Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ultrastructural study confirmed that, in rats, vitamin A deficiency initially caused the sloughing of some spermatids and spermatocytes into the lumina of the seminiferous tubules around day 3 following the initial decrease of body weight. From days 5 to 10, a considerable number of spermatocytes and spermatids, which still remained in the epithelium, underwent necrosis. Several stages of dying spermatocytes and abnormal spermatids were observed. The latter were distinguished by the presence of chromatin aggregating along the nuclear envelopes and highly vacuolated mitochondria. These cells range from single to multinucleate forms. They were incapable of differentiating further into spermatozoa and ultimately degenerated. Within the same period, Sertoli cells exhibited numerous darkly stained lysosome-like inclusions, and the upper part of their cytoplasm appeared as irregular processes, some of which were broken off and resulted in the thinning of the epithelium. From days 10 to 20, the remaining germ cells comprised mainly spermatogonia and few abnormal spermatocytes. The latter appeared enlarged and were very lightly stained. Their nuclei exhibited unusual blocks of heavily condensed chromatin amidst very highly dispersed chromatin fibers. Though their number was reduced, most of the spermatogonia appeared unaltered. Processes of Sertoli cells became even more irregular and were interrupted at certain sites by large empty spaces. Darkly stained inclusions in their cytoplasm were fewer than observed earlier.
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PMID:Cytological changes in the testes of vitamin-A-deficient rats. II. Ultrastructural study of the seminiferous tubules. 41 27

We showed previously that the proliferation of hamster airway secretory cells decreases during vitamin A deficiency (VAD) but later increases when submucosal inflammation develops (Virchows Arch [B] 59:231-242, 1990). This observation has important biological implications since two morphological extremes (atrophy and quiescence versus hyperplasia and hyperproliferation) are reported in the literature for VAD tracheal epithelium in vivo. In the present study, histological slides of tracheal rings from 35-day-old control and VAD hamsters (Virchows Arch [B] 45:197-219, 1984) were reviewed again. Rings from VAD hamsters were selected based on the absence or presence of a florid submucosal inflammation. Quantitative analyses were made on the cartilaginous part of rings from the anterior third of the trachea. When inflammation was absent, a mucociliary pseudostratified epithelium was, for the most part, maintained. The mitotic rate (MR, 6 h colchicine blockade) of secretory cells was markedly reduced (29-fold) but that of basal cells was not changed significantly. Moreover, cell density was not changed by VAD but ciliated cells and secretory cells were decreased and basal cells were increased, proportionally. We call this "minimal morphological change." Thinning (atrophy) of the minimally changed epithelium was associated with focal cell sloughing. Small scattered foci of epidermoid metaplasia (multiple layers of highly keratinized cells which were extremely flat, so that the epithelium was thin and attenuated) were also seen. We call this "atrophic epidermoid metaplasia." When inflammation was present, hyperplastic changes (stratification and epidermoid metaplasia) predominated and cells were in mitosis at all epithelial levels (low, middle, superficial) except in the most superficial (terminally differentiated) squames. The tracheal epithelium was thickened and hypercellular. The cells were piled up at the stratified lesions, and epithelial height, cell density and epithelial MR were significantly increased compared with the non-inflamed VAD epithelium. The effects of VAD and inflammation on cell proliferation were analyzed further by studying 7 h bromodeoxyuridine (BrdU) labelling patterns of cells in VAD tracheal epithelium, with and without submucosal inflammation. In addition, inflammation was induced in "minimally changed epithelium" by mild mechanical injury. The BrdU labelling patterns confirmed that DNA synthesis by secretory cells is reduced markedly by VAD. However, this suppression is overidden by the influx of inflammatory cells (the nature of the stimulus is unknown). The results indicate that the morphological contrasts (atrophy and hyperplasia) seen in the trachea during VAD in vivo are related to extremes in proliferation rates of tracheal secretory cells, regulated by VAD alone (minimal replication) and by inflammation (maximal replication).
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PMID:Vitamin A deficiency and inflammation: the pivotal role of secretory cells in the development of atrophic, hyperplastic and metaplastic change in the tracheal epithelium in vivo. 134 77

The purpose of this research was to determine the effects of vitamin A deficiency on liver and lung morphology and type II pneumocyte function. Weanling rats were fed a retinol-adequate (control) or -deficient diet for 6 wk. Average food intakes and body weights were not different between the vitamin A-deficient and -adequate rats. Histologic examination revealed that the lungs of vitamin A-deficient rats had less collagen in the adventitia of small caliber arteries and arterioles and in the alveolar septa, which appeared thinner than that of controls. Many areas of the lungs of the same rats were also emphysematous (increased size of air spaces distal to the terminal bronchiole, with thinning and partial or total destruction of septal wall). Content of elastin also was lower in the lung parenchyma, as well as in the small arteries and arterioles, but not in the larger ones. Peribronchial collagen was not affected by the deficient diet. Scattered inflammation was observed in most of the vitamin A-deficient rats; a mild inflammatory reaction also was seen in one of the controls. Vitamin A-deficient rats also exhibited hepatocyte vacuolization and mild inflammation in the liver, specifically in the periportal tracts. Surfactant synthesis and ornithine decarboxylase activity were significantly lower in type II pneumocytes isolated from vitamin A-deficient rats. In conclusion, our data provide evidence that vitamin A deficiency produces profound morphologic alterations in liver and lung parenchyma and impairs pneumocyte function.
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PMID:Vitamin A deficiency injures lung and liver parenchyma and impairs function of rat type II pneumocytes. 1080 13