[Gross lung sections--only historical?].
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Biomedical subjects
Publications and source records attributed to W Hartung.
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The authors report on an adenoid cystic carcinoma (ACC) of the lung that had been discovered by chance 14 years before the death of the patient and that had at first been interpreted morphologically as a metastatic lung or as a bronchioalveolar carcinoma. The patient remained without any complaints for 13 years. Diagnosis of ACC became possible only by means of a renewed peripheral lung biopsy. An extrapulmonary primary tumour was excluded by postmortem examination. The disease pattern and the special course of the ACC are described.
Lipid monolayer studies were performed on a Langmuir trough in the absence and in the presence of the plant hormone abscisic acid (ABA). The ABA-induced effects on the lipid monolayers can be summarized as follows: (i) ABA as the free acid (pH below 5.3) increased the molecular area and slightly decreased the surface pressure in the collapse points of monolayers made of saturated, unsaturated and of mixed lipids; ABA as the anion showed only minor effects. (ii) The ABA-induced area increase of the lipid monolayers decreased when the surface pressure increased, but some ABA remained in the monolayers made of unsaturated phospholipids even at collapse pressure. (iii) The incorporation of ABA into the monolayers could be inhibited by adding the plant sterol beta-sitosterol to the monolayer forming phospholipids. (iv) There was no substantial difference of ABA action on plant phospholipids as compared with other phospholipids. (v) ABA had a much stronger influence on unsaturated phospholipids than on saturated ones. (vi) ABA decreased the phase-transition temperature of saturated phospholipids. These results, which agree with those obtained from phospholipid vesicle studies, indicate that the physical state of the lipid is important for the ability of ABA penetrating into the lipid monolayer. Finally, a possible relevance of these results is discussed in terms of the action of ABA on guard cell membranes of plants.
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The spectrum of silicosis of coal miners has changed during the past decades. The life expectancy of the miners suffering from silicosis has been successfully adapted to that of the non-miners as a result of a consistent therapy. Morphologically, the processes involving large callosities have receded markedly; in their place, there has been an increased incidence of generalised focal dust emphysema that are difficult to differentiate clinically from the common chronic obstructive pulmonary diseases. Chronic bronchitis and emphysema are the most important concomitant pulmonary diseases; the incidence of tuberculosis is still enhanced and carcinomas of the lung are only rarely to be acknowledged as so-called carcinomas in scar tissue. Other major diseases that coincide with silicosis are seen in p.m. statistics with customary frequency of incidence (cardiovascular diseases almost 50%, malignant tumours including those of the lung about 25%, other major diseases without respiratory organs about 10%). The main problem in expertising is to differentiate the influence of these diseases from those of silicosis; expertising must employ the legally prescribed terminology. In our own investigations based on 300 postmortem expertises, death as a result of a professionally acquired disease was acknowledged in 48% of all cases of silicosis of severity grades I to III, silicosis being the sole major disease in only half of the cases and in the other cases an essential partial contributor to the cause of death. The significance of the extended generalised dust emphysema as a special type of pneumoconioses that must be classified as grave, is emphasised in contrast to previously compiled statistics.
A woman patient admitted for treatment, who had reached the age of 65 years, had a previous history of an open pulmonary tuberculosis in 1946 that had been treated at that time by means of collapsotherapy and phrenico-exeresis. Pleuropneumonectomy was performed in 1976 because of a residual cavity of a thoracic empyema. Since 1978 the patient suffered from a fistula of the bronchus treated by postural therapy without achieving a cure. In 1989 a fistula formed between oesophagus and pneumonectomy cavity. Clinically this was associated with an increasing reduction of performance and a suddenly ineffective postural drainage, resulting in triphasic and eventually fatal aspiration. Histology revealed a suppurative inflammation in the fistular channel and a slight superficial Candida colonisation of the pneumonectomy cavity, of the fistular channel and of adjacent mucous glands of the oesophagus. Formation of the fistula was probably due to a small traction diverticulum followed by perforation because of obstructed oesophageal passage due to scarified distortions.
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The expression of the small cell carcinoma (SCLC) antigens cluster-5 (antibody LAM8) and cluster-5A (antibody SWA20) was examined on a panel of routinely processed biopsy or surgical specimens of 290 lung tumours by immunoperoxidase staining. Antigen expression was largely restricted to SCLC. Of over 150 tissue samples evaluated, moderate or strong antigen expression was found in 49% (cluster-5) and 45% (cluster-5A). Concordance in expression of the two antigens was seen in 71% of SCLC samples, with 35% expressing both antigens strongly, 8% moderately and 28% being negative for both antigens. Antigen expression was independent of the morphological subtype of SCLC. Primary lung tumours of other histology, including squamous cell carcinoma, large cell carcinoma, adenocarcinoma, mesothelioma or carcinoid had no significant antigen expression. Of 135 tumours, strong or moderate expression of both antigens was seen only in two cases. 20%, mostly carcinoids, were weakly positive for cluster 5 and 4% for cluster 5A antigen. The remainder were antigen negative. No significant antigen expression was seen in 25 normal lung tissues. The membrane antigens of SCLC cluster 5 and 5A are markers for SCLC and their expression in tissues is tumour-associated.
In 6 normal and 7 obstructed excised human lungs the interrupter resistance (APTA, Jaeger Company) with an airway occlusion period of 100 ms was determined, by measuring the equivalent of the alveolar pressure at the end of the occlusion period. To check the pressure equilibration between the tracheal pressure and the alveolar space, catheters were put in the most peripheral layer of the lung. The lungs were ventilated in an artificial thorax. The airway resistance determined from the transbronchial pressure difference by the catheters was taken as a reference. Compared with the reference method, an overestimation of the airways resistance by the interrupter technique in normal lungs was found which was caused by an overshoot of the pressure equilibration during the occlusion period. In contrast, in severely obstructed lungs the pressure equilibration was not complete which led to an underestimation of the airways resistance by the interrupter technique. The best approximation of the airways resistance by the interrupter method was found in lungs with a low degree of obstruction.
Leaves of cotton (Gossypium hirsutum L.) were subjected to overpressures in a pressure chamber, and the exuded sap was collected and analyzed. The exudate contained low concentrations of solutes that were abundant in total leaf extracts, and photosynthetic rates and stomatal conductance were completely unaffected by a cycle of pressurization and rehydration. These criteria and others indicate that the experimental techniques inflicted no damage upon the leaf cells. The pH and abscisic acid (ABA) content of the apoplastic fluid both increased greatly with pressure-induced dehydration. Although ABA concentrations did not reach a steady state, the peak levels were above 1 micromolar, an order of magnitude greater than bulk ABA concentrations of the leaf blades. Treatment of leaves with fusicoccin decreased the K(+) concentration, greatly reduced the pH rise, and completely eliminated the increase in ABA in the apoplast upon dehydration. When water-stressed leaves were pressurized, the pH of the exuded sap was increased by 0.2 units per 1 megapascal decrease in initial leaf water potential. Buffer capacity of the sap was least in the pH range of interest (6.5-7.5), allowing extremely small changes in H(+) fluxes to create large changes in apoplastic pH. The data indicate that dehydration causes large changes in apoplastic pH, perhaps by effects on ATPases; the altered pH then enhances the release of ABA from mesophyll cells into the apoplastic fluid.
Some evidence indicates that photosynthetic rate (A) and stomatal conductance (g) of leaves are correlated across diverse environments. The correlation between A and g has led to the postulation of a "messenger" from the mesophyll that directs stomatal behavior. Because A is a function of intercellular CO(2) concentration (c(i)), which is in turn a function of g, such a correlation may be partially mediated by c(i) if g is to some degree an independent variable. Among individual sunlit leaves in a cotton (Gossypium hirsutum L.) canopy in the field, A was significantly correlated with g (r(2) = 0.41, n = 63). The relative photosynthetic capacity of each leaf was calculated as a measure of mesophyll properties independent of c(i). This approach revealed that, in the absence of c(i) effects, mesophyll photosynthetic capacity was unrelated to g (r(2) = 0.06). When plants were grown in an atmosphere enriched to about 650 microliters per liter of CO(2), however, photosynthetic capacity remained strongly correlated with g even though the procedure discounted any effect of variable c(i). This "residual" correlation implies the existence of a messenger in CO(2)-enriched plants. Enriched CO(2) also greatly increased stomatal response to abscisic acid (ABA) injected into intact leaves. The data provide no evidence for a messenger to coordinate g with A at ambient levels of CO(2). In a CO(2)-enriched atmosphere, though, ABA may function as such a messenger because the sensitivity of the system to ABA is enhanced.
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The aim of general pathology, which following Virchow also should be pathophysiology (and pathobiochemistry), is to elucidate general principles and main mechanisms of diseases. Conceptions like reticulo-endothelial system or coronary insufficiency, inflammations and its mediators, modes of metastasis and many comparable topics are examples of this type of scientific approach, and its tools are careful morphological analysis as well as experimental work of different kinds. In pulmonary pathology the obstruction of airways is one of the most important pathogenetical pathways. Among a broad spectrum of pulmonary diseases it is the main symptom of a developing chronic obstructive pulmonary disease (COPD) and the outstanding cause of cardio-respiratory failure. In German literature the last comprehensive survey on general respiratory pathology was written some twenty years ago and a review of the main techniques of investigation was given at about the same time. Since then - parallel to the invention of new measuring techniques and to the progress in clinical pathophysiology - a rapid further development in the understanding of the pathology of respiratory disorders has taken place, particularly in connection with research in chronic bronchitis and emphysema. Some examples of this development and of the present state of discussion will be reviewed briefly.
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