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Biomedical subjects

W Piacibello

Publications and source records attributed to W Piacibello.

66 records · Page 4Linked to original sources
PubMed1981

Release of platelet-activating factor (PAF) and histamine. II. The cellular origin of human PAF: monocytes, polymorphonuclear neutrophils and basophils.

The origin of platelet activating factor (PAF) from human leucocytes was investigated. Purified monocytes release PAF passively at pH 10.6, when challenged with Ionophore A 23187 or under phagocytic stimuli. Pure preparations of polymorphonuclear neutrophils liberate PAF passively, when challenged with C5a, neutrophil cationic proteins (CP), their carboxypeptidase B derived products (C5a des Arg, CP des Arg) or under phagocytic stimuli. Basophil rich buffy coat cells release PAF when challenged with C5a, CP, anti-IgE (in low amount) or Synacthen concomitantly with basophil degranulation and histamine release. Electron microscopy studies, carried out on Synacthen-stimulated basophil rich buffy coat, provide morphological evidence for platelet-basophil interaction. In conclusion our data demonstrate that PAF can be released from different leucocyte populations. However, the stimuli able to trigger such release appear to have some specificity for the cell target.

Antigen-Antibody Complex↗
PubMed1981

Detection of basophils growing in semisolid agar culture.

The production of basophils in semisolid agar cultures form normal and chronic myeloid leukemia (CML) committed granulocyte-macrophage precursors was investigated using an original whole-dish staining technique with toluidine blue which produces a specific metachromasia in basophils. As additional proof of the basophilic nature of metachromatic cells, their degranulation after challenge with C5a anaphylotoxin and Synachten was observed. Our studies show that few basophils are produced in cultures form normal bone marrow. CML CFUc produce more basophils, their number being roughly correlated with the degree of basophilia. We observed only clusters composed by a pure basophilic population, while larger aggregates in which basophils could be detected were composed also by other granulocytic cells.

Agar↗
PubMed1980

Different kinetic pattern of chronic myeloid leukemia: lymphoblastic and myeloblastic blastic crisis.

Cell kinetic studies were performed in 8 case of lymphoid blastic crisis (BC) of chronic myeloid leukemia at the onset of BC and during subsequent relapses. The results were compared with those found in 7 myeloblastic BC. While in the myeloblastic transformation the labeling index (LI) was always higher in bone marrow than in peripheral blood blasts, suggesting a predominant bone marrow proliferation of the leukemic cells, in the lymphoid transformation a higher LI was often found in peripheral blasts. Moreover, the lymphoblastic transformations were frequently characterized by lymphadenopathy. These findings point to the similarities between lymphoid BC and acute lymphoblastic leukemia, suggesting the possibility that a blastic event may originate in an extramedullary site and that an extramedullary BC is more likely to be lymphoid in nature.

Adult↗
PubMed1980

Insensitivity of chronic myeloid leukemia cells to inhibition of growth by prostaglandin E1.

The influence of E prostaglandins on the in vitro growth of chronic myeloid leukemia (CML)-committed granulopoietic precursors [colony-forming unit-culture (CFU-C)] has been investigated in a double-layer agar system in which CFU-C growth was stimulated by adherent monocytes. Addition of the prostaglandin synthesis inhibitor indomethacin to the feeder layer significantly increased the number of normal CFU-C, whereas CML CFU-C were unaffected. Exogenous prostaglandin E1 inhibited CML CFU-C growth at concentrations 1000-fold higher than those necessary to produce a similar effect on normal CFU-C. These data point to a lower than normal sensitivity of CML-committed granulopoietic precursors. It is suggested that derangement of the responsiveness of CML cells to prostaglandin regulation may play a role in the pathogenesis of uncontrolled leukemic proliferation.

Bone Marrow↗
PubMedDate not supplied

Atypical myeloproliferative disorder associated with a 21 trisomic clone.

The hematological and cytogenetical studies of a case of atypical myeloproliferative disorder are reported. The patient displayed moderate leukocytosis, anemia and thrombocytopenia. Reduced or absent growth of CFU-C was observed in the bone marrow and peripheral blood. The cytogenetical analysis revealed a trisomy 21 limited to the neoplastic clone. The overall results are discussed and compared with the rare cases of acquired trisomy 21 reported in the literature.

Aged↗
PubMedDate not supplied

Different growth factor requirements for the ex vivo amplification of transplantable human cord blood cells in a NOD/SCID mouse model.

The growth factor combination containing early acting cytokines FLT-3 ligand (FL), Stem Cell Factor (SCF) and thrombopoietin (TPO) is able to maintain, for an extended culture period, early stem cells, defined as long-term repopulating NOD/SCID mice (Scid Repopulating Cell-SRC) contained in cord blood (CB). In this culture system, the role of IL-6 and IL-3 has not been clearly established. Using a combination of FL+TPO+SCF with or without IL-6, we were able to form CB CD34+ cells for 30 weeks. The CB CD34+ cells cultured in this system engrafted NOD/SCID mice after 6 weeks of culture; the cells from primary recipients were also able to engraft secondary NOD/SCID mice. When CB CD34+ cells were cultured in the presence of IL-3 in the place of IL-6 we observed an even better expansion of cells and a similar clonogenic progenitor output in the first 8 weeks of culture. However, more primitive LTC-IC output increased up to week 6 with the growth factor combination containing IL-3 and then decreased and disappeared, while with the growth factor combination with or without IL-6 increased up to week 23. Cells cultured for 4 weeks with the 4-factor combination containing IL-3 engrafted NOD/SCID mice less efficiently. Repopulation of NOD/SCID mice was no longer observed when ex vivo expansion was performed for 6 weeks. This study provides some evidence that no differences could be detected in long-term maintenance and even expansion of human primitive cord blood cells cultured with FL+TPO+SCF in the presence or absence of IL-6. Under the culture conditions employed in this study, the presence of IL-3 reduced the repopulating potential of expanded CB CD34+ cells.

Animals↗
PubMedDate not supplied

Differential effect of transforming growth factor beta 1 on the proliferation of human lymphoid and myeloid leukemia cells.

BACKGROUND: Transforming Growth Factor beta (TGF beta) exerts different effects on the hemopoietic system which range from the growth stimulation of more mature myeloid progenitors to the growth inhibition of more immature and multilineage hemopoietic precursors. TGF beta is also an inhibitor of the proliferation and functional activities of normal T and B lymphocytes. The aim of this study was to evaluate its effect on the growth of a human leukemic cells of lymphoid and myeloid origin. METHODS: We tested its activity on the doubling time, the DNA synthesis rate and the clonal growth of a panel of lymphoid and myeloid leukemic cell lines. RESULTS: Among the myeloid cell lines, the proliferation in liquid cultures as well as the clonal growth of KG1, HL60 and U937 were suppressed by TGF beta 1 at doses ranging from 0.025 to 2.5 ng/ml; the degree of inhibition was, however, variable. BV 137, a Ph1-positive cell line derived from a very undifferentiated stem cell, was also highly responsive to TGF beta 1 inhibition. Among the six lymphoid neoplastic cell lines, only Nalm 6, a pre-B leukemic cell line, was consistently and reproducibly inhibited by the same doses of TGF beta 1. Conversely, two Burkitt lymphoma cell lines, Raji and Daudi, and three T-cell leukemias (Molt 4, Jurkat and PF 382) were insensitive to TGF beta inhibition.

Cell Differentiation↗
PubMedDate not supplied

Modulation by retinoic acid of the growth of bone marrow cell progenitors from patients with myelodysplastic syndrome.

The in vitro effect of increasing concentrations of retinoic acid on the growth of day 7 and day 14 CFU-GM and of pre-CFU-GM from patients with myelodysplastic syndromes has been studied. Unlike in normal cells, where retinoic acid enhances the in vitro growth of myeloid progenitors, there was an overall inhibition of bone marrow progenitors from patients with myelodysplastic syndromes at concentrations of 10(-7) to 10(-6) M retinoic acid, with the exception of day 14 CFU-GM whose growth may be enhanced by 10(-7) M retinoic acid.

Bone Marrow↗
PubMedDate not supplied

Expression of the hybrid P210 bcr/abl protein in Philadelphia chromosome positive B-lymphoid cell lines.

An altered c-abl protein (P210) bearing increased tyrosine kinase activity represents the product of the hybrid bcr/c-abl gene arising as a consequence of the Philadelphia (Ph1) chromosome translocation, the consistent cytogenetic abnormality of chronic myelogenous leukemia (CML). Although the chronic phase of this disease is substantially characterized by a marked proliferation of myeloid cells, the Ph1 translocation occurs in an early multipotent stem cell, giving rise to both myeloid and lymphoid cell lineages. Here we show that P210 bcr/abl protein expression varies greatly in different Ph1 chromosome positive B-lymphoid cell lines obtained from Epstein-Barr virus-transformed lymphocytes of a CML patient in the chronic phase. In addition Ph1 positive and Ph1 negative lymphoid cell lines obtained from the same patient were tested for a number of biological properties including the immunophenotype, the capacity to grow in soft agar and possible tumorigenicity in nude mice. No differences were found.

Animals↗