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Takao Sato Tomoki Kameyama Takahisa Noto Teruo Nakadate Hiroshi Ueno Kunihiro Yamada Hiroshi Inoue 《Journal of thrombosis and thrombolysis》2014,37(2):139-147
Present study aimed to investigate the impact of anti-inflammatory cytokines provoked by the hemoglobin scavenger receptor, CD163, on left ventricular (LV) functional recovery after successful reperfusion in patients with acute myocardial infarction (AMI). Intraplaque hemorrhage accelerates plaque destabilization. Extracellular hemoglobin is cleared by CD163, a macrophage scavenger receptor. This process provokes secretion of anti-inflammatory atheroprotective cytokine, interleukin (IL)-10. In 40 patients with the first AMI, coronary atherothrombotic debris was retrieved during percutaneous coronary intervention (PCI), stained with antibodies to CD163 and IL-10. LV function was determined by echocardiography before PCI and 6 months after PCI. %CD163 was defined as ratio of CD163 (+)-cells to whole cells. %IL-10 was expressed as the ratio of positively stained areas per total tissue. Patients were divided into two groups depending on the amount of CD163 (+)-cells: CD163 > 10 % (CD163high, n = 20) and CD163 ≤ 10 % (CD163low, n = 20). CD163high group had significantly higher %IL-10. Final thrombolysis in myocardial infarction (TIMI) flow grade was significantly lower in CD163high group. In subgroups with the final TIMI-3 flow (CD163high-Reflow, n = 15 and CD163low-Reflow, n = 20), the time to reperfusion, infarct size, LV dimensions and fractional shortening (%FS) before PCI were similar. Significant correlation was observed between %IL10 and changes in LV dimensions (diastole, r = ?0.49, P = 0.01; systole, r = ?0.65, P < 0.01) or %FS (r = 0.51, P < 0.01) at 6 months after PCI. Plaque with CD163(+)-macrophages could impair distal flow after primary PCI. However, CD163(+)-macrophages enhance the anti-inflammatory cytokine expression that aids in ventricular functional recovery if distal flow can be achieved by successful reperfusion. 相似文献
995.
Koji Kimura Atsushi Yoshida Fumihiko Katagiri Risa Takayanagi Yasuhiko Yamada 《Biopharmaceutics & drug disposition》2019,40(7):250-261
Infliximab (IFX) is used as a therapeutic agent for ulcerative colitis (UC) and Crohn's disease (CD). Although the dosage regimen has been established through clinical trial experience, it has yet to be assessed with a pharmacokinetic and pharmacodynamic model. The present study analysed sequential changes of clinical response in patients with ulcerative colitis and Crohn's disease following repeated administrations of infliximab using the pharmacokinetic/pharmacodynamic model. In addition, the dosage regimen presently used for patients with ulcerative colitis was evaluated, as well as the potential efficacy gained by increasing the dose and/or reducing the interval of administration for patients with Crohn's disease. Furthermore, the possibility of evaluating the difference between both diseases with regard to the efficacy of infliximab was investigated. Sequential changes in the clinical response values obtained with our model were in good agreement with the observed values following administration of infliximab in patients with ulcerative colitis and Crohn's disease. The results showed the importance of a loading dose for patients with ulcerative colitis, as well as the efficacy of increasing the dose and reducing the interval for patients with Crohn's disease. Also, the efficacy of infliximab for both diseases is suggested to be similar. In conclusion, our results show a possible modeling scenario that can accommodate the clinical response to infliximab administered for ulcerative colitis and Crohn's disease. Furthermore, it provides confirmation for the present dosage regimens given for these diseases. 相似文献
996.
Tadashi Konoshita Takahiro Nakaya Ai Sakai Mika Yamada Mai Ichikawa Satsuki Sato Michiko Imagawa Miki Fujii Katsushi Yamamoto Yasukazu Makino Kenichiro Arakawa Jinya Suzuki Tamotsu Ishizuka 《Medicine》2014,93(29)
The plasma renin activity (PRA) is affected by a number of environmental factors. However, significant heritability has been shown for the activity. A hypothesis that a candidate regulatory single-nucleotide polymorphism, C-5312T, of human renin gene should have a significant effect on PRA was elucidated and updating of independent determinants of PRA was attempted.Cross sectional study.Outpatient study.We enrolled consecutive 810 subjects who had consulted our hospitals for lifestyle-related diseases.Genotypes were assayed with genomic DNA for C-5312T. Among the genetic variants, the difference of PRA was evaluated. Monovariate linear regression analysis was performed to test the correlation between PRA and clinical variables. Finally, stepwise multiple regression analysis was performed to evaluate the independent determinants.On comparing 2 genotype groups, CC/CT and T allele homozygote, the geometric means of PRA were 0.778 and 0.941 ng/ml/h, respectively (F = 5.992, P = 0.015). Monovariate linear regression analysis revealed that a number of variables have a significant correlation with the activity, including urinary salt excretion. A stepwise multivariate regression analysis revealed that renin C-5312T variant (TT) is one of the independent determinants of PRA.Thus, for the first time, a human renin gene variant was associated with a significant increase in PRA as a genetic factor and the independent determinants for the activity were updated including genetic factor. 相似文献
997.
998.
Tomonori Aoki Atsuo Yamada Kazuharu Aoyama Hiroaki Saito Gota Fujisawa Nariaki Odawara Ryo Kondo Akiyoshi Tsuboi Rei Ishibashi Ayako Nakada Ryota Niikura Mitsuhiro Fujishiro Shiro Oka Soichiro Ishihara Tomoki Matsuda Masato Nakahori Shinji Tanaka Kazuhiko Koike Tomohiro Tada 《Digestive endoscopy》2020,32(4):585-591
999.
Ayyappan Anitha Ismail Thanseem Kazuhiko Nakamura Mahesh M. Vasu Kazuo Yamada Takatoshi Ueki Yoshimi Iwayama Tomoko Toyota Kenji J. Tsuchiya Yasuhide Iwata Katsuaki Suzuki Toshiro Sugiyama Masatsugu Tsujii Takeo Yoshikawa Norio Mori 《Journal of psychiatry & neuroscience : JPN》2014,39(5):294-303