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1.
Toshiho Nishita Hidetoshi Oshige Hiroharu Matsushita Yutaka Kano Masao Asari 《The Histochemical journal》1989,21(1):8-14
Summary Carbonic anhydrase III has been localized using the avidin-biotin-glucose oxidase complex (ABC) method in the submandibular gland of the rat and hamster. This isozyme, which is predominant in skeletal muscle, was observed in intercalated duct, striated duct and excretory duct cells in the rat submandibular glands. In contrast, only some striated duct cells in hamster submandibular glands were stained. 相似文献
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Osamu Hori † Masayasu Matsumoto ‡Keisuke Kuwabara Yusuke Maeda †Hirokazu Ueda Toshiho Ohtsuki Taroh Kinoshita Satoshi Ogawa ‡David M. Stern Takenobu Kamada 《Journal of neurochemistry》1996,66(3):973-979
Abstract: Astrocytes exposed to hypoxia (H) or hypoxia/reoxygenation (H/R) maintain cell viability and display changes in protein biosynthesis. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of metabolically labeled astrocytes exposed to H showed induction of an ≈78-kDa polypeptide that demonstrated sequence identity with glucose-regulated protein (GRP) 78. Cell lysates from H/R astrocytes displayed induction of neuroprotective interleukin (IL) 6, which was present in a high-molecular-weight complex also containing GRP78, suggesting that GRP78 might be functioning as a chaperone during cellular stress consequent on H/R. Introduction of anti-sense oligonucleotide to GRP78 into astrocytes prevented expression of the protein and suppressed H/R-induced astrocyte release of IL-6 by ≈50%. These data indicate that modulation of astrocyte properties during oxygen deprivation results, in part, from intracellular glucose depletion and subsequent expression of GRP78, which sustains generation of neuroprotective IL-6 under the stress of H/R. 相似文献
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Metabolic and Biosynthetic Alterations in Cultured Astrocytes Exposed to Hypoxia/Reoxygenation 总被引:7,自引:0,他引:7
Osamu Hori Masayasu Matsumoto† Yusuke Maeda Hirokazu Ueda† Toshiho Ohtsuki David M. Stern† Taroh Kinoshita§ Satoshi Ogawa Takenobu Kamada 《Journal of neurochemistry》1994,62(4):1489-1495
To investigate the astrocyte response to hypoxia/reoxygenation, as a model relevant to the pathogenesis of ischemic injury, cultured rat astrocytes were exposed to hypoxia. On restoration of astrocytes to normoxia, there was a dramatic increase in protein synthesis within 3 h, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis of metabolically labeled astrocyte lysates showed multiple induced bands on fluorograms. Levels of cellular ATP declined during the first 3 h of reoxygenation and the concentration of AMP increased to ± 3.6 nmol/mg of protein within 1 h of reoxygenation. Reoxygenated astrocytes generated oxygen free radicals early after replacement into ambient air, and addition of diphenyliodonium, an NADPH oxidase inhibitor, diminished the generation of free radicals as well as the induction of several bands on fluorogram. Although addition of cycloheximide on reoxygenation resulted in inhibition of both astrocyte protein synthesis and accumulation of cellular AMP, it caused cell death within 6 h, suggesting the importance of protein synthesis in adaptation of hypoxic astrocytes to reoxygenation. Potential physiologic significance of biosynthetic products of astrocytes in hypoxia/reoxygenation was suggested by the recovery of glutamate uptake. These results indicate that the astrocyte response to hypoxia/reoxygenation includes generation of oxygen free radicals and de novo synthesis of products that influence cell viability and function in ischemia. 相似文献
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S Wakasugi T Iwanaga T Inomoto T Tengan S Maeda M Uehira K Araki J Miyazaki K Eto K Shimada 《Developmental genetics》1988,9(3):203-212
We have created a transgenic mouse which showed an autosomal dominant mutation of facial development. This facial malformation was characterized by a short snout and a twisted upper jaw. All offspring showing the dysmorphic phenotype carried the injected gene. In order to analyze the primary cause of this mutation, newborn mice and embryos were examined. The outcome was that the malformation of nasal and premaxillary bone was not the primary defect but was a secondary event. The primary cause of this dysmorphism was a developmental defect in the first branchial arch. Genomic DNA fragments flanking the insertion site of this mutant mouse were cloned. Using these fragments, we have assigned the integration site to chromosome 13. The gene responsible for a previously reported mutant mouse, one which also has a short snout, is also reported to be on chromosome 13. In the fragments flanking the insertion site of the transgenic mouse, at least one fragment was highly conserved in mammals. These results indicate that this malformation is due to the insertional disruption of a host gene. However, the possibility that this mutation is caused by an inappropriate expression of the injected gene still remains to be investigated. 相似文献
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Frequency of duplications in the D-loop in patients with mitochondrial DNA deletions 总被引:3,自引:0,他引:3
Tengan CH Ferreiro-Barros C Cardeal M Fireman MA Oliveira AS Kiyomoto BH Gabbai AA 《Biochimica et biophysica acta》2002,1588(1):65-70
Small duplications (miniduplications) of the D-loop of human mitochondrial DNA (mtDNA) have been described in patients with mtDNA deletions, mtDNA point mutations and in normal aged tissues. The origin of these miniduplications is still unknown but it is hypothesized that they could be formed after oxidative damage. The respiratory chain (RC) is the main source of free radicals in mitochondria and it is believed that a defect in RC increases free radical generation. If miniduplications are originated by oxidative damage, it is expected that they are more abundant in patients with a defect in the RC. We studied the frequency of miniduplications of D-loop in patients with a RC defect due to mtDNA deletions and in controls. We show that four types of miniduplications could be detected with a higher prevalence than in previous studies and that patients with mtDNA deletions did not have higher proportions or increased number of miniduplications, which is against the hypothesis that miniduplications are generated more abundantly in patients with RC defects. We also clearly demonstrate the age-related nature of these miniduplications by a carefully controlled study regarding the age of subjects, which was not considered in other studies on patients with a mitochondrial disease. 相似文献
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Alice Tung Wan Song Evandro Sobroza de Mello Venancio Avancini Ferreira Alves Norma de Paula Cavalheiro Carlos Eduardo Melo Patricia Rodrigues Bonazzi Fatima Mitiko Tengan Maristela Pinheiro Freire Antonio Alci Barone Luiz Augusto Carneiro D'Albuquerque Edson Abdala 《Memórias do Instituto Oswaldo Cruz》2015,110(1):56-64
Histology is the gold standard for diagnosing acute rejection and hepatitis C
recurrence after liver transplantation. However, differential diagnosis between the
two can be difficult. We evaluated the role of C4d staining and quantification of
hepatitis C virus (HCV) RNA levels in liver tissue. This was a retrospective study of
98 liver biopsy samples divided into four groups by histological diagnosis: acute
rejection in patients undergoing liver transplant for hepatitis C (RejHCV+), HCV
recurrence in patients undergoing liver transplant for hepatitis C (HCVTx+), acute
rejection in patients undergoing liver transplant for reasons other than hepatitis C
and chronic hepatitis C not transplanted (HCVTx-). All samples were submitted for
immunohistochemical staining for C4d and HCV RNA quantification. Immunoexpression of
C4d was observed in the portal vessels and was highest in the HCVTx- group. There was
no difference in C4d expression between the RejHCV+ and HCVTx+ groups. However,
tissue HCV RNA levels were higher in the HCVTx+ group samples than in the RejHCV+
group samples. Additionally, there was a significant correlation between tissue and
serum levels of HCV RNA. The quantification of HCV RNA in liver tissue might prove to
be an efficient diagnostic test for the recurrence of HCV infection. 相似文献
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Toshiho Nishita Yuichiro Tomita Takao Imanari Nobutsune Ichihara Kensuke Orito Kazuyoshi Arishima 《Acta veterinaria Scandinavica》2011,53(1):16
Background
Carbonic anhydrase (CA) of the chicken has attracted attention for a long time because it has an important role in the eggshell formation. The developmental profile of CA-II isozyme levels in chicken erythrocytes has not been determined or reported. Furthermore, the relations with CA-II in erythrocyte and egg production are not discussed. In the present study, we isolated CA-II from erythrocytes of chickens and determined age-related changes of CA-II levels in erythrocytes. 相似文献9.
Tengan CH Kiyomoto BH Godinho RO Gamba J Neves AC Schmidt B Oliveira AS Gabbai AA 《Biochemical and biophysical research communications》2007,359(3):771-777
NO has been pointed as an important player in the control of mitochondrial respiration, especially because of its inhibitory effect on cytochrome c oxidase (COX). However, all the events involved in this control are still not completely elucidated. We demonstrate compartmentalized abnormalities on nitric oxide synthase (NOS) activity on muscle biopsies of patients with mitochondrial diseases. NOS activity was reduced in the sarcoplasmic compartment in COX deficient fibers, whereas increased activity was found in the sarcolemma of fibers with mitochondrial proliferation. We observed increased expression of neuronal NOS (nNOS) in patients and a correlation between nNOS expression and mitochondrial content. Treatment of skeletal muscle culture with an NO donor induced an increase in mitochondrial content. Our results indicate specific roles of NO in compensatory mechanisms of muscle fibers with mitochondrial deficiency and suggest the participation of nNOS in the signaling process of mitochondrial proliferation in human skeletal muscle. 相似文献