Biomedical subjects

M Aliaga

Publications and source records attributed to M Aliaga.

At least 19 recordsLinked to original sources

PubMed2002

[Microsatellite analysis of the 3p13-p25 region in renal cell carcinoma in humans].

INTRODUCTION & OBJECTIVES: Interstitial and terminal deletions of different regions of the chromosome 3 have been associated with the development of human nonpapillary renal cell carcinomas. We performed a microsatellite analysis at the region 3p13-p25 to study the role of the short arm of chromosome 3 in the pathogenesis of Renal Cell Carcinomas. MATERIAL & METHODS: Renal tumor specimens and normal kidney tissue from 57 patients were obtained after radical nephrectomy and immediately snap-frozen. Blood samples were also obtained from each patient, immediately processsed and used as normal DNA. To detect allelic loss, we used 8 microsatellite markers covering the region 3p13-p25. Genetic alterations have been correlated with histology, nuclear grade, pathological stage and stromal cell infiltration. RESULTS: A total of 41 cases (71.9%) were clear cell renal cell carcinomas (CCRCC), 7 (12.3%) were chromophobe renal cell carcinomas, 5 (8.8%) were papillary renal cell carcinomas, and 4 (7%) oncocytic tumors. Microsatellite analysis showed loss of heterozigosity (LOH) in 73.2% of the CCRCCs, and in none of the remaining histologic types. Terminal deletions were detected in 53.3% of the nonpapillary RCCs with LOH, and the remaining nonpapillary RCCs showed multiple interstitial deletions (46.6%). A common region of deletion in 3p14.2 has been observed. Due to contamination with normal DNA, when stromal cell infiltration increases, less losses of heterozigosity are detected. We did not find a correlation between LOH at 3p and the nuclear grade, nor between LOH at 3p and the pathological stage. CONCLUSIONS: 1. Microsatellite analysis of LOH at 3p can be used for the differential diagnosis of renal tumors. 2. The evidence of multiple interstitial deletions in a great number of nonpapillary RCCs suggests that more than one gene should be involved in the development of nonpapillary RCC, and already present in early stages of oncogenesis. 3. The common region of deletion 3p14.2 suggests the presence of unstable sequences of DNA that play an important role in the pathogenesis of nonpapillary RCC. 4. LOH at 3p in most nonpapillary RCCs irrespective of the grade and stage, proves that these molecular alterations do not mark a more aggressive behaviour of the tumor.

Carcinoma, Renal Cell↗

PubMed1998

Multicentre survey on compliance with growth hormone therapy: what can be improved?

A survey was undertaken to evaluate compliance in Spanish patients receiving growth hormone treatment. The 28-item structured questionnaire was designed to collect data on compliance, treatment schedule, device used and instruction received. In total, 473 questionnaires were completed in 17 paediatric endocrine units. Compliance was divided into four categories based on percentage of doses omitted, classified as excellent if 0%, good <5%, fair 5-10% and poor >10%. The level of compliance was excellent in 74.0%, good in 20.1%, fair in 3.4% and poor in 2.5%. Compliance was better in those who injected themselves (p < 0.01), were trained by hospital staff (p < 0.01) and used automatic pens (p < 0.05). Patients using conventional syringes were less likely to comply (p < 0.05). More information on growth hormone treatment was requested by 57.6% of patients. The results indicate that the specialist nurse should spend sufficient time with the patients and relatives to ensure a higher compliance rate.

Adolescent↗

PubMed1997

[Mid-term evaluation of a help program for smokers].

BACKGROUND: Medical counsel to smokers is an intervention that has proved useful to motivate smokers to stop smoking. This study pretends evaluate the long-term impact (2 years and 9 months) of systematic and structured health counsel on the smoke habit from the primary health care. MATERIAL AND METHODS: In April 1990, in four primary care centers from Barcelona and Zaragoza, Spain, a program of systematic counselling to stop smoking with an offer of subsequent follow-up was initiated in all adult smokers (15-65 years of age). According to the answer, every patient was classified on one of seven established categories that allowed a individualized follow-up. Data from the total population included in the program from the beginning till January 1993, are analyzed. RESULTS: From 683 known smokers (59.2% males and 40.8% women), 20 were excluded for different reasons and 343 were included in the program (56.4% cover). Average age of included smokers was 35.1 years (SE = 0.6) and average number of visits of 5.3 (SE = 0.2) which was significantly higher than those not included in the program (33.4; SE = 0.6, and 2.7; SE = 0.1). An average follow-up of 14.3 months (SE = 0.5) and of 2.6 (SE = 0.1) interventions on each individual were done. The average daily number of cigarettes was 18.4 (SE = 0.6) in the initial period and 13.3 (SE = 0.6) on the last program evaluation. The final answers showed a 18.1% of quitters and a decrease of more than 50% on the initial consume on 32.6%. In 12% the answer was negative. CONCLUSIONS: Programs of systematic help for smokers show a higher level of favourable responses than does normal counselling.

Adolescent↗

PubMed1992

Model of bronchial allergic inflammation in the brown Norway rat. Pharmacological modulation.

Exposure of non-sensitized Brown Norway (BN) rats to a 10%-ovalbumin aerosol induced an increase in the number of neutrophils in the broncho-alveolar lavage (BAL) fluid 3 and 6 h later but with no change in number of cells at 24 h. When the BN rats were actively sensitized (i.m. injection of 10 mg/kg ovalbumin and i.p. injection of killed Bordetella pertussis) and exposed 12-14 days later to a 10%-ovalbumin aerosol there was an increase in the number of eosinophils in the BAL fluid, maximal 24-48 h after the anaphylactic reaction. The increase in the number of neutrophils in the bronchial lumen 3 and 6 h after the anaphylactic reaction was larger than that obtained in non-specific inflammation and in contrast to this was still present 24-48 h after ovalbumin exposure. In passively sensitized BN rats exposed to ovalbumin aerosol, no inflammation appeared in the BAL fluid 24 h after the anaphylactic reaction. Various drugs, administered twice, 5 min and 5 h after the anaphylactic reaction, have been evaluated for their effects on the 24-h inflammation obtained in actively sensitized rats. Dexamethasone acetate (0.08 mg/kg i.p.) and theophylline (50 mg/kg i.p.) decreased the number of eosinophils and neutrophils. Ketotifen fumarate (12.5 mg/kg), cetirizine dihydrochloride (12.5 mg/kg), salbutamol (2 mg/kg), disodium cromoglycate (50 mg/kg) all given intraperitoneally, reduced the number of eosinophils. Tioxamast decreased the number of eosinophils at 12.5 mg/kg i.p. and by the oral route.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuterol↗

PubMed1991

Pharmacological modulation of a model of bronchial inflammation after aerosol-induced active anaphylactic shock in conscious guinea pigs.

Twenty-four hours after an active anaphylactic shock induced by inhalation of antigen in conscious guinea pigs sensitized by a large dose of ovalbumin in complete Freund's adjuvant, a noteworthy bronchial inflammation, characterized by increased numbers of neutrophils, mononuclear cells and eosinophils in the bronchoalveolar lavage fluid, was observed. Some drugs administered after the anaphylactic shock were investigated using this model. Disodium cromoglycate primarily reduced the number of mononuclear cells and eosinophils. Dexamethasone and theophylline decreased the number of eosinophils. Salbutamol and mepyramine increased neutrophils. Indomethacin did not give rise to any significant effect. This test appears to be of use for the investigation of anti-inflammatory compounds in the prophylactic treatment of asthma.

Albuterol↗

PubMed1991

Theophylline reduces pulmonary eosinophilia after various types of active anaphylactic shock in guinea-pigs.

The action of theophylline was studied on the inflammatory reaction obtained in bronchoalveolar lavage fluid 24 h after an active anaphylactic shock had been induced by ovalbumin inhalation in conscious sensitized guinea-pigs. The compound was administered twice by intraperitoneal administration after the anaphylactic reaction at a dose of 50 mg kg-1. When the guinea-pigs were sensitized by intramuscular injection of 30 mg kg-1 ovalbumin or by ovalbumin aerosol, theophylline reduced the number of eosinophils and mononuclear cells in the fluid. When animals were sensitized by intramuscular injection of 30 mg kg-1 ovalbumin mixed with Freund's complete adjuvant, treatment with the xanthine derivative decreased only the number of eosinophils. In the three models theophylline did not modify significantly the number of neutrophils. Thus theophylline always reduced pulmonary eosinophilia irrespective of the mode of sensitization used to induce anaphylactic shock.

Aerosols↗

PubMed1991

Bronchial inflammation and hyperreactivity after anaphylactic shock in guinea pigs actively sensitized by systemic or aerosol route.

Hyperreactivity and bronchial inflammation resulting from active anaphylactic shock induced by aerosol have been studied in guinea pigs after sensitization by intramuscular injection of large-dose ovalbumin or aerosol ovalbumin. When animals were sensitized by i.m. injection of 30 mg/kg ovalbumin, hyperreactivity to inhalation of histamine was obtained 1-3 h after shock. In bronchoalveolar lavage (BAL) fluid an increase in the number of eosinophils (6-48 h after shock) and neutrophils (6-24 h) was observed. When guinea pigs were sensitized by aerosol route, the hyperreactivity to histamine inhalation appeared 1-6 h after shock. In BAL fluid the number of mononuclear cells dropped (1-3 h) and then increased (24-48 h); the number of neutrophils (6-48 h) and eosinophils (24-48 h) increased. The results observed during these two types of sensitization were compared to those obtained after sensitization by injection of a large dose of ovalbumin mixed with Freund's complete adjuvant.

Aerosols↗

PubMed1990

Model of bronchial hyperreactivity after active anaphylactic shock in conscious guinea pigs.

A model of bronchial hyperreactivity at various times after an active anaphylactic shock in conscious guinea pigs is described. The bronchial inflammation was quantified in parallel by determination of the number of mononuclear cells, neutrophils, and eosinophils in bronchoalveolar lavage (BAL) fluids. The guinea pigs were sensitized by an intramuscular (i.m.) injection of a large dose of ovalbumin in Freund's complete adjuvant. The administration of ovalbumin (to induce anaphylactic shock) and of histamine to investigate bronchial hyperreactivity was by aerosol. The bronchial hyperreactivity to histamine was observed 3-6 hr after the anaphylactic shock. In the BAL fluid a decrease (1-3 hr) and then an increase (24-48 hr) in the number of mononuclear cells was found as well as an increase in neutrophils (3-48 hr) and in eosinophils (6-48 hr). The hyperreactivity was not correlated with changes in one category of cell in the BAL fluid. This model constitutes one simple test for investigating bronchial hyperreactivity in conscious guinea pigs. Further work is needed to try to determine the possible inflammatory parameters responsible for the hyperreactivity.

Administration, Inhalation↗

PubMed1990

Antiallergic and anti-inflammatory action of tioxamast in rats. I. Antiallergic activity in vivo and in vitro.

Tioxamast (F 1865) is an antiallergic drug that, administered systemically, reduces anaphylaxis in various models in rats. This action is due mainly to the inhibition of the synthesis and release of certain mediators. Orally or intraduodenally administered tioxamast inhibits IgE-dependent passive cutaneous anaphylaxis (ED50 = 0.8 mg/kg), IgE-dependent passive pulmonary anaphylaxis (ED50 = 0.5 mg/kg), and IgG-dependent passive cutaneous anaphylaxis (ED50 = 0.6 mg/kg). It has little or not effect on the increase of cutaneous capillary permeability induced by various mediators. In IgE-dependent passive peritoneal anaphylaxis in rats, tioxamast reduces the release of histamine (IC50 = 0.024 micrograms/ml) and of beta-glucuronidase (IC50 = 0.102 micrograms/ml). Also, histamine release is inhibited in IgG-dependent peritoneal anaphylaxis (IC50 = 0.103 micrograms/ml). The antiallergic compound has less effect on the release of histamine induced by the compound 48/80 in the peritoneal cavity of rats (IC50 = 1.67 micrograms/ml). Tioxamast inhibits the synthesis in vitro of leukotriene B4 (LTB4) by peritoneal neutrophils from rats stimulated by A23187 (IC50 = 8.88 micrograms/ml). At higher tioxamast concentrations, metabolites of the cyclo-oxygenase pathway are inhibited at concentrations of the same order of magnitude as those that inhibit Naja naja phospholipase A2 (IC50 = 144 micrograms/ml). Tioxamast also reduces the production of free radicals by leukocytes from the pleural cavity of rats which had phagocytosed opsonized zymosan (IC50 = 5.21 micrograms/ml).

Anaphylaxis↗

PubMed1990

Antiallergic and anti-inflammatory action of tioxamast in rats. II. Anti-inflammatory action in vivo.

Tioxamast is an antiallergic drug that inhibits anaphylaxis in various models in rats, and it inhibits the release and synthesis of certain mediators of inflammation [see Tarayre et al., this issue]. Here we report that the drug also has an anti-inflammatory effect in vivo in various nonimmunological models in rats. It reduces zymosan-induced inflammation in the paw and pleural cavity, starting at doses from 1.5625 to 3.125 mg/kg given intraperitoneally. In pleurisy, tioxamast lowers the concentration of leukotriene B4 (LTB4) in the exudate, at doses from 50 mg/kg i.p. Also, at doses from 12.5 mg/kg i.p., the compound reduced PAF-acether-induced pleurisy and the concentrations of LTB4 and peptidoleukotrienes in the exudate. An anti-inflammatory action against carrageenin-induced edema of the paw was seen only at doses of 50 mg/kg i.p. or more. The anti-inflammatory and antiallergic effect of tioxamast makes it a potentially useful drug in the treatment of allergies in humans.

Animals↗

PubMed1990

Comparative actions of immunosuppressants, glucocorticoids and non-steroidal anti-inflammatory drugs on various models of delayed hypersensitivity and on a non-immune inflammation in mice.

Various models of delayed hypersensitivity (DH) were used in mice: contact hypersensitivity reactions to picryl chloride and oxazolone and reactions to methylated bovine serum albumin (MBSA) and sheep red blood cells (SRBC). Drugs of different classes were tested in these models by systemic treatment around the challenge period: non-steroidal anti-inflammatory drugs (cyclooxygenase inhibitors, and inhibitors of both cyclooxygenase and lipoxygenase); glucocorticoids and immunosuppressants (cyclosporin A. CsA; cyclophosphamide, Cy; methotrexate, Mtx; azathioprine, Aza). These compounds were also studied and compared for their effects on the 3-h and 24-h phase of the carrageenin mouse-paw edema (in which inflammation is maximal after 24 h). Non-steroidal anti-inflammatory drugs (including double inhibitors of cyclooxygenase and lipoxygenase) had little or no effect on DH models, except indometacin. Glucocorticoids inhibited all immune reactions except that to MBSA. Of the immunosuppressants, CsA reduced all the DH reactions while Aza mainly reduced the reaction to SRBC; Cy and Mtx were mainly active on SBRC and MBSA inflammations. On another hand CsA, Cy and Mtx were inactive on the 3-h phase but decreased the 24-h phase of carrageenin edema. At doses active on the DH models and on carrageenin inflammation, Cy induced a lasting blood leukopenia, but CsA and Mtx did not. This combination of tests in the mouse seems to be of interest to demonstrate any action on DH and any anti-inflammatory effect and to suggest whether these activities are related to a possible leukopenic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Hypotheses on a possible role of some mediators in various inflammatory reactions on mouse ear.

Thanks to local application of various compounds that inhibit the effects or the synthesis of histamine, serotonin, prostaglandins, thromboxanes and leukotrienes, hypotheses are proposed about the possible role of these mediators in various experimental inflammations induced on mouse ear: reactions to arachidonic acid, croton oil and cantharidin (6-h and 24-h phases); primary irritation and delayed hypersensitivity reaction to picryl chloride; and semi-delayed (6-h) and delayed (24-h) hypersensitivity to oxazolone. Histamine seems to play a major role in the acute phase (6-h) of the reaction to cantharidin and in the primary irritation due to picryl chloride. Serotonin seems to be more involved in edema due to arachidonic acid and to croton oil and in the semi-delayed phase of hypersensitivity to oxazolone. Leukotrienes seem to have a more pronounced role in arachidonic-acid-induced inflammation and in the primary irritation and delayed hypersensitivity reactions to picryl chloride. Prostaglandins and/or thromboxanes might have some influence in edema due to arachidonic acid and to croton oil, and in the primary irritation reaction to picryl chloride.

Animals↗

PubMed1988

Comparison of the cutaneous/systemic antiinflammatory activity ratios for desonide and hydrocortisone in various experimental models.

The ratios of antiinflammatory activity after oral administration (oral ED50/cutaneous ED50) for desonide (Locapred) and hydrocortisone (hydrocortisone acetate) were compared in various nonimmunological and immunological experimental models on mouse ears: edema induced by croton oil; primary irritation due to picryl chloride; the acute phase (6 h) and the beginning of the chronic phase (24 h) of inflammation due to cantharidin; delayed contact hypersensitivity to picryl chloride; and the semi-delayed (6 h) and delayed (24 h) phases of contact hypersensitivity to oxazolone. These investigations showed that, besides having a better antiinflammatory effect, desonide had a better ratio of local activity to systemic effect in all the models. In addition, by contrast with orally active doses, locally active doses did not induce any thymolytic effect. Such results were confirmed in rats in which desonide reduced 24 h carrageenin abscess after cutaneous application without any significant thymolytic effect. Hydrocortisone was inactive.

Abscess↗

PubMed1987

Pharmacological modulation of PAF-acether-induced pleurisy in rats.

Injection of platelet-activating factor (PAF-acether) into the pleural cavity of rats induced the accumulation of a moderately intense exudate within 30 to 60 minutes. By comparison with animals given injections of the vehicle alone, the animals given this mediator had elevated levels of leukotriene C4-immunoreactive material (LTC4 im) in the exudate and decreased quantities of thromboxane B2 (TxB2) and of 6-Keto-F1 alpha-prostaglandin (6-Keto PGF1 alpha). Nifedipine, verapamil, and diltiazem reduced the pleural exudate with no major effect on the mediators. Both salbutamol and theophylline reduced the exudate and the levels of LTC4 im. Acetylsalicylic acid, phenylbutazone and indomethacin significantly inhibited the exudate, greatly lowered the quantities of cyclooxygenase derivatives and tended to increase LTC4 im. Phenidone, which inhibits the cyclooxygenase and lipoxygenase pathways, decreased the exudate and the three mediators. The phospholipase A2 inhibitor, chloroquine, decreased both the amount of exudate and moderately the concentration of LTC4 im. The glucocorticoids studied had no effect on the exudate or on the mediators. These results suggest that the role of the increased LTC4 im in the induction of the pleurisy is not clear.

6-Ketoprostaglandin F1 alpha↗

PubMed1987

Cutaneously applied erythromycin base reduces various types of inflammatory reactions in mouse ear.

Erythromycin base was tested by brushing a solution onto the skin in various models of non-immune and immune inflammation produced in mouse ear, namely inflammations induced by croton oil and cantharidin, primary irritation by picryl chloride, and contact hypersensitivity reactions to oxazolone and picryl chloride. On the non-immune inflammations, erythromycin displayed a greater effect than indomethacin, phenylbutazone or acetylsalicylic acid, though less than that of hydrocortisone acetate. It inhibited the hypersensitivity reactions less well. These results suggest some participation of an anti-inflammatory mechanism in the clinical effectiveness of cutaneously applied erythromycin base in some forms of acne.

Administration, Topical↗

PubMed1986

Inflammatory action of PAF-acether in the rat pleural cavity.

The injection of PAF-acether into the pleural cavity of the rat induced a maximal exudate after 30-60 min which then decreased and disappeared after 24 hours. In addition, the mediator produced a decrease in the number of leukocytes in the pleural cavity 30 min after injection and an increase in the number of cells after 6 hours.

Animals↗

PubMed1984

Lotifazole (F 1686), a non-steroidal anti-inflammatory agent with an unusual pharmacological spectrum.

Lotifazole (F 1686) - 4-phenyl-2-(2',2',2-trichloroethoxycarboxamido) thiazole - has a range of anti-inflammatory activities in animals that differs from the activities of classic non-steroidal drugs. It reduces carrageenin-induced oedema in rats, UV-induced erythema in guinea pigs, and Arthus pleurisies in rats only at high doses. It does not affect Freund's-adjuvant polyarthritis, and it only slightly affects passive skin anaphylaxis in rats and anaphylactic shock in guinea pigs. Lotifazole does not greatly inhibit prostaglandin synthesis. However, at low doses and after various conditions of treatment, F 1686 reduces PPD- and Bordetella- pertussis-induced delayed-hypersensitivity pleurisy in guinea pigs and rats, respectively, and contact hypersensitivity reactions to picryl chloride and oxazolone in mice. Its action on the two models of delayed-hypersensitivity pleurisy is reflected in a decrease of the pleural exudate and of the number of mononuclear cells in the focus of inflammation. At active doses, Lotifazole does not cause changes in the differential leukocyte count in normal animals. It appears, furthermore, to be a T-lymphocyte stimulant.

Anaphylaxis↗

PubMed1984

Pharmacological study of cantharidin-induced ear inflammation in mice.

Cantharidin applied to the Swiss mouse ear induced a clearly observable inflammatory reaction after 6 hr, maximal after 24 hr, and persisting several days. Desonide and hydrocortisone strongly inhibited the acute (6 hr) and delayed (24 hr) phases after their local application, while, after oral treatment, a reduction in the acute edema was obtained only when using high doses. The cutaneous application of high doses of mepyramine, disodium cromoglycate, methysergide, and (at a quite lower level) cimetidine reduced the 6-hr inflammation. Phenylbutazone and acetylsalicylic acid showed little activity on the same phase after their cutaneous administration. All the nonsteroid compounds produced little or no effect on the 24-hr inflammation after their cutaneous application and were quite inactive on both phases after their systemic treatment. The cantharidin-induced inflammatory reaction in Swiss mouse seems thus to be characterized by two phases. The chronic delayed phase is an example of chronic inflammation without the involvement of immunological processes. Histamine and serotonin might be involved in the acute inflammation.

Administration, Oral↗