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Query: UMLS:C0851184 (thinning)
11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult mallard ducks were fed a diet containing 50 ppm DDT for 6 months. Eggs laid during this period were collected and eggshell weight, thickness, and calcium were determined. Chronic ingestion of DDT resulted in production of eggshells that were significantly thinner and lighter than those of controls. Total calcium of thinned eggshells was also reduced; however, calcium per gram of eggshell was not altered, indicating that other eggshell constituents were not incorporated as well. Calcium adenosine triphosphatase activity in the microsomal fraction of eggshell gland epithelium was assayed in control and DDT-fed ducks. Enzyme activity in DDT-fed ducks was reduced to 65% of control values. Since Ca-ATPase has been shown to be associated with calcium transport, enzyme inhibition may be responsible for decreased eggshell weight and thickness. Electron microscopic evaluation of microsomal fractions showed elements of the plasma membrane, including cilia and microvilli, as well as rough and smooth endoplasmic reticulum. Inhibition of calcium transport at the plasma membrane of mucosal epithelium is proposed as a possible mechanism of DDT-induced eggshell thinning.
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PMID:Effects of DDT on eggshell quality and calcium adenosine triphosphatase. 14 96

Adult male pigeons were fed 500 ppm of nontoxic chlordene per day for 6 weeks. The ultrastructure of hepatic cells of treated pigeons was examined and compared with that of the control birds. Chlordene feeding induced cytological changes in the structure of liver cells. Thinning of the microvilli of bile canaliculi and clear marking of fibrous long spacing and non-fibrous segment long spacing on collagen fibers were noticed. Increase in the number as well as the vacuolation of lipid bodies in certain portions of the cytoplasm, presence of myeloid bodies in mitochondria, and an increase in the smooth-surfaced endoplasmic reticulum were observed in the liver cells of pigeons given chlordene.
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PMID:The hepatic ultrastructure of chlordene-fed pigeons. 19 61

The hormone-induced pigment dispersion in primary cultures of xanthophores of goldfish (Carassius auratus L.) has been shown to involve the dispersion of not only carotenoid droplets but also of smooth endoplasmic reticulum. The dispersion of these organelles is inhibited by cytochalasin B and is accompanied by thinning of the cell body, thickening of the processes, and also overall changes in cellular morphology (process extension) under certain conditions. Electron microscopic examination of heavy meromyosin treated glycerinated xanthophores in scales revealed the presence of actin filaments in these cells.
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PMID:Ultrastructural demonstration of hormone-induced movement of carotenoid droplets and endoplasmic reticulum in xanthophores of the goldfish, Carassius auratus L. 21 Sep 50

Correlative morphological and biochemical studies were made on the adrenal of rats treated with daily subcutaneous injections of testosterone propionate in a dose of 50 mg/kg for 30 consecutive days. Histologically, there is a thinning of the zona fasciculata with a decrease of cell numbers, swelling of the cell body and the occurrence of large lipid droplets in the cytoplasm. Electron microscopic examination revealed swelling of mitochondria with reduction of cristae and hypertrophy of smooth-surfaced endoplasmic reticulum with cluster formation or whirl-like arrangement. In in vitro biochemical experiments, it was noted that conversion of deoxycorticosterone to corticosterone or 18-hydroxydeoxy-corticosterone was decreased to 45% of the control level in the testosterone-treated group.
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PMID:Testosterone-indued focal myocarditis in rats. II. Morphological and biochemical observations of the adrenal in relation to the pathogenetical mechanism of cardiac lesions. 73 65

Seven hundred fifty-two cases of instantaneous sudden cardiac death were studied. Alcoholic cardiomyopathy was found in 127 cases (16.9%), predominantly in men under age 50 (73%). The heart was enlarged, with an average mass of 441 +/- 8 g. Light microscopy revealed uneven thinning and atrophy of the cardiomyocytes, with fatty infiltration and development of fatty tissue around the vessels of the left ventricle and interventricular septum, up to the subendocardial areas. In the majority of cardiomyocytes, electron microscopy showed atrophy of the myofibrils, pronounced dilation of the sarcoplasmic reticulum, lipids in the cytoplasm, mitochondriosis and an increased number of lysosomes and alterations of the mitochondria. Unchanged cardiomyocytes were characterized by hypertrophy and numerous ribosomes, and had developed a granular endoplasmic reticulum. Also observed were interstitial edema, an enlarged cardiomyocyte-capillary space, thinning of the capillary walls, flattening of the endothelium and a plethora and aggregation of erythrocytes. Decreases in mitochondrial enzyme activity were studied by enzyme histochemistry. Analogous pathologic changes may be individually present in other types of myocardial disease, but the complex of changes is specific for alcoholic cardiomyopathy. The frequency of alcoholic cardiomyopathy among victims of sudden death suggests that alcoholic cardiomyopathy is a risk factor for sudden cardiac death.
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PMID:Alcoholic cardiomyopathy and sudden cardiac death. 371 41

In the streptozocin-induced diabetic rat, the placenta is larger and the fetus is smaller than normal. To study cellular differences that might contribute to the size and functional disparity between diabetic and control placentas, a light- and electron-microscopic analysis was performed on 14-, 18-, and 22-day (term) control and diabetic placentas. Diabetic placentas, especially later in gestation, were marked by the presence of large numbers of glycogen-distended cells in the basal zone. Within the placental labyrinth, the trophoblastic layers of the interhemal membrane were significantly thicker in the diabetic placentas on days 18 and 22, and large accumulations of liid droplets were present, especially in the inner two trophoblastic layers. In normal placentas there is a marked thinning of the placental barrier in the labyrinth by day 22 of gestation, making the thickness of the labyrinthine layers in age-matched diabetic placentas even more impressive. Finally, the labyrinth of 22-day diabetic placentas contained more glycogen and rough endoplasmic reticulum in the inner trophoblastic layer, a feature that is found in less-mature (18-day) control placentas. Thus, the diabetic placentas have a number of features that are consistent with functional immaturity/dysmaturity. Cytologic evidence confirms the presence of increased glycogen and lipid reserves in both the junctional zone and the cellular area between maternal and fetal blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fine structural abnormalities of the placenta in diabetic rats. 375 95

Light microscopic and electron microscopic findings in thymuses from 4-week old feline leukemia virus-infected and 4- and 9-week old noninfected kittens were evaluated and found to be morphologically similar to each other. Thymuses from 9-week old feline leukemia virusinfected kittens were markedly atrophied and individual lobules within each thymus varied in the severity of atrophy. Loubules having the least severe atrophy had a moderate thinning of the cortex and a heterogeneous thymuses included intense eosinopoiesis at the corticomedullary junction, increased prominence of vasculature, and enlarged Hassal's corpuscles. In addition to these changes lobules of thymus having the most severe atrophy had a marked cortical thymocyte depletion, lobule collapse, and increased numbers of mast cells. Degeneration of epithelial cells in most lobules was indicated by electronlucency of the cytoplasmic matrix and often greatly dilated rough endoplasmic reticulum.
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PMID:Light and electron microscopic evaluation of thymuses from feline leukemia virus-infected kittens. 624 86

The effects of high toxic doses of the anticancer drugs, etoposide and its phosphate derivative, BMY-40481, on the nervous system of female CD-1 mice were examined by light microscopy (LM) and transmission electron microscopy. Mice were euthanatized 4 wk following a single iv injection of either 0, 50, 100, or 150 mg/kg of BMY-40481 or 44 or 88 mg/kg of etoposide. Mice treated with 100 or 150 mg/kg of BMY-40481 or 88 mg/kg of etoposide had clinical symptomology of progressive ataxia, impaired righting reflex, and splaying and paresis of fore- and hindlimbs at day 8. Similar, dose-related LM changes were observed with both drugs at all doses and consisted of degeneration of dorsal root ganglion cells and axonal degeneration of their distal and proximal processes in peripheral nerves, dorsal spinal roots, and dorsal funiculi of spinal cord. Axonal degeneration was characterized by LM as shrinkage, swelling, and fragmentation of axon cylinders accompanied by secondary demyelination. Degenerative changes in ganglion cell bodies included eccentric nuclei, cytoplasmic vacuolation, central chromatolysis, and peripheral clumping of Nissl's bodies. Ultrastructurally, ganglion cell bodies had focally extensive dilation of the rough endoplasmic reticulum, mitochondrial swelling, increased numbers of phagolysosomes and prominent aggregations of microfilaments (globular filamentous bodies). Ultrastructural axonal changes occurred primarily in large, myelinated fibers and consisted of axonal swelling or loss, thinning of myelin sheaths, and a decrease in the number of organelles. This is the first report of etoposide-related sensory neuropathy in laboratory rats, a model that my be useful for the study of etoposide-related peripheral neuropathy in humans.
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PMID:Etoposide- and BMY-40481-induced sensory neuropathy in mice. 789 82

The pathological changes induced in capillaries by BaH1, a hemorrhagic metalloproteinase isolated from the venom of Bothrops asper, were studied after i.m. injection in mouse gastrocnemius. Hemorrhage was observed macroscopically, and corroborated histologically, within the first 5 min. At the ultrastructural level, the earliest changes in endothelial cells, observed 1 min after toxin administration, consisted of a decrease in the number of pinocytotic vesicles, the presence of blebs and cytoplasmic projections pinching off to the vascular lumen and the detachment of endothelial cells from the surrounding basal lamina. These processes occurred concomitantly with a thinning of endothelial cells. In capillaries undergoing more advanced degenerative stages, there were gaps or breaks in endothelial cells through which erythrocytes were escaping to the extravascular space. In these cells, the basal lamina was usually absent. Throughout this process, intercellular junctions remained apparently intact and no evidence was found of extravasation through widened intercellular junctions. In addition to this morphological pattern of degeneration, some capillaries presented swollen endothelial cells with dilated endoplasmic reticulum and lacking pinocytotic vesicles. Many capillaries contained platelet plugs and fibrin. Thus, hemorrhage induced by BaH1 occurs per rhexis, as has been also described for other venoms and hemorrhagic toxins.
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PMID:Pathological changes induced by BaH1, a hemorrhagic proteinase isolated from Bothrops asper (Terciopelo) snake venom, on mouse capillary blood vessels. 798 2

A single injection of peroxidase-labelled Ricinus communis agglutinin (RCA-HRP) was given intracerebrally in 5-day old postnatal rats to determine its effects on neural tissues. The rats were sacrificed at various time intervals ranging from 1 hour to 8 weeks after the injection. 5 days after the injection, the lateral ventricle ipsilateral to the injection was progressively enlarged. The size of the ventricle continued to expand so that 10-15 days after the injection the ventricle on the contralateral side was also affected. In longer surviving rats, i.e 3-8 weeks after the injection, both the ventricles were extremely dilated resulting in the thinning of the cerebral cortex. Scanning electron microscopy of the dilated ventricles showed signs of disruption of the ependyma in some regions. A number of cells including macrophages, neurons, glioblasts, astrocytes and oligodendrocytes were present on the ependyma. Their identification was confirmed by scanning- and transmission electron microscopy. Transmission electron microscopy of the cerebral cortex subjacent to the dilated ventricles showed the presence of many degenerating neurons, 2-5 hours after the injection of RCA-HRP. The neurons displayed typical features of degeneration, i.e. displacement of nucleus, dilatation of cisternae of rough endoplasmic reticulum, and swelling and disintegration of mitochondria. In conclusion, following a single intracerebral injection of RCA-HRP, drastic neuronal degeneration was elicited near the site of injection and this resulted in the dilatation of the lateral ventricles similar to hydrocephalus.
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PMID:Induced hydrocephalus in postnatal rats following an intracerebral injection of ricin. 830 63


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