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Biomedical subjects

G Lust

Publications and source records attributed to G Lust.

At least 91 records · Page 5Linked to original sources
PubMed1988

Immunohistochemical localization of fibronectin and chondronectin in canine articular cartilage.

We compared the distribution of fibronectin and chondronectin within the matrix of canine articular cartilage. Fibronectin was found throughout the matrix as well as pericellularly. In contrast, chondronectin was observed predominantly associated with the cell or pericellular matrix. Interactions of these molecules with matrix components in the pericellular matrix probably differs, however, since concentrations of hyaluronidase which prevented detection of pericellular fibronectin allowed detection of chondronectin. Chondronectin and fibronectin were detected in osteoarthritic cartilage as well as in disease-free cartilage. Penetration of biotinylated fibronectin into cartilage from the external medium occurred only in osteoarthritic cartilage and proceeded only from the articular surface. Disease-free cartilage appeared to maintain a barrier to fibronectin penetration from the articular surface which was sustained even after the proteoglycan content was markedly depleted by incubation of cartilage with catabolin or lipopolysaccharide. In cartilage that was proteoglycan-depleted, the only detectable penetration of external fibronectin was from the cut surface.

Animals↗
PubMed1987

Plasma relaxin levels in pregnant and lactating dogs.

The pattern of plasma relaxin has been studied during pregnancy and following parturition in two breeds of dogs, Labrador retrievers and beagle hounds. Blood samples were collected at weekly intervals following mating and during pregnancy, parturition, and lactation. Relaxin, progesterone, and estradiol-17 beta were determined by specific double antibody radioimmunoassays. Immunoreactive relaxin (IR) was not detectable in plasma of male dogs, bitches in anestrous, or pseudopregnant bitches that had undergone an infertile mating. IR was first detectable in plasma in the third or fourth week of gestation in retrievers and beagles. IR levels rose to a peak of 4-5 ng/ml in both breeds. The peak plasma levels were reached 2-3 wk before whelping and declined significantly prior to that event. IR then persisted during lactation at a level of 0.5-2 ng/ml for 4-9 wk, but was significantly higher (p less than 0.01) at all time periods and persisted longer in labradors than in beagles. The secretion of relaxin did not parallel that of progesterone, which was highly elevated in the first samples drawn (during the first week of pregnancy), remained high through 5 or 6 wk of gestation, then slowly declined until the time of parturition, becoming undetectable during lactation. Plasma estradiol-17 beta was low after the second week of pregnancy in both breeds of dogs and became undetectable during lactation. The source of relaxin in the dog is not known currently, and its sites of secretion and role in pregnancy are currently under investigation in our laboratories. The dog is the first species in which plasma IR is detectable during lactation using antibody R6.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Fibronectin as a marker for osteoarthritis.

Abnormal cartilage from osteoarthritic canine joints contained up to 20 times more fibronectin than did disease-free cartilage. Fibronectin synthesis in osteoarthritic cartilage was increased and more of the newly made protein accumulated in this cartilage. Data suggested that fibronectin content was increased in cartilage with early osteoarthritic changes whereas glycosaminoglycan content remained unchanged. Immunoperoxidase studies revealed that fibronectin was distributed throughout the matrix of both normal and osteoarthritic cartilage. Fibronectin concentration was increased twofold in synovial fluid from osteoarthritic joints.

Animals↗
PubMed1986

Incorporation of purified plasma fibronectin into explants of articular cartilage from disease-free and osteoarthritic canine joints.

The purpose of this study was to determine if articular cartilage was able to accumulate fibronectin, a large molecule of 440,000 daltons, from the external medium, and if so, to compare the extent of accumulation by normal and osteoarthritic cartilage and to localize the sites of fibronectin accumulation within the articular cartilage. The uptake of canine serum albumin, another protein present in plasma and synovial fluid with a lower molecular weight (67,000 daltons) and a lower pI, was compared. Purified plasma fibronectin and canine albumin were labelled with 125I or N-hydroxysuccinimidobiotin by standard procedures and incubated with articular cartilage explants. The 125I-fibronectin that had bound to cartilage components was extracted with 4 M urea, and both extract and cartilage residues were counted. Cartilage accumulated fibronectin to a greater extent than albumin. For normal cartilage, a level of saturation appeared to be reached at an external concentration for fibronectin of about 150 micrograms/ml. Degenerated cartilage accumulated about 10-fold more fibronectin than normal cartilage. Biotinylated fibronectin was localized within frozen sections of articular cartilage by probing with peroxidase-linked avidin. Fibronectin accumulation in normal cartilage was restricted to the articular surface and the cut edge. In degenerated cartilage, penetration of fibronectin was more extensive but proceeded only from the articular surface. Staining of adjacent sections with peroxidase-linked antifibronectin antibody confirmed previous observations that endogenous fibronectin is present throughout the cartilage matrix. The possibility that synovial fluid fibronectin could be a source of cartilage fibronectin, especially in degenerated cartilage, was discussed.

Animals↗
PubMed1986

Fibronectin and water content of articular cartilage explants after partial depletion of proteoglycans.

The aim of this study was to test the hypothesis that fibronectin in cartilage of osteoarthritic joints accumulates in increased quantities in response to a reduction in proteoglycan content in the matrix. We determined fibronectin content in an ELISA system, uptake of plasma 125I-fibronectin from the medium, and glycosaminoglycan content by a dye method. The proteoglycan content of canine articular cartilage was reduced by co-incubation of the cartilage with canine synovium, partially purified catabolin, or retinoic acid. Data suggested that proteoglycan loss alone was not sufficient to result in the increased fibronectin accumulation that has been reported in the deteriorating articular cartilage of osteoarthritic joints. Cartilage that lost as much as 75% of its proteoglycan content did not have increased fibronectin content and did not take up more fibronectin from the external medium. A related goal of this study was to evaluate the percentage of water in proteoglycan-depleted but disease-free cartilage, as the percentage of water is known to be elevated in osteoarthritic cartilage. Data indicated that the percentage of water in the depleted cartilage increased in proportion to the decrease in proteoglycan content, but the total amount of water in the cartilage did not increase; water content appeared to be unchanged. Under the conditions used, the proteoglycan content was reduced and the percentage of water was elevated, but fibronectin content was not increased. Thus, the cartilage incubated in vitro did not mimic osteoarthritic cartilage.

Animals↗
PubMed1986

Presence of fibronectin in articular cartilage in two animal models of osteoarthritis.

Fibronectin content was determined in articular cartilage in a spontaneous dog model and in a meniscectomy rabbit model of osteoarthritis. Determination of the fibronectin content of urea extracts of articular cartilage by an enzyme linked immunosorbent assay (ELISA) disclosed that degenerated cartilage contained from 10- to 40-fold more fibronectin than normal cartilage. The finding that cartilage fibronectin content was increased in both animal models suggests that elevated cartilage fibronectin content is a general feature of the osteoarthritic process. Immunoperoxidase studies disclosed that fibronectin was distributed throughout the matrix in hyaluronidase treated normal and osteoarthritic cartilage from both animal models, but quantitative differences in fibronectin were not observed by these techniques.

Animals↗
PubMed1985

Deposition of fibronectin in articular cartilage of canine osteoarthritic joints.

Deposition of fibronectin was examined in articular cartilage of healthy and osteoarthritic joints of Labrador Retriever dogs. Abnormal cartilage from osteoarthritic joints contained up to 20 times more fibronectin than did disease-free cartilage. Compared with normal cartilage, the rate of fibronectin synthesis in osteoarthritic cartilage was increased and a greater proportion of the newly made fibronectin accumulated in the lesion cartilage matrix. The rate of release of endogenous prelabeled [3H]fibronectin from disease-free explants was similar to the rate of release from degenerated cartilage explants into incubation media. Concentrations of fibronectin were greater in synovial fluid from osteoarthritic joints than in synovial fluid from healthy joints, but both types of fluid had less fibronectin than in blood plasma.

Animals↗
PubMed1984

Synthesis of fibronectin in normal and osteoarthritic articular cartilage.

The content and the biosynthesis of fibronectin was examined in disease-free articular cartilage and in articular cartilage from osteoarthritic canine joints. Fibronectin content was increased in extracts of cartilage from osteoarthritic joints. Incubation of cartilage in vitro with [3H]phenylalanine and subsequent isolation of [3H]fibronectin from a gelatin affinity column and characterization by SDS-polyacrylamide gel electrophoresis and by immunoprecipitation indicated that disease-free and osteoarthritic cartilage explants synthesized fibronectin. About 50% of the [3H]fibronectin was recovered in the incubation medium. The osteoarthritic cartilage synthesized and accumulated up to 5-fold more [3H]fibronectin than disease-free cartilage.

Cartilage, Articular↗
PubMed1983

Degenerative joint disease: multiple joint involvement in young and mature dogs.

Radiologic, pathologic, and ancillary methods were used to determine the occurrence of degenerative joint disease involving multiple joints of immature and adult dogs. Animals were selected for the development of hip joint dysplasia and chronic degenerative joint disease. Of disease-prone dogs, 82% (45 of 55 dogs) had radiologic changes, indicative of hip dysplasia, by 1 year of age. At necropsy, more abnormal joints were identified than by radiographic examination. Among 92 dogs between 3 to 11 months of age that had joint abnormalities, 71% had hip joint involvement; 38%, shoulder joint involvement; 22%, stifle joint involvement; and 40% had multiple joint involvement. Polyarthritis was asymptomatic and unexpected. Radiographic examination of older dogs also revealed evidence of degenerative joint disease in many joints. Multiple joint involvement was substantiated at necropsy of young and mature dogs. A similar pattern of polyarticular osteoarthritis was revealed in a survey (computer search) of necropsy reports from medical case records of 100 adult and elderly dogs. Usually, the joint disease was an incidental observation, unrelated to the clinical disease or to the cause of death. The frequent occurrence of degenerative changes in several joints of dogs aged 6 months to 17 years indicated that osteoarthritis may be progressive in these joints and raises the possibility that systemic factors are involved in the disease process.

Age Factors↗
PubMed1982

Reduced deposition of collagen in the degenerated articular cartilage of dogs with degenerative joint disease.

Collagen metabolism in the focal degenerated cartilage from immature dogs with degenerative joint disease was compared with that in the adjacent 'normal' cartilage of the same joint surface. The deposition of collagen into the cartilage in vitro as measured by accumulation of hydroxy[14C]proline was decreased in the early and in advanced stages of cartilage degeneration. The deposition of collagen into cartilage in vivo as measured by the accumulation of hydroxy[3H]proline (intravenously injected [3H]proline) also was reduced in the degenerated cartilages of a dog with degenerative joint disease. Gel electrophoretic analysis revealed that degenerated cartilage contained less alpha 1 II collagen chains, but increased amounts of larger proteins. Degenerated cartilage contained more water, increased amounts of unidentified, non-collagenous protein, increased collagenolytic enzyme activity and fewer chondrocytes. Decreased deposition of collagen would result in collagen depletion in the foci of degenerated cartilage in joints of dogs with degenerative joint disease.

Animals↗
PubMed1982

The type of collagen made by the articular cartilage in joints of dogs with degenerative joint disease.

The collagen in the degenerated articular cartilage from dysplastic canine hip joints was characterized as to type by examining cartilage directly and also after labeling cartilage slices with 14C-proline in vitro. Collagen analysis was by sodium dodecylsulfate-polyacrylamide gel electrophoresis of 14C-labeled collagen, and of 14C-peptides which had been cleaved by cyanogen bromide. Amino acid analysis was done on hydrolysates of whole cartilage and of purified collagens to quantify the ratio of hydroxyproline to hydroxylysine. Data revealed that type II collagen was the radiolabeled product synthesized in all samples of degenerated cartilage and was the only collagen detected in biochemical tests in the cartilage of joints with degenerative joint disease as well as in disease free hip joints. Results suggested that chondrocytes in degenerated cartilage of canine joints did not switch their collagen phenotype, but continued to synthesize type II collagen. Cartilage degeneration in joints of dogs with hip dysplasia proceeded without a change in collagen phenotype.

Animals↗
PubMed1982

Ultrastructure of the articular cartilage and synovium in the early stages of degenerative joint disease in canine hip joints.

A combined light and electron microscopic study recorded the developing degenerative changes in the hip joints of dogs with spontaneous joint disease. Synovium from joints with normal articular cartilage contained 33% type A and 64% type B cells. The 1st evidence of articular cartilage degeneration was loss of the surface amorphous layer and disruption of collagen fibrils. In the face of the earliest focal cartilage defects, the number of type A cells decreased (P less than 0.01) and remained low. Necrotic synoviocytes and synoviocytes of uncertain type increased as articular cartilage lesions progressed. The earliest pathologic changes in the synovium and the articular cartilage surface were evident only on ultrastructural examination.

Animals↗
PubMed1981

Increased pyrophosphate in fibroblasts and lymphoblasts from patients with hereditary diffuse articular chondrocalcinosis.

The metabolic and genetic factors leading to deposition of calcium pyrophosphate crystals in cartilage of patients with chondrocalcinosis are not well understood. Analysis of cultured fibroblasts and lymphoblasts from 12 affected members of a large kindred showed a mean concentration of intracellular inorganic pyrophosphate two times greater than that in cells from unaffected family members or normal, unrelated volunteers. Increased intracellular pyrophosphate may, therefore, be a biochemical marker for the heterozygous expression of the chondrocalcinosis gene.

Cells, Cultured↗
PubMed1981

Evidence of a generalized metabolic defect in patients with hereditary chondrocalcinosis. Increased inorganic pyrophosphate in cultured fibroblasts and lymphoblasts.

A gene in the heterozygous state appears responsible for a 2-fold increase in pyrophosphate content of both fibroblasts and lymphoblasts cultured from patients who have dominantly inherited chondrocalcinosis. Cells from unaffected family members of this large kindred showed a pyrophosphate content in the same range as was found in unaffected, unrelated controls. Similar cells from individuals homozygous for the gene would be useful in delineating the precise biochemical abnormality responsible for the increased pyrophosphate content.

Adult↗
PubMed1981

Early, asymptomatic stage of degenerative joint disease in canine hip joints.

The early stages of degenerative joint disease were investigated in coxofemoral joints from dogs with a hereditary predisposition to hip dysplasia. Alterations observed included mild nonsuppurative synovitis, increased volume of both synovial fluid and the ligamentum teres, and focal degenerative articular cartilage lesions. On radiologic examination, subluxation of the femoral head was seen, but only in the most severely affected joints. Synovial inflammation with increased synovial fluid and ligament volumes were indicators of early degenerative joint disease in dogs. These changes seemed to coincide with, or perhaps to precede, microscopic evidence for articular cartilage degeneration and occurred before radiologic abnormalities were detected.

Animals↗