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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five cases with collapse of a vertebral body due to malignancy were surgically treated. A posterior exposure was adequate for removal of the tumor within the vertebral body; and stabilization of the spine appears to have been achieved satisfactorily with Harrington rods. The indications for surgical treatment and the results are discussed. In selected cases, this procedure has been worthwhile. It has relieved pain, restored ambulation, and allowed a normal existence for patients who otherwise would have been bedridden.
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PMID:The treatment of malignancy of a vertebral body. 615 22

Treatment of epithelial African green monkey kidney (BSC-1) cells with the potent tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induces a rapid and reversible redistribution of actin and vinculin that is detectable after only 2 min of treatment. Within 20-40 min, stress fibers disappear, while at the same time large actin-containing ribbons resembling ruffles develop both at the cell periphery and in more central regions. Vinculin is associated with these actin ribbons or bands in a punctate or patchy staining pattern. Adhesion to the substratum is changed from predominantly focal contacts associated with stress fiber ends in untreated cells to broad zones of close contact after TPA treatment. High voltage electron microscopic observations disclose the ribbons to consist of highly cross-linked actin filament networks. Thus, association of vinculin with filament networks, rather than (the ends of) filament bundles, is demonstrated. The integrity of microtubules and vimentin filaments is not affected by TPA treatment, but their distribution is altered to conform with the highly distorted cell shape. The response to TPA is neither prevented nor modified by nocodazole-induced depolymerization or taxol-induced stabilization of microtubules. An intact intermediate filament network seems not required either since colcemid-induced collapse of vimentin filaments towards the nucleus does not affect the cell's response to TPA. Rapid redistribution of actin and vinculin also takes place in enucleated cells and in the presence of cycloheximide, but is prevented by dinitrophenol or oligomycin. TPA-induced cytoskeletal alterations are independent of fibronectin expression and not mimicked, modified, or prevented by calmodulin inhibitors or experimentally elevated levels of calcium and cyclic AMP. Thus the morphological response to TPA involves rapid redistribution of actin and vinculin independent of transcription and translation, fluctuations in the levels of calcium or cyclic AMP, or changes in the organization of microtubules, intermediate filaments, and fibronectin.
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PMID:A tumor promoter induces rapid and coordinated reorganization of actin and vinculin in cultured cells. 620 76

The computed tomographic (CT) appearance of lobar collapse has yet to be defined. In an attempt to determine the characteristic appearance of collapse 95 cases were reviewed retrospectively in a wide variety of clinical settings over a 3 year period ending January 1983. In this report 38 cases of lobar collapse secondary to endobronchial occlusion are analyzed; the appearance of collapse without endobronchial obstruction forms the basis of a subsequent report. Computed tomography was accurate in determining the site of bronchial occlusion in all cases. In 36 of 38 cases collapse was caused by endobronchial tumors, including bronchogenic carcinoma, bronchial carcinoids, endobronchial metastases, and lymphoma. Differentiation between these tumors was not feasible with CT. Most cases of collapse were caused by central tumor. In those cases in which a bolus of contrast material was used differentiation between tumor mass and collapsed pulmonary parenchyma was possible. Two of 38 cases were found to have benign bronchial occlusion. In one case a mucous plug obstructing the left lower lobe bronchus was accurately defined. In another case a bronchial stricture occluded the right lower lobe bronchus. This represented the only false positive case in this series. It is concluded that CT is an accurate means for establishing the diagnosis of endobronchial obstruction. In most cases the diagnosis of neoplasia was possible, provided a bolus of contrast material was used to define tumor mass. The potential role of CT in evaluating patients with lobar collapse is discussed.
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PMID:Computed tomography of lobar collapse: 1. Endobronchial obstruction. 630 26

Aggregation of the receptor for IgE on mast cells, basophils, and a tumor analog, rat basophilic leukemia (RBL) cells, induces a calcium-dependent degranulation of the cells. We have measured the membrane potential (delta psi) of RBL cells during this reaction by using the tetraphenylphosphonium ion (Ph4P+) equilibration technique. We observed a 20-45% reduction in ionophore-sensitive Ph4P+ accumulation. The phenomenon persisted under conditions expected to collapse the mitochondrial membrane potential, consistent with the effect being due to a change in delta psi of the plasma membrane. We estimated that the change reflects a depolarization of 20 mV (from -90 to -70 mV, interior negative). Whereas degranulation fails to occur in the absence of external Ca2+, this was not true of the depolarization, indicating that the latter was not a consequence of secretion. When aggregation of the receptor is induced by reaction of the cell-bound IgE with a multivalent antigen, the secretory reaction can be halted by adding a univalent hapten. In this case, complete repolarization occurs. Equivalent depolarization was observed in the absence of Na+ but was diminished when both Ca2+ and Na+ were absent. Together, the data suggest that aggregation of the receptor opens ion channels and that the latter disappear promptly when the receptors are disaggregated. It is plausible that formation of these channels leads to the entry of Ca2+ and is an early and critical consequence of the aggregation of the receptors, thereby leading to degranulation.
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PMID:Crosslinking of the receptors for immunoglobulin E depolarizes the plasma membrane of rat basophilic leukemia cells. 631 May 90

Proton beam irradiation resulted in clinical and/or histopathological regression of large ciliary body and choroidal melanomas in three eyes. Enucleations were performed 6 1/2 weeks, five months, and 11 months after irradiation for angle-closure glaucoma from total retinal detachment, increase in retinal detachment, and neovascular glaucoma, respectively. A direct relationship was found between the length of the interval from irradiation to enucleation and the degree of histologic changes. Vascular changes in the tumors included endothelial cell swelling and decreased lumen size, basement membrane thickening, collapse of sinusoidal vessels, and thrombosis of vessels. Although apparently unaltered tumor cells remained, degenerative changes occurred in some melanoma cells, including lipid vacuoles in cytoplasm, pyknotic nuclei, and balloon cell formation. Patchy areas of necrosis and proteinaceous exudate were present. Pigment-laden macrophages were found near tumor vessels and all had a substantial chronic inflammatory infiltrate. The effect of proton beam irradiation on tumor vessels probably plays an important role in uveal melanoma regression.
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PMID:Ciliary body and choroidal melanomas treated by proton beam irradiation. Histopathologic study of eyes. 631 Nov 46

A sixty-year-old man experienced successively over two years several episodes of circulatory collapse and meningeal hemorrhage, a myocardial infarction, an episode of ketoacidosis and a seizure before acute abdominal pain with fever related to the sudden, partial, necrosis of his tumor, led to the discovery of a pheochromocytoma. This observation exemplifies the multiple clinical aspects and diagnostic pitfalls of this secreting tumor. It underscores the misleading nature of normotensive pheochromocytomas.
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PMID:[Pheochromocytoma and its diagnostic pitfalls]. 632 Apr 24

Many nonpulmonary diseases may present with respiratory manifestations or may involve the lungs later in the disease course. The mechanisms by which such involvement occurs are almost as diverse as the diseases themselves and include the following. Hematogenous spread of disease is one of the most common mechanisms of lung involvement, for example, lung involvement by metastatic malignant disease. Cytotoxic factors from another anatomic location may be deposited in the alveolar basement membranes and cause pulmonary damage, for example, pulmonary hemorrhage associated with Goodpasture's syndrome. The pulmonary vasculature may prominently manifest generalized disease, as frequently occurs in Wegener's granulomatosis. Toxins accumulated as a result of disease in another organ system may damage the alveolar capillaries and result in pulmonary edema, as can occur in patients with severe azotemia due to renal failure. Depletion of lung surfactant as a consequence of disease in another organ system may produce alveolar collapse and respiratory failure; a disease that can have this effect is acute pancreatitis. The lungs may be the first organs to exhibit, through unknown mechanisms, underlying systemic diseases such as the collagenoses. Humoral factors released in another anatomic site may cause pulmonary problems; for example, bronchospasm may develop in patients with carcinoid of the intestine as a result of serotonin released by the tumor. Injury to another organ system can produce lung damage by complex mechanisms; an excellent example is the occasional development of neurogenic pulmonary edema in patients with trauma to the brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory manifestations of systemic disease. 3. Neurologic, skeletal, dermatologic, gynecologic, and gonadal diseases and disorders of pregnancy. 647 14

A case of acute intestinal vascular necrosis in a 19-year-old user of oral contraceptives (OCs) is described, and hypotheses explaining the digestive complications of synthetic estrogens are reviewed. The patient had originally presented with a violent gastric pain that subsequently spread to the entire abdomen. An abrupt worsening of her condition involved cardiovascular collapse associated with a peritoneal syndrome, vomiting and dehydration, and hyperleukocytosis. Emergency opening of the peritoneum was followed by evacuation of a large quantity of fetid gas and alimentary debris, and observation of a completely necrosed stomach. A careful lavage of the entire intestinal cavity led to temporary improvement, but it became clear during an attempt at gastrectomy that further treatment would be unavailing and the patient died shortly thereafter. Estrogens were believed to be responsible for the digestive necrosis because it occurred in a young woman who had used an estrogen-rich OC for 3 years and who smoked; a hapatic biopsy confirmed the diagnosis. No traces of other risk factors such as hypertension, hyperlipidemia, diabetes, neoplasia, or obesity were observed. Recent publications indicate that OCs are responsible for a certain number of digestive problems, which may include acceleration of intestinal transit, severe diarrhea, rectorrhagia, ischemic or ulcerative colitis, intestinal infarct which is usually localized, and hepatocellular problems ranging from moderate hepatic insufficiency to malignant tumor and Budd-Chiari syndrome. OCs do not modify hemodynamic regimes, but they may cause elevation of fibrinogen and thrombin, diminution of antithrombin III acitivty, increased platelet adhesivity, and decreased fibrinolysis leading to hypercoagulability. These modifications in hemostasis occur in all OC users and are not statistically correlated with occurence of thrombotic accidents. OCs are probably responsible for parietal vascular lesions; experimental injection of synthetic estrogens is associated with both arterial and venous lesions. The most characteristic anomaly is at the level of the intima, with proliferation of smooth muscle cells and increased conjunctive tissue fibers associated with proliferation of the media or the endothelium. The absence of lipid deposits, the simultaneous appearance of arterial and venous lesions, and other evidence argues against and atheromatous origin of parietal lesions. A significant correlation has been found between high levels of anti-synthetic ethinyl estradiol antibodies and the presence of vascular lesions. It is hypothesized that these circulating immune complexes penetrate the vascular walls of OC users and produce lesions, which may depend on factors such as smoking.
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PMID:[Digestive complications of oral contraceptives: a case of extensive digestive necrosis in a young woman]. 647 54

The term cybernosis was proposed by Meerloo (1971) in order to designate the cybernetic functional disorders in senescence. Blocking cybernosis or bloking negative feedback is the term used for negative feedback perturbation in a neuro-endocrine subsystem caused by factors dwelling inside or outside it. Using the hypothalamo-hypophyso-adrenocortical subsystem as a model, the author shows that due to an excessive and anarchic secretion of corticoids by a tumor developed in the adrenocortical, the hypothalamo-hypophyseal control centers are blocked. A similar blockade occurs after longterm administration of high doses of a steroid, similar or identical to the natural corticoid hormone, which retro-acts like the latter. In the first case we deal with tumoral blocking cybernosis, in the second, with an iatrogenic one. As in both cases the subsystems are turned off without structural desorganization, the term blockade is more appropriate than that of disorder which implies the existence of a certain functional disability. Tumoral blocking cybernoses were seen by us in thyroid toxic adenoma, corticosteroid secreting adenomas and ovarian tumors; iatrogenic cybernoses occur in the long-term corticosteroid therapy in dermatoses, hirsutism, etc. Blocking cybernoses, both tumoral and iatrogenic, require great caution in their correction. Sudden removal of the blockade is followed by severe disorders producing collapse and coma with their implicit risk.
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PMID:Blocking cybernosis in endocrine glands pathology. 653 45

Round atelectasis is a little-known form of peripheral pulmonary collapse which may mimic a neoplastic tumor. Usually the atelectasis forms a well-demarcated round or oval intrapulmonary pleural-based mass at the basal, posterior or interlobar pleura. It is thought to be a sequela of a pleural effusion. If the radiographic features are characteristic, and fine-needle biopsy finding negative, the diagnosis of round atelectasis can be made with assurance, and unnecessary procedures such as thoracotomy and pulmonary resection can be avoided. In this paper experiences of 11 patients with this condition are presented. In 4 the diagnosis was established by surgery and in 7 a long-term follow-up confirmed the diagnosis of a nonmalignant intrapulmonary lesion. The pathogenesis, clinical and radiological features, and the diagnostic workup are discussed.
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PMID:Round atelectasis. 668


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