. CKD at levels of 1.5 and 3.0% was added to a corn-soybean meal-oats-whey-type diet containing inadequate amounts of Ca (.4% of the diet) to provide final dietary Ca levels of .85 and 1.3%. A diet containing 3% limestone (1.3% dietary Ca) served as a positive control. Body weight gain was depressed by 3.0% CKD, and histopathological lesions of the humerus, not typical of nutritional secondary hyperparathyroidism or rickets, were observed. The lesions detected were osteonecrosis, thinning of the cortex and reduction in the width of the epiphyseal cartilage. Width of the proximal epiphyseal plate and cortical index of the humerus (width of cortex divided by total diameter at narrowest point of diaphysis) were smaller in pigs fed 3% CKD than in pigs fed 3% limestone. CKD contained 2.3% A1, 15 ppm Cd and 110 ppm Pb, providing 690, .45 and 3.3 ppm of A1, Cd and Pb, respectively, in the diet containing 3% CKD. Kidney, liver and bone ash concentrations of these three minerals were not increased by CKD, and typical toxicity signs were absent. It is concluded that CKD may contain one or more factors that interfere with normal bone metabolism in growing pigs when the diet contains 3.0% CKD.

Animals↗
PubMed1982

Glucocorticoid-induced inhibition of osteolysis and the development of osteopetrosis, osteonecrosis and osteoporosis.

Changes in the developing femoral epiphysis, especially those concerning the osteocytes, were examined in pony foals systemically treated with daily intramuscular injections of either 0.5 or 5.0 mg of dexamethasone per 100 kg bodyweight for either 3, 8 or 11 months. Midsagittal sections of proximal femur from animals treated for 3 months contained significantly more bone tissue subchondrally and epiphyseally than did sections from untreated ponies. Large portions of the bone tissue appeared necrotic, although osteoblasts and patent capillaries were abundant. After 8 months the bone sections revealed marked osteoporosis. Abnormally dense bone was again observed after 11 months. There were significant increases in the severity of these changes in bone from the animals treated with the higher dosage. Calcium kinetics studies revealed an inhibition of calcium deposition (bone formation) in the treated animals after 2 and 7 months. However, calcium removal (bone resorption) was inhibited to a greater extent. Osteopetrosis (radiographic sclerosis) resulted from the initial resorption/formation imbalance, and was accompanied by osteonecrosis and osteocyte death. Continued treatment resulted in osteopenia, caused by the removal of necrotic bone debris and the inhibition of new bone formation. The primary event in the development of glucocorticoid-induced bone disease was shown to be suppression of osteolysis with the development of osteonecrosis.

Animals↗