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Biomedical subjects

P Gentile

Publications and source records attributed to P Gentile.

At least 19 recordsLinked to original sources
PubMed2006

Reconstruction of the nasal dorsum with autologous rib cartilage.

The authors present their experience with the correction of deformities of the nasal saddleback using rib cartilage grafts. They present a review of international literature on this topic, analyzing 33 patients selected from 452 cases of rhinoplasties performed between January 1990 and December 2004 at the Department of Plastic and Reconstructive Surgery of the University of Rome "Tor Vergata." Nasal saddleback is one of the most complicated defects to correct surgically. It can be a consequence of nasoethmoid-orbital fractures and is in this case associated with other evident signs like telecanthus, teleorbitism, or orbital dystopia. It can be also a consequence of surgical procedures in the nasal area where a loss of bone or septal cartilaginous support has occurred. They compare the techniques employed in the reconstruction and describe the advantage of the use of cartilage from the 11th rib and evaluate the results of an engineering analysis of tension forces on the rib cartilage. Of the total number of patients treated, good cosmetic results were obtained in 84% of the cases and excellent functional results in almost all of the cases (94%).

Adult↗
PubMed1997

Polymorphous low-grade adenocarcinoma: flow cytometric, p53, and PCNA analysis.

Polymorphous low-grade adenocarcinoma of minor salivary glands (terminal duct carcinoma, lobular carcinoma) was first defined more than a decade ago. A 17% recurrence rate and a 9% metastasis rate have been reported. Fifteen formalin-fixed, paraffin-embedded archival cases were analyzed. Ploidy and proliferative activity were evaluated with flow cytometric analysis. Demonstration of an abnormal p53 gene product and proliferative cell nuclear antigen analyses were also performed with routine immunohistochemical procedures. The purpose of this investigation was to evaluate these parameters and determine if a correlation existed. Flow cytometry was performed on 10 cases; 3 showed an aneuploid cell line (mean, S-phase diploid tumor cells 5.9%; S-phase aneuploid 26.7%). Products of a mutation of the p53 tumor suppressor gene have been noted to accumulate in salivary gland tumors, both benign and malignant. Qualitative assessment revealed p53 positive staining in 4 of 15 tumors; positive cells comprised 5% to 10% of the tumor. The percentage of tumor cells positive for proliferative cell nuclear antigen staining ranged from 0.5% to 70%. There was no correlation between proliferative activity as determined by proliferative cell nuclear antigen when compared with results of flow cytometric analysis except for one case that exhibited p53 staining, a 26% proliferative cell nuclear antigen fraction, and a distinct aneuploid cell line.

Adenocarcinoma↗
PubMed1996

Differentiating agents do not induce a true hairy cell phenotype in B-CLL cells in vitro.

B-Chronic lymphocytic leukemia (B-CLL) and hairy cell leukemia (HCL) are both differentiated B-cell lymphoproliferative disorders. Prior studies have suggested that phorbol esters and the macrocyclic lactone Bryostatin-1, which are both protein kinase-C activators, can induce the differentiation of B-CLL cells into HCL cells in vitro, as evidenced by morphology, phenotype and TRAP activity. The differentiating effect of all-trans retinoic acid on B-CLL cells has been less extensively studied. We studied the effects of incubating adherence purified B-CLL cells with phorbol myristic acetate (PMA), all-trans retinoic acid (ATRA), and Bryostatin-1. None of these agents induced a true HCL phenotype (CD5-, CD11c/CD25 coexpression) under the conditions studied.

Acid Phosphatase↗
PubMed1996

Malignant mesothelioma: immunohistochemistry and DNA ploidy analysis as methods to differentiate mesothelioma from benign reactive mesothelial cell proliferation and adenocarcinoma in pleural and peritoneal effusions.

OBJECTIVE: To determine whether malignant mesotheliomas can be differentiated from adenocarcinomas and benign reactive mesothelial cells in pleural and peritoneal fluids using immunohistochemical analysis in conjunction with DNA ploidy analysis. DESIGN: Sixteen cases of malignant mesothelioma, including epithelial, sarcomatous, and biphasic types, were collected. DNA analysis using flow cytometry and/or image analysis was performed on paraffin-embedded tissue from 15 of the mesothelioma cases, as well as on cytospin cell preparations from samples of pleural and peritoneal fluids from cases with either cytologically proven adenocarcinoma (seven cases) or benign reactive mesothelial cells (seven cases). Immunohistochemical studies were done in 15 mesotheliomas, 5 adenocarcinomas, and 4 benign reactive mesothelial cell effusions. RESULTS: All malignant mesotheliomas tested (100%) stained positively for prekeratin, whereas stains for carcinoembryonic antigen, B72.3, Leu-M1, and Ber-EP4 were negative. Stains vimentin, epithelial membrane antigen, and CA125 were positive in 75%, 75%, and 25% of cases tested, respectively. Benign reactive mesothelial cell cases stained similarly. Adenocarcinomas were more likely to react positively with B72.3, Ber-EP4, and carcinoembryonic antigen, and negatively with vimentin. DNA analysis showed that all benign cases were diploid, while all adenocarcinomas were nondiploid. Fifty-three percent of the malignant mesotheliomas were nondiploid. Sensitivity for detection of nondiploidy was greater for image analysis than for flow cytometry (100% vs 75%). CONCLUSIONS: B72.3, Ber-EP4, carcinoembryonic antigen, and vimentin are useful immunohistochemical markers in differentiating malignant mesotheliomas from adenocarcinomas, whereas immunohistochemistry does not reliably distinguish malignant from benign hyperplastic mesothelial cells. The addition of DNA ploidy studies is useful for differentiating the latter two groups.

Adenocarcinoma↗
PubMed1991

Interleukin-6 ablates the accessory cell-mediated suppressive effects of lactoferrin on human hematopoietic progenitor cell proliferation in vitro.

LF, an iron-binding glycoprotein, has myelosuppressive effects in vitro and in vivo. The present study evaluated the mode of LF action in vitro and the effects of various recombinant CSFs and ILs on this action. Normal human low-density BMC, at 2 x 10(6)/ml, were exposed to purified and endotoxin-depleted iron-saturated LF for 2 h, washed three times, and plated for CFU-GM and BFU-E in the presence of rhuCSFs (e.g., GM-CSF, Epo, IL-3) and in the absence and presence of rhuIL-6, rhuIL-1 alpha, or rhuIL-1 beta. LF caused a 40-65% plateau curve of inhibition for CFU-GM and BFU-E that was not apparent when adherent mononuclear cells (monocytes) were removed from the target population of cells. This myelosuppression was ablated by rhuIL-6, but not by rhuIL-1 alpha or rhuIL-beta. These results suggests a role for IL-6 in the accessory cell-mediated suppressive effect of LF on CFU-GM and BFU-E and open up the possibility that IL-6 may have stimulatory/enhancing or cofactor activities necessary for optimal proliferation of hematopoietic progenitor cells.

Animals↗
PubMed1987

Approaches to ablating the myelotoxicity of chemotherapy.

Myelotoxicity remains a significant dose-limiting side effect of chemotherapy contributing to the morbidity and mortality of patients undergoing treatment for cancer. A number of different experimental approaches are being studied, both in the clinic and in the laboratory, in an attempt to prevent this iatrogenic complication. The present review provides a synopsis of the various myeloprotective strategies now being employed in experimental trials. Emphasis is placed on the use of putative physiologic bioregulatory molecules (lactoferrin, prostaglandin E, interferon) to prevent or lessen chemotherapy-induced myelotoxicity, with consideration also given to other promising treatment modalities (i.e., adenosine, lithium, diethyldithiocarbanate).

Adenosine↗
PubMed1987

The opposing actions in vivo on murine myelopoiesis of purified preparations of lactoferrin and the colony stimulating factors.

The actions of purified iron-saturated human lactoferrin (LF), purified preparations of human MiaPaCa colony stimulating factor-1 (CSF-1), and recombinant murine interleukin-3 (IL-3) were evaluated in vivo in mice. Studies in vitro were compared at lowered (5%), as well as at normal incubator (20%), oxygen (O2) tension because of the potentially greater physiologic relevance of in vitro studies performed at lowered O2 tension. The results demonstrate that 1) increased release of granulocyte-macrophage colony stimulating factor (GM-CSF) in vitro from pokeweed mitogen stimulated mouse spleen cells and from human mononuclear blood cells occurred at lowered O2 tension, and that human mononuclear blood leukocytes were more sensitive to the LF-induced suppression of GM-CSF release when cells were cultured at 5%, compared to 20%, O2 tension; 2) LF administered intravenously (IV) to mice pretreated with sublethal intraperitoneal dosages of Cytoxan decreased the cycling status of marrow and spleen granulocyte-macrophage (CFU-GM), erythroid (BFU-E-2 and BFU-E-1) and multipotential (CFU-GEMM) progenitor cells and the absolute numbers of these progenitors; these effects were most noticeable if care was taken to deplete endotoxin from the LF samples prior to testing LF in vivo and if the control medium was endotoxin free; 3) endotoxin-depleted LF decreased the cycling status of marrow and spleen CFU-GM, BFU-E, and CFU-GEMM and the numbers of these progenitors in the marrows of mice previously untreated with Cytoxan; these effects were most apparent when assessment of progenitor cells and their cycling rates were evaluated in vitro at lowered (5%) O2 tension; 4) purified natural human CSF-1 increased the absolute numbers of marrow CFU-GM and the cycling status of marrow CFU-GM and CFU-GEMM in mice pretreated with LF; and 5) purified recombinant murine IL-3 stimulated proliferation of day 8 and day 12 CFU-S (colony forming unit-spleen) in mice not previously treated with Cytoxan. These results substantiate the in vivo myelosuppressive effects of LF on CFU-GM and extend these effects to erythroid and multipotential progenitor cells, provide evidence that human CSF-1 has an in vivo action in mice, and confirm the studies of others showing that IL-3 stimulates the proliferation of CFU-S in vivo.

Animals↗
PubMed1985

Abnormalities in myelopoietic regulatory interactions with acidic isoferritins and lactoferrin in mice infected with Friend virus complex: association with altered expression of Ia antigens on effector and responding cells.

The regulation of myelopoiesis was evaluated in B6D2F1 mice inoculated with Friend virus complex (spleen focus-forming virus plus helper virus) or helper virus alone by analyzing acidic isoferritin (AIF) and lactoferrin (LF) interactions with target cells. Under normal conditions, AIF suppresses colony and cluster formation by an Ia-antigen-positive cycling subpopulation of mouse granulocyte-macrophage progenitor cells (CFU-GM). Under the same conditions, the release of AIF-inhibitory activity and granulocyte-macrophage colony stimulatory factors (GM-CSF) from an Ia-antigen-positive subpopulation of monocytes and macrophages is suppressed by LF. Within one to two days after inoculation in vivo with Friend virus complex or helper virus, mouse CFU-GM become insensitive in vitro to suppression by purified human AIF as well as crude mouse AIF, and by four days, bone marrow, spleen, and thymus cells of these mice release much greater quantities of AIF-inhibitory activity than the cells from mice injected with control medium. The Friend virus complex itself has no influence in vitro on CFU-GM from normal mice. In addition, the release of AIF-inhibitory activity from bone marrow, spleen, and resident peritoneal cells and the release of GM-CSF from resident peritoneal cells of mice infected with Friend virus complex are not suppressed by LF. The inability of AIF to suppress colony formation by bone marrow and spleen CFU-GM from mice infected with Friend virus complex is associated with the loss of Ia (I-A subregion) antigens from CFU-GM, even though CFU-GM are in cycle. The nonresponsiveness of bone marrow, spleen, and peritoneal cells from these mice to LF suppression of AIF release and the inability of LF to influence GM-CSF release from peritoneal cells is associated with loss of Ia antigens from these cells. The above abnormalities are similar to the defects noted using cells from patients with leukemia. These results suggest that mice infected with Friend virus complex can serve as a model for investigating abnormalities in cell regulation and their relationships to disease progression.

Animals↗
PubMed1984

Functional activities of acidic isoferritins and lactoferrin in vitro and in vivo.

The functional activities of acidic isoferritins (AIF) and lactoferin (LF) were evaluated. The inhibitory activity of AIF (AIFIA) was inactivated by preincubation with a monoclonal antibody (2A4) against AIF, but AIFIA was not inactivated by another monoclonal antibody against AIF (1C5), by a monoclonal antibody (3A5) against basic isoferritins, or by a heteroantiserum (LFT) against basic isoferritins. Monoclonal 2A4 also inactivated the inhibitory activity against colony formation by granulocyte-macrophage (CFU-GM) progenitor cells that was constitutively released by human monocytes or induced by human monocytes in the presence of OKT4+ lymphocytes. In addition to OKT4+ lymphocytes, the release of AIFIA from human monocytes was modulated by iron-saturated human LF and OKT8+ lymphocytes, both of which suppressed the release of AIFIA. Evidence for the physiologic relevance of AIF as a regulator of myelopoiesis was presented, in that human AIF suppressed the numbers of CFU-GM, BFU-E, and CFU-GEMM per femur and the cycling status of these cells in mice recovering from a sublethal dosage of Cytoxan. Abnormalities in LF and AIF interactions were found with cells from a pediatric patient with neutrophilia of unknown etiology that were consistent with the disease manifestations of neutrophilia. Polymorphonuclear neutrophils (PMN) from the patient contained low levels (1%-10% of control) of immunologically reactive LF and the LF found was ineffective as a suppressor molecule for the release of GM-CSF from normal mononuclear blood cells. In addition, the patient's GM-CSF releasing mononuclear blood cells were insensitive to the suppressive effects of purified LF, and colony formation by the patient's CFU-GM, but not BFU-E or CFU-GEMM, were insensitive to the suppressive effects of purified AIF. When the activity of purified AIF was assessed against mouse bone marrow cells under serum-free conditions, it was apparent that serum was not needed for the suppressive activity of AIF and that in some cases, serum actually masked the effects of AIF. Human monoblast cell line U937 was found to be a good model in vitro for the actions of LF and AIF; U937 cells induced for Ia-antigens by human gamma interferon were separated into populations of Ia-antigen+ and Ia-antigen- cells by fluorescence activated cell sorting (FACS), and LF and AIF suppressed colony formation only by the Ia-antigen+ U937 cells. A comparative analysis of bovine and human LF against release of GM-CSF from human mononuclear cells demonstrated that both were active in their iron-saturated form.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

In vivo modulation of murine myelopoiesis following intravenous administration of prostaglandin E2.

The effects of in vivo administration of prostaglandin E2 (PGE2) on several hematologic parameters were investigated in intact mice under both steady-state conditions and in mice hematopoietically rebounding following a sublethal injection of cyclophosphamide. Intravenous injection of native PGE2, or 16,16 dimethyl-PGE2, an enzymatically stable analog of PGE2, resulted in the significant suppression of nucleated bone marrow and splenic cellularity, total resident nucleated peritoneal cells, and the absolute number of detectable granulocyte-macrophage progenitor cells (CFU-GM) per femur or spleen when administered for 3 or 7 consecutive days. The in vivo effects of 16,16 dimethyl-PGE2 were more pronounced on the cyclophosphamide-treated mice. Dose titration analysis of the effects of 16,16 dimethyl-PGE2 revealed significant suppression of hematologic parameters over a concentration range of 10 micrograms-10(-5) micrograms/mouse/day (10(-5) M-10(-11) M). The reduction in total nucleated marrow, splenic, and peritoneal cellularity observed following PGE2 administration resulted from a selective effect on nonspecific esterase-positive cells. In situ morphological analysis of the progeny of CFU-GM proliferating in cultures established from mice treated with PGE2 in vivo indicated that the reduction in absolute CFU-GM observed resulted from a preferential effect on those colony-forming cells restricted to monocyte-macrophage differentiation. Prostaglandin F2 alpha was without stimulatory or inhibitory effects in vivo on the hematopoietic parameters investigated.

16,16-Dimethylprostaglandin E2↗
PubMed1983

Suppression of mouse myelopoiesis by administration of human lactoferrin in vivo and the comparative action of human transferrin.

Purified human lactoferrin was assessed for its influence in vivo in untreated mice and in mice undergoing rebound myelopoiesis after sublethal dosages of Cytoxan. Fully iron-saturated lactoferrin suppressed the numbers of granulocytes and monocytes per femur, the numbers of granulocyte-macrophage progenitor cells (CFU-GM) per femur and spleen, and decreased the cycle status of femoral and splenic CFU-GM. These effects were detected after administration of lactoferrin i.v. or i.p. into untreated and Cytoxan-treated mice. The suppressive effects on cellularity and numbers of CFU-GM per femur were apparent to a greater degree in mice treated with Cytoxan, and the i.v. route appeared preferable to the i.p. route. Heat-treated lactoferrin, inactive in vitro, was inactive in vivo, but iron-depleted (apo-) lactoferrin, inactive in vitro, was active in vivo, suggesting that the apo-lactoferrin acquired the iron in vivo that was necessary to change it into an active form. Titration of the effects of lactoferrin in Cytoxan-treated mice demonstrated a plateau curve of suppression of nucleated cells and CFU-GM per femur with dosages ranging from 100 micrograms to 10(-4) micrograms lactoferrin per mouse, with loss of activity at 10(-5) micrograms. The suppressive effect of lactoferrin on cycle status of CFU-GM required concentrations of 10 micrograms or higher. The effects of lactoferrin were reversible with time, with the suppressive influence on cycling status being lost before that on numbers of CFU-GM per femur. Purified human transferrin was also assessed for its influence in mice undergoing rebound myelopoiesis. Transferrin decreased the nucleated cellularity and the number of CFU-GM per femur and per spleen, but had little or no influence on the cycling status of CFU-GM and differed in its temporal effect on myelopoiesis from that of lactoferrin. These results suggest that lactoferrin and transferrin suppress the number of progenitor cells moving into the CFU-GM compartment and lactoferrin suppresses the cycling status of cells within the CFU-GM compartment. These effects are probably mediated by an action on the production of factors necessary for movement of cells into, and cell cycling within, the CFU-GM compartment.

Animals↗
PubMed1983

Lactoferrin, transferrin and acidic isoferritins: regulatory molecules with potential therapeutic value in leukemia.

In the process of evaluating roles for purified preparations of lactoferrin, transferrin and acidic isoferritins in the regulation of myelopoiesis, it was found that: (1) values reported for lactoferrin in the serum and plasma of normal donors are in most cases an over-estimation, (2) lactoferrin suppresses the production/release of granulocyte-macrophage colony stimulatory factors (GM-CSF) from monocytes in the absence of T-lymphocytes and also suppresses the production/release of acidic isoferritin-inhibitory activity from monocytes, (3) lactoferrin, transferrin and acidic isoferritins act on their specific target cells which express Ia-like antigens, (4) lactoferrin and transferrin act in vivo to suppress rebound myelopoiesis in mice recovering from sublethal dosages of Cytoxan, with preliminary observations suggesting that lactoferrin has a greater apparent effect on the bone marrow and transferrin has a greater apparent effect on the spleen, (5) active lactoferrin derives from Fc receptor positive subpopulations of PMN from patients with CML as well as from normal donors, but the percentage of Fc receptor containing PMN is lower in CML, as is the amount of active lactoferrin found in their PMN, and (6) lactoferrin, transferrin and acidic isoferritins suppress the colony formation of U937 clonogenic cells, with lactoferrin and transferrin decreasing the release of growth factors from U937 cells which are needed to stimulate U937 colony formation, and lactoferrin and acidic isoferritins suppress the colony formation of WEHI-3 cells, with lactoferrin decreasing the release of growth factors from WEHI-3 cells which are needed to stimulate WEHI-3 colony formation. Speculation on the potential usefulness of these iron binding glycoproteins to control of disease progression is given in the discussion.

Animals↗
PubMedDate not supplied

Breast asymmetries: a brief review and our experience.

The authors describe their personal experience with the management of mammary asymmetries. A review of their database from January 1998 to January 2005 identified 177 patients with idiopathic breast asymmetries. All these cases had been classified previously into six groups. Bilateral asymmetric hypertrophy and unilateral hypertrophy were treated with reduction mammaplasty. Unilateral hypertrophy with amastia or hypoplasia of the contralateral side was managed with reduction and augmentation mammaplasty. Unilateral amastia or hypoplasia (Poland's syndrome) was treated with a single monopedicle transverse rectus abdominis muscle (TRAM) flap, and asymmetric bilateral hypoplasia was managed with augmentation mammaplasty. Unilateral mammary ptosis was treated with mastopexy and augmentation mammaplasty. The proposed classification, derived from the authors' experience in this field, gives an idea of how they usually treat these patients. It is useful for a first evaluation, but after that, every treatment must always be individualized on a patient-by-patient basis.

Breast↗