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Although the cat visual system has been the subject of intensive investigation, little attention has been given to the morphological features of ganglion cell projections to the suprachiasmatic nucleus. The present study has utilized anterograde transport of horseradish peroxidase and wheat germ agglutinin–conjugated horseradish peroxidase to label ganglion cell terminals in the cat suprachiasmatic nucleus. Visualization of the reaction product was facilitated through the use of gold-substituted silver intensification. Ganglion cell terminals were found to be morphologically diverse, making both asymmetric and symmetric contacts with postsynaptic processes. Synaptic vesicles were either scattered or densely packed, sometimes forming paracrystalline arrays. In contrast to other retinorecipient areas in which ganglion cell terminals have, been characterized by the presence of lightly staining mitochondria, many of the retinal terminals in the suprachiasmatic nucleus were seen to contain darkly stained mitochondria. Postembedding antiglutamate immunocytochemistry was used to evaluate the level of endogenous glutamate in these ganglion cell terminals. Although morphologically diverse, all of the retinal terminals in the suprachiasmatic nucleus were glutamate positive, consistent with the postulated role of glutamate as the neurotransmitter of retinal ganglion cells. © 1995 Wiley-Liss, Inc. 相似文献
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Oncocytosis and oncocytomas have attracted attention because on the one hand there have been reports of the favourable prognosis and generally benign nature of oncocytic tumours, while on the other hand, Hurthle cell change in thyroid neoplasms have been reported to be correlated with aggressive biological behaviour and a significantly worse clinical course. Presently, there appear to be two schools of thought on the significance of oncocytosis: (i) a process where there is redifferentiation of cells with involvement in the pathogenesis of cancer; and (ii) a compensatory process for ‘functional exhaustion’ of the cell. Many aspects of oncocytosis seem unclear. In this study, transmission electron microscopy is used to demonstrate the presence of thyroid oncocytes in the hemithyroidectomy specimen of a patient with focal lymphocytic thyroiditis. Tissue sections from this specimen did not display preferential uptake of neutral red dye, a distinctive characteristic of M-phase cancer cells which was previously reported. The findings seem to suggest that oncocytes are not cells with distinctive proliferative potentials. If that were the case, then oncogenesis or cancer cell progression and oncocytosis may not be convergent processes. 相似文献
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Redox regulation of hepatocyte apoptosis 总被引:1,自引:0,他引:1
Carmen Garcia-Ruiz José C Fernández-Checa 《Journal of gastroenterology and hepatology》2007,22(S1):S38-S42
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Stable isotope methodologies offer a number of possibilities for the nutritional assessment of many different processes and metabolic pathways. The application of stable isotopes has been boosted by the development of new mass spectrometers, lower costs of probes, and the risks associated with radioactive tracers. The use of 13 C as a tracer offers all the advantages of stable isotopes and has been widely applied for measuring various types of metabolic processes. This review is focused on clinical and nutritional assessments using 13 C breath tests. 相似文献
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EMILIO SIENDONES YOLANDA JIMÉNEZ-GÓMEZ JOSÉ LUÍS MONTERO CONSUELO GÓMEZ-DÍAZ JOSÉ MANUEL VILLALBA JORDI MUNTANÉ 《Journal of gastroenterology and hepatology》2006,20(1):108-116
Background and Aim: PGE1 reduces in vivo and in vitro D-galactosamine (D-GalN)-induced cell death in hepatocytes. The present study was undertaken to elucidate the intracellular pathway by which D-GalN induces cell death in cultured hepatocytes. In addition, we evaluated if PGE1 was able to modulate different parameters related to D-GalN-induced apoptosis in cultured rat hepatocytes.
Methods: Hepatocytes were isolated from male Wistar rats (225–275 g) by the classical collagenase procedure. PGE1 (1 µM) was administered 2 h before D-GalN (5 mM) in primary culture of rat hepatocytes. Apoptosis was determined by DNA fragmentation and caspase-3, -6, -8 and -9 activation in hepatocytes. Caspase activation was evaluated by the detection of the related cleaved product and its associated activity. Cell necrosis was determined by the measurement of lactate dehydrogenase (LDH) activity in culture medium. To elucidate the role of mitochondria, we measured neutral (nSMase) and acid (aSMase) sphingomyelinase, as well as the expression of cytochrome c in mitochondria and cytoplasm fractions from D-GalN treated hepatocytes.
Results: D-GalN induced caspase-3 activation and DNA fragmentation in hepatocytes. This apoptotic response was not associated with the activation of caspase-6, -8 or -9. The use of specific inhibitors confirmed that only caspase-3 was involved in D-GalN-induced apoptosis. D-GalN did not modify nSMase and aSMase activities, nor mitochondrial cytochrome c release in hepatocytes.
Conclusions: D-GalN induced apoptosis through caspase-3 activation but without modification of the activity of caspase-6, -8, -9, SMases or cytochrome c release. PGE1 appears to prevent D-GalN-induced apoptosis by a mitochondria-independent mechanism. 相似文献
Methods: Hepatocytes were isolated from male Wistar rats (225–275 g) by the classical collagenase procedure. PGE
Results: D-GalN induced caspase-3 activation and DNA fragmentation in hepatocytes. This apoptotic response was not associated with the activation of caspase-6, -8 or -9. The use of specific inhibitors confirmed that only caspase-3 was involved in D-GalN-induced apoptosis. D-GalN did not modify nSMase and aSMase activities, nor mitochondrial cytochrome c release in hepatocytes.
Conclusions: D-GalN induced apoptosis through caspase-3 activation but without modification of the activity of caspase-6, -8, -9, SMases or cytochrome c release. PGE
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Reduced peripheral blood mitochondrial DNA content is not a risk factor for Type 2 diabetes. 总被引:1,自引:0,他引:1
AIMS: Mitochondrial depletion in pancreatic beta cells is known to reduce glucose stimulated insulin secretion. We aimed to determine whether the offspring of patients with early onset Type 2 diabetes had reduced peripheral blood mitochondrial content relative to control subjects and whether this could lead to a predisposition to type 2 diabetes in later life. METHODS: We measured the levels of mitochondria relative to a single copy genomic target by real time polymerase chain reaction in a series of peripheral blood samples taken from the offspring of Caucasian patients with Type 2 diabetes and matched controls. Measures of insulin sensitivity and beta cell function were also taken. RESULTS: In contrast with previous studies, mitochondrial DNA content was not decreased in the offspring of patients with Type 2 diabetes relative to matched controls in our cohort. Conversely, we noted a small proliferation in mitochondrial numbers in our case subjects. In agreement with these findings, no correlations with either insulin sensitivity or beta cell function were noted. CONCLUSIONS: Our results indicate that reduced mitochondrial DNA content in peripheral blood is not a risk factor for the development of Type 2 diabetes in the offspring of patients with early onset Type 2 diabetes. 相似文献
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心磷脂(CL)是维持线粒体能量代谢所必需的一种磷脂,参与了众多重要生理过程。此文对CL的结构、合成和转化;在维持线粒体正常功能中的作用;缺血/再灌注(I/R)损伤中的改变以及和线粒体功能的关系等作了逐一阐述,说明CL与I/R损伤导致的细胞死亡关系密切,CL量或性质的改变在细胞凋亡中处于中心地位。 相似文献