Biomedical subjects
Publications and source records attributed to D Marranca.
We investigated the expression of different cell adhesion molecules on cord blood (CB) and bone marrow (BM) CD34+/CD38+ and CD34+/CD38- cells. CD11a and CD62L were more expressed in CB than in BM CD34+/CD38- subset, suggesting a possible advantage in homing and engraftment. A short exposure to various cytokines increased CD62L expression only in the more differentiated CB and BM CD34+/CD38+ cells.
A high number of stem cells migrate in fetal blood and, at birth, the number of progenitors in cord blood equals or exceeds that of adult bone marrow. Recently hemopoiesis has been successfully reconstituted with the infusion of cord blood cells. It is important to clearly define the quantity and quality of cord blood totipotent and multilineage progenitors to evaluate the possibility of their utilization in transplants. Our first aim was to study the growth characteristics of cord blood progenitors. We have evaluated the number of cycling cells with the thymidine suicide technique and the production, by phytohemagglutinin (PHA) stimulated cord blood mononuclear cells, of some cytokines involved in the proliferation of progenitor cells, such as granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin 6 (IL-6) and leukemia inhibitory factor (LIF). We have also studied by flow cytometry the CD34+CD33-, CD34+CD33+ cell subsets and the presence of the c-kit receptor in order to quantitate the number of earlier progenitors. Our second aim was to elucidate whether the cord blood totipotent stem cell population or the committed progenitors could be expanded in vitro. Our results showed that in cord blood the number of early progenitors, as evaluated by the number of mixed lineage colony forming units (CFU-Mix), by the CD34+CD33- subsets and the expression of the c-kit, is higher than in bone marrow. We have also demonstrated the possibility in vitro of increasing the number of progenitors by more than 30-fold by utilizing stem cell factor (SCF) in association with other cytokines.(ABSTRACT TRUNCATED AT 250 WORDS)
The hypothesis has been made that inhibition of prostacyclin (PG12) production may play a role in the pathogenesis of thrombosis in patients with the lupus anticoagulant (LA), but so far no evidence of reduced PG12 levels in vivo has been produced. We have tested the plasma levels of PG12 and thromboxane A2 (TXA2) and the platelet sensitivity to PG12 in 14 patients with and without LA and in 14 healthy controls. No significant difference in the prostanoid basal levels was detected among the groups; however, in some patients PG12 increments seemed to parallel the clinical course of the disease. Platelet sensitivity to exogenous PG12 was significantly enhanced in the LA + patients and correlated with PG12 values. We suggest that in these subjects additional factors, other than reduced PG12, may predispose to thrombosis.
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Desferrioxamine (DFO) has shown anti-proliferative and cytotoxic effects on several tumor cells. DFO is used at present in the treatment of neuroblastoma in combination with chemotherapy (D-CECaT regimen: cyclophosphamide, etoposide, carboplatin, and thiotepa). We compared the effect of continuous or intermittent exposures to DFO on 3H-thymidine uptake, viability, and cell cycle of human neuroblastoma (NB) cell lines. Our results show that continuous exposures to DFO cause dose- and time-dependent cytotoxicity of NB cells, while intermittent exposures result in significant NB cell toxicity only when using high DFO concentrations. By 3H-thymidine uptake, a significant inhibition of proliferation was observed only in continuous exposures. In addition, a consistent arrest in G1 phase was detected only in cultures treated continuously with high DFO concentrations. Our data indicate that 3H-thymidine uptake, viability, and cell cycle changes are proportional to the extent of exposure and concentration of DFO, suggesting that in vivo DFO continuous infusion may improve anti-neuroblastoma activity.
BACKGROUND: Parathyroid hormone (PTH) has important applications in the nephrological clinical practice. Because assays of Intact PTH (I-PTH) are liable to interferences by N-truncated fragments, a novel method for whole-(1-84) PTH has been proposed. This study is aimed at comparing the latter with some of the previous I-PTH assays. For each method the results are referred to pertinent markers of mineral metabolism. METHODS: We enrolled 171 subjects, including 56 healthy controls (C), 65 calcium stone- formers (CaSF), 40 haemodialysis patients (HD), 10 with primary hyperparathyroidism (PHP). On blood samples we measured: I-PTH by four methods (N-Tact, Advantage, Elecsys, Scantibodies), whole-(1-84) PTH, defined as CAP (Cyclase Activating PTH), total and ionised calcium, phosphate, vitamin D, osteocalcin and Crosslaps. The difference between I-PTH and CAP Scantibodies is defined as CIP (Cyclase Inhibiting PTH). RESULTS: Despite relating to each other (r>0.97) PTH values varied remarkably among methods. For all methods, the reference intervals differed from those provided by the producer. Assuming these new ranges, 10 CaSF had over-range values not always associated with abnormalities of mineral metabolism. One of the PHP patients was normal for I-PTH with 2/4 methods. In HD the differences among methods were even greater, there were inverse (p<0.05) and direct (p<0.001) relationships with ionised calcium and osteocalcin-crosslaps, respectively. The CAP/CIP ratio was lower in low bone turnover patients, but the two subgroups widely overlapped. CONCLUSIONS: This study indicates that the reliability of I-PTH assays is still unsatisfactory, and none of the four methods emerged as the best. Assay for CAP only improves diagnostic efficiency, whereas the CAP/CIP ratio does not exhibit powerful discriminating capacity. Our suggestion is that each Centre should establish its own reference ranges. PTH assay should always be coupled with measurements of other markers of mineral metabolism as well as renal function.