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Karl Jungmann

Publications and source records attributed to Karl Jungmann.

2 recordsLinked to original sources

Upper airway epithelial structural changes in obstructive sleep-disordered breathing.

The etiology of upper airway collapsibility in patients with snoring and obstructive sleep apnea (OSA) remains unclear. Structural mucosal changes could be contributory factors. The objective of this study was to determine whether pathologic changes in the epithelium or the epithelial-connective tissue interface are present in patients with snoring and/or OSA by means of scanning electron microscopy and immunohistochemistry. Uvulae were obtained by uvulopalatopharyngoplasty from three patients with habitual snoring and nine patients with mild to severe OSA, as well as by dissection from 43 nonsnoring body donors. Scanning electron microscopy revealed structural changes in the epithelial-connective tissue boundary that significantly differed from age-related changes in the control subjects. The immunohistochemical staining with antibodies against epithelial cytokeratins showed differences in the expression pattern of cytokeratin 13 between patients and control subjects. No differences were found in the distribution pattern of laminin. Analysis of defense cells revealed a significant diffuse infiltration of leukocytes, mainly T cells, inside the lamina propria of the patient group, which was not observed in the control group. In conclusion, these results support the hypothesis that progressive structural changes in the mucosa caused by the trauma of snoring are a possible contributory factor to upper airway collapsibility.

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Morphological studies of the optic canal.

BACKGROUND: In some cases of closed head injuries after minor blunt trauma, an amaurosis can occur. Our knowledge concerning the pathophysiological mechanisms of traumatic optic neuropathy is limited. The aim of this study is to analyze the morphology of the optic canal in order to understand the effect of mechanical forces in the optic canal and the consecutive injuries. METHODS: Forty-one optic canals from body donors were analyzed by light microscopic, polarization microscopic, immunohistochemical and scanning electron microscopic techniques. RESULTS: In the optic canal, collagen fibrils of the dural sheath are organized in a scissor-like pattern. Within this collagen network multiple vessels are integrated. The main component of the extracellular matrix is collagen type I. The dural sheath and pial sheath are connected by collagen bundles. Parallel to these bundles, small vessels form anastomoses between the dural and pial vessel systems. In the arachnoidea, no blood vessels can be detected by immunohistochemical techniques. CONCLUSIONS: Based on morphological findings, the following pathophysiological mechanisms can be discussed in cases of blunt closed head injury with consecutive amaurosis: 1. Squeezing and rupture of nutritive vessels by transduction of shearing forces via the scissor-like collagen network. 2. Atrophy by pressure of the optic nerve after injury to the microvasculature followed by formation of microhematomas and reactive edema. 3. Direct injury of axons of the optic nerve by shearing forces within the optic canal. These mechanisms should be studied further in the future.

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