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1.
Environ Pollut ; 266(Pt 3): 115134, 2020 Nov.
Article in English | MEDLINE | ID: mdl-32663630

ABSTRACT

Airborne particulate matter can represent a serious issue for human health, especially in densely populated urban areas. Moreover, the inhalation of particulate can be more harmful with decreasing particles diameter. Vegetation can provide many ecosystem services to the citizens, including the removal of many different pollutants in the air, but while the effect on many gaseous compounds has already been widely proved, the capability of particulate matter (PM) sequestration driven by vegetation and its resulting benefit on air quality has not been deeply investigated yet at larger spatial scale, especially in Mediterranean environment. This study was conducted in the Real Bosco di Capodimonte, a green area of about 125 ha located inside the urban area of Naples (Italy) containing different species typical of the Mediterranean forest ecosystem. To better understand the interaction between PM and the park area, we measured fluxes of PM10, PM2.5 and PM1 with a fast acquisition analyser, according to the Eddy Covariance technique. We found that the particle deposition was higher during the central hours of the day and it was more evident for smaller size particles. Furthermore, the daily PM fluxes found accorded with evapotranspiration and carbon sequestration operated by plants, suggesting a possible active role of vegetation on the particulate deposition.


Subject(s)
Air Pollutants/analysis , Particulate Matter/analysis , Ecosystem , Environmental Monitoring , Humans , Italy , Parks, Recreational , Particle Size
2.
Int J Biol Markers ; 22(4): 302-6, 2007.
Article in English | MEDLINE | ID: mdl-18161662

ABSTRACT

Mutations in the TP53 gene are the most common genetic alterations in cancer. Accumulation of mutated protein may induce circulating anti-p53 antibodies (anti-p53Ab) in sera of cancer patients. The aim of our work was to evaluate the presence and prognostic value of anti-p53Ab in gastric cancer patients and to investigate whether their presence is related to p53 overexpression in tumor tissue. Anti-p53Ab were analyzed in sera from 111 patients with gastric carcinoma and from 64 healthy donors by ELISA. p53 expression was also quantified by ELISA in biopsies of 54 gastric cancers and 22 healthy gastric mucosas. Significant anti-p53Ab levels were found in 15.3% of patients, whereas none of the 64 donor sera were positive. High levels of p53 expression were detected only in tumor tissue, in 72.2% of cases. A significant correlation was observed between anti-p53Ab and high levels of mutated p53 in tissue (p<0.05). The survival time of serum-positive patients was significantly longer than that of patients with low/negative serum levels, with a survival rate of 41.2% and 14.9%, respectively, over 48 months (p<0.05). Thus, detection of serum anti-p53Ab in gastric cancer patients can be useful to identify a subset of patients with better prognosis.


Subject(s)
Adenocarcinoma/blood , Adenocarcinoma/diagnosis , Gene Expression Regulation, Neoplastic , Genes, p53 , Stomach Neoplasms/blood , Stomach Neoplasms/diagnosis , Tumor Suppressor Protein p53/chemistry , Adenocarcinoma/genetics , Adult , Aged , Biopsy , Case-Control Studies , Disease Progression , Female , Genetic Predisposition to Disease , Humans , Male , Middle Aged , Prognosis , Stomach Neoplasms/genetics , Tumor Suppressor Protein p53/immunology
3.
Int J Cancer ; 72(1): 133-41, 1997 Jul 03.
Article in English | MEDLINE | ID: mdl-9212234

ABSTRACT

Cytofluorimetric and reverse-transcription polymerase chain reaction (RT-PCR) analysis showed that adriamycin-resistant (ADRR), but not sensitive (WT), MCF-7 human mammary carcinoma cell lines express alpha4beta1 and alpha5beta1 integrins. ADR(R) cells adhere to fibronectin (FN), and only alpha5beta1 is involved in cell adhesion to this glycoprotein, while alpha4beta1 mediates cell binding to the cellular counter-receptor VCAM-1. Proliferation assays showed that FN, but not VCAM-1, delivers a mitogenic signal to quiescent ADR(R) MCF-7 cells. The activating signal is mediated by alpha5beta1, since cell proliferation is inhibited in the presence of RGD peptide or specific antibody. Cell cycle analysis demonstrated that cell/FN interaction induces the re-entry of ADR(R) MCF-7 into S phase, and prevents them from undergoing serum deprivation-induced apoptosis. Our data suggest that the presence of alpha5beta1 on the resistant cells enables them to draw advantage from FN for both cell growth and survival.


Subject(s)
Breast Neoplasms/metabolism , Doxorubicin/pharmacology , Integrin beta1/metabolism , Receptors, Fibronectin/metabolism , Breast Neoplasms/drug therapy , Cell Adhesion , Cell Division , Drug Resistance, Neoplasm , Humans , Integrin beta1/physiology , Polymerase Chain Reaction , Receptors, Fibronectin/physiology , Tumor Cells, Cultured , Vascular Cell Adhesion Molecule-1/pharmacology
4.
Anticancer Res ; 16(2): 581-8, 1996.
Article in English | MEDLINE | ID: mdl-8687101

ABSTRACT

Cytofluorimetric and biochemical analysis in two different grade human bladder cancer cell lines showed that G3 EJ cells exhibited higher levels of alpha5beta1 and alpha6beta1 heterodimers, and the G2 RT112 cell line higher levels of alpha2beta1. Alpha6/beta4 receptor was detected only in RT112 cells. Adhesion assays with extracellular matrix proteins indicated that both cells bound to fibronectin, laminin and collagen 1, the adhesive properties being related to the integrin profile. Inhibition tests revealed that alpha5beta1 mediated adhesion to fibronectin, alpha3beta1 and alpha6beta1 to laminin, and that alpha2beta1 was the main mediator of adhesion to collagen I in both cell lines. In EJ but not in RT112 cells, tumor necrosis factor-alpha induced the upregulation of alpha2, which mediated increased adhesion to collagen I. The different effects of TNFalpha on the two cell lines were not attributable to differences in tumor necrosis factor responsiveness, as both cells expressed comparable levels of tumor necrosis factor receptor-1 and the tumor necrosis factor-inducible intercellular adhesion molecule-1.


Subject(s)
Carcinoma, Transitional Cell/metabolism , Integrin beta1/metabolism , Neoplasm Proteins/metabolism , Receptors, Antigen/physiology , Urinary Bladder Neoplasms/metabolism , Cell Adhesion/drug effects , Collagen/metabolism , Fibronectins/metabolism , Humans , Laminin/metabolism , Tumor Cells, Cultured , Tumor Necrosis Factor-alpha/pharmacology
5.
Anticancer Res ; 14(3A): 905-13, 1994.
Article in English | MEDLINE | ID: mdl-8074492

ABSTRACT

The modulatory activity of the polar solvent N-methylformamide (NMF) on the effects of hyperhermic treatment was investigated on a human melanoma cell line (M14). Cells treated with NMF alone (1% for 20 h), hyperthermia (Hyp) alone (42.5 degrees C for 2 h) and with the two different sequences of treatment (NMF-->Hyp and Hyp-->NMF) were analysed by scanning electron microscopy and fluorescence microscopy. Moreover, their clonogenic efficiency and adherence properties were assessed. The results obtained can be summarized as follows. (a) The sequence Hyp-->NMF appeared to be more cytotoxic than the reverse sequence or NMF and Hyp given alone. (b) Heat induced cell swelling and detachment from the substrate. The pretreatment with the polar solvent was capable of preventing such alterations. (c) Fluorescence microscopy revealed remarkable changes induced by hyperthermia on actin network, vimentin distribution and vinculin expression. NMF administration proved to be capable of modulating these changes. In particular, the actin and vimentin networks showed a quite normal arrangement in NMF-->Hyp treated cells and very altered patterns in cells treated with the reverse sequence. Concerning the effects on the adhesion plaques, revealed by vinculin labeling, a considerable increase in the expression of these structures was observed after NMF treatment. (d) A remarkable increase of the attachment to collagen I and laminin molecules was revealed in NMF treated cells, whereas heat exposure reduced the number of adherent cells. Considered all together, the results obtained indicate that the administration of NMF after hyperthermia enhances the cytotoxic effect and modifies cell adherence properties, responsible for dissemination and metastasis.


Subject(s)
Antineoplastic Agents/pharmacology , Formamides/pharmacology , Hot Temperature , Melanoma/pathology , Cell Adhesion/drug effects , Cell Survival/drug effects , Humans , Hyperthermia, Induced , Melanoma/ultrastructure , Tumor Cells, Cultured
6.
Anticancer Res ; 10(3): 565-77, 1990.
Article in English | MEDLINE | ID: mdl-2369079

ABSTRACT

The treatment of exponentially-growing B16 melanoma cells with teniposide causes a dose- and time-dependent decrease of cell survival. By means of the nucleoid technique, the formation of double strand breaks was demonstrated in the nuclei of the treated cells, indicating a possible involvement of topoisomerase II. DNA double strand breaks were rapidly but ineffectively repaired. Morphometric and densitometric analyses showed that teniposide treatment causes a considerable increase of nuclear area, nuclear DNA and cell size, associated with a lowering of the mitotic index to less than one hundredth of that of the controls. The cytocidal effect of VM-26 can be potentiated by the addition of a non-lethal dose of lonidamine, whose synergism is particularly evident at low teniposide concentrations.


Subject(s)
Antineoplastic Agents/pharmacology , Indazoles/pharmacology , Podophyllotoxin/analogs & derivatives , Pyrazoles/pharmacology , Teniposide/pharmacology , Tumor Cells, Cultured/drug effects , Animals , Cell Division/drug effects , Cell Line , Cell Nucleus/drug effects , Cell Nucleus/ultrastructure , Cell Survival/drug effects , Clone Cells , Drug Interactions , Drug Screening Assays, Antitumor , Melanoma, Experimental , Mice , Mitotic Index/drug effects , Tumor Cells, Cultured/cytology
7.
Invasion Metastasis ; 10(3): 142-69, 1990.
Article in English | MEDLINE | ID: mdl-2139872

ABSTRACT

Papain-immunized mice possess serum antibodies which cross-react with cathepsin-B- and cathepsin-H-like endopeptidases isolated from B16 melanoma cells. The growth rate, invasion and metastasis of both the B16 melanoma and the Lewis lung carcinoma were inhibited in mice immunized with papain. These animals presented an increased mean survival time as compared to the tumor-bearing nonimmunized controls. Quantitative microscopy suggested that vasodilation and edema, associated with tumor invasion, are, at least partially, sustained by proteolytic enzymes, being strongly reduced when tumor cells were inoculated in papain-immunized mice.


Subject(s)
Cysteine Endopeptidases , Lung Neoplasms/immunology , Melanoma, Experimental/immunology , Papain/immunology , Abdominal Muscles/anatomy & histology , Abdominal Muscles/pathology , Animals , Antibodies/immunology , Antibody Formation/drug effects , Caseins/metabolism , Cathepsin D/blood , Cathepsin D/immunology , Cathepsin D/metabolism , Cathepsin H , Cathepsins/immunology , Cathepsins/metabolism , Cell Division/drug effects , Cross Reactions/immunology , Electrophoresis, Polyacrylamide Gel , Immunization , Injections, Intraperitoneal , Lung Neoplasms/enzymology , Lung Neoplasms/pathology , Lung Neoplasms/secondary , Melanoma, Experimental/enzymology , Melanoma, Experimental/pathology , Mice , Neoplasm Invasiveness , Neoplasm Metastasis , Papain/metabolism , Transplantation, Heterologous
8.
Oncology ; 44(1): 17-23, 1987.
Article in English | MEDLINE | ID: mdl-3561923

ABSTRACT

Flunarizine, a calcium antagonist commonly employed in therapy for vascular diseases, enhances the in vitro and in vivo antitumor activity of vincristine on B16 melanoma cells. In the presence of flunarizine higher intracellular levels of vincristine were observed in vitro and for a longer time. B16 melanoma bearing mice treated with both the drugs presented a median survival time that was significantly longer than that of the controls. The possible mechanism of the enhancement is herein discussed.


Subject(s)
Flunarizine/pharmacology , Melanoma/pathology , Vincristine/pharmacology , Animals , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Cell Division/drug effects , Cell Line , Drug Resistance , Drug Synergism , Flunarizine/administration & dosage , Melanoma/drug therapy , Melanoma/mortality , Mice , Mice, Inbred C57BL , Vincristine/administration & dosage
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