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G Carulli

Publications and source records attributed to G Carulli.

84 records · Page 5Linked to original sources
PubMedDate not supplied

[P-glycoprotein and treatment with plicamycin + hydroxyurea in myeloid blastic crisis of chronic myeloid leukemia].

The authors studied P-glycoprotein (P-gp) expression in three patients affected by myeloid blast crisis of chronic myeloid leukemia undergoing chemotherapy with plicamycin + hydroxyurea. P-gp is the molecular marker of multidrug resistance (MDR), and is able to promote the efflux of various drugs (including plicamycin) from the neoplastic cell. When resistance towards plicamycin and hydroxyurea association was observed, the blasts obtained from the three patients were found to express P-gp. Although P-gp may be not the unique mechanism responsible for resistance towards plicamycin and hydroxyurea association, the MDR phenotype may play an important role in the resistance towards this treatment protocol in the blast crisis of chronic myeloid leukemia.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

[Aggregation of human neutrophils induced by phytohemagglutinin].

Phytohemagglutinin-induced aggregation of circulating neutrophils was studied in 13 normal subjects. The interference caused by various drugs (vinblastine, cytochalasin B, indomethacin, nicardipine and flunarizine) was tested. The modifications in the aggregation values induced by these drugs are in favour of an evident dependence of the phenomenon upon the trans-membrane flow of calcium ions and the calmodulin function and of a limited dependence upon the microtubular function.

Adult↗
PubMedDate not supplied

Granulocyte colony-stimulating factor (G-CSF) administration increases PMN CD32 (FcRII) expression and FcR-related functions.

The phenotypical and functional properties of circulating neutrophils from ten patients suffering from intermediate- and high-grade non-Hodgkin lymphoma were investigated before and after rhG-CSF administration (5 micrograms/kg/day subcutaneously for 5 days). The following parameters were studied: flow cytometry evaluation of surface CD32, CD16, CD11b and CD18 by means of a whole blood method; whole blood phagocytosis by means of a flow cytometric assay; whole blood chemiluminescence using opsonized zymosan as a stimulus. A significant increase in the expression of surface CD32 was detected in all patients, while CD11b expression was found to be increased in only four of them. CD16 and CD18 expression did not change. A significant enhancement of phagocytosis and phagocytosis-associated chemiluminescence was also observed. These results show that rhG-CSF administration can increase both FcRII expression and FcR-related functions.

Adult↗
PubMedDate not supplied

Effects of recombinant human granulocyte colony-stimulating factor administration on neutrophil phenotype and functions.

BACKGROUND AND OBJECTIVE: Recombinant human granulocyte colony-stimulating factor (rhG-CSF) is currently used for treatment of various types of neutropenia, treatment of aplastic anemia, mobilization of peripheral blood progenitor cells. However, rhG-CSF is not only a growth factor for the myeloid lineage, but it also acts as a modulator of neutrophil behavior. The aim of the present review article is to examine the following aspects of rhG-CSF therapy: 1) does rhG-CSF influence neutrophil functions, and in particular their microbicidal properties? 2) does rhG-CSF modify neutrophil phenotype? 3) If so, what are the mechanisms potentially involved? EVIDENCE AND INFORMATION SOURCES: The author of the present article has been working in the field of rhG-CSF effects on neutrophil function, contributing original papers in peer-reviewed journals. In addition, the present review critically examines articles and abstracts published in journals covered by the Science Citation Index and Medline. STATE OF ART AND PERSPECTIVES: Treatment with rhG-CSF causes enhancement of functions such as phagocytosis, superoxide anion generation, chemiluminescence, bacterial killing, and ADCC. Neutrophil phenotype changes after rhG-CSF administration: immediate effects cause direct activation of circulating neutrophils, but delayed effects are characterized by increased surface expression of important effector molecules directly involved in neutrophil functions, such as CD14, CD32, CD64. These effects may have useful clinical consequence in patients who show an increased risk of infections, such as cancer patients, subjects with hematologic diseases (myelodysplasia, aplastic anemia), congenital diseases characterized by neutropenia, and patients with AIDS. Other changes which characterize neutrophils after rhG-CSF administration are represented by significant impairment of CD16 expression, chemotaxis, and reduced in vivo migration of neutrophils to inflammatory sites. These effects may be explained by bone marrow modification due to rhG-CSF therapy. In fact, treatment with rhG-CSF causes a significant acceleration of transit time of cells belonging to the myeloid lineage, along with amplification of the mitotic pool and a relative decrease of elements of the post-mitotic pool. It is possible that, because of the accelerated bone marrow transit time of myeloid cells, rhG-CSF causes a relative immaturity of circulating neutrophils. It is known that both CD16 expression and chemotaxis properties are acquired by neutrophils in the late stages of maturation, but the time necessary to acquire full functional maturity seems to be shortened by rhG-CSF administration, and this kinetic aspect may play a non-negligible role in the modification of neutrophil behavior.

Animals↗