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991.
Hospital Volume and Cardiac Complications of Endomyocardial Biopsy: A Retrospective Cohort Study of 9508 Adult Patients Using a Nationwide Inpatient Database in Japan
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Yuki Mori Daichi Tomonaga Anastasia Kalashnikova Fumihiko Furuya Nozomi Akimoto Masataka Ifuku Yuko Okuno Kaoru Beppu Kyota Fujita Toshihiko Katafuchi Hiroki Shimura Leonid P. Churilov Mami Noda 《Glia》2015,63(5):906-920
l ‐tri‐iodothyronine (3, 3', 5–triiodothyronine; T3) is an active form of the thyroid hormone (TH) essential for the development and function of the CNS. Though nongenomic effect of TH, its plasma membrane–bound receptor, and its signaling has been identified, precise function in each cell type of the CNS remained to be investigated. Clearance of cell debris and apoptotic cells by microglia phagocytosis is a critical step for the restoration of damaged neuron‐glia networks. Here we report nongenomic effects of T3 on microglial functions. Exposure to T3 increased migration, membrane ruffling and phagocytosis of primary cultured mouse microglia. Injection of T3 together with stab wound attracted more microglia to the lesion site in vivo. Blocking TH transporters and receptors (TRs) or TRα‐knock‐out (KO) suppressed T3‐induced microglial migration and morphological change. The T3‐induced microglial migration or membrane ruffling was attenuated by inhibiting Gi/o‐protein as well as NO synthase, and subsequent signaling such as phosphoinositide 3‐kinase (PI3K), mitogen‐activated protein kinase (MAPK)/extracellular signal‐regulated kinase (ERK). Inhibitors for Na+/K+‐ATPase, reverse mode of Na+/Ca2+ exchanger (NCX), and small‐conductance Ca2+‐dependent K+ (SK) channel also attenuated microglial migration or phagocytosis. Interestingly, T3‐induced microglial migration, but not phagocytosis, was dependent on GABAA and GABAB receptors, though GABA itself did not affect migratory aptitude. Our results demonstrate that T3 modulates multiple functional responses of microglia via multiple complex mechanisms, which may contribute to physiological and/or pathophysiological functions of the CNS. GLIA 2015:63:906–920 相似文献
996.
RhoA/ROCK pathway mediates p38 MAPK activation and morphological changes downstream of P2Y12/13 receptors in spinal microglia in neuropathic pain
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Emiko Tatsumi Hiroki Yamanaka Kimiko Kobayashi Hideshi Yagi Masafumi Sakagami Koichi Noguchi 《Glia》2015,63(2):216-228
Recent studies have indicated an important role of ATP receptors in spinal microglia, such as P2Y12 or P2Y13, in the development of chronic pain. However, intracellular signaling cascade of these receptors have not been clearly elucidated. We found that intrathecal injection of 2‐(methylthio)adenosine 5′‐diphosphate (2Me‐SADP) induced mechanical hypersensitivity and p38 mitogen‐activated protein kinase (MAPK) phosphorylation in the spinal cord. Intrathecal administration of P2Y12/P2Y13 antagonists and Rho‐associated coiled‐coil‐containing protein kinase (ROCK) inhibitor H1152 suppressed not only p38 MAPK phosphorylation, but also mechanical hypersensitivity induced by 2Me‐SADP. In the rat peripheral nerve injury model, intrathecal administration of antagonists for the P2Y12/P2Y13 receptor suppressed activation of p38 MAPK in the spinal cord. In addition, subarachnoidal injection of H1152 also attenuated nerve injury‐induced spinal p38 MAPK phosphorylation and neuropathic pain behavior, suggesting an essential role of ROCK in nerve injury‐induced p38 MAPK activation. We also found that the antagonists of the P2Y12/P2Y13 receptor and H1152 had inhibitory effects on the morphological changes of microglia such as retraction of processes in both 2Me‐SADP and nerve injured rats. In contrast these treatments had no effect on the number of Iba1‐positive cells in the nerve injury model. Collectively, our results have demonstrated roles of ROCK in the spinal microglia that is involved in p38 MAPK activation and the morphological changes. Inhibition of ROCK signaling may offer a novel target for the development of a neuropathic pain treatment. GLIA 2015;63:216–228 相似文献
997.
Hiroki Tsuka Koji Morita Kan Kato Hiromichi Kawano Hitoshi Abekura Kazuhiro Tsuga 《Journal of oral biosciences / JAOB, Japanese Association for Oral Biology》2017,59(4):231-236
Objectives
The purpose of this study was to evaluate the bond strength of polyetheretherketone (PEEK) to resin-based luting material.Methods
Eighty PEEK specimens were randomly divided into two groups (n = 40/group): no treatment and sandblasting. Each of the 40 specimens of dental gold-silver-palladium alloy (PALLAZ12-n; Yamamoto Precious Metal Co., Ltd., Osaka, Japan), zirconia (Aadva Zirconia; GC, Tokyo, Japan), and hybrid composite resin (CERASMART; GC, Tokyo, Japan) was used as a control material for PEEK. Each group was divided into four subgroups (n = 10) for the different resin-based luting materials: Panavia® V5 (Kuraray Medical, Tokyo, Japan), RelyXTM Ultimate Resin Cement (3M ESPE, St Paul, MN, USA), G-CEM Link Force (GC, Tokyo, Japan), and Super-Bond C&B (Sun Medical, Siga, Japan). The resin-based luting materials were bonded onto the specimens. All specimens were stored in distilled water at 37 °C for 24 h. Bond strength was measured with a shear test, and failure modes were assessed by stereomicroscopy. The surfaces were observed by scanning electron microscopy after the various pretreatments.Results
Compared with the control group, the PEEK group showed a significantly lower (p < 0.05) shear bond strength for most of the specimens. Among PEEK groups, the most frequent failure mode was adhesive failure between the material and the resin-based luting material.Conclusions
This study found that the bond strength between PEEK and resin-based luting materials was not adequate for clinical use of PEEK. 相似文献998.
Hisao Hayashi Yasuaki Tatsumi Shinsuke Yahata Hiroki Hayashi Kenji Momose Ryohei Isaji Youji Sasaki Kazuhiko Hayashi Shinya Wakusawa Hidemi Goto 《临床与转化肝病杂志(英文版)》2015,3(4):239-245
Background and Aims: Wilson disease (WD) is an inherited disorder of copper metabolism, and an international group for the study of WD (IGSW) has proposed three phenotypes for its initial presentation: acute hepatic, chronic hepatic, and neurologic phenotypes. Characterization of the acute hepatic phenotype may improve our understanding of the disease. Methods: Clinical features of 10 WD patients with the acute hepatic phenotype and characteristics of chronic lesions remaining in survivors were assessed by the European Association for the Study of the Liver (EASL) guidelines. Results: All six patients younger than 30 years had survived an acute episode of hemolytic anemia with residual liver disease of cirrhosis or chronic hepatitis. The acute episode was self-limiting in two of the four patients over the age of 30 years and progressed to acute liver failure in the other two patients. One of the two survivors had residual liver disease of chronic hepatitis, while the other had chronic hepatitis and neurologic disease. Neurologic disease remained in a patient who successfully received a liver transplantation. During acute episodes, serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) changed rapidly along with anemia. Liver-specific ALT levels were age-dependently correlated with hemoglobin (Hb) concentrations. Enzyme reduction was milder for AST than ALT, which resulted in a high AST/ALT ratio in the anemic stage. The anemic stage in two patients transformed to acute liver failure. Conclusions: All survivors of an acute episode of the acute hepatic phenotype had residual liver disease or both liver and neurologic diseases. The rapid changes in liver enzymes during the acute episode and the liver and neurologic diseases remaining in survivors may provide a better understanding of WD. 相似文献
999.
Tomokatsu Saijo Nobuhiko Joki Yoji Inishi Mikako Muto Motohiko Saijo Hiroki Hase 《Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy》2015,19(2):125-130
Hepatitis B surface antigen is widely used in hepatitis B virus surveillance; patients who test negative for the antigen are judged to be uninfected. However, occult hepatitis B virus infection has been confirmed with hepatitis B virus DNA at low levels in the liver and peripheral blood in patients positive for hepatitis B core antibody or hepatitis B surface antibody, even if they test negative for hepatitis B surface antigen. To investigate the prevalence of occult hepatitis B virus in hemodialysis patients, we performed cross‐sectional analysis of 161 hemodialysis patients in two related institutions for hepatitis B surface antigen, hepatitis B core antibody, and hepatitis B surface antibody. Hepatitis B surface antigen, hepatitis B core antibody, or hepatitis B surface antibody was present in 45 patients (28.0%). Hepatitis B virus DNA was present in six patients (3.7%), all of whom also tested positive for hepatitis B core antibody. Hepatitis B surface antibody positivity was unrelated in only one of the six patients. Four of the six patients were positive for hepatitis B surface antigen; however, two (1.3%) of these with occult hepatitis B virus infection were found to be hepatitis B surface antigen negative. Occult hepatitis B virus infection may be missed in hepatitis B virus surveillance using hepatitis B surface antigen alone; therefore, routine hepatitis B core antibody screening is necessary. Patients who test positive for hepatitis B core antibody should undergo further hepatitis B virus DNA testing to enable accurate hepatitis B virus screening. 相似文献
1000.
Shinji Watanabe Takahisa Gono Kumiko Nishina Naohiro Sugitani Eri Watanabe Hiroki Yabe Chihiro Terai 《BMC immunology》2017,18(1):53