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K Morgenroth

Publications and source records attributed to K Morgenroth.

At least 19 recordsLinked to original sources
PubMed1992

Recognition of SV40-VP2 in the infected cell by antipeptide antibodies.

Antipeptide antibodies were elicited against two synthetic peptides corresponding to amino acids 47-55 and 98-103 of the structural protein VP 2 of SV 40. The induced antibodies proved to be VP 2-specific in an immunoblot. In immunofluorescence these antibodies showed a discrete nuclear and perinuclear staining pattern. In immune electron microscopy studies the induced antibodies did not bind to major virions suggesting that VP 2 is not present at the surface of SV 40 particles.

Animals↗
PubMed1992

[Pulmonary fibrosis after inhalation of amorphous silicic acid].

Light- and scanning electron microscopical studies with energy dispersive x-ray microanalysis were performed on biopsy material obtained from two patients with longstanding occupational exposure to amorphous silica, in whom radiologically interstitial pulmonary fibrosis in vicinity of dust deposits, which could be identified as amorphous and rarely as crystalline silica, was found. The direct topographical relationship between the dust deposits and the tissue reaction indicate that the amorphous silica incorporated in the fibrotic foci is responsible for the development of the fibrosis.

Adult↗
PubMed1990

[Pulmonary risks caused by exposure to glass fiber dust].

We observed two patients who, after inhaling glass fibre dust for 14 and 16 years, respectively, developed a cough and dyspnoea on exertion. Our investigation of transbronchially obtained lung tissue with the aid of light microscopy, electron microscopy and energy-dispersive x-ray micro-analysis revealed fibrosis of mild extension in immediate topographical relationship to phagocytosed fragments of glass fibre. We conclude from these findings that inhaled glass fibre dust can develop a fibrogenic effect.

Biopsy↗
PubMed1990

[Roentgen microanalysis of dust particles in histologic sections of pneumoconiosis].

We investigated the significance of X-ray element analysis of histological sections obtained from 26 patients with pneumoconiosis (occupations, etc. mining, quartz processing, metal polishing, exposure to aluminium dust, exposure to asbestos dust). Aluminium-containing or, in the case of asbestosis, magnesium-containing silicates were the most commonly found minerals. Iron and titanium were detected in particular in the sections obtained from metal polishers. X-ray micro-analysis permits a more accurate determination of dust exposure, and an improvement in the description of the pneumoconiosis presenting.

Asbestosis↗
PubMed1989

[Changes in the bronchial musculature in chronic obstructive respiratory tract diseases].

Changes in the bronchial musculature in patients with chronic obstructive lung disease, were submitted to a systematic electron-microscopic investigation. A marked interstitial fibrosis with degenerative changes affecting the muscle cells was observed. The formal pathogenetic course of these changes can be reconstructed on the basis of numerous individual findings. The muscle cells are progressively "ensheathed" in a disorderly fine-filamentous basic structure (matrix), and in collagenous fibres. As a result, the contact surfaces between the muscle cells are disturbed, and the nerve endings "displaced" from the muscle cells. This fibrosis is associated with a protracted "shrivelling" of the individual muscle cells. The changes involving the muscles of the bronchial wall are comparable with those seen in the smooth muscles of blood vessels involved in arteriosclerosis. The morphological changes to the muscles of the bronchi described in this paper strongly suggest that protracted fibrosis formation, coupled with the degradation of muscle cells, contribute to a loss of elasticity of the bronchial wall in chronic obstructive lung disease.

Adult↗
PubMed1988

[Campylobacter pylori--status of knowledge from the morphologic viewpoint].

The morphological alterations of the gastric mucosa due to Campylobacter pylori (C.p.) were examined with high resolution light microscopy, scanning electron microscopy, and transmission electron microscopy. On the ultrastructural level the number and distribution of bacteria were correlated to the extent of the inflammatory resp. degenerative epithelial alterations. Intestinal metaplasia was always free of bacteria, even with strong colonization of the residual mucosa. In comparison to the gastric mucosa in the IM the cellular disintegration was less strongly developed. The topographical distribution of C.p. was studied on two ulcer resection specimens and documented by means of "campylobacter-mapping". Contrary to the subjective impression made by stomach biopsies, the bacterial colonization examined was not patchy, but rather it was evenly distributed. The association between C.p. and duodenal ulcer, made in most literature, relies primary on cultural, or morphological studies of the antrum mucosa, thereby actually representing the correlation of C.p. to the accompanying gastric inflammation. An analysis of the detection methods--morphological, cultural, and the urease-test--confirms the significance of morphological methods in the diagnosis of C.p.-infection.

Campylobacter↗
PubMed1987

[Causative relations between infections and allergies in obstructive respiratory tract diseases in childhood].

Obstructive bronchitis of young babies and infants is most often caused by respiratory-syncytial (RS)- and parainfluenza viruses, to a certain extent by adenoviruses. In the school age-group rhinoviruses and to a smaller extent mycoplasma pneumoniae gain further importance. All the viruses may cause or deteriorate asthmatic attacks, as well as during common cold or on the basis of documented allergies. Proposed mechanisms of viral-infection-induced obstructive airway disease are distinct lesions of bronchial-epithelium, followed by enhanced allergen-resorption and sensitization of submucosal mast cells, establishing an allergy. Following epithelial discontinuation airway irritant receptors which are raised in sensitivity by viral toxins are exposed and stimulated. Via vago-vagal reflexes this leads to bronchoconstriction. Furthermore, in the development of bronchial hyperresponsiveness there may be participation of virus-induced blockage of adrenoceptors, basophilic and mast-cell release of mediators as well as induction of specific IgE antibodies against RS- and/or Para-influenza-viruses. Viral airway infections are supposed to influence the immunological response of T-lymphocytes and probably macrophages selectively, e.g. to regulate IgE-antibody production. Especially in children with an atopic family history the RS-viruses cause obstructive airway disease. During acute respiratory-virus infections using electron microscopy marked pathological changes of bronchial-epithelium can be demonstrated causing disturbance or even stopage of mucus-transport. These changes are fully reversible within weeks after airway infection. Although there is no doubt about a causative relation between respiratory-tract infection and allergy, hardly any prediction for development of asthma bronchiale in later life, after having suffered from virus-induced obstructive airway disease early in life, can be made.(ABSTRACT TRUNCATED AT 250 WORDS)

Asthma↗
PubMed1986

Leukotriene synthesis by human gastrointestinal tissues.

The prostaglandin and leukotriene synthesizing capacity of human gastrointestinal tissues obtained at surgery was investigated using radioimmunoassay for prostaglandin E2, leukotriene B4 and sulfidopeptide leukotrienes. The leukotriene immunoassay data were validated by high-pressure liquid chromatography (HPLC). During incubation at 37 degrees C, fragments of human gastric, jejuno-ileal and colonic mucosa released considerably larger amounts of prostaglandin E2 than of leukotriene B4 and sulfidopeptide leukotrienes. Gastrointestinal smooth muscle tissues released even larger amounts of prostaglandin E2, but smaller amounts of leukotrienes than the corresponding mucosal tissues. Adenocarcinoma tissue released larger amounts of leukotriene B4, sulfidopeptide leukotrienes and prostaglandin E2 than normal colonic mucosa. Ionophore A23187 (5 micrograms/ml) did not stimulate release of prostaglandin E2 from any of the tissues investigated, but enhanced release of leukotriene B4 and sulfidopeptide leukotrienes. HPLC analysis demonstrated that immunoreactive leukotriene B4 co-chromatographed almost exclusively with standard leukotriene B4, while immunoreactive sulfidopeptide leukotrienes consisted of a mixture of leukotrienes C4, D4 and E4. Leukotriene synthesis by human gastrointestinal tissues was inhibited by the lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA) and the dual enzyme inhibitor BW755C (3-amino-1-(trifluoromethylphenyl)-2-pyrazoline hydrochloride). Synthesis of prostaglandin E2 was inhibited by the cyclooxygenase inhibitor indomethacin as well as by BW755C. Incubation of gastrointestinal tissues in the presence of glutathione decreased the amounts of leukotrienes D4 and E4, while release of leukotriene C4 was simultaneously increased. On the other hand, incubation of tritiated leukotriene C4 with incubation media from human gastric or colonic mucosa resulted in conversion of the substrate to [3H]leukotriene D4 and [3H]leukotriene E4. The results indicate the capacity of human gastrointestinal tissues to synthesize the 5-lipoxygenase-derived products of arachidonate metabolism, leukotriene B4 and sulfidopeptide leukotrienes, in addition to larger amounts of prostaglandin E2. Furthermore, considerable activities of the sulfidopeptide leukotriene-metabolizing enzymes gamma-glutamyl transpeptidase and dipeptidase were detected in human gastrointestinal tissues. These enzymes might play an important role in biological inactivation and/or change of biological profile of sulfidopeptide leukotrienes generated in the human gastrointestinal tract.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗