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Biomedical subjects

A Gabrielli

Publications and source records attributed to A Gabrielli.

At least 109 records · Page 6Linked to original sources
PubMed1982

HLA and psoriasis (with or without arthropathy).

30 probands affected by psoriasis, with or without arthropathy, and their relatives were typed for HLA-A, -B and -C antigens. Association of HLA-B16 and HLA-B17 with psoriasis was confirmed. One third of probands was without any known HLA-A, -B, -C marker. Considering probands with at least one HLA-B marker, we found that 50% of their sibs carrying marker is affected and the remaining 50% is healthy. To explain the weak association observed, an attempt to propose a model is made: such a model postulate a gene interaction between the HLA marker gene and an hypothetic "Ps (Psoriasis susceptibility) gene". The model, described in detail in this work, tries to explain why a large part (1/3) of probands is affected even if they do not carry any HLA marker and why 50% of marker positive sibs of marker positive probands are healthy.

Adult↗
PubMed1977

[Lymphocyte typing in chronic lymphoid leukemia].

We used the membrane fluorescence and the rosette formation test to study the lymphocyte populations in 25 patients with untreated chronic lymphocytic leukemia (CLL). The results show a significant increase, absolute and percent of S-Ig bearing cells, whereas the E and EA rosette forming cells are decreased in per cent, increased in absolute. The number of lymphocytes with the receptor for the Fc fragment of IgG, is unchanged. The lymphocytosis causes mainly a significant decrease in percentage of E rosette forming cells. A big splenomegaly and a bad clinical stage, according to Rai et al. classification, are responsible for a decrease of E, EA, EAC rosette forming cells; unchanged the percentage of S-Ig bearing cells. Such a modification of the surface receptor pattern is present not only in those CLL more advanced in clinical stage and with hyperleucocitosis and/or splenomegaly, but also in those forms with worse clinical feature and prognosis. Our work confirms that CLL is mainly a B proliferative disease; we observed only one case due to T cell proliferation. Four cases were impossible to classify immunologically: one had no cells bearing the markers, three had a subnormal surface receptor pattern.

Adult↗
PubMedDate not supplied

Essential cryoglobulinemia: a therapeutic dilemma.

Our data confirm those already reported in the literature. There is no univocal therapy for essential cryoglobulinemia. Several therapeutic strategies may be employed according to severity of the clinical picture. Skin and articular involvement may benefit from the administration of non-steroidal antiinflammatory drugs. The presence of visceral involvement requires steroids and/or immunosuppressive drugs. Plasma-exchange should be used in patients with severe progressive disease. However, data showing that anyone of the proposed treatment could irreversibly stop the clinical course of the disease are lacking. Immunological parameters except serum viscosity cannot help in the decision to initiate a plasma-exchange program and in monitoring its efficacy.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Viral load in samples from hepatitis C virus (HCV)-infected patients with various clinical conditions.

Molecular methods for the absolute quantitation of nucleic acids present in biological samples have recently been developed and applied in basic and in medical virology; these studies indicated that competitive polymerase chain reaction (PCR) and competitive reverse transcription PCR (cRT-PCR)-based methodologies are currently the methods of choice for quantifying DNA and RNA species present in clinical samples at low concentration. Recently, quantitative molecular techniques were developed to study the hepatitis C virus (HCV) pathogenic potential, the natural history of HCV-infected patients and the efficiency of antiviral therapies in real time. The pilot study reported here was carried out using a cRT-PCR application for the direct quantitation of HCV RNA molecules in plasma samples of infected individuals which was recently developed in our laboratory. Although sharp individual variability of viral load was documented in this study, the mean HCV RNA copy number detected in samples from untreated HCV-infected patients with various clinical conditions (chronic active hepatitis, cirrhosis, cryoglobulinaemia and chronic hepatitis) was substantially similar, with only one exception: in samples from patients tested positive for anti-liver-kidney microsomal (anti LKM1) auto-antibodies, a significantly lower HCV viraemia level was revealed. Additionally, HCV viraemia was monitored in four patients with sustained biochemical and histological response (at least 12 months) following interferon-alpha discontinuation.

Evaluation Studies as Topic↗
PubMedDate not supplied

Human monoclonal recombinant Fabs specific for HCV antigens obtained by repertoire cloning in phage display combinatorial vectors.

Molecular cloning of the antibody repertoire in phage display combinatorial vectors is a powerful method enabling the dissection of the immunoresponse against a given pathogen. In this paper we describe the construction of a combinatorial library displayed on phage surface, containing the antibody repertoire of a patient with high serological response against hepatitis C virus (HCV) antigens. Following selection of the library against solid-phase-bound antigen, sixteen human antibody Fab fragments able to bind to HCV-specific antigens were generated and studied for binding characteristics. The majority of them appeared to have specificity for the HCV c33 peptide. All the clones reacting with the c33 peptide shared the same heavy-chain CDR3 sequence. This is the first report of molecular cloning in a combinatorial phage display vector of the antibody repertoire of an anti-HCV-positive patient.

Amino Acid Sequence↗
PubMedDate not supplied

Probing the natural antibody repertoire by combinatorial cloning of IgM and IgD isotypes in phage display vectors.

It is well known that immunoglobulins with no identifiable immunogenic origin, called natural antibodies, are present in the sera of healthy individuals and their role as a defence against important pathogens has been proposed. Unfortunately, the studies are hampered by the fact that these immunoglobulins seem to have low affinity and to be polyreactive, and are commonly available in polyclonal preparations. Lately, new technologies for the production of monoclonal antibodies became available, and in particular the cloning of genes coding for antibody fragments in combinatorial phage display vectors provided a handy tool for the selection of human monoclonal antibodies. In this work, we describe the successful development of a technology for the molecular cloning of combinatorial phage display libraries containing genes coding exclusively for antibody fragment of the IgM or IgD phenotype. These libraries can be useful for molecular cloning of monoclonal antibodies of the IgM and IgD phenotype and can help elucidate the role played by natural antibodies in defence against infectious agents.

Antibodies, Monoclonal↗
PubMedDate not supplied

Piascledine modulates the production of VEGF and TIMP-1 and reduces the invasiveness of rheumatoid arthritis synoviocytes.

BACKGROUND: In rheumatoid arthritis (RA), hypertrophy of the synovial membrane generates a tumour-like pannus that invades the joint cavity and erodes cartilage and bone. Invasion of the extracellular matrix (ECM) is accompanied by angiogenesis, in which vascular endothelial growth factor (VEGF) and tissue inhibitors of metalloproteinases (TIMPs), produced by synoviocytes lining the pannus, have a primary role. Piascledine (PSD) is used in the treatment of osteoarthritis and has anti-inflammatory effects in vitro. OBJECTIVE: To study the effects of PSD on levels of VEGF and TIMP-1 and chemoinvasion in RA synoviocytes and healthy controls. METHODS: The effects of PSD 5, 10, and 20 microg/mL were evaluated, with/without interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNFalpha) 20 ng/mL, on synoviocytes. The levels of VEGF and TIMP-1 were assayed in the culture medium by enzyme-linked immunosorbent assay (ELISA). Chemoinvasion was measured by the Boyden chamber invasion assay. RESULTS: RA synoviocytes treated with PSD showed, compared to basal, lower levels of VEGF (41080+/-830 vs. 79210+/-920 pg/106 cells, p<0.001) and increased levels of TIMP-1 (23540+/-93.2 vs. 12860+/-42.9 ng/106 cells, p<0.001). PSD decreased dose-dependently IL-1beta and TNFalpha induced migration. CONCLUSIONS: In RA synoviocytes, and also to a lesser extent in control cells, PSD modulates VEGF and TIMP-1 and decreases chemoinvasion. PSD might have a role in the treatment of RA synovitis controlling invasiveness.

Arthritis, Rheumatoid↗