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Biomedical subjects

M Selman

Publications and source records attributed to M Selman.

At least 109 records · Page 6Linked to original sources
PubMed1985

A new model of diffuse interstitial pulmonary fibrosis in the rat.

We have produced experimental diffuse interstitial pulmonary fibrosis in rats with a combination of low and repeated doses of paraquat plus continuous exposure to normobaric 74% O2 in the breathing air for several weeks. Pulmonary fibrosis was evaluated histologically and biochemically, through the determination of total collagen content in the lung. Our procedure is characterized by low initial mortality, the development of extensive distortion of the pulmonary architecture, and the presence of severe and diffuse interstitial fibrosis. The model was compared with bleomycin-induced pulmonary fibrosis in the same rat strain, in which the process is focal and leaves most of the lung unaffected. We conclude that lung damage produced by the combination of low doses of paraquat plus normobaric 74% O2 concentration in the breathing air is an adequate experimental model of diffuse interstitial pulmonary fibrosis as it occurs in many of the human cases of this condition.

Animals↗
PubMed1985

The duration of the pulmonary paraquat toxicity--enhancement effect of O2 in the rat.

The duration of the pulmonary paraquat toxicity-enhancement effect of O2 has been examined in Wistar rats. In one experiment, various groups of normal animals were given a single dose (5 mg/kg body wt) of paraquat and after different periods were exposed to continuous breathing of normobaric 74% O2 in airtight chambers until dead or up to 10 days. In a reverse experiment, a large number of rats were first exposed for 6 days to continuous breathing of normobaric 74% O2 and were then separated into various groups which received a single dose of paraquat (5 mg/kg body wt) after various periods of breathing normal air, ranging from 0 to 96 hr. The extent of pulmonary damage in both experiments was evaluated by histologic examination and by biochemical determination of total collagen content of the lungs. It was found that the duration of the pulmonary damage induced by paraquat that is enhanced by continuous breathing of high O2 concentration lasts 24 to 48 hr. It was also observed that 12 to 24 hr after paraquat administration and continuous breathing of high O2 concentration pulmonary lesions are severe and extensive, and in animals surviving 6 or more days there was also incipient interstitial fibrosis. The reverse sequence of treatment (O2 + paraquat) resulted in no mortality and no pulmonary lesions. Additional controls treated with each of the pulmonary toxins alone also revealed no lung changes.

Animals↗
PubMed1985

Increase of unidentified HLA antigens in pulmonary tuberculosis.

We studied the HLA-A, B,C and DR antigens in 50 patients with advanced pulmonary tuberculosis in an effort to detect some genetic factors which may predispose to the development of this disease. We found a decrease in HLA-A3, A9, B5, B8, B13, B17 and B27. The incidence of "double blank" antigens in the locus A was 18% (2.5% in controls, p less than 0.0005) in the locus B 16% (1.5% in controls, p less than 0.0005) and 28% in the DR locus (7% in controls, p less than 0.0005). Our results suggest that the cells responsible for the immune response in patients with tuberculosis appear to have a diminished number of HLA antigens serologically determined. That phenomenon could be explained by several hypothesis like poor expression of these proteins or masking for another substance. In spite of the mechanism, this abnormal membrane expression of HLA antigens could be important for the development of the disease since the cell-cell interactions critical for the mounting of an adequate immune response might not be appropriate.

Female↗
PubMedDate not supplied

Evaluation of adenosine deaminase activity in the Mycobacterium tuberculosis culture supernatants.

BACKGROUND: Adenosine deaminase (ADA) catalyzes hydrolytic and irreversible deamination of deoxyadenosine into deoxyinosine and of adenosine into inosine, and is related to lymphocytic proliferation and differentiation. The measurement of ADA activity in body fluids is a useful tool in the evaluation of mycobacterial infections. Elevated ADA activity has been found in pleural effusions of patients with pleural tuberculosis relative to those from patients with nontuberculous pleural diseases, and is mainly associated with cellular host factors such as monocyte-macrophages or lymphocytes. In contrast, there is little information about ADA activity measurement in mycobacteria culture supernatants. METHODS: We evaluated ADA activity as described by Giusti in the culture supernatants of eight Mycobacterium tuberculosis isolates. RESULTS: Mycobacteria culture supernatants did not display any ADA activity. CONCLUSIONS: This result supports the notion that Mycobacterium tuberculosis is not the source of ADA activity. However, increased ADA activity in biological fluids from tuberculosis patients might be due to the interaction of the mycobacterium with host factors.

Adenosine Deaminase↗
PubMedDate not supplied

Preoperative risk factors associated with mortality in lung biopsy patients with interstitial lung disease.

The objective of this study was to evaluate the risk factors associated with mortality in interstitial lung disease patients. We performed a retrospective study of 722 consecutive patients submitted for lung biopsy during the 1986-1990 period. Twenty-two (3%) died within the 30 days following surgery. Forty-four patients who survived after the surgery for the same time span were randomly chosen as control group. Dyspnea at rest was present in 18/44 of surviving group (SG) and in 18/22 of the nonsurviving group (NSG) (OR 6.5, 95% CI 1.8-22.4,p = .001). Systemic diseases (i.e., diabetes, systemic arterial hypertension)were mainly present in the NSG (OR 7.2, 95% CI 2.3-22.8, p < .001). The SG displayed significantly less respiratory insufficiency with a PaO2 of 52.2 + 8.4 versus 38.5 i 9.4 mm Hg, and PaCO2 of 28.8 i 4.5 versus 38.5 +/- 9.2 mm Hg, respectively (p < .001). Likewise, the SG exhibited a PaCO2/PaO2 ratio of 0.5 - 0.1, while in the NSG it was of 1 +/- 0.4 (p < .001), showing a sensitivity of 84% and specificity of 93% for mortality. Multiple logistic regression analysis for these variables showed that log likelihood was still significant for PaCO2 > 34 mm Hg, PaO2 <48 mm Hg, and comorbid diseases. Logistic regression analysis of these three variables showed the greatest sensitivity and specificity (84 and 750/0,respectively) for prediction of mortality. However, the strongest association was found when PaCO2/PaO2 ratio was analyzed alone (OR 21,073,CI 95% 28-15,946,357, p < .005). These data suggest that PaCO2/PaO2 ratio appears to be a predictor of mortality in this subset of patients. Its prospective use has reduced early mortality after surgery less than 1% in the last decade.

Adult↗
PubMedDate not supplied

[Hypersensitivity pneumonitis in Mexico City].

OBJECTIVE: To investigate the association between the urban area of origin of patients and the prevalence of hypersensitivity pneumonitis (HP), induced by avian antigens. MATERIAL AND METHODS: A case-control study was conducted in 1999 at the National Institute of Respiratory Diseases (NIRD). Cases were 109 consecutive HP patients and controls were 184 patients: 39 with idiopathic pulmonary fibrosis (IPF), 63 with pulmonary tuberculosis (PTB), and 82 with asthma. Mexico City and surrounding counties (SC) were divided into 5 geographical areas: 1) Downtown; 2) North-East (NE); 3) South-East (SE); 4) North-West (NW) and 5) South-West (SW). Statistical analysis consisted of calculation of disease prevalence by urban area; associations were assessed with odds ratios and 95% confidence intervals. Multivariate analysis with multiple logistic regression was performed to adjust for age, gender and socioeconomic level. RESULTS: Eighty HP cases were located in the NE southernmost and SE northernmost areas of Mexico City (48 and 32, respectively) (OR = 3.86; 95% CI 2.17-6.96). Thirty-six controls with asthma came from the SW area, (where NIRD is located) (p < 0.05), and four from SC. Controls with PTB and IPF were scattered throughout the study area. CONCLUSIONS: The NE southernmost and SE northernmost areas were associated with HP. The cause of HP may not be geographical; a garbage dump used to be located in this area, suggesting that exposure to organic particles might contribute to the development of HP in susceptible individuals.

Adult↗
PubMedDate not supplied

Propranolol-induced hyperreactivity in guinea-pig lung parenchyma strips: possible role of histamine.

In vivo and in vitro studies have demonstrated that beta-adrenoceptor blockers enhance the airway smooth muscle contraction to antigen, but the mechanisms are not fully understood. In the present work, we corroborated that propranolol (3.9 x 10(-6) M, 30 min incubation) induces hyperreactivity to antigenic challenge (cumulative concentration-response curve to ovalbumin, 0.01 to 100 micrograms/ml) in lung parenchyma strips from sensitized guinea-pigs. This hyperreactivity was enhanced by indomethacin (3.2 x 10(-5) M) and was unaffected by the lipoxygenase/cyclooxygenase inhibitor phenidone (1 x 10(-4) M). However, the histamine H1 receptor antagonist pyrilamine (1 x 10(-6) M) reduced the potentiation effect of propranolol. These results suggest that bronchoconstrictor prostaglandins, thromboxane A2 and leukotrienes, are not involved in the propranolol-induced lung parenchyma strips hyperreactivity to antigen in vitro, and that histamine may account, at least in part, for such propranolol effect.

Animals↗
PubMedDate not supplied

Role of leukotriene C4 and edema in the acute allergic bronchoconstriction in the guinea pig.

In vitro studies have suggested that leukotrienes are involved in acute allergic bronchoconstriction, though this has not been definitively corroborated yet in in vivo studies. On the other hand, edema production during antigenic challenge could be an additional factor favouring such bronchoconstriction. In the present work we quantified immunoreactive leukotriene C4 (iLTC4) concentrations in bronchoalveolar lavages during allergic bronchoconstriction induced by 1 mg/kg i.v. ovalbumin (OA) in immunized guinea pigs, as well as water content in guinea pig lung fragments obtained before and during this bronchoconstriction. We found that basal concentrations of iLTC4 (median 1.06 ng/ml) were not significantly modified at 2, 5 and 10 min (median 1.10, 0.29 and 1.37 ng/ml, respectively) of the bronchoconstrictor response. Water content in lung fragments did not change among non-immunized guinea pigs, immunized ones and at 15 min of bronchoconstriction (mean +/- SEM 79.32% +/- 0.18, 79.10% +/- 0.31 and 79.13% +/- 0.40%, respectively). In addition, isoproterenol (20 micrograms/kg, i.v.) rapidly reverted about 70% of the bronchoconstriction induced by a higher antigenic dose (OA, 3.1 mg/kg i.v.); residual obstruction was not associated with increased water content in lung fragments (78.13% +/- 0.43). These results suggest that in this model, acute allergic bronchoconstriction is not due to an increased iLTC4 release or to edema production, and that airway smooth muscle contraction is the main component of this response.

Animals↗
PubMedDate not supplied

Mutilans arthropathy in systemic lupus erythematosus.

The rare association of resorptive arthropathy with systemic lupus erythematosus is described in a 37-year-old female patient in order to emphasize the occurrence of aggressive joint abnormalities of the disease. This patient developed mild articular manifestations at the onset of the disease and 8 years later we detected mutilans changes in the DIP joints. Other diseases in which similar articular findings have previously been noted, were ruled out through the follow-up.

Adult↗
PubMedDate not supplied

Circulating autoantibodies in patients with pigeon breeder's disease.

Sera from 19 patients with hypersensitivity pneumonitis induced by avian antigens were studied in order to determine the presence of circulating autoantibodies. IgM and IgG rheumatoid factors were positive in 68% and 100% of the cases respectively. IgM-rheumatoid factor was detected with at least two methods, showing titers between 1:20 and 1:1280 by the latex agglutination test and between 140 and 579 IU/ml by nephelometry test. The IgG rheumatoid factor was studied by the indirect immunofluorescence technique, showing positive determinations in all of our hypersensitivity pneumonitis patients. Titers of these autoantibodies ranged from 1:80 to 1:640. In addition, we studied the presence of antinuclear, anti-nDNA, anti-mitochondrial, and anti-smooth muscle antibodies by the immunofluorescence test using HEp-2 cells, mouse kidney, and Crithidia luciliae targets. Sera from all of our hypersensitivity pneumonitis patients have negative results of autoantibodies to these antigens. Negative results of autoantibodies to the nRNP, Sm, SS-A(Ro) and SS-B(La) nuclear antigens by counterimmuno-electrophoresis and double immunodiffusion techniques were also obtained. As controls we studied 14 healthy individuals and 8 subjects exposed to avian antigens but without hypersensitivity pneumonitis symptoms and no positive determinations for rheumatoid factor, antinuclear antibodies, as well as to anti-mitochondrial and anti-smooth muscle antibodies, were found. These findings support that different immune abnormalities are present in patients with hypersensitivity pneumonitis induced by avian antigens. One of these immune alterations or a combination of them may promote or facilitate the acute interstitial lung injury and/or perpetuate a chronic inflammatory process.

Adult↗
PubMedDate not supplied

Rating of breathlessness at rest during acute asthma: correlation with spirometry and usefulness of breath-holding time.

We studied 13 patients with acute attacks of asthma to test the hypothesis that magnitude of dyspnea at rest correlates well with spirometry and with breath-holding time. Dyspnea ("falta de aire" in Spanish) was quantitated with a linear numerical scale from 0 to 10. We measured breath-holding time, breathing frequency (f), and FEV1 and FVC both expressed as percent of normal. Measurements were done on the patient's arrival and were repeated 3 to 6 times until dyspnea at rest disappeared or was minimal. Dyspnea magnitude, f, and breath-holding time correlated well with FEV1% and FVC% (r between 0.65 and 0.78), and better with changes in FEV1% and FVC% with respect to initial values (delta FEV1 y delta FVC; r between 0.80 and 0.89). Breath-holding time and f changed in proportion to magnitude of dyspnea (r = -0.85 and 0.87 respectively). Regression equations were: dyspnea = 6.34 -0.16 (delta FEV1) r = 0.80, and dyspnea = 7.82-0.105 (FEV1%) r = 0.62. Using multiple regression we improved prediction of FEV1% with easily obtained variables (R = 0.76). These results suggest that: 1) magnitude of dysnea, f, and breath-holding time correlate with severity of airflow obstruction in acute asthma attacks associated with dyspnea at rest; and 2) breath-holding time varies inversely with dyspnea magnitude when it is present at rest.

Acute Disease↗