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Biomedical subjects

J Wolf

Publications and source records attributed to J Wolf.

At least 19 recordsLinked to original sources
PubMed1992

Growth of Hodgkin cell lines in severely combined immunodeficient mice.

No animal model exists for the in vivo growth of Hodgkin's-lymphoma-derived cells. Neither unmanipulated Hodgkin's-disease(HD)-derived cell lines nor primary biopsy tissue could be grown in nude mice. Since the severe combined immunodeficient (SCID) mouse has been reported to be a better recipient for transplanted human lymphatic tissue than the nude mouse, we tested whether SCID mice provide suitable conditions for the in vivo growth of HD cell lines. Tumorigenicity of HD cells was tested in untreated and pre-treated SCID mice and in another combined immunodeficient mouse strain, beige/nude/X-linked immunodeficient (BNX) mouse. SCID mice supported in vivo growth of the 6 HD cell lines tested (L428, L540, L591, DEV, HD-LM2, KM-H2). Only one of the 6 lines (DEV) was tumorigenic in BNX mice. No HD cell line proliferated in T-cell-deficient nude mice. Thus, in vivo growth of HD cell lines appeared to be related to the degree of host immunodeficiency. Additional growth supportive treatments such as fibrosarcoma co-transplantation, intraperitoneal mineral oil injection or immunosuppressive pre-treatment (anti-asialo-GMI-antibody injection) permitted growth of 3 additional HD cell lines in BNX mice. The immunophenotype and karyotype of explanted graft cells were identical to the original cell lines. Our experiments describe an effective and reproducible xenograft model for growth of Hodgkin's-disease-derived cell lines. This may be of value for elucidating the growth characteristics of Hodgkin's-lymphoma-derived cells as well as for testing new therapeutic regimens.

Animals↗
PubMed1992

Local growth of a Burkitt's lymphoma versus disseminated invasive growth of the autologous EBV-immortalized lymphoblastoid cells and their somatic cell hybrids in SCID mice.

Specific host-graft interactions, as well as intrinsic properties of transferred cell, determine tumorigenicity in xenogeneic systems. We compared the growth characteristics of human B-lymphoid cell lines in SCID mice with the well characterized growth pattern in nude mice and observed striking differences in malignancy in the respective hosts. Two cell lines derived from the same individual, the Epstein-Barr-virus(EBV)-positive Burkitt's lymphoma BL 60 (BL) and the autologous EBV-immortalized lymphoblastoid cell line IARC 277 (LCL) were used. In addition, we tested somatic cell hybrids (HYB) of both cell lines, which despite the LCL-like differentiation phenotype show the de-regulated c-myc expression pattern of the parental BL line, assumed to be a critical factor in BL pathogenesis. Subcutaneously (s.c.) injected BL cells produced local progressively growing tumor masses at the injection site without distant metastases in both nude and SCID mice. Although both mouse strains possess the same genetic background (BALB/c) and differ only in the B-cell sub-set, the growth patterns of the LCL and hybrids were completely different. In contrast to the regressive behaviour of LCL and hybrids in nude mice, these lines show invasive and disseminated progressive growth in SCID mice. Peripheral lymph nodes an thymic tissue were preferentially colonized, whereas mucosal-associated lymphoid tissue (Peyer's patches and appendix) and spleen were not infiltrated. The preferential migration of lymphocytes to certain tissues is termed homing in a syngeneic system and mediated by homing receptors and vascular addressins. The "homing" of LCL and hybrids into lymphoid SCID mouse tissue suggests a strong interaction with the endothelial cells of the host. Detailed phenotypic analysis of BL, LCL and 3 different hybrids was performed using an antibody panel against differentiation and adhesion markers. Overall dominance of the LCL phenotype was observed in the hybrids, as indicated by cytology, tumor growth, dissemination and the pattern of surface-marker expression. The c-myc activation in hybrids does not appear to influence growth behavior.

Animals↗
PubMed1992

Proton-induced X-ray emission analysis of atherosclerotic plaques of the carotid bifurcation.

The trace elements of both calcified atherosclerotic plaques and plaque-free vessel walls of the carotid bifurcation from 31 autopsies were investigated using the proton-induced X-ray emission (PIXE) method. The trace elements studied were phosphorus (P), calcium (Ca), chrome (Cr), iron (Fe), copper (Cu), zinc (Zn), lead (Pb), selenium (Se), bromine (Br), strontium (Sr), and rubidium (Rb). All samples contained Fe and Zn. Mercury (Hg) was not detected in any of the samples studied. All plaque-free samples contained Cu and almost all Br and Ca, none Sr. All calcified atherosclerotic plaques contained Ca and almost all Br and Sr. The relative levels of Ca were higher in the calcified plaques than in the plaque-free vessel walls. The relative value of Ca in calcified and uncalcified samples was greatest in the group who had died because of cardiovascular disorders and smallest in the group who had died from other causes. There was a strong positive correlation between the Ca and Sr of the plaque samples and between the P and Br of the plaque-free samples.

Aged↗
PubMed1992

Fibronectin mediates anchorage-dependent focus formation in cultured human synoviocytes.

To determine the effect of extracellular matrix proteins on synoviocyte phenotype, a serum-free, defined-medium culture system was established. Rheumatoid synoviocytes maintained on type I collagen appeared monolayered, whereas cells maintained on fibronectin showed focus formation. Focus formation was abrogated by maintaining cells in the presence of antifibronectin. Focus formation was associated with a fibronectin-rich extracellular matrix, whereas monolayer morphology was associated with matrices containing a greater proportion of collagen. The abundant amount of fibronectin present in the synovial microenvironment may be partially responsible for the transformationlike phenotype displayed by rheumatoid synoviocytes.

Arthritis, Rheumatoid↗
PubMed1992

Preliminary report: growth of Hodgkin's lymphoma derived cells in immune compromised mice.

Until now there has been no satisfactory animal host for the in vivo growth of Hodgkin lymphoma cells. With the exception of one mutant subline (L540Cy) none of the other Hodgkin derived cell lines nor Hodgkin's disease (HD) derived lymphatic tissue could be propagated in suitable animal systems such as the T-cell deficient nude mouse. Recently, the severe combined immunodeficient (SCID-) mouse has been demonstrated as a possible recipient for human lymphatic tissue. In the present study, we have evaluated the SCID mouse as a possible in vivo model for Hodgkin's lymphoma. I) We demonstrate that seven permanent cell lines derived from patients with Hodgkin's disease grow progressively in SCID mice after subcutaneous and intraperitoneal inoculation. II) In addition, after intravenous injection, two of these lines (L540, L540Cy) show a disseminated growth pattern resembling the distribution of HD cells in man (involvement of lymph nodes, liver and bone marrow but not of spleen). The observed reproducible disseminated tumor growth establishes the SCID mouse as a new animal model for experimental treatment strategies in Hodgkin's lymphoma. III) We present preliminary results of the transplantation of primary material from 13 patients with Hodgkin's disease. Material from two patients induced human tumors in the SCID mice recipients, whereas material from two others led to the induction of mouse lymphomas. The human tumors showed three distinct histological patterns: 1) Lymphoproliferative disease (LPD); 2) anaplastic large cell lymphomas (ALCL); 3) Hodgkin like lesions (HLL). In vitro cell lines established from human SCID mouse tumors were of B-lymphoid origin, were EBV-positive and showed numerical and some structural chromosomal aberrations of varying degree.

Animals↗
PubMed1991

Regressing nude mouse grafts of Burkitt's lymphoma x lymphoblastoid cell hybrids show deregulation of the c-myc gene and expression of the EBV latent membrane protein.

Somatic cell hybrids between the malignant Burkitt lymphoma cell line BL 60 and the non-malignant Epstein-Barr virus (EBV) immortalized lymphoblastoid cell line (LCL) IARC 277 demonstrate the deregulated c-myc transcription pattern of the parental BL cell line during exponential growth in tissue culture. Subcutaneous nude mouse grafts of these hybrids, however, completely regress after an initial growth phase. To investigate whether regression of these grafts is mediated by a down-regulation of the BL-60-derived deregulated c-myc gene in vivo, c-myc transcription was analyzed in growing versus regressing hybrid grafts. In the initial growth phase as well as during regression, these grafts showed the deregulated c-myc expression pattern of the parental BL cell line with highly abundant c-myc transcripts originating from the BL specific translocation chromosome 8q+. Our results question the significance of c-myc deregulation for an unlimited in vivo growth potential of B-lymphoblastoid cells. To further characterize the hybrids, surface expression of B-cell-specific antigens was analyzed on the hybrids and shown to correspond to that of the parental LCL. In addition, transcription of the gene encoding for the EBV latent membrane protein (LMP) as well as histological features were analyzed in growing versus regressing hybrid grafts. The LMP gene, which is down-regulated in the tumors produced by the parental BL cells, was expressed in the hybrid grafts as well as in the parental LCL grafts. This finding might be compatible with a host response of the nude mouse against LMP. The histological analysis, however, which revealed massive necrosis in the center of the regressing grafts without pronounced inflammatory infiltrates, rather points to a hypoxemic process leading to graft regression.

Animals↗
PubMed1991

Three main arteries of the face and their tortuosity.

The anatomy of the facial, transverse facial and infraorbital arteries and their tortuosity was studied in 69 human cadavers (age range 18-95 years). The types of facial vascularisation were divided into four categories according to the gradually diminishing relative dominance of the facial artery. Type A, in which the facial artery was dominant, comprised 22% of the cases; type B 49%; type C 20%; and the variant of the hypoplastic facial artery, type D, 9% of the cases. The type of vascularisation was not dependent on age or sex. The tortuosity of all three arteries showed a statistically significant increase with age. A weak correlation was found between the relative dominance and the tortuosity of the facial artery.

Adolescent↗
PubMed1991

Plasma renin activity in renal transplant patients with hypertension.

Chronic renal allograft rejection (CR) is the major cause of graft loss after 1 year following transplantation. Hypertension (HTN) and proteinuria (Up) are the hallmarks of this immunologic allograft response. Over 1 year, 23 patients posttransplantation and with HTN (diastolic greater than 95 mm Hg) were examined. Serial serum creatinine (Scr), Up, urine creatinine (Ucr), and resting and enalapril challenged (EC) plasma renin activity (PRA) were all determined. Renal artery stenosis was excluded by noninvasive imaging. Of the 23 patients, eight eventually lost their renal allografts, while 15 maintained satisfactory renal function (Scr less than 2.5). Results of this study show that: 1) worsening renal function (RF) increases EC reactivity; 2) the presence of proteinuria is not itself related to increase in EC activity; 3) renin before and after EC was higher (P = .06) in the allograft loss group. In this study, patients with high PRA represent the highest EC responses. Therefore, they display not macrovascular lesions, but microvascular intrarenal disease; this defect is most likely secondary to chronic immunologic insult.

Adult↗
PubMed1991

Distribution of type VI collagen expression in synovial tissue and cultured synoviocytes: relation to fibronectin expression.

Type VI collagen has recently been shown to be an important component of connective tissue. Double label immunofluorescence procedures were used to immunolocalize type VI collagen in normal and rheumatoid synovium and its distribution was compared with that of fibronectin. In normal synovium type VI collagen is expressed in the synovial membrane but not in the interstitium of the villus. In rheumatoid synovium, however, type VI collagen is extensively deposited in both the interstitial connective tissue and along the lining of the synovial membrane. Cultured rheumatoid and normal synoviocytes produce type VI collagen and fibronectin and incorporate them into their extracellular matrix. These data suggest that type VI collagen may play a part in matrix remodelling of the inflamed joint.

Arthritis, Rheumatoid↗
PubMed1991

Detection of C trachomatis in urogenital specimens by polymerase chain reaction.

OBJECTIVE: To establish a polymerase chain reaction (PCR) protocol for the detection of urogenital C trachomatis infection and to compare it with the detection in cell culture. SPECIMENS: Urethral specimens were collected from 62 male patients and cervical specimens from 106 female patients. SETTING: Department of Dermatology and Venereology, Ruprecht-Karls-Universität, Heidelberg. METHODS: Urogenital specimens were simply boiled for 15 minutes and subsequently subjected to amplification without prior extraction of nucleic acid. The DNA sequence selected for amplification is located in the third open reading frame of the ubiquitous C trachomatis plasmid pCTT1. The amplified products were demonstrated by agarose gel electrophoresis followed by Southern blot hybridization. In addition, specimens were investigated with cell culture. MAIN OUTCOME MEASURES: Results of PCR and cell culture. RESULTS: PCR detected all C trachomatis serovars relevant for urogenital infections (D-L2). Serial dilution experiments revealed that the PCR procedure was 100 fold more sensitive than cell culture. The investigation of 168 urogenital specimens showed that the PCR confirmed all 30 cell culture positive results, however, out of the 138 cell culture negative specimens 16 were positive using the PCR. CONCLUSIONS: A substantial number of urogenital C trachomatis infections detectable by PCR may be missed by the cell culture technique.

Bacteriological Techniques↗
PubMed1991

Radiographic signs in the temporomandibular and hand joints in patients with psoriatic arthritis.

The temporomandibular (TMJ) and hand joints of 64 patients with psoriatic arthritis (PA) were examined radiographically with panoramic tomography and dorsovolar projection. The associations between radiographic signs in the condyle of the TMJ and finger joints were analyzed with Pearson's product-moment correlation coefficient. Twenty-six patients (41%) had radiographic signs in their TMJs. Arthritic signs were seen in 14 (22%) and degenerative signs in 12 (19%) patients. Fifty-five patients (86%) had radiographic signs in their hands; 33 patients (52%) had arthritic and 22 (34%) degenerative signs. In the TMJ statistically significant correlations were found among erosion, flattening, and cortical sclerosis and also between osteophyte and cortical sclerosis. In the finger joints erosion correlated significantly with dislocation and loss of space. Erosion in the condyle of the TMJ was the only sign that correlated with changes in the finger joints such as erosion, dislocation, and ankylosis. Erosion in the TMJ also correlated with erosion in the metacarpophalangeal joint and wrist.

Adult↗
PubMed1991

[Invasive, metastatic growth of lymphoblastoid B cells in immunodeficient SCID mice].

A Burkitt's lymphoma (BL, EBV +, 8/22 translocation), the EBV immortalized lymphoblastoid cell line from the same individual (LCL) and somatic cell hybrids (HYB) between both cell lines were inoculated in immunedeficient scid mice. Subcutaneous injected BL cells produced local tumor masses without distant metastases. In contrast LCL and hybrids show invasive and disseminated growth. Peripheral lymph nodes and thymic tissue were preferentially colonized. A detailed phenotypic analysis of BL, LCL and 3 different hybrids was performed using differntiation and adhesion molecules. The preferential "homing" of LCL and hybrids seem to be correlated with the expression of the lymphocyte homing receptor (CD44). The growth of LCL in scid mice shows, that additional genetic alterations are not necessary to cause a malignant phenotype. Activation of myc seem to play a minor role, because hybrids mimic the LCL phenotype and distribution pattern.

Animals↗
PubMed1990

Suppression of the malignant phenotype in somatic cell hybrids between Burkitt's lymphoma cells and Epstein-Barr virus-immortalized lymphoblastoid cells despite deregulated c-myc expression.

To approach the question whether the absence of specific cellular gene functions may be involved in Burkitt's lymphoma pathogenesis, somatic cell hybrids were established between a malignant Epstein-Barr virus (EBV) positive Burkitt's lymphoma cell line (BL 60) and a nonmalignant EBV-immortalized lymphoblastoid cell line (IARC 277) derived from the same individual. The hybrids revealed a near tetraploid karyotype including one copy of the 8q+ chromosome resulting from the Burkitt's lymphoma-specific translocation t(8;22) in addition to three apparently normal copies of chromosome 8. Although the hybrid cells exhibited the deregulated c-myc expression pattern of the parental Burkitt's lymphoma cell line with highly abundant transcripts originating from the 8q+ chromosome, their growth characteristics in tissue culture as well as in nude mice were identical to that of the parental nonmalignant lymphoblastoid cell line. These data indicate that, at least in the system described here, the malignant phenotype of Burkitt's lymphoma cells can be suppressed by introduction of an additional set of apparently normal chromosomes from the same individual and that EBV infection and c-myc deregulation may not be sufficient for maintenance of the malignant phenotype.

Animals↗
PubMed1990

The mandibular infected buccal cyst (paradental cyst). A radiographic and histological study.

Mandibular infected buccal cysts occur on the buccal and distal aspects of the roots of partly or fully erupted mandibular molars with vital pulps. In the present investigation six cases associated with mandibular first and second molars were studied. The cysts were lined with a non-keratinised squamous epithelium with a mixed inflammatory cell infiltrate in the connective tissue. The clinical and microscopic features were similar to those of previously reported paradental cysts. The inflammation always present in these cysts may have an important role in their pathogenesis. It may induce periodontal pocketing, which may lead to hyperplasia and cyst formation in adjacent odontogenic epithelium, which may be either remnants of the reduced enamel epithelium or cell rests of Malassez.

Adolescent↗