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Biomedical subjects

E Alesse

Publications and source records attributed to E Alesse.

48 records · Page 3Linked to original sources
PubMed1984

[Effect of calcium ionophore (A23187) on the production of thromboxane B2 in human polymorphonuclear cells in vitro].

Polymorphonuclear leukocytes (PMN) are capable to produce prostaglandins in vivo and in vitro, and thromboxane B2 (TXB2) which is the main metabolite of arachidonic acid in these cells. In the present work we studied, with radioimmunoassay method, the effect of calcium ionophore A23187 on PMN. This substance is capable to stimulate TXB2 release by PMN and its effect is inhibited by indomethacin.

Calcimycin↗
PubMed1983

Reduced mitogenic stimulation of human lymphocytes by extremely low frequency electromagnetic fields.

Blastogenesis of human peripheral blood lymphocytes stimulated in vitro by non-specific mitogens (PHA, ConA, PWM) upon exposure to extremely low frequency EMF has been studied. Different frequencies of square waveforms have been used. PHA-stimulation resulted in strong inhibitions as measured by [3H]thymidine incorporation. A frequency window (3-50 Hz) within which ConA-induced blastogenesis was significantly inhibited has been individuated. The mitogenic effect of PWM was significantly affected only at 3 Hz.

Adult↗
PubMed1983

Effect of salicylates on lymphocyte blastogenesis in vitro: association with other non-steroid anti-inflammatory drugs.

High concentrations of the non-steroid anti-inflammatory drugs, alone and in association, reduce the blastogenesis of human lymphocytes in vitro. This effect is probably due to the toxicity of these agents and not to the inhibition of prostaglandin (PG) prosuction. Therefore drugs, such as, salicylates and associations of salicylates with other non-steroid anti-inflammatory drugs, which have a weak action on PG-synthesis, also inhibit proliferation of lymphocytes.

Anti-Inflammatory Agents↗
PubMed1982

[Effect of the association of caffeine-indomethacin on the production of prostacyclin in the rat stomach].

Prostaglandin (PG) E1, PGD2 and the unstable PGI2 are inhibitors of human platelet aggregation and increase the concentration on cAMP in human platelets, presumably by stimulation of the adenylate cyclase. Methylxanthines exert their antiaggregatory effect by inhibiting the platelet cAMP phosphodiesterase. We examined whether caffeine-indomethacin is able to block PGI2 release from gastric mucosa less than the administration of indomethacin alone. PGI2 production was determined on aliquots of incubated mucosal strips, tested for ADP-induced aggregation of human platelet rich plasma. The obtained data indicate that the PGI2 production found in rats treated with the association was higher than that observed in rats treated with indomethacin alone. The present preliminary findings suggest that caffeine when given together with indomethacin reduces the indomethacin-induced inhibition of PGI2 release from the gastric mucosa.

Animals↗
PubMed1982

[Action of some salicylates associated with other non-steroidal anti-inflammatory drugs on the release of prostacyclin from the gastric mucosa of the rat].

In the present work it has been tested if associations of indomethacin or aspirin with diflunisal or sodium salicylate block PGI2 release from gastric mucosa less than the administration of the compounds alone. PGI2 production was determined on aliquots of incubated mucosal strips, tested for ADP-induced aggregation of human platelet rich plasma. The obtained data indicate that PGI2 generation found in rats treated with indomethacin or aspirin associated with diflunisal or sodium salicylate was higher than that found in rats treated with indomethacin or aspirin alone. This effect may be likely explained by competition between salicylates and other non steroidal anti-inflammatory drugs for binding sites on PG-synthetase and plasma proteins.

Animals↗
PubMed1980

["Granuloma pouch" reduction after treatment with indomethacin and diflunisal and collateral effects of these drugs on gastric mucosa].

In the present work it was determined the ability of non-steroidal anti-inflammatory drugs (Diflunisal and Indomethacin) to inhibit formation of "granuloma pouch" exudate induced in rats. This study shows that the combined administration of Diflunisal and Indomethacin exerts similar anti-inflammatory activity as the single drugs. There does not seem to be additive anti-inflammatory effects of the drugs in combination but, if anything, a weak antagonism. The association of the two compounds produces a reduced harmful effect on the gastric mucus.

Animals↗
PubMed1980

[The influence of levamisole in vitro on lymphocytes from an immunodeficient patient].

Cultures of lymphocytes from a patient with a suppressed immune-system were set up, and a low response was seen after treatment with mitogenic substances such as PHA and ConA. Other lymphocyte cultures from the same patient were treated with Levamisole, and after this it was noted that the percentage of T-cell rosettes with sheep erythrocytes was increased.

Animals↗
PubMedDate not supplied

In vivo cadmium treatment alters natural killer activity and large granular lymphocyte number in the rat.

The effects of oral exposure for nearly 6 months to Cd (200 or 400 ppm) on rat natural killer (NK) activity were investigated. No significant differences in body and thymus weights were observed. Peripheral blood lymphocyte (PBL) number was consistently higher in treated rats throughout the treatment; the number of spleen cells decreased during the first 50 days, and then reached a level higher than in controls. NK activity, evaluated in a 4-h chromium release assay against YAC-1 target cells, was altered in treated rats: lower up to day 30, and then higher. In parallel, a reduction of the large granular lymphocytes (LGL) was found initially in the peripheral blood of Cd-treated rats, followed by a persistent marked increase. These changes were closely correlated with the altered distribution of CD8+ aGM1+ CD5- cells, which mostly consist of NK cells. Fluorescence-activated cell sorter (FACS) analysis revealed a decrease of cell subset with a typical NK phenotype during the first 30 days of treatment and a clear increase thereafter. Post-exposure observations indicated that all these effects disappeared with a return to control values 2 months after cessation of treatment. These findings suggest that in vivo administration of Cd induces both inhibitory and stimulatory effects on rat NK cell number and cytotoxic activity, depending on time of exposure.

Animals↗
PubMedDate not supplied

Cadmium inhibits spontaneous (NK), antibody-mediated (ADCC) and IL-2-stimulated cytotoxic functions of natural killer cells.

Cadmium (Cd2+), an environmental contaminant, has been shown to inhibit, even if not totally, natural killer (NK) cell-mediated cytotoxicity and antibody-dependent cellular cytotoxicity (ADCC) of human peripheral blood lymphocytes in a dose- and time-dependent manner. The presence of Cd2+ during the early period of the cytotoxic assay was needed to obtain maximal inhibition. Preincubation of either effector or target cells with Cd did not result in any inhibitory effect. Cd2+ also inhibited the cytotoxic activities of effector cells prestimulated with IL-2 for 18 h or 4 days, which mostly consist of NK cells. Our results indicate that Cd2+ did not block effector-target conjugate formation, but rather interfered with the hydrolysis of phosphoinositides, as shown by the decrease of inositol trisphosphate (IP3), which is known to release stored Ca2+.

Antibody-Dependent Cell Cytotoxicity↗
PubMedDate not supplied

Combination therapy with cyclosporine and methotrexate in patients with early rheumatoid arthritis soon inhibits TNFalpha production without decreasing TNFalpha mRNA levels. An in vivo and in vitro study.

OBJECTIVE: To evaluate the ability of two different combination therapies with prednisone (PDN), methotrexate (MTX) and cyclosporine (CSA) to modulate both TNFalpha transcription and production in early rheumatoid arthritis (RA). METHODS: 24 patients with early RA received a step-down bridge therapy with MTX and PDN (group A). Twelve patients out of the 24 randomly received also CSA (group B). Blood samples and peripheral blood mononuclear cells (PBMC) were collected at different times. TNFalpha levels were measured both in sera and in PBMC supernatants. TNFalpha mRNA was assessed by use of RT-PCR. RESULTS: 10 patients in group A and 9 in group B improved. At baseline, RA patients serum TNFalpha levels were increased compared to controls (p < 0.001) and did not correlate with clinical and serological parameters. These levels decreased within the first month of therapy in both groups, the lower levels being observed in the sera of CSA treated patients. After 30 days of therapy, TNFalpha levels in group B supernatants were significantly lower than those observed in group A, both after 24 and 48 hours of PHA stimulation (p < 0.03 and p < 0.05 respectively). TNFalpha mRNA levels never differed between patients and controls, independently of both the clinical picture and the assigned therapy. CONCLUSION: The addition of CSA to a treatment regimen of PDN + MTX lowers TNFalpha production in vitro without decreasing TNFalpha mRNA expression. This effect could help to induce early immunosoppressive and therapeutic effects during RA.

Adult↗