Biomedical subjects

A Zettl

Publications and source records attributed to A Zettl.

At least 55 records · Page 3Linked to original sources

PubMed2000

Electron spin density distribution in the polymer phase of CsC60: assignment of the NMR spectrum.

We present high resolution 133Cs-13C double resonance NMR data and 13C-13C NMR correlation spectra of 13C enriched samples of the polymeric phase of CsC60. These data lead to a partial assignment of the lines in the 13C NMR spectrum of CsC60 to the carbon positions on the C60 molecule. A plausible completion of the assignment can be made on the basis of an ab initio calculation. The data support the view that the conduction electron density is concentrated at the C60 "equator," away from the interfullerene bonds.

Journal Article↗

PubMed2000

Recurrent genetic aberrations in thymoma and thymic carcinoma.

Apart from single reported aberrant karyotypes, genetic alterations in thymic epithelial neoplasms have not been investigated so far. In this study, 12 World Health Organization classification type A thymomas (medullary thymomas), 16 type B3 thymomas (well-differentiated thymic carcinomas), and nine type C thymomas, all of them primary thymic squamous cell carcinomas, were analyzed by comparative genomic hybridization and fluorescence in situ hybridization. With the exception of one single case, type A thymomas did not reveal chromosomal gains or losses in comparative genomic hybridization. In contrast, all type B3 thymomas showed chromosomal imbalances, with gain of 1q, loss of chromosome 6, and loss of 13q occurring in 11 (69%), six (38%), and five (31%) of 16 cases, respectively. In primary thymic squamous cell carcinoma, the most frequent chromosomal losses were observed for 16q (six of nine cases, 67%), 6 (4 of 9, 44%), and 3p and 17p (three of nine each, 33%), whereas recurrent gains of chromosomal material were gains of 1q (5 of 9, 56%), 17q, and 18 (three of nine each, 33%). This study shows that the distinct histological thymoma types A and B3 exhibit distinct genetic phenotypes, whereas type B3 thymoma and primary thymic squamous cell carcinoma partially share genetic aberrations. In addition to the possible tumorigenic role, the deletion in type B3 thymoma of chromosome 6, harboring the HLA locus, might play a role in the pathogenesis of paraneoplastic autoimmunity characteristic of thymoma.

Adult↗

PubMed2000

Genetic imbalances in primary gastric diffuse large B-cell lymphomas: comparison of comparative genomic hybridization, microsatellite, and cytogenetic analysis.

Extranodal malignant non-Hodgkin's lymphomas account for about 40% of lymphoid neoplasms, but few data are available concerning the genetic background of primary gastric diffuse large B-cell lymphoma (DLBCL). A study was performed of 27 primary gastric DLBCLs and 5 gastric DLBCLs with a concomitant low grade component of mucosa-associated lymphoid tissue-type lymphoma using comparative genomic hybridization (CGH), microsatellite studies, classic cytogenetics, and fluorescence in situ hybridization (FISH) to search for specific genetic aberrations. The most frequent aberrations were losses of material on chromosome 6q and gains of parts of chromosome 3. In three cases, a total of six high level DNA amplifications were detected, with five of them involving chromosomal regions not having been reported before in gastric DLBCL. A high overall concordance of 91.4% between microsatellite analysis and CGH was observed using DNA extracted from the same tissue block. The concordance achieved using DNA from different tissue blocks of the same patient was 85%. Microsatellite studies, CGH, FISH, and classic cytogenetics represent complementary techniques that facilitate a comprehensive view of genetic alterations in malignancies such as primary gastric DLBCL.

Adult↗

PubMed1998

T cell receptor repertoire in rheumatoid arthritis.

CD4+ T cells are a major component of the inflammatory infiltrate in rheumatoid synovitis. Within synovial lesions, clonal CD4+ T cell populations are detectable, supporting the notion of an antigen specific recognition even in the joint. In general, the clonal size of individual T cell clones is small and does not lead to a marked distortion of the synovial T cell receptor (TCR) repertoire. Comparison of TCR sequences derived from different patients has not provided evidence for common sequences. Either multiple antigens are recognized or the TCR repertoire is sufficiently plastic with a multitude of different TCR structures responding to the same antigen(s). However, within one individual, the repertoire of clonal T cell populations is restricted. Identical T cell clones can be identified in different joints and at different timepoints of the disease, emphasizing that the spectrum of antigens recognized is conserved over time and that the T cell response pattern is not subject to evolution. Characterization of antigens involved in the latter stages of the disease may thus provide critical information on disease-initiating events. Recent data have led to the new concept that the role of T cells in rheumatoid arthritis (RA) is not limited to synovial inflammation. Evidence has been provided that the premorbid TCR repertoires of RA patients and normal controls can be distinguished. The T cell repertoire in RA patients is prone to recognize certain microbial products and autoantigens. The selection of this response pattern can only partially be attributed to the disease associated HLA-DRB1 alleles. Additional factors common in RA patients but not in HLA-DR matched control individuals seem to be important in shaping the TCR repertoire. Furthermore, the repertoire of mature T cells in RA patients is characterized by oligoclonality which involves T cells in the peripheral blood compartment. Possibly, these clonal T cell populations react to widespread autoantigens, raising the possibility that RA patients have a defect in controlling peripheral tolerance and an anomaly of lymphoproliferation. In contrast to joint residing CD4+ T cells, expanded clonotypes isolated from the blood of different patients have been described to share TCR beta chain structures. How these characteristic features of the global TCR repertoire in RA patients translate into mechanisms of disease remains to be elucidated.

Arthritis, Rheumatoid↗

PubMed1997

Single-Electron Transport in Ropes of Carbon Nanotubes

The electrical properties of individual bundles, or "ropes," of single-walled carbon nanotubes have been measured. Below about 10 kelvin, the low-bias conductance was suppressed for voltages less than a few millivolts. In addition, dramatic peaks were observed in the conductance as a function of a gate voltage that modulated the number of electrons in the rope. These results are interpreted in terms of single-electron charging and resonant tunneling through the quantized energy levels of the nanotubes composing the rope.

Journal Article↗

PubMed1997

Multiple mechanisms support oligoclonal T cell expansion in rheumatoid synovitis.

BACKGROUND: The synovial T cell infiltrate in rheumatoid arthritis (RA) is diverse but contains clonally expanded CD4+ populations. Recent reports have emphasized that RA patients have a tendency to develop CD4+ T cell oligoclonality which also manifests in the peripheral blood. Clonal dominance in the tissue may thus result from antigen specific stimulation in the synovial membrane or may reflect the infiltration of expanded clonotypes present throughout the lymphoid system. We have explored to what extent clonal populations amongst tissue CD4+ T cells display joint specificity as defined by their restriction to the joint, their persistence over time, and their expression of markers indicative for local activation. MATERIALS AND METHODS: Matched samples of peripheral blood and synovial fluid or synovial tissue were collected from 14 patients with active RA and CD4+ IL-2R+ and CD4+ IL-2R- T cells from both compartments were purified. Clonal populations of CD4+ T cells were detected by RT-PCR amplification of T cell receptor (TCR) transcripts with BV and BJ specific primers followed by size fractionation and direct sequencing of dominant size classes of TCR transcripts. RESULTS: Clonal CD4+ T cells were detected in the synovial fluid and synovial tissue of all patients. All patients carried synovial clonotypes that were undetectable in the blood but were present in independent joints or at several non-adjacent areas of the same joint. These joint restricted CD4+ clonotypes were generally small in size, were preferentially found in the IL-2R+ subpopulation, and persisted over time. A second type of clonogenic T cells in the synovial infiltrate had an unrestricted tissue distribution and was present at similar frequencies amongst activated and nonactivated T cells in the blood and affected joints. Ubiquitous clonotypes isolated from two different patients expressed sequence homologies of the TCR beta chain. CONCLUSIONS: Two types of expanded CD4+ clonotypes contribute to the T cell infiltrate in rheumatoid synovitis. Differences in the distribution pattern and in molecular features suggest that distinct mechanisms are supporting the clonal outgrowth of these two groups of clonotypes. Clonally expanded T cells restricted to the joint but present in several independent joints appear to respond to locally residing antigens. Clonogenic cells with an unrestricted distribution pattern and widespread activation in the blood and tissue may react to a different class of antigens which appear to be shared by multiple patients. T cell recognition in RA may be involved at several different levels and may be related to more than one pathomechanism.

Adult↗

PubMed1996