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J L Pujol

Publications and source records attributed to J L Pujol.

At least 109 records · Page 6Linked to original sources
PubMed1990

Interleukin-1 release by alveolar macrophages in asthmatic patients and healthy subjects.

A thymocyte proliferative response assay was used to compare spontaneous and lipopolysaccharide (LPS)-induced interleukin-1 (IL-1) release by alveolar macrophage (AM) in asthmatic patients and normal subjects. Twelve asthmatic patients and seven nonsmoking healthy subjects underwent a bronchoalveolar lavage (BAL). All asthmatic patients had a reversible airway obstruction and 7/12 were allergic. BAL AM were separated by adherence on tissue culture plates in medium RPMI-1640 supplemented with antibiotics and fetal calf serum, and were incubated with or without 10 micrograms/ml LPS for 20 h. Free-cell supernatants were tested by C3H/HeJ mice thymocyte proliferative assay. Unstimulated AM supernatant IL-1 activity was significantly higher in asthmatic patients (mean +/- SEM: 47.8 +/- 11.9 units/10(6) AM) in comparison with healthy subjects (4.8 +/- 2.3 units/10(6) AM; p less than 0.05, Mann-Whitney U test) but did not significantly differ between allergic (42.2 +/- 15.5 units/10(6) AM) and intrinsic asthmatic patients (55.8 +/- 20.7 units/10(6) AM). For healthy subjects, IL-1 activity was significantly higher in LPS-stimulated AM supernatants (85 +/- 20 units/10(6) AM, p less than 0.05; Mann-Whitney U test) in comparison with unstimulated ones; for asthmatic patients, unstimulated and LPS-stimulated AM supernatant IL-1 activity did not significantly differ. This finding is in accordance with previous work suggesting that AM from asthmatic patients have a weak suppressive activity upon lymphocyte proliferation and emphasize the enhanced AM releasability in asthma.

Adolescent↗
PubMed1990

Interstitial pulmonary disease induced by occupational exposure to paraffin.

An occupational interstitial pulmonary disease was observed in a 59-year-old workman after five years of massive exposure to aerosolized paraffin. Histologic studies of open-lung biopsy showed a lipoid pneumonia characterized by (1) alveolitis involving large lipid-laden macrophages and (2) interstitial fibrosis. Electron microscopy of AMs disclosed features of paraffin-laden cytoplasmic vacuoles. Successive treatments included prednisolone and cyclophosphamide. Despite these treatments and withdrawal from exposure, the pulmonary function became impaired progressively, resulting in restrictive syndrome and severe exertional dyspnea. Concomitantly, PMNs harvested by BAL increased, whereas initial lymphocytosis decreased. This is the first case observed of occupational interstitial fibrosis in which electron-microscopic findings clearly established a relationship with an exposure to paraffin. This observation also emphasizes the switch from alveolitis to fibrosis in the pathogenesis of interstitial pulmonary disease.

Humans↗
PubMed1990

A vision for excellence.

One hospital integrates employee relations, customer service and commitment to quality into one successful, award-winning program. Employees at AMI Palmetto General are motivated to constantly consider the hospital's goals and strive for excellence.

Florida↗
PubMed1989

Phenotypic heterogeneity studied by immunohistochemistry and aneuploidy in non-small cell lung cancers.

Non-small cell lung cancers (non-SCLC) differ from small cell lung cancers (SCLC) by many clinical features and prognosis. However, recent studies suggest that lung cancer heterogeneity frequently leads to the association of SCLC and non-SCLC in the same tumor. This phenotypic heterogeneity can be analyzed by immunohistochemistry using monoclonal antibodies (Mab) raised against differentiation related antigens. It may have clinical relevance inasmuch as the diversification of malignant cells is a well-known factor of tumor progression and may be due to chromosomal instability because inappropriate gene expression leads to the formation of antigens unrelated to cell lineage. Chromosomal instability in cancer leads to aneuploidy detectable by cell DNA content analysis. In a prospective study, we analyzed, in parallel, the expression of neuroendocrine related antigens by immunohistochemistry and the cell DNA content in frozen specimens from 40 patients who underwent complete surgical resection of primary non-SCLC in an attempt (a) to characterize the phenotypic heterogeneity and (b) to determine whether this heterogeneity is correlated with aneuploidy and clinical staging. Three Mabs were used in association as a marker of neuroendocrine antigen expression (S-L 11.14, MOC-1, and NE-25); reactivity of these Mabs in 9 SCLC and 3 lung carcinoid tissue sections was used as positive control. All SCLC and 2 of 3 lung carcinoids tested were homogeneously positive with Mabs S-L 11.14, MOC-1, and NE-25; 13 of 40 non-SCLC were homogeneously positive and 11 additional specimens focally positive with Mabs S-L 11.14, MOC-1, and NE-25. The frequency of this abnormal phenotype was significantly higher in poorly differentiated squamous cell carcinomas (chi 2 10.08; P less than 0.005), in clinical stage III non-SCLC (chi 2 5.93; P less than 0.02), and in tumors involving mediastinal lymph nodes (chi 2 5; P less than 0.03). The percentage of cells in the modal DNA of G0-G1 phase was significantly lower in non-SCLC homogeneously positive with Mabs S-L 11.14, MOC-1, and NE-25 [27.4 +/- 10.3% (SD)] in comparison with non-SCLC negative with these same Mabs [56.8 +/- 21.3%; P less than 0.01, Mann-Whitney U test]. We conclude that (a) mixed SCLC-non-SCLC differentiation is frequent and can be assessed by immunohistochemistry, (b) neuroendocrine differentiation in non-SCLC is mainly observed in poorly differentiated tumors and in advanced clinical stages, and that (c) this heterotopic phenotype is correlated with aneuploidy and has clinical implications.

Adult↗
PubMed1989

Platelet function: aggregation by PAF or sequestration in lung is not modified during immediate or late allergen-induced bronchospasm in man.

Among the mediators involved in the pathophysiologic mechanisms that underly the reactions of the acute and delayed phases of bronchospasm induced by allergens in man, platelet-activating factor (PAF) could play an important role, in particular by its effects on platelets. In animals, inhalation or injection of PAF causes a platelet-dependent bronchoconstriction that is blocked by prior administration of an antiplatelet antiserum and accompanied by platelet accumulation in the pulmonary vessels. In man, inhalation of PAF causes a bronchospasm and induces a bronchial hyperreactivity. Abnormalities of platelet aggregation and the secretion into plasma of platelet factor 4 and beta-thromboglobulin have been described in patients with asthma during induced bronchospasm. Platelet functions have been studied in 15 patients with asthma before and after allergen bronchial provocation tests. There was no difference between platelet counts, plasma concentrations of platelet factor 4 and beta-thromboglobulin, and platelet aggregation induced by several agonists (adrenaline, arachidonic acid, or PAF) before and immediately after the allergen bronchial provocation test. There was no platelet pulmonary sequestration as studied with 111Indium-labeled platelets during 24 hours after the antigen challenge, and the life span of circulating platelets was normal. Our results do not support an important direct role for PAF in the pathophysiology of asthma. It is still possible that the current methodology is too insensitive to detect amounts of PAF in the circulation or that PAF is acting locally.

Adolescent↗
PubMed1989

Substance P activation of bronchoalveolar macrophages from asthmatic patients and normal subjects.

The role of substance P in the pathogenesis of asthma is unclear. Animal studies suggest that it may be important, whereas human studies do not confirm this. Alveolar macrophages can be recovered easily by bronchoalveolar lavage (BAL) and stimulated in vitro. To assess the role of substance P in humans, we tested its ability to stimulate alveolar macrophages from six normal subjects and seven asthmatic patients. BAL cells were separated by adherence and alveolar macrophages constituted 95% of the adherent cell population. Four concentrations of substance P were used (10(-7), 10(-6), 10(-5), 10(-4) M). To assess the non-specific activation of alveolar macrophages we used three concentrations of lipopolysaccharides (LPS) (5, 10, 20 micrograms/ml). The stimulation of alveolar macrophages was assessed by the release of thromboxane B2 by radioimmunoassay. This study indicates that alveolar macrophages are stimulated by LPS but are poorly activated or not at all by substance P.

Adolescent↗
PubMed1989

Identification of an alveolar macrophage-derived activity in bronchial asthma that enhances leukotriene C4 generation by human eosinophils stimulated by ionophore A23187 as a granulocyte-macrophage colony-stimulating factor.

Incubation of eosinophils (EOS) with alveolar macrophage (AM) supernatants isolated from asthmatic subjects followed by stimulation with the calcium ionophore A23187 resulted in enhancement of the capacity of EOS to elaborate leukotriene C4 (LTC4) (mean enhancement 169 +/- 37%, n = 31). Pretreatment of EOS with AM supernatants derived from normal individuals did not enhance LTC4 generation as compared with control medium. Enhancement was maximal when EOS were preincubated with a 1:6 dilution of AM supernatants for 5 min at 37 degrees C and were then stimulated with 5 microM A23187 for 15 min. Separation of AM supernatants by size-exclusion HPLC using a TSK G3000 SW column resulted in a peak of enhancing activity with an estimated molecular mass of approximately 30,000 D. Further purification by anion exchange HPLC using a TSK DEAE 5PW column (pH 7.4) resolved the activity into a minor peak at 0.17 M NaCl and a major peak at 0.2 M NaCl. The activities were distinct from interleukin-1 and tumor necrosis factor. Resolution of the major peak of activity by reverse-phase HPLC using a C18 spherisorb ODS column and a slope gradient of 0 to 100% acetonitrile/0.1% trifluoroacetic acid demonstrated a single peak of activity that eluted at 41% acetonitrile. The enhancing activity was sensitive to trypsin and heat and was neutralized by a specific antibody to granulocyte-macrophage colony-stimulating factor (GM-CSF). Pretreatment of EOS with recombinant GM-CSF primed the cells for enhanced LTC4 generation following subsequent stimulation with A23187. GM-CSF may play a role in the amplification of the eosinophilic inflammation in asthmatic airways.

Adolescent↗
PubMed1989

[Results of a phase II study of the combination of cis-platinum and 5-FU in epidermoid or undifferentiated large cell bronchial cancer].

The aim of this study was to test cisplatinum and 5-FU chemotherapy. Thirty-five patients with epidermoid or undifferentiated lung carcinoma were entered in a multicentric phase II trial, in an attempt to further define the activity and toxicity of this association. None of them had been previously treated by chemotherapy. The dosage schedule was cisplatinum 100 mg/m2 D1 and 5-FU 1 g/m2 D1 to D5 every 3 weeks for 3 courses before evaluation. There were CR: 2, PR: 10, for a total response rate of 35%. Median survival was 7 months. Tolerance was acceptable. We conclude that this association can be safely administered, but that the results are not superior to others previously reported. Further studies are required to define the activity of a cisplatinum, 5-FU and radiotherapy association.

Adult↗
PubMed1989

[Physiopathology of asthma].

Bronchial asthma is a unique disease; knowledge of the pathophysiology increases rapidly and underlines that is more a syndrome than a disease. Indeed a new definition has been recently proposed: desquamative eosinophilic chronic bronchitis. The airway obstruction, which is responsible for the wheezing breathlessness, is the consequence of a spasm but also an inflammation. After activation of the resident cells in the airways (mast cells, epithelial cells and alveolar macrophages), mediators are released and - in cooperation with the nervous system-recruit inflammatory cells from blood and bone marrow (mainly eosinophils). A kind of vicious circle seems to amplify the initial (allergic or not) event. Desquamation of the epithelium and disposition of collagen on the basement membrane take a quite long time to be cleared after an asthma attack. Mechanisms of repair must be studied in order to improve treatment. Bronchial asthma is not really a disease; indeed a lot of precipitating agents are able to induce and increase bronchial hyperreactivity. Allergy is the most important factor; but environment, hormones and other infectious agents could be quite important in many patients.

Allergens↗
PubMed1989

[Should the development of virological diagnostic methods influence our practical approach?].

Respiratory viral infections which occur in patients with spontaneous or therapeutic immunodepression are frequent and serious. Apart from these acute situations, viruses are responsible for some chronic respiratory pathologies which affect the functional prognosis, as illustrated by the relationship between the respiratory pathologies demands an accurate diagnosis. Two methods can be used routinely to demonstrate the presence of a virus in bronchoalveolar lavage fluid or in transbronchial biopsy: (1) direct immunofluorescence or immunoenzymatic technique; the concomitant finding of a cytopathogenic effect on the cells that constitute the sample makes this method more sensitive and confirms the pathogenic character of viruses demonstrated by immunological techniques; (2) isolation of the virus from cell cultures; the sensitivity of this method can be increased by an immunological search for the virus (fast culture). Hybridization in situ is a new and promising method where a DNA probe complementary to viral nucleic acids is used to evidence the viral genome in the infected cells. Serum IgM assays, which provide proof of an active infection, should be preferred to conventional serology, although seroconversion is inconstant in immunodepressed patients. Improvements in virological diagnostic methods should result in the future use of new antiviral treatments.

Biopsy↗
PubMed1987

[Inflammatory mechanisms of bronchial asthma].

The definition of asthma brings with it the idea of inflammation, as bronchial obstruction, which characterises it, is associated with bronchospasm, hypersecretion and oedema. In the asthmatic, awareness of the bronchial inflammation at the time of diagnosis is essential, as it contributes to prognosis and therapeutic orientation. The diagnosis of bronchial inflammation begins with the clinical assessment, such as cough, expectoration and the worsening of symptoms in the morning alerts the clinician. In the course of certain clinical forms of asthma the absence of any relief of airflow obstruction by bronchodilators, although it is proved to be reversible after a few days of glucocorticoids, is evidence of inflammation. Fibreoptic bronchoscopy extends the clinical examination and enables a direct observation of airways inflammation. In addition it allows sampling, such as bronchial biopsy and/or broncho-alveolar lavage. The mechanism of bronchial inflammation are well understood; some mastocytes (mucous) are present in the broncho-alveolar contents and are probably the origin of inflammatory reaction, whether the stimulus be allergenic or not. The mediators liberated lead in part to the bronchial obstruction but equally to cellular recruitment and thus to an amplification of the initial reaction. Probably the eosinophils play a fundamental role ar this stage. The alveolar macrophages are equally implicated in this inflammatory reaction. Bronchial inflammation appears as a result of complex cellular reactions, regulated by chemical mediators. The most obvious consequence of bronchial inflammation is the delayed bronchial reaction. The experimental model contributes to physio-pathological understanding and a characterisation of the inflammatory components is observed principally in those patients with severe asthma. Agents capable of causing or aggravating bronchial hyper-reactivity can also induce bronchial inflammation. From this observation the idea is born of a relation between the concept of bronchial hyper-reactivity and bronchial inflammation. Acquired bronchial hyper-reactivity evolves in parallel to the symptoms and its intensity is correlated with the severity of the asthma. An understanding of the inflammatory mechanisms without doubt will bring new therapeutic perspectives.

Asthma↗
PubMed1987

[Pleural and mediastinal metastases from a malignant mesothelioma of testicular vaginalis membrane].

The authors describe an original observation of secondary intrathoracic metastases due to a malignant adenomatoid tumour or mesothelioma of the testicular tunica vaginalis. The hypothesis of a primary pleural mesothelioma could be excluded here as could secondary pleural deposits from another neoplasm. The exceptionally malign potentialities of this common tumour of the testicular adnexae were reviewed as well as the extremely poor prognosis.

Adult↗
PubMed1985

[Invasive aspergillar pneumopathy during the treatment of microcellular bronchial cancer. Efficacy of early antifungal treatment].

The invasive aspergillus pneumonias have been described particularly in chemotherapy for patients with haematological disorders. In respiratory disorders such cases are exceptional. The authors report a case of invasive aspergillus pneumonia, occurring during treatment of a small cell cancer; the rapid commencement of anti-fungal treatment by Amphotericin "B" and Flucytosine enabled an apparent cure of the tumour by radiotherapy and chemotherapy. The authors stress the difficulty of definitive diagnostic criteria at the beginning of the disorder and also the need to start anti-fungal treatment as soon as possible.

Amphotericin B↗
PubMed1976

Fibrous histiocytoma of the lung.

A case of asymptomatic fibrous histiocytoma of the lung is described in a 14-year-old girl. A left thoracotomy was performed followed by partial resection of the lingula. Postoperative progress was uneventful.

Adolescent↗
PubMedDate not supplied

Cyfra 21-1, neuron specific enolase and prognosis of non-small cell lung cancer: prospective study in 621 patients.

BACKGROUND: CYFRA 21-1, a serum cytokeratin 19 fragment, and neuron specific enolase (NSE), the gamma-subunit of enolase, are putative markers of lung cancer. Their clinical applicability as prognostic factors in non-small cell lung cancer (NSCLC) would need an appraisal by simultaneous evaluation of other known survival determinants in a large population followed over a long period. AIM: To determine the prognostic value of different clinical and routine biological variables at presentation with particular attention paid to the above-mentioned markers. METHODS: 621 histologically proven and previously untreated NSCLC patients have been prospectively studied (seven were lost to follow-up). Median follow-up was 4 years and 2 months. At presentation, 16 clinical and biological variables were recorded. Serum NSE and CYFRA 21-1 were assayed blind without any clinical information given. RESULTS: The serum CYFRA 21-1 distribution differed significantly according to histology, disease stage and performance status, with the highest levels observed in squamous cell carcinomas, metastatic stage, positive mediastinal nodal status and poor performance status. However, the respective "receiver operating characteristic" curves showed that the CYFRA 21-1 serum level did not accurately predict tumour stage. Serum NSE distribution correlated neither with tumour stage nor with performance index and its sensitivity in the whole NSCLC was low. In the Cox proportional hazard model, the following variables were independent determinants of a poor outcome: performance status 2 or 3, hazard ratio (HR): 2.25; Nodal status N(2-3), HR: 1.84; Metastatic disease, HR: 1.73; NSE>12.5 ng/ml, HR: 1.52; CYFRA 21-1>3.6 ng/ml, HR: 1.41 and Tumour status T(3-4), HR: 1.31. When the survival analysis was restricted to the 274 patients affected by a metastatic stage, we observed that performance status, nodal status, NSE and CYFRA 21-1 remained prognostic determinants with similar hazard ratios. CONCLUSION: The prognostic information given by a high serum CYFRA 21-1 level is independent from other well-known variables such as performance status and disease stage and is perennial throughout extended follow-up period. A high NSE level also prognosticates a poor outcome probably by reflecting tumour heterogeneity and underestimated neuroendocrine differentiation.

Aged↗