Biomedical subjects

H J Kahn

Publications and source records attributed to H J Kahn.

75 records · Page 5Linked to original sources

PubMedDate not supplied

"Aberrant elastic" in elastofibroma: an immunohistochemical and ultrastructural study.

Elastofibroma is a rare lesion characterized by the presence of abundant abnormal elastic fibers with a unique morphology, fibroblastic proliferation, and collagen deposition. Whether the altered morphology of the elastic fibers is a degenerative phenomenon or is due to abnormal elastogenesis is controversial. We studied fetal skin and three cases of elastofibroma by light microscopy and immunohistochemistry using an antibody to lysozyme, and one case of elastofibroma by electron microscopy (EM). Our previous studies have shown that normal elastic fibers in adult skin do not stain for lysozyme whereas abnormal elastic fibers in solar elastosis and pseudoxanthoma elasticum react positively for lysozyme. In the fetal skin and all three cases of elastofibroma the elastic fibers were negative for lysozyme. EM showed the abnormal flowerlike configuration of the elastic fibers, which consisted of a central core of normal or degenerating elastin surrounded by radiating spokes of granular and filamentous material of variable electron densities, suggesting that the structure and organization of the microfibrils is abnormal. The absence of lysozyme in the aberrant elastic did not differentiate whether there was excessive production of fetal or adult elastic. However, the excessive amount of microfibrils seen at the ultrastructural level suggests that there may be excessive fetal elastic production. The elastic fibers were intimately related to the fibroblasts and were often present within their caveolae, suggesting that the abnormal elastic fibers are produced by the fibroblast. Our study suggests that abnormal elastogenesis with subsequent degeneration plays a role in the production of the abnormal elastic fibers in elastofibroma.

Elastic Tissue↗

PubMedDate not supplied

The effects of nicotine on Parkinson's disease.

Post-mortem studies have demonstrated a substantial loss of nicotinic receptors in Parkinson's disease (PD), which may be at least partially responsible for some of the cognitive, motoric, and behavioral deficits seen in this disorder. Epidemiologic studies have suggested that cigarette smoking is a strong negative risk factor for the development of PD. We have previously shown that blockade of central nicotinic receptors produces cognitive impairment in areas of new learning, short-term memory, and psychomotor slowing with increasing dose sensitivity with age and disease. Studies of acute stimulation of nicotinic receptors in Alzheimer's disease with nicotine and the novel agonist ABT-418 in our laboratory and others have shown improvements in several measures of cognitive function. Prior studies of the effects of nicotine in PD have suggested some improvements in clinical symptomatology. We have begun quantitative studies of both acute and chronic nicotine in PD to assess both cognitive and motor effects. Fifteen (15) nondemented subjects (age 66 +/- 5.3; M/F = 11/4) with early to moderate PD (mean Hoehn-Yahr stage = 1.77; MMSE = 28.6) received a dose-ranging study of intravenous nicotine up to 1.25 microg/kg/min, followed by chronic administration of nicotine by transdermal patch with doses ranging up to 14 mg per day for 2 weeks. Testing occurred both during drug administration and up to 2 months after drug cessation to look for prolonged effects. Preliminary analysis shows improvements after acute nicotine in several areas of cognitive performance, particularly measures such as reaction time, central processing speed, and decreased tracking error. Improvements in attention and semantic retrieval were not seen. After chronic nicotine, improvements were seen in several motor measures suggesting improved extrapyramidal functioning. This appeared to be sustained for up to 1 month after drug. The treatment was well tolerated. Nicotinic stimulation may have promise for improving both cognitive and motor aspects of Parkinson's disease.

Aged↗

PubMedDate not supplied

The ultrastructure of metastatic adenocarcinoma in serous fluids. An aid in identification of the primary site of the neoplasm.

Identification of the primary sites of metastatic adenocarcinomas is a diagnostic problem, particularly in cases of occult primary neoplasms. We studied the ultrastructural morphology of 16 metastatic adenocarcinomas that presented as effusions to establish organ-specific features that would characterize adenocarcinomas from various sites. The nine cases in which the site of the primary carcinoma was known included seven derived from the breast, one from the ovary and one from the colon. The primary site was unknown in seven cases at the time of presentation. After investigations, the primary site became known in five cases (lung, colon and appendix, one case each, and the ovary in two cases). Ultrastructurally diagnostic features could be detected in gastrointestinal, ovarian, bronchioloalveolar-cell and breast carcinomas. In gastrointestinal carcinomas, the presence of short microvilli with long rootlets was specific for the group. The lamellar inclusions of type II pneumocytes were diagnostic of bronchioloalveolar-cell carcinoma. The microvilli in ovarian carcinomas were long, slender and bushy, as in mesotheliomas; however, the cells lacked the perinuclear condensation of tonofilaments seen in the latter. Breast carcinomas were associated with numerous intracytoplasmic lumina, electron-dense granules and aggregates of small vesicular bodies. We conclude that ultrastructural examination of adenocarcinomas in serious fluids can help to identify the primary site of certain neoplasms or at least shorten the list of possibilities. This may reduce costs and minimize the discomfort patients have to undergo by curtailing extensive invasive investigations in search of unknown primary neoplasms.

Adenocarcinoma↗