27 research outputs found

    Analyses of Histocompability and Isozyme Variations in Triploid Fish, Carassius auratus langsdorfii

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    Clonal diversity of triploid gynogenetic fish, Carassius auratus langsdorfii, was examined by tissue grafts and electrophoreses of several enzymes and muscle protein. The hypervariabilities of histocompatibility clones and electromorph clones were observed in wild-caught specimens. The ratio of DNA value of each specimen to control diploid fish varied from 1.38 to 2.01. Unidirectional histocompatibility and protein variations in histocompatibility clones were the characteristics of this gynogenetic fish. These facts seem to indicate the divergence of a clone. Tissue-incompatibility was observed betweeen F脀 progeny of triploid ginbuna × Shubunkin. Some of offspring expressed the male-dependent transparent-scaled character. This indicates the fact that fusions of female and male pronuclei must have occured. In the other strain, random reductions of DNA values were observed. The divergence of a clone must have been caused by the gene addition or loss.Article信州大学理学部紀要 19(1): 9-25(1984)departmental bulletin pape

    Tsumura-Suzuki obese diabetic mice-derived hepatic tumors closely resemble human hepatocellular carcinomas in metabolism-related genes expression and bile acid accumulation

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    Background and aims Tsumura-Suzuki obese diabetic (TSOD) is a good model of metabolic syndrome showing typical lesions found in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis, and develops spontaneous hepatic tumors with a high frequency. Majority of the developing tumors overexpress glutamine synthetase (GS), which is used as a marker of hepatocellular carcinoma (HCC). The aim of this study is to assess the status of expression of metabolism-related genes and the level of bile acids in the TSOD mice-derived tumors and to determine the association with metabolic dysregulation between human HCC and TSOD mice-derived tumors. Methods GS-positive hepatic tumors or adjacent normal tissues from 71-week-old male TSOD mice were subjected to immunohistochemical staining (IHC), quantitative RT-PCR (qRT-PCR), quantitation of cholic acid and taurocolic acid. Results We found that downregulation of the rate-limiting enzyme for betaine synthesis (BADH), at both mRNA and protein levels in GS-positive TSOD mice-derived tumors. Furthermore, the bile acid receptor FXR and the bile acid excretion pump BSEP (Abcb11) were found to be downregulated, whereas BAAT and Akr1c14, involved in primary bile acid synthesis and bile acid conjugation, were found to be upregulated at mRNA level in GS-positive TSOD mice-derived tumors. BAAT and Akr1c14 was also overexpressed at protein levels. Total cholic acid was found to be increased in GS-positive TSOD mice-derived tumors. Conclusion Our results strongly support the significance of TSOD mice as a model of spontaneously developing HCC

    Proximal Vertebral Body Fracture after 4-Level Fusion Using L1 as the Upper Instrumented Vertebra for Lumbar Degenerative Disease: Report of 2 Cases with Literature Review

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    Some cases with lumbar degenerative diseases require multi-level fusion surgeries. At our institute, 27 and 4 procedures of 3- and 4-level fusion were performed out of a total 672 posterior lumbar interfusions (PLIFs) on patients with lumbar degenerative disease from 2005 to 2010. We present 2 osteoporotic patients who developed proximal vertebral body fracture after 4-level fusion. Both cases presented with gait disability for leg pain by degenerative lumbar scoliosis and canal stenosis at the levels of L1/2-4/5. After 4-level fusion using L1 as the upper instrumented vertebra, proximal vertebral body fractures were found along with the right pedicle fractures of L1 in both cases. One of these patients, aged 82 years, was treated as an outpatient using a hard corset for 24 months, but the fractures were exacerbated over time. In the other patient, posterolateral fusion was extended from Th10 to L5. Both patients can walk alone and have been thoroughly followed up. In both cases, the fracture of the right L1 pedicle might be related to the subsequent fractures and fusion failure. In consideration of multi-level fusion, L1 should be avoided as an upper instrumented vertebra to prevent junctional kyphosis, especially in cases with osteoporosis and flat back posture

    Description of the Diversity in Surgical Indication and Surgical Strategies for Primary Spinal Cord Tumors: A Nationwide Survey by the Neurospinal Society of Japan

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    Objective To assess the current management of primary spinal cord tumors (PSCTs) and determine whether and to what extent there are differences in surgical strategies for PSCTs. Methods The Neurospinal Society of Japan conducted a survey between April 1 and 30, 2021. Certified spine surgeons were requested for information on the frequency of surgeries in 2020 and the surgical strategies adopted for each PSCTs. The following tumor histologies were focused: schwannoma, meningioma, and cauda equina tumor as extramedullary tumors; and ependymoma, hemangioblastoma, astrocytoma, and cavernoma as intramedullary tumors. The participants were divided according to their response as follows: experts, who had experienced ≥ 100 surgeries for PSCTs, and nonexperts. Results Among 308 participants (63%), 35 (11%) were experts. The total number of PSCTs in 2020 was 802 of which 564 tumors were extramedullary and 223 were intramedullary. Schwannoma accounted for 53% of the extramedullary tumors, and ependymoma accounted for 39% of the intramedullary tumors. Surgical strategies significantly differed among both the experts and nonexperts groups. Some discrepancies in the adopted surgical strategies were observed between groups. Some of the nonexperts, and none of the experts, ruled out surgery for schwannomas (Eden type 4), astrocytomas, or cavernomas. Five nonexperts (2.2%), and none of the experts, resected the entire dura for meningiomas. Conclusion A nationwide survey revealed that a sufficient consensus did not exist regarding surgical strategies for PSCTs. A disease-specific registry for PSCTs is necessary in academic societies

    Dystrophin deficiency in canine X-linked muscular dystrophy in Japan (CXMDJ) alters myosin heavy chain expression profiles in the diaphragm more markedly than in the tibialis cranialis muscle

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    <p>Abstract</p> <p>Background</p> <p>Skeletal muscles are composed of heterogeneous collections of muscle fiber types, the arrangement of which contributes to a variety of functional capabilities in many muscle types. Furthermore, skeletal muscles can adapt individual myofibers under various circumstances, such as disease and exercise, by changing fiber types. This study was performed to examine the influence of dystrophin deficiency on fiber type composition of skeletal muscles in canine X-linked muscular dystrophy in Japan (CXMD<sub>J</sub>), a large animal model for Duchenne muscular dystrophy.</p> <p>Methods</p> <p>We used tibialis cranialis (TC) muscles and diaphragms of normal dogs and those with CXMD<sub>J </sub>at various ages from 1 month to 3 years old. For classification of fiber types, muscle sections were immunostained with antibodies against fast, slow, or developmental myosin heavy chain (MHC), and the number and size of these fibers were analyzed. In addition, MHC isoforms were detected by gel electrophoresis.</p> <p>Results</p> <p>In comparison with TC muscles of CXMD<sub>J</sub>, the number of fibers expressing slow MHC increased markedly and the number of fibers expressing fast MHC decreased with growth in the affected diaphragm. In populations of muscle fibers expressing fast and/or slow MHC(s) but not developmental MHC of CXMD<sub>J </sub>muscles, slow MHC fibers were predominant in number and showed selective enlargement. Especially, in CXMD<sub>J </sub>diaphragms, the proportions of slow MHC fibers were significantly larger in populations of myofibers with non-expression of developmental MHC. Analyses of MHC isoforms also indicated a marked increase of type I and decrease of type IIA isoforms in the affected diaphragm at ages over 6 months. In addition, expression of developmental (embryonic and/or neonatal) MHC decreased in the CXMD<sub>J </sub>diaphragm in adults, in contrast to continuous high-level expression in affected TC muscle.</p> <p>Conclusion</p> <p>The CXMD<sub>J </sub>diaphragm showed marked changes in fiber type composition unlike TC muscles, suggesting that the affected diaphragm may be effectively adapted toward dystrophic stress by switching to predominantly slow fibers. Furthermore, the MHC expression profile in the CXMD<sub>J </sub>diaphragm was markedly different from that in <it>mdx </it>mice, indicating that the dystrophic dog is a more appropriate model than a murine one, to investigate the mechanisms of respiratory failure in DMD.</p

    SV40 miR-S1 and Cellular miR-1266 Sequester Each Other from Their Targets, Enhancing Telomerase Activity and Viral Replication

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    Virus-encoded microRNAs (miRNAs) target viral and host mRNAs to repress protein production from viral and host genes, and regulate viral persistence, cell transformation, and evasion of the immune system. The present study demonstrated that simian virus 40 (SV40)-encoded miRNA miR-S1 targets a cellular miRNA miR-1266 to derepress their respective target proteins, namely, T antigens (Tags) and telomerase reverse transcriptase (TERT). An in silico search for cellular miRNAs to interact with viral miR-S1 yielded nine potential miRNAs, five of which, including miR-1266, were found to interact with miR-S1 in dual-luciferase tests employing reporter plasmids containing the miRNA sequences with miR-S1. Intracellular bindings of miR-1266 to miR-S1 were also verified by the pull-down assay. These miRNAs were recruited into the Ago2-associated RNA-induced silencing complex. Intracellular coexpression of miR-S1 with miR-1266 abrogated the downregulation of TERT and decrease in telomerase activity induced by miR-1266. These effects of miR-S1 were also observed in miR-1266-expressing A549 cells infected with SV40. Moreover, the infected cells contained more Tag, replicated more viral DNA, and released more viral particles than control A549 cells infected with SV40, indicating that miR-S1-induced Tag downregulation was antagonized by miR-1266. Collectively, the present results revealed an interplay of viral and cellular miRNAs to sequester each other from their respective targets. This is a novel mechanism for viruses to manipulate the expression of viral and cellular proteins, contributing to not only viral lytic and latent replication but also cell transformation observed in viral infectious diseases including oncogenesis

    Dystrophin deficiency in canine X-linked muscular dystrophy in Japan (CXMD) alters myosin heavy chain expression profiles in the diaphragm more markedly than in the tibialis cranialis muscle-1

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    <p><b>Copyright information:</b></p><p>Taken from "Dystrophin deficiency in canine X-linked muscular dystrophy in Japan (CXMD) alters myosin heavy chain expression profiles in the diaphragm more markedly than in the tibialis cranialis muscle"</p><p>http://www.biomedcentral.com/1471-2474/9/1</p><p>BMC Musculoskeletal Disorders 2008;9():1-1.</p><p>Published online 9 Jan 2008</p><p>PMCID:PMC2257929.</p><p></p>sitive fiber. Furthermore, fast (white), hybrid (gray), or slow MHC myofibers (black) were analyzed among populations of muscle fibers with non-expression of developmental MHC (A, B) or with expression of developmental MHC (C) in terms of fiber numbers (see Table 1) and fiber sizes (A-C). Note that larger sizes of slow MHC fibers were noticeable in populations of muscle fibers expressing fast and/or slow MHC(s) but not developmental MHC of affected muscles (B)

    Dystrophin deficiency in canine X-linked muscular dystrophy in Japan (CXMD) alters myosin heavy chain expression profiles in the diaphragm more markedly than in the tibialis cranialis muscle-5

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    <p><b>Copyright information:</b></p><p>Taken from "Dystrophin deficiency in canine X-linked muscular dystrophy in Japan (CXMD) alters myosin heavy chain expression profiles in the diaphragm more markedly than in the tibialis cranialis muscle"</p><p>http://www.biomedcentral.com/1471-2474/9/1</p><p>BMC Musculoskeletal Disorders 2008;9():1-1.</p><p>Published online 9 Jan 2008</p><p>PMCID:PMC2257929.</p><p></p>scle and diaphragm of a normal (A) or an affected dog (B, C) at adolescent (2 or 4 months old) or adult stages (10 or 11 months old). The numbers under the ages show total fibers examined. MHC expression between two groups (normal, dMHC (-) affected, dMHC (-); affected, dMHC (-) affected, dMHC (+)), between muscles (TC muscle diaphragm), or among ages (2, 4, and 10 or 11 months) was analyzed by Yates's chi-square test. Significant differences (< 0.05) were detected in all tests, except for no significant differences between 4 and 10 months old in normal TC muscles or diaphragms. Note that slow MHC fibers were consistently larger than other fibers, in populations of muscle fibers without developmental MHC of affected diaphragms. In populations of muscle fibers co-expressing developmental MHC and other MHC isoform(s), slow MHC and hybrid fibers were increased markedly in the affected diaphragm at 4 and 11 months old, unlike TC muscles

    Dystrophin deficiency in canine X-linked muscular dystrophy in Japan (CXMD) alters myosin heavy chain expression profiles in the diaphragm more markedly than in the tibialis cranialis muscle-3

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    <p><b>Copyright information:</b></p><p>Taken from "Dystrophin deficiency in canine X-linked muscular dystrophy in Japan (CXMD) alters myosin heavy chain expression profiles in the diaphragm more markedly than in the tibialis cranialis muscle"</p><p>http://www.biomedcentral.com/1471-2474/9/1</p><p>BMC Musculoskeletal Disorders 2008;9():1-1.</p><p>Published online 9 Jan 2008</p><p>PMCID:PMC2257929.</p><p></p
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