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Biochemical mechanisms underlying acrylamide induced neurotoxicity were examined using an in vitro model consisting of sagittal slices of rat brain. Incubation of brain slices under oxygen in artificial cerebrospinal fluid containing acrylamide produced a dose and time dependent inhibition of glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Lysosomal enzymes, acid phosphatase, N-acetyl glucosaminidase and beta-glucuronidase decreased in a similar manner, while no changes were observed in the activity of Na+K+ATPase, cytochrome c oxidase and lactate dehydrogenase. Incubation of slices with two structurally related compounds, acetamide (a non-neurotoxic amide) and methylene bis-acrylamide (a weak neurotoxin), indicated that acrylamide selectively inhibited GAPDH, enolase and N-acetyl glucosaminidase at low concentration; similar doses of acetamide and methylene bis-acrylamide did not have the same effect on brain slices. Incubation with acrylamide depleted glutathione levels in slices, and the addition of glutathione to the incubation medium prevented acrylamide induced inhibition of GAPDH and lysosomal enzymes. Time dependent inhibition of lysosomal enzymes was also observed in vivo, in the brain and sciatic nerve of rats following a single dose of acrylamide. These results demonstrate that both in vitro and in vivo, lysosomal enzymes are also inhibited following acrylamide exposure. The rat brain slice model exhibits both selectivity and sensitivity towards neurotoxicants and hence, may prove to be an useful in vitro model for the mechanistic evaluation of neurotoxicity. 相似文献
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An ankylosed tooth can be suitable for obtaining orthodontic anchorage. However, if such a tooth lacks adequate clinical crown height, the anchorage will not be effective. In those situations surgical luxation or restorative crown augmentation is suggested. This case report is about the restorative treatment of an ankylosed, infraoccluded tooth to enhance the anchorage for forced orthodontic eruption of impacted maxillary canines. A crown augmentation in the form of a modified bilayered (sandwich) restoration using GIC, Composite resin and Silver amalgam on left maxillary first molar (26) was successful in sustaining the anchorage for forced eruption and alignment of impacted canines. 相似文献
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Monoclonal antibody K1 reacts with epithelial mesothelioma but not with lung adenocarcinoma. 总被引:8,自引:0,他引:8
K Chang L H Pai H Pass H W Pogrebniak M S Tsao I Pastan M C Willingham 《The American journal of surgical pathology》1992,16(3):259-268
Immunoperoxidase histochemical staining of cryostat sections from human tumor tissues revealed that a murine monoclonal antibody (MAb), K1, can distinguish epithelial mesotheliomas from lung adenocarcinomas. All of 15 epithelial-type mesotheliomas and all four mixed type mesothelioma samples, but none of 23 lung adenocarcinomas with different degrees of histologic differentiation demonstrated reactivity with antibody K1. Of the cell populations in each mesothelioma tested, 80% to 100% showed strong and homogeneous staining with MAb K1. Immunofluorescence analysis of live cultured cells from an epithelioid mesothelioma (H-meso) and several lung carcinoma cell lines as well as a pleural effusion of a patient with mesothelioma also showed selective reactivity of K1 with the mesothelioma cells. These data indicate that K1 can be useful as a mesothelial cell marker for the differential pathological diagnosis of the epithelial form of mesothelioma; K1 may also be useful in the study of the pathogenesis, immunodiagnosis, and immunotherapy of epithelial-type and mixed-type human malignant mesothelioma. 相似文献
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BACKGROUND: Chronic renal failure (CRF) is associated with an atherogenic
lipid profile and an increased risk of ischaemic cardiovascular disease.
The associated hyperlipidaemia is reportedly ameliorated by erythropoietin
(Epo) therapy. According to a recent report, rats studied 3 weeks after 5/6
nephrectomy and fed a high- protein diet exhibited increased activities of
hepatic HMG-CoA reductase (HMG-CoAR) and cholesterol 7 alpha-hydroxylase
(Ch-7 alpha- H), despite normal corresponding mRNA values. DESIGN AND
METHODS: This study was designed to examine the effects of naturally
progressing CRF of longer duration as well as those of Epo therapy on gene
expressions of the key factors involved in hepatic cholesterol metabolism,
i.e., LDL receptor (LDLR), HMG-CoAR, and Ch-7 alpha-H. Sprague-Dawley rats
were randomized to the CRF group (5/6 nephrectomy), Epo-treated CRF group
(given Epo 150 U/kg/twice weekly) and sham-operated, placebo- treated
normal controls. They were allowed free access to regular rat chow and
studied 6 weeks after surgery. Liver mRNAs and protein mass or activities
of the above factors were studied. RESULTS: Plasma cholesterol
concentration was significantly increased in the CRF group (P < 0.001)
and was modestly lowered (P < 0.05) by Epo therapy. However, microsomal
cholesterol concentration and LDLR, HMG-CoAR, and Ch-7 alpha-H mRNA as well
as HMG-CoAR activity, and Ch-7 alpha-H and LDLR protein mass measurements
were virtually identical in the three groups. Thus, hepatic LDLR, HMG-CoAR,
and Ch-7 alpha-H mRNA and protein measurements in rats with CRF were
similar to those of the normal control group representing an inappropriate
response to the associated hypercholesterolemia. Epo therapy led to partial
amelioration of CRF- associated hypercholesterolaemia with no discernible
effect on hepatic tissue expression of the above factors.
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