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651.
Wakao N Imagama S Zhang H Tauchi R Muramoto A Natori T Takeshita S Ishiguro N Matsuyama Y Kadomatsu K 《Neuroscience letters》2011,488(3):299-304
Hyaluronan is a component of the extracellular matrix of the central nervous system, and forms perineuronal nets around neurons. It has been recently reported that the hyaluronan-degrading enzyme hyaluronidase promotes lateral mobility of AMPA-type glutamate receptors and enhances synaptic plasticity. However, the biological significance of hyaluronan-degrading products (oligosaccharides) has not been studied in depth. Here we investigated the effects of hyaluronan oligosaccharides on motor function recovery after spinal cord injury in rats. The disaccharide HA2 and especially the tetrasaccharide HA4, significantly improved motor function, unlike the case with oligosaccharides composed of 6-12 saccharides. Consistent with this finding, HA4 treatment enhanced axonal regeneration/sprouting, as assessed by corticospinal tract tracer fiber counts. HA4 treatment also significantly suppressed accumulation of Iba-1-positive cells in a lesion two weeks after injury. In vitro experiments demonstrated that NMDA-induced neuronal cell death was partly blocked by HA4, but not by other oligosaccharides, whereas proteoglycan-mediated inhibition of neurite outgrowth was not affected by treatment with any oligosaccharide examined. Taken together, the present results revealed that due in part to its neuroprotective activity, HA4 promotes motor function recovery after spinal cord injury. 相似文献
652.
Vahl TP Tauchi M Durler TS Elfers EE Fernandes TM Bitner RD Ellis KS Woods SC Seeley RJ Herman JP D'Alessio DA 《Endocrinology》2007,148(10):4965-4973
Glucagon-like peptide-1 (GLP-1) is an intestinal hormone that is secreted during meal absorption and is essential for normal glucose homeostasis. However, the relatively low plasma levels and rapid metabolism of GLP-1 raise questions as to whether direct endocrine action on target organs, such as islet cells, account for all of its effects on glucose tolerance. Recently, an alternative neural pathway initiated by sensors in the hepatic portal region has been proposed to mediate GLP-1 activity. We hypothesized that visceral afferent neurons in the portal bed express the GLP-1 receptor (GLP-1r) and regulate glucose tolerance. Consistent with this hypothesis, GLP-1r mRNA was present in the nodose ganglia, and nerve terminals innervating the portal vein contained the GLP-1r. Rats given an intraportal infusion of the GLP-1r antagonist, [des-His(1),Glu(9)] exendin-4, in a low dose, had glucose intolerance, with a 53% higher glucose excursion compared with a vehicle-infused control group. Infusion of [des-His(1),Glu(9)] exendin-4 at an identical rate into the jugular vein had no effect on glucose tolerance, demonstrating that this dose of GLP-1r antagonist did not affect blood glucose due to spillover into the systemic circulation. These studies demonstrate that GLP-1r are present on nerve terminals in the hepatic portal bed and that GLP-1 antagonism localized to this region impairs glucose tolerance. These data are consistent with an important component of neural mediation of GLP-1 action. 相似文献
653.
654.
Sakamoto S Iijima K Mochizuki D Nakamura K Teshigawara K Kobayashi J Matsuura S Tauchi H Komatsu K 《Oncogene》2007,26(41):6002-6009
The proteins responsible for radiation sensitive disorders, NBS1, kinase ataxia-telangiectasia-(A-T)-mutated (ATM) and MRE11, interact through the C-terminus of NBS1 in response to the generation of DNA double-strand breaks (DSBs) and are all implicated in checkpoint regulation and DSB repair, such as homologous recombination (HR). We measured the ability of several NBS1 mutant clones and A-T cells to regulate HR repair using the DR-GFP or SCneo systems. ATM deficiency did not reduce the HR repair frequency of an induced DSB, and it was confirmed by findings that HR frequencies are only slightly affected by deletion of ATM-binding site at the extreme C-terminus of NBS1. In contrast, The HR-regulating ability is dramatically reduced by deletion of the MRE11-binding domain at the C-terminus of NBS1 and markedly inhibited by mutations in the FHA/BRCT domains at the N-terminus. This impaired capability in HR is consistent with a failure to observe MRE11 foci formation. Furthermore, normal HR using sister chromatid was completely inhibited by the absence of FHA/BRCT domains. These results suggested that the N- and C-terminal domains of NBS1 are the major regulatory domains for HR pathways, very likely through the recruitment and retention of the MRE11 nuclease to DSB sites in an ATM-independent fashion. 相似文献
655.
656.
Reizo Baba Kazuo Tsuyuki Yasuo Kimura Kenji Ninomiya Masahiko Aihara Kunio Ebine Nobuo Tauchi Kenji Nishibata Masami Nagashima 《European journal of applied physiology》1999,80(5):397-401
In this study we aimed to elucidate the validity and usefulness of the oxygen uptake efficiency slope (OUES) in the evaluation
of adult cardiac patients. Cardiopulmonary exercise tests were performed on a treadmill by 50 adult patients with chronic
heart failure. The OUES was calculated from data for the first 75%, 90%, and 100% of exercise duration. The OUES is derived
from the following equation: V˙O2=a× logV˙
E+b, where V˙O2 is oxygen uptake (ml/kg/min), V˙
E is minute ventilation (l/kg/min), and the constant “a” represents OUES. We also determined the ventilatory anaerobic threshold
(VAT). The correlation coefficient of the logarithmic curve-fitting model was [mean (SD)] 0.986 (0.009). The OUES could be
used to discriminate effectively between New York Heart Association functional classes (P < 0.001). OUES and maximum V˙O2 were significantly correlated (r=0.78, P < 0.01). Agreement between the OUES values for the first 90%, 75%, and 100% of the exercise was excellent (intraclass correlation
coefficient = 0.99). Our results suggest that OUES is applicable to adult cardiac patients as an objective, effort-independent
estimation of cardiorespiratory functional reserve.
Accepted: 7 September 1998 相似文献
657.
658.
Tomoko Sugiyama Takuma Tajiri Makiko Kurata Shinichiro Hiraiwa Hirotaka Fujita Tomohisa Machida Hiroyuki Ito Takashi Muraki Hisamichi Yoshii Hideki Izumi Takayoshi Suzuki Masaya Mukai Naoya Nakamura 《Pathology international》2023,73(7):306-316
The utility of endoscopic ultrasound fine-needle aspiration cytology (EUS-FNAC) or endoscopic ultrasound fine-needle aspiration biopsy (EUS-FNAB) for diagnosis of small and large pancreatic ductal adenocarcinomas (PDACs) remains in question. We addressed this by analyzing 97 definitively diagnosed cases of PDAC, for which both EUS-FNAC and EUS-FNAB had been performed. We subclassified the 97 solid masses into small (n = 35) or large (n = 62) according to the maximum tumor diameter (<24 mm or ≥24 mm) and compared the diagnostic sensitivity (truly positive rate) of EUS-FNAC and of EUS-FNAB for small and large masses. Diagnostic sensitivity of EUS-FNAC did not differ between large and small masses (79.0% vs. 60.0%; p = 0.0763). However, the diagnostic sensitivity of EUS-FNAB was significantly higher for large masses (85.5% vs. 62.9%; p = 0.0213). Accurate EUS-FNAC-based diagnosis appeared to depend on the degree of cytological atypia of cancer cells, which was not associated with quantity of cancer cells. The accuracy of EUS-FNAB-based diagnosis appeared to depend on cancer cell viability in large masses and cancer volume in small masses. Based on the advantages or disadvantages in each modality, both modalities play an important role in the qualitative diagnosis of PDAC as a complementary procedure. 相似文献