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Biomedical subjects

C Kuhn

Publications and source records attributed to C Kuhn.

At least 199 records · Page 11Linked to original sources

Reactive eosinophilic pleuritis: a lesion to be distinguished from pulmonary eosinophilic granuloma.

Pleural nodules or sheets of histiocytes, admixed with eosinophils, giant cells, and other inflammatory cells are observed frequently in patients with spontaneous pneumothorax. This reaction, designated reactive eosinophillic pleuritis (REP), can closely resemble eosinophilic granuloma. Reactive eosinophilic pleuritis was found in pleural tissue of 22 of 57 patients with spontaneous pneumothorax in whom tissue was available for study. None of these patients had clinical or radiographic evidence of interstitial lung disease. Follow-up of 20 patients with REP ranged from six months to five years. None developed evidence of eosinophilic granuloma. Electron microscopy of one case did not show the Langerhans granules characteristic of the histiocytoses, including eosinophilic granuloma. Reactive eosinophilic pleuritit appears to be a nonspecific reaction to pleural injury, and is not a prodromal feature of pulmonary eosinophilic granuloma.

Diagnosis, Differential↗

[Skin wound granulation from contact with synthetic foil of teflon-polyurethane type].

When a plastic-foil consisting of teflon-polyurethan foam is applied to ulcer cruris and to polyurethan foam is applied to ulcera cruris and to combusted skin, pronounced granulation and formation of new capillaries and collagen fibers are observed in the contact area. The tightly adhering foils are tolerated by the wounds for more than 40 days with continous granulation. An adverse reaction against the foreign material and development of eosinophils and giant cells is not observed, though the polyurethan-foam of the foil was burst by the ingrowing granulation tissue. When the wound surface is clean, change of the dressing with this foil is necessary only every second or third day.

Bandages↗

Emphysema-like changes in the lungs of the blotchy mouse.

The Blotchy allele is one of several mutations at the Mottled locus on the mouse X-chromosome. Affected males and heterozygous females within the several allelic groups possess varying degrees of connective tissue abnormalities similar to those found in copper-deficient and lathyritic animals, including aortic aneurysms and reduced skin tensile strength. There is evidence that defective inter- and intramolecular cross-links in collagen and elastin account for these abnormalities. The lung of the Blotchy mouse is also structurally and functionally abnormal. Hemizygous males have larger total lung volumes, markedly increased mean linear intercepts, and diminished internal alveolar surface area when compared to normal control animals. Light microsbopy and scanning electron microscopy show abnormal architecture with enlargement of air spaces and effacement of alveolar septa. Static air and saline pressure-volume curves show that lungs of Blotchy mice have decreased elastic recoil and are significantly more compliant than normal. These abnormalities in the lung of the Blotchy mouse suggest that the defects of the connective tissue proteins described in skin and aorta also involve the lung. The Blotchy strain may be a useful model in which to investigate how abnormalities of connective tissue proteins influence pulmonary structure and function.

Animals↗

The scanning electron microscopy of elastase-induced emphysema. A comparison with emphysema in man.

Emphysema was produced in hamsters by a single intratracheal injection of 25 units of porcine pancreatic elastase. The lungs were examined by scanning electron microscopy at intervals from 24 hours to 1 year after the injection, and the appearance was compared to examples of human emphysema. Within 24 hours of injection, the alveolar ducts were dilated and air spaces were of more variable size than normal. Fibrin strands, erythrocytes and phagocytic cells were present in air spaces. By a week the hemorrhage and exudate had resolved, but adnormal air spaces continued to enlarge over the period of study. The abnormal airspaces formed by progressive dilation of alveolar ducts with shortening and occasionally effacement of interalveolar septa. Interalveolar pores were occasionally enlarged but only focally increased in number. The appearance of single examples of human congenital lobar emphysema and panlobular emphysema resembled the animal model. Abnormal air spaces were formed by dilated alveolar ducts with retraction of interalveolar septa. In contrast, in some cases of centrolobular emphysema marked fenestration of alveolar septa occurred and large air spaces were often traversed by threadlike strands of tissue remnants of some preexisting alveolar walls. The results suggest that there are at least two morphogenetic processes leading to emphysema. One is the coalescence of fenestrations leading to destruction of alveolar walls, and the other is a gradual remodeling of lung structure by mechanisms still to be defined.

Adult↗

The induction of emphysema with elastase. II. Changes in connective tissue.

Both clinical and experimental evidence implicate proteolytic enzymes active against elastin in the pathogenesis of emphysema. Paradoxically, however, the elastin content of emphysematous human lungs at autopsy has been normal. When emphysema was produced in hamsters by a single intratracheal injection of 25 units of porcine pancreatic elastase, the elastin content of the lungs was reduced from 1.40 +/- 0.22 mg. in controls to 0.43 +/- 0.10 mg. 24 hours after injection, and histologic sections showed that many elastic fibers had disappeared. The elastin content of the lungs gradually increased, approaching normal values by 2 months after injection. The incorporation of 14C-proline into elastin was markedly elevated during the first 2 weeks after injection, decreasing nearly to normal by 2 months. The synthesis of collagen was also increased, indicated by an increase in the collagen content of the lung, an increase in the prolyl hydroxylase activity, and an increase in incorporation of labeled proline into collagen. During the period of active resynthesis of elastin, small clumps of microfibrils and elastic fibrils were visible by electron microscopy within grooves on the surface of septal connective tissue cells in the lungs. Many elastic fibers seen in histologic sections up to 4 months after injection were of abnormal configuration and disorganized.

Animals↗

Clonal growth of hamster free alveolar cells in soft agar.

Free alveolar cells obtained from healthy unstimulated hamsters were tested for their ability to form colonies in soft agar. Every bronchial washing so far tested contained colon-forming cells. The average plating efficiency was 8.1% (2.4-18.3%). Alveolar colony-forming cells were characterized by having a long initial lag period (4-8 days) and only mononuclear phagocytes were found in the colony. Medium conditioned by baby hamster kidney cells or other cells was required for the initiation and maintenance of their growth. Alveolar cells from normal mice and rats also formed colonies under appropriate culture conditions.

Agar↗

Size and distribution of SV 40 DNA Sequences covalently linked with the DNA of permissive mammalian cells.

CV-1 cells productively infected with SV 40 contain viral DNA which is covalently linked with the host cell DNA. These linear duplex viral-host DNA molecules are replicated during the infectious cycle. They can be selectively isolated and purified by two successive cycles of DNA-DNA hybridization and elution steps using first CV-1 cell and then SV 40-DNA immobilized on filters. In an attempt to clarify the nature of the host DNA sequences neighbouring the viral DNA it was found that reiterated host DNA must be within the range of 800 bases from the viral sequences. Reassociation kinetics and treatment of the reassociated viral-host DNA sequences with single strand-specific S1 nuclease have shown that unique host DNA sequences are always present in close neighbourhood of the viral DNA. Most of the SV 40 DNA sequences are probably intergrated as fragments of subgenomic length.

Animals↗

The fine structure of so-called minute pulmonary chemodectomas.

Electron microscopy was performed on several minute tumors of the type called chemodectomas, all from the lung of a single patient. The cells had a whorling pattern with extensive interdigitating cytoplasmic processes joined by desmosomes. Except for tangles of cytoplasmic fibrils, the tumor cells had few distinctive organelles. They had no endocrine-like granules and were not associated with nerves or basement membranes. The tumors had little resemblance to paragangliomas, but displayed a puzzling similarity to meningiomas. Our observations permit no definite conclusions as to the histogenesis of these lung tumors. Viewed in the light of recent physiologic studies, they cast doubt on the presence of special chemoreceptive paraganglia in the lung.

Aged↗

Scanning electron microscopy of mast cell degranulation.

Scanning and transmission electron microscopy were used to study the morphologic changes occurring in isolated mast cells after stimulation by compound 48/80. Two approaches were used to obtain cells for scanning electron microscopy. Cells incubated in suspension were collected on Millipore filters and air-dried from isopropyl alcohol. Other cells were allowed to attach to cover slips, stimulated, fix in situ, and dried from Freon at its critical point. Resting mast cells prepared by the latter method were covered by a tracery of shelflike ridges, whereas cells prepared by the first method had no ridges but presented a bumpy surface disclosing the underlying granules. Stimulation by compound 48/80 caused marked changes in the surface configuration of the cells, with loss of the regular pattern of ridges, extrusion of granules, and the appearance of openings leading to the interior of the cell. Correlation with transmission electron microscopy indicates that these openings lead to channels containing granules and lined by an intact membrane. These openings give extracellular cations access to granules within the confines of the cell, where the cations may exchange for histamine.

Animals↗