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Biomedical subjects

S Ferrara

Publications and source records attributed to S Ferrara.

30 records · Page 2Linked to original sources
PubMed1995

Treatment with ribavirin+alpha interferon in HCV chronic active hepatitis non-responders to interferon alone: preliminary results.

Alpha interferon (IFN-alpha) represents the best therapy for HCV active chronic hepatitis, but only 25% of treated patients achieve a complete recovery. Several attempts have been made to increase this percentage. The objective of our study is to verify whether the combination ribavirin (R)+ IFN-alpha can lead to positive results in non-responders to treatment with IFN-alpha alone. The preliminary results for 5 subjects, all non-responders to IFN, treated with R+ IFN for 60 days and then IFN alone for 4 months more show that during the R+IFN treatment, 2 subjects presented a reduction in transaminase; a month after the suspension of R, ALT returned to pre-treatment values. The results are preliminary but we can say that this combination in the proposed doses and times in these subjects, cannot be considered adequate to modify the natural course of this disease.

Adult↗
PubMed1995

Bell's palsy and visualization of the facial nerve by MRI.

A group of patients complaining of facial nerve palsy (Bell's palsy) were evaluated with MRI using a 0.5 unit and high resolution T1-weighted images, in order to evaluate the efficacy of Gd-DTPA enhancement in depicting the degree of nerve damage: MRI examination was performed within 24 hours to two weeks after the onset of palsy. The authors describe the results obtained from the analysis of 11 cases of Bell's palsy, discussing the prognostic and clinical significance.

Adolescent↗
PubMed1994

B cell dysfunction after bone marrow transplantation is associated with decreased Ca2+ flux upon membrane Ig crosslinking.

Patients undergoing bone marrow transplantation have a long-lasting defect of B cell-mediated immunity. Both quantitative (decreased blood B cell counts) and qualitative (decreased Ig production) abnormalities of B cells have been described. To better understand the mechanism of the qualitative defect and its potential relation to B cell immaturity, we studied the in vitro responsiveness of B cells to polyclonal stimuli in patients at 2-12 months post-transplant and in normal neonates. Several key steps of the B cell program were deficient in the patients while they were relatively normal in the neonates. These included (i) early activation as assessed by Ca2+ flux; (ii) late activation as assessed by the increase in cell size and upregulation of the activation antigens CD25 and CD71; and (iii) proliferation as assessed by the number of cycling cells after stimulation. We conclude that the functional B cell defect during the early (< 1 year) post-transplant period extends back to the level of early activation and cannot be simply attributed to the relative immaturity of post-transplant B cells.

Adolescent↗
PubMed1994

Abundance of a restricted fetal B cell repertoire in marrow transplant recipients.

Patients undergoing bone marrow transplantation are humorally immunodeficient for one or more years post-transplant. This immunodeficiency could be partially caused by B cell repertoire restriction similar to that observed in ontogeny. To test this idea, the abundance of rearranged genomic segments bearing five variable heavy chain (VH) genes was compared in patients at several timepoints post-transplant and in immunologically normal neonates, infants and adults. The genes evaluated in the study (VH6, VH4-58p2, VH3-56p1, VH3-20p1 and VH3-13-2) were selected from those commonly utilized by fetal B cells. The assay employed quantitative PCR and oligonucleotide hybridization detection under conditions designed to detect relatively unmutated forms of these genes. In blood B cells from early post-transplant (2-5 months) patients, these VH genes were markedly overutilized compared with normal adults. B cells from late post-transplant (6-21 months) patients and from normal neonates and infants also overutilized these genes; however, to a lesser degree than early post-transplant B cells. The data suggest that, as in ontogeny, the B cell repertoire is strikingly restricted to fetal-type VH genes early post-transplant, and may become normal only very late (years) post-transplant.

Adult↗
PubMed1993

B cell reconstitution after human bone marrow transplantation: recapitulation of ontogeny?

Patients undergoing BMT have a long-lasting defect of B cell-mediated immunity, especially if chronic GVHD ensues. It has been postulated that the post-transplant B cell abnormalities can be explained by the recapitulation of B cell ontogeny. To test this hypothesis, we studied the quantitative and phenotypic reconstitution of circulating B cells in 24 transplant recipients and compared it with normal ontogeny. The results confirm that a second round of ontogeny occurs in transplant recipients without chronic GVHD. This was evidenced by the pattern of quantitative B cell reconstitution (low-->high-->normal B cell counts), large B cell size and a high proportion of B cells overexpressing CD38, membrane IgM (mIgM) and membrane IgD (mIgD). The recapitulation of ontogeny was blunted in most patients with chronic GVHD, as evidenced by the absence of the overshoot of total B cells and by the relative lack of CD38high, mIgMhigh and mIgDhigh B cells. We conclude the post-transplant B cell development in patients without chronic GVHD parallels ontogeny. The limited ability of patients with chronic GVHD to re-enact B cell ontogeny may contribute to their longer-lasting and more severe humoral immunodeficiency.

Adult↗
PubMed1992

A novel B cell stimulation/proliferation assay using simultaneous flow cytometric detection of cell surface markers and DNA content.

Assessment of the specific B cell proliferative response by thymidine incorporation following polyclonal stimulation (e.g. with pokeweed mitogen or B cell growth factor) is problematic whenever the proportion of B cells in a particular sample is low as in blood samples. Here we describe a simple assay consisting of identifying the cultured B cells with anti-CD19/CD20 fluorescein-conjugated antibody and simultaneously using propidium iodide DNA staining to determine the percent of S/G2/M phase cells among the gated B cells. This assay can be used to determine B cell responsiveness even in individuals with very low blood B cell counts (e.g., in recipients of bone marrow transplant), does not require laborious B cell purifications and does not involve radiation hazard.

Adult↗
PubMed1992

Recovery of mononuclear cell subsets after bone marrow transplantation: overabundance of CD4+CD8+ dual-positive T cells reminiscent of ontogeny.

Patients after bone marrow transplantation are immunodeficient for months to years. To understand better the pathogenesis of this immunodeficiency, we studied quantitative reconstitution of blood monocytes, natural killer (NK) cells, T cells, and B cells at 2-22 months post-transplant. The results indicate monocyte and NK counts generally recover within 2 months, followed by CD4-CD8+ T cell, B cell, and finally (after > 1 year) CD4+CD8- T cell numbers. Dual-positive CD4+CD8+ T cells (which were barely detectable in normal adults), CD4-CD8+ T cells and B cells transiently reached supranormal levels during recovery. Both CD4+CD8- and CD4-CD8+ T cells were larger than controls throughout the 2-year follow up. Comparison with neonatal and infant mononuclear cell subsets suggested the reconstitution of CD4+CD8+ T cells and B cells is similar to ontogeny. In contrast, the reconstitution of CD4+CD8- T cells did not resemble ontogeny.

B-Lymphocytes↗
PubMedDate not supplied

Mandibular metastatic hepatocellular carcinoma: report of a case involving severe and uncontrollable hemorrhage.

Hepatocellular carcinoma (HCC) is a malignant tumor with a marked tendency to spread through the portal system. Metastases from HCC usually involve lungs, surrenal glands, the skeletal and gastroenteric systems, spleen, heart and kidneys. Secondary localizations to the mandible are rare. Generally, bone metastases from HCC appear as osteolytic lesions more likely localized to the ribs, spine, femor, omer, sternum, and then to the mandible. Mandibular metastatic HCC is hemorrhagic in nature because of its hypervascularity. Any diagnostic maneuver that could end in bleeding should be avoided. Non-invasive diagnostic procedures such as computer tomography (CT) scan should be preferred. Among the invasive diagnostic procedures, only fine needle biopsy should be attempted and palliative radiotherapy could be useful for the control of local symptoms. A case report of a hemorrhagic mandibular metastatic HCC that had to be treated surgically, in order to control the severe and profuse bleeding, is presented.

Carcinoma, Hepatocellular↗