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Biomedical subjects

R Ferlinz

Publications and source records attributed to R Ferlinz.

At least 37 records · Page 2Linked to original sources
PubMed1994

In vitro study of human alveolar macrophage and peripheral blood mononuclear cell reactive oxygen-intermediates release induced by sulfur dioxide at different concentrations.

Sulfur dioxide (SO2) is a major air pollutant in urban areas. Alveolar macrophages (AM) located on the alveolar surface are in direct contact with this inhaled gas. We evaluated the dose-dependent effect of SO2 exposure on the oxidative metabolism of AM and peripheral blood mononuclear cells (PBMNC) by measuring the spontaneous and stimulated reactive oxygen intermediates (ROI) release. AM or PBMNC were placed on a polycarbonate membrane, which was in direct contact with the surface of a nutrient reservoir. For exposure of the cells to SO2 a special chamber was employed, in which humidified standard air with 5% CO2 at 37 degrees C was mixed with SO2 at the desired concentration. Periods of time between 30 and 120 minutes and concentrations between 0.3 and 1.5 ppm SO2 were chosen for exposure. Thirty minutes exposure of AM to SO2 (0.3-1.5 ppm) yielded a dose-dependent stimulation of ROI release; 2.0- to 3.6-fold of control (r = 0.965, p < 0.005). An exposure of 120 minutes to SO2 resulted in a similar ROI production of about 2.5-fold at all tested concentrations. These experiments provide evidence that AM and PBMNC become activated by SO2 producing large amounts of ROI.

Bronchoalveolar Lavage Fluid↗
PubMed1994

Oncogene overexpression in non-small-cell lung cancer tissue: prevalence and clinicopathological significance.

In contrast to small-cell lung cancer, few data are available on the role of oncogene overexpression in non-small-cell lung cancers (NSCLC). To determine the prevalence and extent of the transcriptional activation of cancer genes in NSCLC we investigated the level of mRNA of the three important cellular oncogenes--erbB2, Ki-ras, and c-myc--in 39 surgically or endoscopically obtained tumor samples and 24 samples of normal bronchopulmonary tissue taken from the same patients. Tissue RNA was prepared and the specific mRNA analyzed by the highly sensitive nuclease S1 protection assay. Oncogene mRNA in the tumors was quantified by comparison with the homogeneously weak signals in normal lung tissue preparations with densitometry. The presence of two- to four-fold excess RNA was defined as moderate and a greater than fourfold RNA amount as strong gene overexpression. In contrast to normal tissue the oncogene mRNA amount varied considerably among tumors, showing increases up to 64-fold in erbB2, 13-fold in Ki-ras, and 57-fold in c-myc. Moderate and strong (in brackets) mRNA overexpression occurred with 33% (33%) in erbB2, 36% (18%) in Ki-ras, and 18% (23%) in c-myc. Simultaneous overexpression of two genes was observed with 41% and increased mRNA of all genes tested with 20% of the NSCLC samples. Augmented oncogene mRNA was observed most frequently in large-cell carcinoma. The c-myc overexpression was significantly more prevalent in large-cell cancer than in adenocarcinoma. Tumor differentiation was negatively correlated with c-myc mRNA amounts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

An experimental model for the exposure of human ciliated cells to sulfur dioxide at different concentrations.

Mucociliary transport is an important nonimmunological defense mechanism of the respiratory tract. The aim of this study was to investigate the effect of sulfur dioxide (SO2) at different concentrations on ciliary beat frequency (CBF). Ciliated cells were obtained from 12 volunteers by nose brush. CBF was quantified using video-interference microscopy. The cells were placed on a polycarbonate membrane in contact with the surface of a reservoir filled with RPMI 1640 (bicarbonate buffered) or Ringer's (electrolyte) solution, allowing the cells to be supplied by capillarity. In an exposure chamber the cells were exposed for 30 min to SO2 2.5-12.5 ppm at 37 degrees C and 100% air humidity. SO2 induced a dose-dependent decrease in CBF of the cells cultured in Ringer's solution. SO2 at 2.5 ppm caused a 42.8% decrease and at 12.5 ppm a 96.5% decrease (8.1 +/- 0.24 versus 0.28 +/- 0.20 Hz). CBF of cells cultured in RPMI 1640 was reduced only moderately after 12.5 ppm SO2 exposure (7.9 +/- 0.26 versus 6.70 +/- 0.30 Hz). In Ringer's solution a decrease in pH was observed after 30 min of SO2 exposure to 12.5 ppm to a minimum value of 3.6. By contrast, the pH of RPMI 1640 remained constant at 7.5 under identical conditions. After adding RPMI 1640 to Ringer's solution, CBF increased in parallel to the pH to control values (5.0 ppm: 4.64 +/- 0.45 to 8.51 +/- 0.60 Hz). These data suggest that the highly water-soluble SO2 reversibly eliminates CBF in correlation with a decrease in pH.

Adult↗
PubMed1994

Effect of sulfur dioxide on mucociliary activity and ciliary beat frequency in guinea pig trachea.

The effects of 30 min exposure to sulfur dioxide on mucociliary activity (MCA) and ciliary beat frequency (CBF) were studied in 31 guinea pig tracheas. MCA was measured by recording the light reflected from ciliated mucous membranes using an infrared bar code reader. CBF of single ciliated cells obtained by brushing was measured with phase-contrast microscopy. Each tracheal sample was exposed to SO2 at concentrations ranging from 2.5 to 12.5 ppm, or to air for control purposes. MCA and CBF were measured before and immediately after gas exposure. A reduction in mean MCA of 63% (P = 0.0007) and statistically insignificant changes in CBF (P > 0.05) were recorded at concentrations of 2.5 ppm SO2. Higher SO2 concentrations caused a further impairment of MCA as well as a dose-dependent decrease in CBF (P = 0.002). A concentration of 12.5 ppm SO2 induced a decrease from baseline values of approximately 80% in mean MCA and of roughly 70% in mean CBF. This study demonstrates a dose-dependent SO2-induced decrease in MCA of guinea pig tracheas. The decrease in MCA was associated with an impairment of CBF only at SO2 concentrations higher than 5.0 ppm.

Animals↗
PubMed1994

[New approaches to evaluation of nonspecific inhalation provocation (dose-response relationship) in the comparative evaluation of bronchial hyperreactivity within the scope of clinical trials].

For the performance of clinical drug trials in the therapy for bronchial hyperresponsiveness, unspecific inhalatory provocation tests are generally employed to judge therapeutic success. In particular, the parameter-specific provocation doses are considered to be the main target values. However, it must be considered that these provocation doses are not equally calculable for every patient in the same way and at any examination time. This leads to the fact that the number of evaluable case studies is often appreciably lower than the number of test participants and that a meaningful therapy group comparison may even not be possible under certain circumstances. An evaluation model is presented here in order to fully exploit the obtained data; in this the percentile changes of the function parameters (estimated by linear regression) at a defined dose of the provocation substance are analyzed. In analogy, a survival time model and, as a supplement, a best case/worst case analysis are performed for further statistical evaluation. With the present procedure, an evaluation with inclusion of all test participants is possible. In contrast to the previously used evaluation procedures, this allows a reliable statistical confirmation of the results of clinical tests in the therapy for bronchial hyperresponsiveness.

Aerosols↗
PubMed1994

[In vitro studies of modification of mucociliary clearance by guinea pig tracheas by exposure to air pollutants of sulfur or nitrogen dioxide].

We studied the effect of sulfur dioxide (SO2) and nitrogen dioxide (NO2) on mucociliary activity (MCA) and ciliary beat frequency (CBF) in 63 guinea pig tracheas. The tracheas were placed in a gas cylinder and exposed for 30 minutes to SO2 concentrations ranging from 2.5 to 12.5 ppm or to NO2 concentrations ranging from 3.0 to 15.0 ppm. Control experiments were performed with exposure of the tracheas to synthetic air. MCA was measured by recording the light reflected from ciliated mucous membranes using an infrared barcode reader and CBF using video-interference microscopy. The exposure to 2.5 ppm SO2 caused a reduction in mean MCA of 63% and no significant changes in CBF. Higher SO2 concentrations caused a further impairment of MCA as well as a dose-dependent decrease in CBF. 10.0 or 12.5 ppm SO2 induced a decrease from baseline values to approximately 20% in MCA and to roughly 30% in mean CBF. The exposure to NO2 at concentrations ranging from 3.0 to 15.0 ppm did not induce any changes in MCA or CBF of the guinea pig tracheas. Our results show that exposure to SO2 for 30 minutes is able to depress the mucociliary clearance of guinea pig tracheas, whereas the exposure to equivalent NO2 concentrations for the same time do not alter the mucociliary transport.

Air Pollutants↗
PubMed1994

[Development of tuberculosis in Germany--a comparison between former West and East Germany].

The development of tuberculosis in both parts of Germany between 1950 and 1990 is compared. From 1950-1965 morbidity and mortality were significantly greater in the former GDR than in the FRG. Figures have somewhat increased in the FRG since 1965; a breakdown according to indigenous and alien population shows that the development of the disease among Germans has been approximately the same in both parts of Germany. For the last ten years the proportion of cases of acute infectious tuberculosis has remained almost unchanged in both the GDR and the FRG. A comparison of the development of infant tuberculosis does not disclose any influence exercised by BCT vaccination on the epidemiology.

Cross-Cultural Comparison↗
PubMed1994

[Toxic lung damage caused by mitomycin C].

Lung toxicity is one of the rare side effects of mitomycin C (MMC), an effective antineoplastic agent. There have been only few reports on pulmonary damage after MMC monotherapy. We describe a case of a pulmonary reaction following MMC monotherapy. The patient was examined including bronchoalveolar lavage (BAL) and transbronchial lung biopsy. BAL yielded the diagnosis of a lymphocyte alveolitis with normal CD4/CD8 ratio within the T lymphocytes. Histologically a florid alveolitis was diagnosed. Radiological and CT findings including HR-CT are described.

Aged↗
PubMed1993

[In vitro studies of the beat frequency of ciliary cell cultures after short-term exposure to SO2 and NO2].

Mucociliary transport is an important defense mechanism of the respiratory tract. The aim of this study was to investigate the effect of SO2 and NO2 at different concentrations on ciliary beat frequency (ZSF). Single ciliated cells were obtained from 25 volunteers by nose brush. ZSF was quantified using video-interference-microscopy. The cells were placed on a polycarbonate membrane, which was in contact with the surface of a reservoir filled with RPMI medium (bicarbonate buffered) or electrolyte solution (Ringer), allowing the cells to be supplied by capillarity. In an exposure chamber the cells were exposed for 30 to 120 min to SO2 2.5 to 15.0 ppm at 37 degrees C. SO2 induced a dose dependent decrease in ZSF of the cells, supported by Ringer solution. 2.5 ppm SO2 caused a 42.8%, 12.5 ppm a nearly 100% decrease (8.10 +/- 0.24 vs. 0.28 +/- 0.20 Hz). ZSF of cells cultured in RPMI medium was reduced moderately after 12.5 ppm SO2 exposure (7.90 +/- 0.26 vs. 6.66 +/- 0.31 Hz). In Ringer solution we observed a decrease of pH after 30 min SO2 exposure with 12.5 ppm to a minimum value of 3.6. In marked contrast, the pH of RPMI medium remained constant at 7.5 under identical conditions. After adding RPMI medium to Ringer solution, ZSF increased in parallel to the pH (5.0 ppm: 2.77 +/- 0.37 to 7.97 +/- 0.49 Hz). After an initial increase in ZSF, 120 min NO2 exposure to 15.0 ppm yielded a decrease in ZSF of 23.3% under conditions of constant pH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Pulmonary toxicity caused by nitrofurantoin].

Nitrofurantoin is used in the treatment of, and to prevent, urinary tract infections. Since this chemotherapeutic agent was introduced in the fifties, quite a number of cases of acute and chronic pulmonary damage have been reported that were conditioned by nitrofurantoin. This is a report on three cases of pulmonary nitrofurantoin reactions, one of them acute and two chronic. All three patients were examined with the inclusion of bronchoalveolar lavage and transbronchial lung biopsy. In all three cases alveolitides of varying activity were confirmed. The radiological and CT findings are described.

Adult↗
PubMed1993

[Reference controlled, randomized double-blind study of the effectiveness of a salbutamol/DNCG DA combination in bronchial hyperreactivity in comparison with salbutamol DA alone (parallel group comparison)].

We examined 20 patients in whom bronchial hyperreactivity and positive inhalative methacholine provocation test (dosage-effect curve) had been known for at least 3 months at the time of study. The patients received randomised either DA Salbutamol/DNCG (0.1 mg Salbutamol and 1.0 mg DNCG/puff) or DA Salbutamol alone (0.1 mg Salbutamol puff). In each case the therapy consisted of 4 x 2 puffs daily. The minimum treatment time was 14 days. The average treatment time was 16 days in both groups. The major aim of the study was to find out whether treatment with the combination preparation in the inhalative methacholine test would lead to a higher provocation dose (PD) for the Rt value and/or sGaw and/or FEV1 representing an alleviation of bronchial hyperreactivity, compared with the pre-examination and with the control group with Salbutamol monotherapy. In addition, the effectivity was to be documented by means of peak-flow values to be measured by the patient himself. The results show in both groups a mild but statistically not significant reduction of the provocation reaction in the inhalative methacholine provocation test in the sense of an improvement in bronchial hyperreactivity. No significant difference between the therapy groups, and especially no superiority of the combination treatment, is evident.

Adult↗
PubMed1993

[Realistic in vitro study of oxygen radical liberation by alveolar macrophages and mononuclear cells of the peripheral blood after short-term exposure to SO2].

Alveolar macrophages (AM) located on the alveolar surface are directly exposed to air pollutants. We evaluated the effect of exposure to SO2 on the oxidative metabolism of AM and peripheral blood mononuclear cells (PBMNC) by measuring the spontaneous and stimulated reactive oxygen-intermediates (ROI) release. AM or PBMNC were placed on a polycarbonate membrane, which was in contact with the surface of a reservoir filled with RPMI 1640 allowing the cells to be supplied with nutrients by capillarity. For SO2 exposure times of 10, 20 and 30 minutes and concentrations of 2.5, 7.5 and 12.5 ppm were chosen. A 10-minute SO2-exposure up to 12.5 ppm induced a dose dependent maximal 3.6 fold increase of spontaneous ROI-production (r = 0.876; p < 0.005). A 30-minute exposure of 12.5 ppm SO2 exhibited a cytotoxic effect inducing the death of 62 +/- 9% of AM and caused a 63% decrease of ROI-release compared to 2.5 ppm SO2-exposure under identical conditions (r = -0.96; p < 0.005). These experiments demonstrate that AM and PBMNC are activated by SO2 and that concentrations in the range of 12.5 ppm SO2 are toxic and induce a decrease in ROI-release after 30 minutes exposure of these cells.

Aged↗
PubMed1993

[Alveolar macrophages and mononuclear cells of the peripheral blood in sulfur dioxide and chrysotile B exposure: a realistic in vitro test of oxygen free radical liberation].

Sulfur dioxide (SO2) and Asbest are frequently found at workplaces. They can induce airway and lung parenchymal injury. Alveolar macrophages (AM) play an important and decisive role in the damage of respiratory tissue. We evaluated the reactive oxygen intermediates (ROI) production of AM and peripheral blood mononuclear cells after exposure with SO2 and Chrysotile B. The cells were exposed in a special gas exposure chamber at 37 degrees C and 100% air humidity for 30 minutes to 1.5 or 2.5 ppm SO2. Afterwards they were incubated for one hour with 100 micrograms or 200 micrograms Chrysotile B. Control experiments were performed with cell exposure to synthetic air without SO2 and Chrysotile B. Spontaneous and phorbol myristate acetate (PMA) stimulated ROI-release were measured by chemiluminescence and the cell toxicity was evaluated with the trypan blue exclusion test. Our results show a dose-dependent increase of the spontaneous ROI-production of AM after SO2 and Chrysotile B exposure. Exposure to 100 micrograms Chrysotile B caused an 1.5 fold, exposure to 1.5 or 2.5 ppm SO2 plus 100 micrograms Chrysotile B resulted in an 2.4 respectively 3.3 fold increase in ROI-release compared to control experiments. Exposure of AM to 200 micrograms Chrysotile B yielded an 1.9 fold, exposure to 2.5 ppm SO2 plus 200 micrograms Chrysotile B a 3.9 fold elevation in the spontaneous ROI-production compared to control experiment with standard air. A similar reaction pattern was observed in PMA-stimulated AM and in peripheral blood mononuclear cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Lung-restricted activation of the alveolar macrophage/monocyte system in pulmonary sarcoidosis.

An activation of T-cells that is restricted to the lung has been demonstrated in pulmonary sarcoidosis. The role of blood monocytes (MO) and alveolar macrophages (AM) in this concept of compartmentalized inflammation has not yet been evaluated. In order to elucidate this question, we measured the release of tumor necrosis factor alpha (TNF alpha) and interleukin-1 (IL-1) by peripheral blood mononuclear cells (PBMNC) and AM in 43 patients with sarcoidosis (32 with active, 11 with inactive disease) without therapy and correlated the spontaneous monokine release to parameters of the T-cell alveolitis and the course of the disease. TNF alpha as well as IL-1 were spontaneously released by AM of the active group, i.e., 2,385 +/- 735 pg/ml/10(8) cells/24 h and 7/12 (IL-1+/total), respectively. Autologous PBMNC were quiescent, releasing only baseline levels of any monokine. AM were not activated in the inactive group, releasing 500 +/- 212 pg/ml/10(6) cells/24 h TNF alpha, whereas 1/5 were IL-1-positive (p less than 0.05 in both comparisons), which is within the range of the control group. Kinetic experiments revealed that the TNF alpha gene of AM is activated in vivo, resulting in TNF alpha mRNA-positive, TNF alpha-releasing cells that, cultured in vitro, regulate the TNF alpha gene transcription down and cease to release TNF alpha. Interestingly, there is no stringent correlation between the spontaneous release of TNF alpha by AM and signs of T-cell activation as soluble interleukin-2 (IL-2) receptor serum concentration, release of IL-2, and expression of IL-2 receptor by alveolar T-cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1992

Fibrosing alveolitis responsive to corticosteroids following Legionnaires' disease pneumonia.

Two male patients ages 54 and 58 years had persisting pneumonia with dry cough, dyspnea, weight loss, and fever up to 39 degrees C that did not respond to erythromycin treatment. There was extensive restrictive impairment of ventilation and loss of diffusing capacity for carbon monoxide. Histologic examination of the basal pulmonary infiltrates showed fibrosing alveolitis. Serologic titers indicated that the patients had suffered from Legionella pneumophila infection. We believe that Legionella had caused the fibrosing alveolitis since there was absence of any other causative agents or factors. Both patients responded to corticosteroid treatment with rapid clinical improvement but delayed radiologic regression.

Humans↗
PubMed1992

[Pulmonary infiltrations with eosinophilia (pulmonary eosinophilia)].

The pulmonary eosinophilias are characterised by radiographic lung shadows with either a peripheral blood eosinophilia of more than 450/microliter or histologic abnormalities consisting of both interstitial and intraalveolar accumulations of eosinophils and macrophages. We describe the clinical features, radiographic changes, results of bronchoscopy and follow-up studies of three women with chronic eosinophilic pneumonia of unknown aetiology. In all patients the illness resolved rapidly after treatment with corticosteroids, however one patient experienced a second episode after treatment withdrawal. We demonstrate the wide differential diagnosis of the syndrome of pulmonary eosinophilia.

Adult↗
PubMed1992

[Primary pulmonary nodular amyloidosis and multiple emphysematous bullae in Sjögren syndrome].

The authors report on a very rare case of an isolated primary nodular pulmonary amyloidosis with multiple emphysematous bullae in Sjögren's syndrome. The circular foci present in both lungs in disseminated form were immunohistochemically speaking amyloid deposits of the AL-lambda type. There were no pointers to other organ manifestations or monoclonal immunoglobulins in the serum and/or urine.

Amyloid↗