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991.
A. M. Diehl MD M. A. Chacon PhD J. J. Potter MS D Rolfes MD D. F. Cruess MD E Mezey MD 《Alcoholism, clinical and experimental research》1987,11(4):385-391
It has been suggested that pyridoxine deficiency may potentiate ethanol-induced liver injury. Our purpose was to clarify the effect of pyridoxine deficiency on ethanol-associated liver injury by comparing liver histology, serum liver enzymes, and the viability of cultured hepatocytes from pyridoxine-deficient and pyridoxine-sufficient rats that had been chronically fed ethanol-enriched diets. Our data fail to substantiate that pyridoxine-deficient animals are more susceptible to the hepatotoxic effects of ethanol than pair-fed pyridoxine-sufficient controls. Furthermore, the addition of pyridoxine to hepatocyte cultures fails to prevent in vitro cytotoxicity of added ethanol. Pyridoxine deficiency may augment ethanol-induced enhancement of hepatic urea synthesis. These data suggest that pyridoxine deficiency may contribute to the abnormal plasma amino acid profiles and nitrogen balance of chronic alcoholics, but that it does not potentiate ethanol-induced liver injury. 相似文献
992.
Screw-fixated and hydroxyapatite-coated press-fit cups were studied using radiostereometry in 29 revision and 14 primary arthroplasties. The acetabular defects in the revision cases varied from none to type 3 (wall defects) according to Gustilo—Pasternak. Morsellized allograft was used in 25 revisions. Nine of these cups rested on less than 50% living bone. After 2 years, the mean migration in the revised group reached 0.36, 0.21, and 0.49 mm in the horizontal, longitudinal, and anteroposterior (AP) directions. The mean rotations varied between 0.5° and 0.7° depending on direction. The primary implants displayed smaller mediolateral migration and AP tilt. The mean proximal wear rate for the whole group was 0.11 mm/y. A central gap on the postoperative AP view implied less migration. The size of the preoperative bone defects or amount of bone—graft used had no influence on the migration. Despite extensive use of morsellized allograft, this implant displayed the smallest migration so far reported in revision hip arthroplasty. 相似文献
993.
Fokko Bosker Dorien Vrinten André Klompmakers H. Westenberg 《Naunyn-Schmiedeberg's archives of pharmacology》1997,355(3):347-353
The modulation of extracellular 5-hydroxytryptamine (5-HT) in the central nucleus of the amygdala (CeA) by 5-HT1A receptors was studied by intracerebral microdialysis in awake and freely moving rats. Local administration of 1 μM tetrodotoxin
(TTX), 60 mM K+ and perfusion with Ca2+-free Ringer containing EGTA confirmed that the major part of dialysate 5-HT levels from the CeA is of neuronal origin. Administration
of 300 nM of RU 24969, a 5-HT1B receptor agonist, through the probe into the CeA decreased dialysate 5-HT levels to 67.2% of the baseline value. Systemic
administration of the 5-HT1A receptor agonists 8-OH-DPAT and flesinoxan dose-dependently decreased 5-HT levels in the CeA. The effect of 0.3 mg/kg of
flesinoxan could be completely antagonized by systemic administration of 0.05 mg/kg WAY 100635, a 5-HT1A receptor antagonist. WAY 100635 alone had only minimal effects at this dose. These data show that a major part of the extracellular
5-HT in the CeA stems from 5-HT neurons and that the amount of 5-HT released into this brain region can be modulated by 5-HT1A receptors.
Received: 11 September 1996 / Accepted: 25 November 1996 相似文献
994.
Elyse Y. Bissonnette PhD A.Dean Befus PhD 《The Journal of allergy and clinical immunology》1997,100(6):825-831
β2-Agonists inhibit the release of preformed mediators such as histamine and newly synthesized mediators such as prostaglandin D2 from mast cells. However, although mast cells have been identified as an important source of several cytokines including tumor necrosis factor-α (TNF-α), there is no information about their regulation by β2-agonists. Thus given the importance of TNF-α in inflammation and the widespread use of β2-agonists, we investigated the effect of long-acting (salmeterol) and short-acting (salbutamol) β2-agonists on the secretion of TNF-α from human skin mast cells. Treatment of mast cells with salmeterol or salbutamol (100 nmol/L) inhibited the IgE-dependent release of TNF-α (82% and 74%, respectively). Moreover, 2-hour treatment with salmeterol, isoproterenol, or salbutamol inhibited mast cell cytotoxicity against a TNF-α–sensitive cell line, WEHI-164, with an IC50 of 71, 50, and 29 nmol/L, respectively. Specificity for β-adrenergic receptors was shown with propranolol. The inhibitory effect of β2-agonists was observed after only 20 minutes of treatment but was lost by 24 hours after removal of salbutamol and isoproterenol (7% and 11% inhibition remaining, respectively). In contrast, the inhibition of TNF-α release was increased 1 hour after removal of salmeterol and remained significant 24 hours later. Furthermore, β2-agonists did not show tachyphylaxis for the inhibition of TNF-α release. Thus selective β2-agonists demonstrate anti-inflammatory activity by inhibiting the release of TNF-α from mast cells stimulated through their IgE receptor or by a tumor target cell. This inhibitory effect of β-agonists may be important in their mode of action in the treatment of allergic diseases. (J Allergy Clin Immunol 1997;100:825-31.) 相似文献
995.
Respiratory failure with diffuse patchy lung infiltrates: an unusual presentation of squamous cell carcinoma
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Marc Meysman Danny F Schoors Hendrik Reynaert Marc Noppen Erwin Pierre Walter Vincken 《Thorax》1994,49(12):1271-1272
The case history is presented of a patient with squamous cell carcinoma of the lung with diffuse bilateral pulmonary shadowing mimicking bronchioloalveolar cell carcinoma which led to type I respiratory failure. 相似文献
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