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Biomedical subjects

A Grilli

Publications and source records attributed to A Grilli.

At least 37 records · Page 2Linked to original sources
PubMed1999

Impact of extremely low frequency electromagnetic fields on CD4 expression in peripheral blood mononuclear cells.

There is increasing evidence suggesting that extremely low frequency electromagnetic fields (ELF-EMF) may influence several cell functions. Here the effects of ELF-EMF were studied on the expression of CD4+ cell surface receptors of human peripheral blood mononuclear cells (PBMC) using fluorescence-activated cell sorter (FACScan). The expression of CD4+ in ELF-EMF exposed (24, 48 and 72 h) and not exposed PBMC were not statistically significant. In addition, a flow cytometric analysis was determined by using a fluorescent labeled antibody, at 24 and 72 h incubations. The amount of bound antibody was distributed with a slight difference in the ELF-EMF-exposed PBMC compared to the not exposed cells. Moreover, DNA CD4+ expression in PBMC strongly increased in exposed cells, resting and activated with Phytohaemaglutinin (PHA). When polymerase chain reaction was performed on CD4+ mRNA of PBMC an increase of CD4+ mRNA expression was found after the resting cells were exposed to ELF-EMF at 24 h compared to not exposed cells, while at 48 and 72 h no difference was found. In the cell cycle progression analysis, the PBMC exposed to ELF-EMF presented a significant increase of percentage expression of cell cycle progression in the S phase compared to not exposed cells; while in G1 and G2 phases, there were no differences. Our results provide new evidence that ELF-EMF can affect CD4+ expression in PBMC and describe an additional biological activity for ELF-EMF affecting CD4+ transcription and translation protein and the increase of the percentage expression of the cell cycle progression of the S phase.

Blotting, Western↗
PubMed1999

Immunocytochemical localization of phospholipase C isozymes in cord blood and adult T-lymphocytes.

The response of T-cells to peptide antigen plus major histocompatibility complex (MHC) consists of a series of cellular events collectively called T-cell activation. An essential component of this pathway is phospholipase C (PLC)gamma1, whose hydrolytic activity increases rapidly after binding of ligands to the T-cell receptor (TCR) and consequent activation of tyrosine kinases. Recent studies also suggest a GTP binding protein-dependent activation of PLCbeta during the early steps of T-cell activation. On the basis of these findings, we first checked the expression of PLC isoforms by Western blotting and by confocal and electron microscopy techniques, and then we looked for the phosphoinositide breakdown induced by CD3 engagement in cord and adult T-lymphocytes. Our results indicated that PLCbeta1 was almost exclusively expressed in cord T-cells, whereas PLCbeta2 was more strongly represented in the adult. The amount of PLCgamma1 was found to be larger in the adult than in cord cells. No significant differences were found in PLCgamma2 and delta2 expression. PLCdelta1 was scarcely detectable. On CD3 stimulation, adult lymphocytes gave rise, as expected, to a dramatic increase in phosphoinositide breakdown, whereas in cord cells this response was scarcely detected. These results indicate that a shift in PLC expression occurs in the postnatal period and that this change is associated with induction of the capability to respond to CD3 engagement with phosphoinositide hydrolysis.

Adult↗
PubMed1998

Does chronic hypoxia increase rat carotid body nitric oxide?

The carotid body plays an important role in ventilatory adaptation during chronic hypoxia. Nitric oxide (NO) may act as a regulator in neurotransmission, influencing the carotid body chemosensory discharge. The aim of the study was to understand if NO could contribute to the adaptation process during chronic hypoxia. The rats were kept in chronic hypoxia (10-11% inspired oxygen) for 12 days, while the controls were kept in room air (21% O2). The distribution for diaphorase activity and immunohistochemistry for nitric oxide synthase (NOS) showed that chronic hypoxia induces an increase in NOS activity in the carotid body. It was concluded that NO release increased during chronic hypoxia and causes an inhibitory effect on carotid chemosensory discharge of the rat carotid body.

Adaptation, Physiological↗
PubMed1998

Mast cell recruitment after subcutaneous injection of RANTES in the sole of the rat paw.

The effect of hrRANTES was studied after the injection in the sole of the rat paw, an area particularly rich in mast cells. Subcutaneous injections of RANTES 50 ng/10 microl produced an erythematous reaction which was inhibited by anti-RANTES antibody 50 microg/rat injected in the tail vein 30 min before hrRANTES 50 ng/10 microl was injected. In another set of experiments the animals were injected subcutaneously in the sole of the paw with PBS 10 microl (control), LPS (100 ng/10 microl) hrRANTES 50 ng/10 microl or anti-RANTES 50 microl/rat injected in the tail vein 30 min before hrRANTES 50 ng/10 microl was injected. The biopsies were analysed after 4 h and counted in an optic field. hrRANTES produced a strong recruitment of mast cells selectively coloured with 0.1% toluidine blue and inhibited by anti-RANTES antibody. In addition to the optical and electron microscope study, in some of the excised tissue Northern blot analysis for histidine decarboxylase (HDC) mRNA was performed to estimate the amount of histamine generation in the tissue of the injection sites. We found that subcutaneous injections of hrRANTES 50 ng/10 microl in the sole of the rat paw produced an accumulation of a great number of mast cells compared to PBS 10 microl (negative control) or LPS 100 ng/10 microl (positive control) after 4 h. The hrRANTES effect was inhibited by anti-RANTES antibody injected in the tail vein 30 min before hrRANTES exposure. Moreover, hrRANTES increased HDC mRNA and histamine generation.

Animals↗
PubMed1998

An emerging superbug. Staphylococcus aureus becomes less susceptible to vancomycin.

The name staphylococcus aureus comes from the Greek, staphyle (a bunch of grapes), kokkos (berry shaped), and aureus (golden). Morphologically, the pathogen resembles grapelike clusters of gram-positive cocci. The illustration here shows the bacteria infecting nasal epithelial tissue, and causing cell damage and inflammation. S. aureus has been knocking down our antibiotic defenses one by one, with some strains becoming dangerously less susceptible to vancomycin. Epidemiologists warn that these strains are coming soon to a hospital near you; be prepared by knowing how to identify the bug, notify infection control authorities, and use basic infection control procedures.

Anti-Bacterial Agents↗
PubMed1997

Massive infiltration of basophilic cells in inflamed tissue after injection of RANTES.

Regulated upon activation normal T expressed and secreted (RANTES) is a new inducible protein member of the human C-C branch of chemokines. RANTES is a potent monocyte and lymphocyte chemoattractant and is a mediator of inflammatory responses. In these studies we found that RANTES 10 ng/50 microl chemoattracts basophilic cells in a dose-dependent manner 4 h after an intradermal injection in rat skin sites, as revealed by optic microscopy. Moreover, in biopsy specimens from rat skin injection sites histamine release was significantly higher (P < 0.05) than in controls (PBS 50 microl) after 4 h from RANTES treatment. The presence of basophilic cells in rat skin injection sites after RANTES-treatment was also confirmed by electron microscopy studies. In addition, histidine decarboxylase (HDC) mRNA was increased in rat skin sites injected with RANTES compared to sites injected with PBS (controls). Our report describes additional biological activities for RANTES, suggesting that this human chemoattractant protein may play a fundamental role in histamine and HDC generation, along with basophilic cell recruitment.

Animals↗
PubMed1996

Vanadate as factor of cardiovascular regulation by interactions with the catecholamine and nitric oxide systems.

The effects of 1 microgram/mL of vanadium, given for 12 mo as sodium metavanadate in drinking water, on cardiovascular and biochemical indices of male rabbits were investigated. At the end of the exposure period, vanadium was more accumulated in bones and kidneys than in spleen and liver; the cardiac ventricles and the aorta contained similar amounts of this element. Blood pressure and heart rate were unchanged in the vanadate-exposed animals since the observed decrease of both cardiac inotropism and stroke volume was counteracted by an increase of peripheral vascular resistance, with reduction of arterial blood flow. The arterial levels of sodium, potassium and aldosterone were unmodified by vanadate which, however, strongly raised those of noradrenaline, adrenaline, L-DOPA, and dopamine. Vanadate caused a marked increase of the activity of monoamine oxidase in renal tubules and liver (probably in relation to the increased plasma catecholamine levels) and a reduction of that of glucose-6-phosphate dehydrogenase in the kidney. There was also evidence that vanadium reduces synthesis and/or release of nitric oxide, the endothelium-derived vasodilating factor, likely through a reduced formation from bradykinin. It was concluded that vanadium may represent an environmental factor of altered cardiovascular homeostasis.

Animals↗
PubMed1993

Inhibition of granuloma formation induced by potassium permanganate in the mouse by a specific human recombinant receptor antagonist for interleukin-1 (hrIL-1ra).

Interleukin-1 (IL-1) is a polypeptide which mediates several systemic changes associated with infection, inflammation and injury, such as fever, neutrophilia, increased acute phase protein synthesis, and arachidonic acid metabolites. Recently, a natural inhibitor of IL-1 has been cloned, called IL-1 receptor antagonist (IL-1ra), which prevents Escherichia coli-induced shock in rabbits and blocks PGE2 induced by IL-1. In this report we study the effect of human recombinant (hr) IL-1ra on chronic inflammation induced by dorsal injections of 200 microliters of a 1:40 saturated crystal solution of potassium permanganate (KMnO4) in mice. After 7 days, all mice developed a subcutaneous granulomatous tissue indicative of a chronic inflammatory response, at the site of injection. KMnO4-treated mice, injected intraperitoneally twice with hrIL-1ra, 20 micrograms/dose (the first at the same time of induction of the granuloma and the second 24 hr later), show significant decreases in size and weight of the granuloma when compared to mice not treated with hrIL-1ra (controls); the inhibitory effect was approximately 32-46 and 25-51%, respectively. In addition, in all mice treated with hrIL-1ra, there was a strong inhibition of PGE2 and LTB4 on assay of freshly minced granuloma tissue. Moreover, when hrIL-1 beta (1.0 ng/ml) or LPS (100 ng/ml) were added overnight to the minced granuloma tissue cultures, these compounds enhanced the production of LTB4 and PGE2 from the untreated mice, whereas in IL-1ra-treated mice they failed. In the histological studies of the granuloma, animals treated with hrIL-1ra show a lesser degree of mononuclear cell (MC) accumulation. The inhibitory effect of hrIL-1ra on PGE2 production was also confirmed on peritoneal macrophages from untreated mice, stimulated overnight with hrIL-1 beta or LPS in vitro. The resulting inhibition was dose-dependent. In these studies we show, for the first time, the anti-inflammatory effect of hrIL-1ra on chronic inflammation as assessed by the inhibition of granuloma formation, PGE2, LTB4, and white cell accumulation in inflamed tissue.

Animals↗
PubMed1993

Human recombinant interleukin-1 receptor antagonist (hrIL-1RA) inhibits prostaglandin E2 (PGE2) generation but not alkaline phosphatase activity in in vivo chronic granulomatous tissue induced by KMnO4.

Interleukin-1, a soluble polypeptide, plays an important role in inflammatory reactions by increasing prostaglandin E2 (PGE2) generation. Human recombinant IL-1 receptor antagonist (hrIL-1ra) is a natural inhibitor of IL-1 which blocks its activity in several inflammatory states. In these studies we found that hrIL-1ra (250 mg/ml) inhibits the generation of PGE2, as measured by RIA method, in minced mouse granuloma tissue (700 mg) treated overnight with LPS (10-1000 ng/ml) or hrIL-1 beta (0.1-10 ng/ml). In addition, we show that hrIL-1ra (250 ng/ml) strongly inhibited IL-1 alpha and IL-1 beta, as measured by ELISA method, in the minced granuloma tissue treated overnight with LPS 1 micrograms/ml or IL-1 beta (10 ng/ml). The granuloma tissue induced in mice by a dorsal subcutaneous injection (0.2 ml) of a saturated solution (1:40 dilution) of KMnO4 crystals, presented an alkaline phosphatase activity which was not inhibited by two intraperitoneal administrations of hrIL-1ra 20 micrograms/200 ml bolus injections (given at the same time as KMnO4 injection and one 24 h later). These results show for the first time that hrIL-1ra blocks PGE2, IL-1 alpha and IL-1 beta but not alkaline phosphatase activity, which is a marker in growing bone and in calcific and inflamed tissue.

Alkaline Phosphatase↗
PubMed1992

[Participation of tyrosine residues of myoglobin in the disproportionateness reaction of heme iron (II) and (IV)].

By means of the comparison of the constant oxidation reactions of both the myoglobin modified by N-acetylimidazole and the intact myoglobin in the presence of H2O2 or ferrylmyoglobin we characterized the role of the tyrosine residues (Tyr) of myoglobin in the synproportionation reaction between heme iron (II) of one molecule and heme iron (IV)--of another. It was demonstrated that Tyr derivatization resulted in the decrease of the velocity of redox interaction between deoxymyoglobin (II) and ferrylmyoglobin (IV) and led to the decrease of the efficiency of oxymyoglobin deoxygenation. The effects were shown to be independent on Tyr quantity in myoglobin molecule and to have the same character for both the sperm-whale myoglobin and the horse myoglobin.

Animals↗
PubMed1991

Basophil-bound and serum immunoglobulin E directed against Helicobacter pylori in patients with chronic gastritis.

The immunoglobulin (Ig) E immune response in patients with Helicobacter pylori-associated chronic gastritis has been evaluated. Of 26 patients with H. pylori infection, 22 (84%) tested positive for basophil-bound specific IgE (determined by the histamine release test) and 18 (69%) for serum specific IgE (determined by an enzyme-linked immunosorbent assay). In contrast, only 1 of 17 persons in whom the bacterium was not detected presented cell-bound and serum specific IgE. In the 4 histamine release test--positive but enzyme-linked immunosorbent assay--negative patients, removal of antibody from the basophil surface by acid elution showed that histamine release occurred through an IgE-dependent mechanism. When normal basophils, passively sensitized with serum from IgE-positive patients, were exposed to the H. pylori antigen, a significant release was observed, confirming the class specificity of the response. Inhibition experiments with bacteria other than H. pylori showed that the IgE antibody was specifically directed against this organism. The percentage of antigen-induced histamine release did not correlate with serum specific IgE level. However, the response of basophils to antigenic challenge was proportional to IgE-dependent cellular releasability. This finding suggests that target cell sensitivity may be the most important factor in determining the entity of biological response to the antigenic challenge. The ability of H. pylori to induce a specific IgE immune response could answer key questions regarding the mechanisms inducing gastric inflammation.

Chronic Disease↗
PubMed1991

The serological diagnosis of human hydatid disease by time-resolved fluoroimmunoassay.

The use of a new immunoassay, time-resolved fluoroimmunoassay (TR-FIA), in the diagnosis of human hydatid disease has been evaluated. This technique, which is based on the labelling of antibodies with europium (Eu), was compared with a well-established method, the enzyme linked immunosorbent assay (ELISA). Of 102 patients with hydatid disease, 97 (95.1%) were positive according to TR-FIA and 83 (81.4%) according to ELISA. The rate of non-specificity for other parasitic infections (n = 206) was 8.7% for TR-FIA and 17.5% for ELISA. It is concluded that TR-FIA is more sensitive and more specific than ELISA in the diagnosis of human hydatid disease.

Animals↗
PubMed1991

Glutathione transferase isoenzymes in normal and neoplastic human kidney tissue.

Glutathione transferase (GST) activity in the cytosolic fractions of renal cortex tumour was found to be significantly lower (215 +/- 156 mU/mg) than that present in the corresponding non-tumour (466 +/- 278 mU/mg) tissues. Using the immunoblotting technique, glutathione transferase isoenzymes expression in both tumour and non-tumour kidney was investigated. Alpha and pi class glutathione transferases were the most abundant enzymes in non-tumour kidney and were expressed by all samples investigated. Immunofluorescence analysis indicated that the pi class enzymes are localized mainly in the distal convoluted tubules, whereas alpha class enzymes are localized in the proximal tubules. In the tumour moiety the alpha class GST appears to be absent or expressed at low level as compared with non-tumour samples. On the contrary, no significant differences in the expression of pi class GST were found in tumour as compared with non-tumour tissues. Mu class GST protein was detected in 12 of 26 samples tested. When present, mu class GST constitutes a few per cent of total GST protein. Immunofluorescence studies indicate that mu class GSTs are localized within the distal convoluted tubules. According to the electrophoretic mobility at least two different mu GST subunits (26.5 and 27.5 kd) were found. In one sample only the faster mu class GST subunit was present, two samples expressed both types of GST subunits, whereas nine samples expressed only the slower GST subunit. With the exception of one sample, a reduction of mu class GST expression was seen in tumour as compared with non-tumour tissues. The decrease of activity seen in the cytosolic fraction of tumour kidney must be ascribed mainly to a reduction or to a lack of expression of alpha class GST and to a lesser extent of mu class GST.

Adult↗
PubMed1990

Glutathione transferase isoenzymes from human prostate.

By using affinity-chromatography and isoelectric-focusing techniques, several forms of glutathione transferase (GSTs) were resolved from human prostate cytosol. All the three major classes of GST, i.e. Alpha, Mu and Pi, are present in human prostate. However, large inter-individual variation in the qualitative and quantitative expression of different isoenzymes resulted in the samples investigated. The most abundant group of prostate isoenzymes showed acid (pI 4.3-4.7) behaviour and were classified as Pi class GSTs on the basis of their immunological and structural properties. Immunohistochemical staining of Pi class GSTs was prevalently distributed in the epithelial cells surrounding the alveolar lumen. Class Mu GSTs are also expressed, although in small amounts and in a limited number of samples, by human prostate. The major cationic isoenzyme purified from prostate, GST-9.6; (pI 9.6; apparent subunit molecular mass of 28 kDa), appears to be different from the cationic GST alpha-epsilon forms isolated from human liver and kidney as evidenced by its structural, kinetical and immunological properties. This enzyme, which accounts for about 20-30% (on protein basis) of total amount of GSTs, is expressed by only 40% of samples. GST-9.6 has the ability to cross-react in immunoblotting analysis with antisera raised against rat liver GST 2-2, rather than with antisera raised against members of human Alpha, Mu and Pi class GSTs. Although prostate GST-9.6 shows close relationship with the human skin GST pI 9.9, it does not correspond to any other known human GST.

Aged↗
PubMed1990

Basophil releasability in human hydatidosis.

We studied immunoglobulin E (IgE)- and non-IgE-mediated releasability in basophils from 31 patients with hydatidosis. Histamine release to non-IgE-dependent stimuli did not differ significantly between normal individuals and patients with hydatidosis. On the contrary, an increased histamine liberation was obtained by challenging basophils from hydatid patients with anti-human IgE. It is concluded that Echinococcus granulosus infection induces an enhanced sensitivity of basophils to IgE-dependent stimuli.

Animals↗