[Thoracopulmonary actinomycosis, a difficult differential diagnosis in suspected tumor].
Explore the source record for details and available documents.
Actinomycosis↗
Biomedical subjects
K Kienast
Publications and source records attributed to K Kienast.
Respiratory epithelium exposed to sulfur dioxide--functional and ultrastructural alterations.
The value of morphological investigations of airway mucosa should be compared to a functional method when estimating the toxicity of airborne pollutants. In 34 guinea pig tracheas, mucociliary activity was measured using a modified light beam reflex method before and following exposure to sulfur dioxide for 30 minutes in concentrations ranging between 7.5 and 37.5 mg/m3. Exposure to air served as a control. Simultaneously, specimens were taken for light and electron microscopy. Mucociliary activity decreased from 8.4 +/- 2.9 Hz (control exposure) to 4.0 +/- 2.9 Hz following exposure to 7.5 mg/m3, to 3.4 +/- 2.7 Hz at 15 mg/m3 sulfur dioxide, to 1.8 +/- 2.2 Hz at 22.5 mg/m3 sulfur dioxide, to 1.5 +/- 1.8 Hz at 30 mg/m3 sulfur dioxide, and to 2.0 +/- 1.2 Hz at 37.5 mg/m3 sulfur dioxide, respectively (P < .01). Despite a 56% decrease in mucociliary activity, only minor morphological alterations were observed following exposure to 7.5 mg/m3 sulfur dioxide. However, following exposure to 15 mg/m3 sulfur dioxide or higher, structural alterations of respiratory mucosa such as epithelial sloughing, intracellular edema and mitochondrial swelling, widened intercellular space, and ciliary cytoplasmic extrusions were found. Thus measurement of mucociliary activity proved to be a more sensitive indicator of airway toxicity than structural investigations alone.
Animals↗
[Clinical late manifestation of Ondine's syndrome with pronounced primary, especially sleep related alveolar hypoventilation].
We report on a very rare case of a primary, alveolar hypoventilation syndrome (Ondine's Curse syndrome) in a female patient who was first treated at the age of 26 years as a result of an influenza infection; however, the case history revealed a decreased performance in comparison to similar aged children from earliest childhood onwards as well as an intermittent zyanosis of the lips and distal extremities. Other diseases which could explain a global respiratory insufficiency and/or pulmonary arterial hypertension were excluded.
Adult↗
[Experimental determination of equivalent percentage changes in measurement parameters of dose-response relations with the inhaled methacholine provocation test].
For the experimental determination of equivalent changes of the measurement parameters in the non-specific inhalative provocation test with metacholine, 26 persons with exogenous allergic asthma bronchiale were examined during the symptom-free interval. The inhalative provocation test was performed as dose-response relationship. Linear regressions were calculated with the data obtained. The percentage change of the measurement parameters that occurred with a quantity of 400 micrograms of aerosolised methacholine was calculated on the basis of the regression equation. These changes correspond to equivalent changes of the individual measurement parameters compared with each other. Generally, a drop in FEV1 by 20% is demanded for a positive provocation test. If this value is defined as "gold standard", the measured data allow derivation of the equivalent changes. Our studies showed that an increase of Rt by 195% (triplication), a sGaw drop by 44%, a PEF drop by 20% and a drop of MEF75, MEF50 by 30% each, compared with the original value, is equivalent to a significant change in the sense of a positive inhalative provocation test.
Adolescent↗
[In vitro exposure of a human bronchial epithelial cell line with nitrogen dioxide induces enhanced transcription and liberation of pro-inflammatory cytokines].
Studies of in vivo inhalation of nitrogen dioxide (NO2) have demonstrated a transient pulmonary inflammation. This study was done to determine the contribution of airway epithelial cells to the release of inflammatory mediators following NO2 exposure. Confluent cultures of the human bronchial epithelial cell line BEAS-2B on Transwell-Col filters were exposed for 1 h to air or NO2 up to 1.5 ppm with the apical fluids removed with 5% CO2 at 37 degrees C. The cells were hydrated with Hanks' Balanced Salt Solution (HBSS) in the basolateral compartment. Sequential reverse transcription and quantitative cDNA amplification (RT-PCR) was used to measure inflammatory mediator mRNA abundance in BEAS-2B cultures. When compared to air-exposed cells, NO2 induced increases in IL-6 (23.4-fold) and IL-8 (30.9-fold) mRNA abundance. The NO2-dependent increases in mRNA expression reached a maximum between 0 and 1 h post exposure and returned to baseline levels within 24 h. IL-6 and IL-8 proteins as measured by enzyme-linked immunosorbent assays (ELISA) were also elevated in supernatants recovered from NO2-exposed BEAS-2B cells. These studies suggest that exposure to NO2 induces the synthesis and release of inflammatory mediators from airway epithelial cells that may participate in the pathogenesis of airway disease.
Bronchi↗
[61-year-old patient with rapidly progressive cerebellar symptoms].
The rare case of a paraneoplastic, cerebellar degeneration is reported. In addition to the valuable early diagnosis of tumor disease, this paraneoplastic occurrence can also lead to false diagnoses in regard to both the underlying disease and the staging of the tumor. In the cases of known tumor disease, the assumption of cerebral metastasis is also possible.
Autoantibodies↗
[The chemotactic behavior of alveolar macrophages and blood monocytes after exposures to different NO2 concentrations].
The chemotaxis of alveolar macrophages (AM) and blood monocytes (BM) is important in the elimination of particles and microorganisms which have invaded the lung. The effect of nitrogen dioxide (NO2) on chemotaxis was tested on AM obtained by diagnostic bronchoscopy from five patients suspected of having bronchial carcinoma (four men, one woman; mean age 59 +/- 10 years). Blood monocytes were also studied with blood from seven healthy subjects (five men, two women; mean age 32 +/- 10 years). These cells were placed on polycarbonate membranes for 15 min each, exposed to NO2 concentrations between 1.0 and 5.0 parts per million (ppm), and then incubated with complement component C5a as chemotactically active agent. The number of AM or BM which actively migrated through the polycarbonate membrane under the influence of C5a was measured by means of a light microscope. The migration rate of AM (compared to air exposure) was reduced by 33% with 1.0 ppm NO2 and by 61% with 5.0 ppm. The migration rate of BM in similar conditions was reduced by as much as 55%. There was no significant cytotoxic effect of NO2 exposure at 1.0 and 3.0 ppm. With 5.0 ppm 13.0 +/- 3.0 cells were no longer viable. These results indicate that NO2 concentrations relevant to indoor conditions affect the chemotaxis of AM and BM after short-time NO2 exposures. The data further suggest that NO2 exposures of these cells depressed chemotactic mechanisms without relevant cytotoxicity.
Aged↗
['94 pneumology update. Progress and perspectives in pneumology. Paradigm of change (I)].
Explore the source record for details and available documents.
Diagnostic Imaging↗
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↗
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↗
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↗
[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↗
An in vitro model to study effects of airborne pollutants on human ciliary activity.
A method to study the effects of airborne pollutants on ciliary activity of isolated human respiratory cells is presented. Human respiratory cells were scraped from nasal cavities of 25 healthy volunteers and washed in Ringer's solution. The cells were placed on polycarbonate membranes (3 microns pore size) and kept in macroplate holders swimming on Ringer's solution. Cells were thus kept humid and were supplied with nutrients through the pores of the membrane by capillary forces, while their surface was exposed to the gaseous environment. Isolated respiratory cells were exposed to SO2, NO2, and mixtures of SO2 and NO2 in various concentrations for 30 min and for 2 h. Exposure to synthetic air served as control. Ciliary beat frequency was measured using video-interference contrast microscopy, before and after exposure to the various gases. Exposure of isolated respiratory cells to a non-toxic gaseous environment resulted in a 20% reduction of ciliary beat frequency. A concentration-dependent decrease of ciliary beat frequency following exposure to SO2 in concentrations ranging between 2.5 and 12.5 ppm was found. Exposure to NO2 up to 2 h in concentrations ranging between 3 ppm and 15 ppm did not decrease ciliary beat frequency. No cumulative effect was found, if a mixture of SO2 (2.5 ppm) and NO2 (12 ppm) was applied.
Adult↗
[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↗
[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↗
[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↗
[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↗
[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↗