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G Weseloh

Publications and source records attributed to G Weseloh.

At least 37 records · Page 2Linked to original sources
PubMed1999

Hepatocyte growth factor in human osteoarthritic cartilage.

OBJECTIVE: Hepatocyte growth factor/scatter factor is a potent mitogen, morphogen and motogen for a variety of mainly epithelial cells. Hepatocyte growth factor is synthesized by mesenchymal cells and can be found in various tissues. The objective of this study was to investigate the expression and distribution patterns of this pleiotropic growth factor and its receptor, the product of the proto-oncogene c-met in normal and osteoarthritic human knee cartilage. METHODS: Five normal and 14 osteoarthritic human cartilage samples graded histomorphologically by Mankin Score, were studied by radioactive in-situ hybridization and immunohistochemistry for the expression of Hepatocyte growth factor and the c-met receptor. RESULTS: Hepatocyte growth factor could be found by immunohistochemistry in the territorial matrix surrounding the chondrocytes of calcified cartilage and within the deep zone of normal cartilage. Chondrocytes of these cartilage zones showed also positive c-met receptor-staining. Moreover, a small number of chondrocytes in the superficial and intermediate zone showed c-met staining. In accordance with the increased hepatocyte growth factor staining of osteoarthritic cartilage, an enhanced expression of hepatocyte growth factor-RNA by chondrocytes of the deep zone as well as the deeper mid zone was observed. Contrary to normal cartilage, c-met was identified immunohistochemically in osteoarthritic chondrocytes of all cartilage zones. CONCLUSION: These results indicate that hepatocyte growth factor seems to be acting in an autocrine/paracrine manner in normal and osteoarthritic cartilage. The ubiquitous presence of the HGF/HGF-receptor complex in osteoarthritic chondrocytes suggests that hepatocyte growth factor may contribute to the altered metabolism in osteoarthritic cartilage.

Cartilage, Articular↗
PubMed1998

Increased content of type-VI collagen epitopes in human osteoarthritic cartilage: quantitation by inhibition ELISA.

Type-VI collagen is an integral part of the extracellular cartilage matrix. However, the exact amounts of type-VI collagen in normal and osteoarthritic human cartilage still are not known. In this study, we describe an inhibition enzyme-linked immunosorbent assay that was developed to quantitate type-VI collagen epitopes found in guanidinium chloride extracts from normal and osteoarthritic human cartilage. In 31 cartilage samples from various localizations of healthy adult human knees, type-VI collagen epitopes accounted for approximately 0.40% of the total collagen content. Interestingly, type-VI collagen epitopes increased about 4-fold in osteoarthritic cartilage. A statistically significant increase of type-VI collagen epitopes was found during early stages of the disease, with only a superficial roughening of the cartilage surface and a loss of proteoglycans. Thus, these findings indicate that type-VI collagen is a minor component of normal human articular cartilage and that the amount of type-VI collagen epitopes increases significantly during early stages of osteoarthritis.

Adult↗
PubMed1996

Cartilage thickness measurement in magnetic resonance imaging.

To assess the accuracy of cartilage thickness measurements in magnetic resonance imaging (MRI), we compared data obtained by cartilage thickness measurements in MRI with corresponding histological sections of 14 human proximal tibial articular surfaces. Each proximal tibial articular surface was cut into five medial and lateral slices and each of these slices was divided into three sectors providing 420 sectors, 406 of which were evaluated in our study. The overall correlation coefficient (r) was 0.96. Topographical differences were found. The lowest correlation coefficient in our series was observed in the anterior part of the medial tibial plateau (r = 0.88). Cartilage thickness measurements in MRI were more accurate in cartilage thicker than 2 mm (r = 0.94) than in thinner cartilage layers (r = 0.73). There were no significant differences in cartilage thickness measurements in different grades of osteoarthritis. However, the mean percentage difference between cartilage thickness in MRI and histology was about 10% in our series.

Cartilage, Articular↗
PubMed1995

Comparison of low-field (0.2 Tesla) and high-field (1.5 Tesla) magnetic resonance imaging of the knee joint.

In order to evaluate the reliability of low-field magnetic resonance imaging (MRI), we examined 22 patients using a 0.2-Tesla magnet unit in comparison with a 1.5-Tesla system. The MRI findings were compared with the intraoperative findings. Concerning the diagnosis of meniscal tears, the gradings of both systems differed only in three cases. The specificity was 97% (both systems), the sensitivity 83% (1.5 T) versus 75% (0.2 T). The sensitivity and specificity for detection of tears of the anterior cruciate ligament were 100% and 75%, respectively, for both systems. The gradings differed only in two cases. In our series we found 6 full-thickness cartilage defects that were all detected with the high-field imaging system. They were missed by the low-field imaging system in 5 cases. The results suggest that both systems are reliable in diagnosing meniscal tears and ruptures of the anterior cruciate ligament.

Adolescent↗
PubMed1995

Synovial fibroblast-like cells strongly express jun-B and C-fos proto-oncogenes in rheumatoid- and osteoarthritis.

To identify recently activated cells in the synovial membrane (SM) of patients with rheumatoid arthritis (RA), the in situ expression of the proto-oncogenes jun-B, c-jun, jun-D, and c-fos was assessed by means of immunohistochemistry and in situ hybridization techniques. SM from patients with osteoarthritis (OA) or joint trauma (JT), as well as from normals (No) were used as controls. Numerous cells expressing high levels of jun-B and c-fos were found within lining layer and diffuse infiltrates in the vicinity of inflammatory cells, but only a few in lymphoid follicles and endothelia. The positive cells were spindle-shaped, CD14- and CD3-negative and, in addition, expressed mRNA for collagen alpha 2 (I) and alpha 1 (III), indicating that they were fibroblasts. In control OA, JT, and even No SM, individual fibroblast-like cells stained as strongly as in RA; however, the density of positive cells was substantially lower. In RA SM, fibroblasts, but not lymphocytes or macrophages, appear to undergo in situ activation. Quantitative differences among RA, OA, and JT may be related to different degrees of inflammatory infiltration.

Arthritis, Rheumatoid↗
PubMed1993

Biased T cell receptor V gene usage in rheumatoid arthritis. Oligoclonal expansion of T cells expressing V alpha 2 genes in synovial fluid but not in peripheral blood.

OBJECTIVE: To analyze the T cell receptor (TCR) variable (V) region gene usage in the rheumatoid joint. METHODS: Monoclonal antibodies (MAb) were used to determine the prevalence of selected V elements on T cells in synovial fluid (SF) from rheumatoid arthritis (RA) patients and in peripheral blood (PB) from RA patients and normal controls. V alpha 2-positive PB and SF T cells from 1 patient were cloned by immediate limiting-dilution and analyzed by restriction mapping. RESULTS: In 9 of 14 RA patients, SF was enriched in at least 1 of the selected V elements, compared with PB. TCR genes of the V alpha 2 family were the most frequently overrepresented in the SF (4 patients). The expanded V alpha 2-positive cells were oligoclonal in SF but heterogeneic in PB. CONCLUSION: Our data showing biased and clonally restricted TCR elements in the rheumatoid joint indicate major histocompatibility complex-restricted antigen recognition, rather than a "superantigen," in the pathogenesis of RA.

Adult↗
PubMed1993

Independent expression of fibril-forming collagens I, II, and III in chondrocytes of human osteoarthritic cartilage.

Normal and osteoarthritic human articular cartilage was investigated by in situ hybridization for expression patterns of the fibrillar collagens type I, II, and III to evaluate phenotypic changes of articular chondrocytes related to the disease. In 11 out of 20 samples, a defined subset of chondrocytes in the superficial and upper middle zone of osteoarthritic cartilage showed significant levels of cytoplasmic alpha 1 (III) mRNA, whereas strong signals of alpha 1 (II) mRNA were found in the upper and lower middle zone, partially overlapping with the zone of alpha 1 (III) mRNA-expressing cells. The extent of type II and III collagen expression depended on the integrity of the extracellular matrix surrounding the chondrocytes, and the location within the articular cartilage. No alpha 1 (I) mRNA was detectable in osteoarthritic original articular cartilage. The alpha 1 (I) probe did, however, reveal signals in pannus-like tissue, osteophytes, and bone cells. In normal articular cartilage, no detectable levels of cytoplasmic mRNA for alpha 1(I), alpha 2 (I), or alpha 1 (III) were seen. Using specific mono- and polyclonal antibodies, we found deposition of type III collagen but hardly any of type I collagen in the superficial zone of osteoarthritic cartilage that is consistent with the in situ hybridization results. These results indicate a phenotypic alteration in a defined subset of chondrocytes in conditions of diseased cartilage, expressing and synthesizing collagen type III independently from type I collagen, but in part simultaneously with type II collagen.

Adult↗
PubMed1992

Type X collagen synthesis in human osteoarthritic cartilage. Indication of chondrocyte hypertrophy.

OBJECTIVE: To investigate the appearance of hypertrophic chondrocytes in osteoarthritic (OA) cartilage, using type X collagen as a specific marker. METHODS: The biosynthesis of type X collagen was examined by metabolic labeling of freshly isolated articular chondrocytes with 3H-proline, immunoprecipitation, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the synthesized collagens. Extracellular deposition of types X and II collagen was analyzed immunohistochemically. RESULTS: Immunostaining revealed an irregular distribution of type X collagen, which was localized around chondrocyte clusters in fibrillated OA cartilage, but was absent from the noncalcified region of normal articular cartilage. Freshly isolated OA chondrocytes synthesized predominantly type X collagen, while control chondrocytes synthesized mostly type II collagen. CONCLUSION: Our findings indicate focal premature chondrocyte differentiation to hypertrophic cells in OA cartilage.

Adult↗
PubMed1992

Activation of collagen type II expression in osteoarthritic and rheumatoid cartilage.

In situ hybridization and immunohistochemical techniques were applied to investigate gene expression and extracellular deposition of collagen type II in normal, osteoarthritic and rheumatoid human articular cartilage. Normal cartilage showed an essentially even extracellular distribution of type II collagen with poly- and monoclonal antibodies, while only a few cells were positive for alpha 1(II) collagen mRNA. In situ hybridization of osteoarthritic and rheumatoid cartilage, however, showed strong enhancement of type II collagen gene expression; transcripts were observed predominantly in the upper middle zone of the articular cartilage while the upper layer was mostly negative and correlated with a zone of reduced proteoglycan staining. The elevated mRNA levels frequently coincided with pericellular immunostaining for type II collagen, indicative for enhanced synthesis of the protein. In two samples, however, pericellular loss of collagen type II staining was found despite positive cytoplasmic signals with the alpha 1(II) RNA probe, suggesting enhanced collagen destruction. Control hybridization with a probe for 18S rRNA revealed very few negative cells throughout both normal and arthritic cartilage samples, ruling out major cell necrosis in the specimens investigated. Thus, our observations identify sites of activated type II collagen synthesis in osteoarthritic cartilage that were predicted by previous biochemical studies and support the notion that damaged cartilage attempts to restore matrix by enhanced synthesis of its components.

Adolescent↗
PubMed1991

Expression of the CD2 activation epitope T11-3 (CD2R) on T cells in rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, and Lyme disease: phenotypic and functional analysis.

CD2R is an activation-associated epitope unmasked by a conformational change of the CD2 cell-surface glycoprotein. In spite of elaborate studies on the role of CD2 and CD2R in adhesion and stimulation of T cells in vitro, no instances of CD2R expression in vivo were known to date. We report high levels of CD2R observed on blood and synovial fluid T cells in rheumatoid arthritis and on peripheral blood T cells in juvenile rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, and Lyme disease. In vivo, expression of CD2R was restricted to T cells, not limited to a particular T-cell subset and not correlated with the expression of p55 interleukin 2R (IL-2R) (CD25) or major histocompatibility complex (MHC) class II molecules. When stimulated to proliferation via CD2 or CD3, ex vivo CD2R+ T cells showed the same basic activation requirements as CD2R-T cells.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1987

Changes in cell surface antigen expression on human articular chondrocytes induced by gamma-interferon. Induction of Ia antigens.

Ia antigens (class II HLA molecules) have been detected on cells eluted from affected human cartilage in certain disease states, but not on normal cartilage cells. Because the presence of Ia antigens on chondrocytes may play an important role in rheumatic diseases, we investigated the induction of these molecules by gamma-interferon (gamma-IFN), a potent Ia-inducing lymphokine. Human articular chondrocytes were incubated with recombinant gamma-IFN, and the expression of Ia antigens was studied by cell sorter analysis, using a panel of reagents that detect monomorphic and polymorphic specificities of the DR and DQ Ia antigen families. While the induction of DR antigens, including polymorphic DR specificities, was readily obtained with gamma-IFN (50-95% positive cells), DQ antigens were negative or were displayed only on a lower percentage of chondrocytes (5-60%). In addition, incubation with gamma-IFN led to an increased expression of HLA class I antigens. The expression of various other surface markers either remained unchanged (as in 4F2 and BA-2) or showed tendencies toward decreased percentages (as in 83c2) or increased percentages (as in M phi R-17). No apparent change in cell morphology or growth pattern was observed.

Antigens, Surface↗
PubMed1986

Intraarticular T lymphocytes in monoarticular and oligoarticular inflammatory joint diseases. Normal subset distribution and less numbers of activated T cells indicate major differences as compared to rheumatoid arthritis.

T lymphocyte subpopulations and the expression of T cell activation antigens were determined in peripheral blood, synovial fluid and/or synovial tissues of patients with recurring monoarticular arthritis and patients with HLA-B27 associated oligoarthritis in comparison to patients with rheumatoid arthritis (RA). In individuals with monoarthritis or oligoarthritis, there was a normal T cell subset distribution, both in peripheral blood and in intraarticular sites, with only a small number of T cells bearing Ia antigens. This was in marked contrast to the patient group with RA that demonstrated a significantly decreased ratio of T helper/inducer to T suppressor/cytotoxic cells in addition to large numbers of Ia+ T cells in intraarticular sites. The expression of the Tac antigen was similar in all disease groups.

Adolescent↗
PubMed1978

[Frequency of necroses of the head of the femur in the treatment of the so-called congenital dislocation of the hip joint according to Hoffmann-Daimler (author's transl)].

The article reports on the results which can be obtained with the method described by Hoffmann-Daimler regarding the functional treatment of the so-called congenital dislocation of the hip joint. The report is based on a patient material of 110 children with 159 dislocated hips treated at the Orthopaedic University Clinic at Erlangen between 1971 and 1976. Observation of the course of the disease revealed a much lower rate of incidence of necrosis of the head of the femur than stated in literature, using the Hoffmann-Daimler method. The incidence of necrosis on pre-treatment of most children with other therapeutic methods, was 2.3% at the beginning of the Hoffmann-Daimler treatment, and increased to 12.7% up to the end of the treatment, dropping to 9.3% at the time of the follow-up examination.

Child, Preschool↗