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91.
Kanamaru Y Arcos-Fajardo M Moura IC Tsuge T Cohen H Essig M Vrtovsnik F Loirat C Peuchmaur M Beaudoin L Launay P Lehuen A Blank U Monteiro RC 《European journal of immunology》2007,37(4):1116-1128
Myeloid cells bear Fc receptors (FcR) that mediate inflammatory signaling through the ITAM-containing FcRgamma adaptor. They express FcRgamma-associated FcalphaRI, which modulate either activating or inhibitory signaling depending on the type of ligand interaction. The role of FcalphaRIgamma in disease progression remains unknown, notably in IgA nephropathy (IgAN), one of major causes of end-stage renal disease, in which large amounts of circulating IgA-immune complexes (IC) may mediate receptor activation. To analyze the involvement of FcalphaRI activation in glomerulonephritis (GN), we generated Tg mice expressing a mutated, signaling-incompetent, human FcalphaRI(R209L) that cannot associate with FcRgamma. Like FcalphaRI(wt)-Tg mice, they developed mesangial IgA deposits but not macrophage infiltration. FcalphaRI activation in FcalphaRI(wt), but not in FcalphaRI(R209L), Tg mice resulted in marked inflammation with severe proteinuria and leukocyte infiltration in spontaneous IgAN or anti-glomerular basement membrane Ab-induced GN models. Receptor triggering of syngenically transferred FcalphaRI(wt) Tg macrophages into non-Tg animals induced their recruitment into injured kidneys during GN development. FcalphaRI(wt) cross-linking on macrophages activated MAP kinases and production of TNF-alpha and MCP-1. Moreover, IgA-IC from IgAN patients activated FcalphaRI and induced TNF-alpha production. Thus, FcalphaRI activation mediates GN progression by initiating a cytokine/chemokine cascade that promotes leukocyte recruitment and kidney damage. 相似文献
92.
Nami Ogawa Takashi Mori Ichiro Fujishima Hidetaka Wakabayashi Masataka Itoda Kenjiro Kunieda Takashi Shigematsu Shinta Nishioka Haruka Tohara Minoru Yamada Sumito Ogawa 《Journal of the American Medical Directors Association》2018,19(6):516-522
Background
Sarcopenic dysphagia is characterized by difficulty swallowing due to a loss of whole-body skeletal and swallowing muscle mass and function. However, no study has reported on swallowing muscle mass and quality in patients with sarcopenic dysphagia.Objective
To compare the differences in swallowing muscle mass and quality between sarcopenic and nonsarcopenic dysphagia.Method
A cross-sectional study was performed in 55 older patients, who had been recommended to undergo dysphagia assessment and/or rehabilitation. Sarcopenic dysphagia was diagnosed using a diagnostic algorithm for sarcopenic dysphagia. The thickness and area of tongue muscle and geniohyoid muscle (coronal plane and sagittal plane), and the echo-intensity of the tongue and geniohyoid muscles were examined by ultrasound.Results
The study participants included 31 males and 24 females (mean age of 82 ± 7 years), with 14 having possible sarcopenic dysphagia, 22 probable sarcopenic dysphagia, and 19 without sarcopenic dysphagia. The group with sarcopenic dysphagia had a significantly lower cross-sectional area and area of brightness of the tongue muscle than that observed in the group without sarcopenic dysphagia. The most specific factor for identifying the presence of sarcopenic dysphagia was tongue muscle area (sensitivity, 0.389; specificity, 0.947; cut-off value, 1536.0), while the factor with the highest sensitivity was geniohyoid muscle area brightness in sagittal sections (sensitivity, 0.806; specificity, 0.632; cut-off value, 20.1). Multivariate logistic regression analysis showed that the area of the tongue muscle and its area of brightness were independent risk factors for sarcopenic dysphagia. However, geniohyoid sagittal muscle area and area of brightness showed no significant independent association with sarcopenic dysphagia.Conclusion
Tongue muscle mass in patients with sarcopenic dysphagia was smaller than that in patients without the condition. Sarcopenic dysphagia was also associated with increased intensity of the tongue muscle. 相似文献93.
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96.
Chris Hoi Houng Chan Masataka Inoue Katrina K. Ki Tomotaka Murashige John F. Fraser Michael J. Simmonds Geoff D. Tansley Nobuo Watanabe 《Artificial organs》2020,44(12):1286-1295
Nonsurgical bleeding is the most frequent complication of left ventricular assist device (LVAD) support. Supraphysiologic shear rates generated in LVAD causes impaired platelet aggregation, which increases the risk of bleeding. The effect of shear rate on the formation size of platelet aggregates has never been reported experimentally, although platelet aggregation size can be considered to be directly relevant to bleeding complications. Therefore, this study investigated the impact of shear rate and exposure time on the formation size of platelet aggregates, which is vital in predicting bleeding in patients with an LVAD. Human platelet-poor plasma (containing von Willebrand factor, vWF) and fluorochrome-labeled platelets were subjected to a range of shear rates (0-10 000 s−1) for 0, 5, 10, and 15 minutes using a custom-built blood-shearing device. Formed sizes of platelet aggregates under a range of shear-controlled environment were visualized and measured using microscopy. The loss of high molecular weight (HMW) vWF multimers was quantified using gel electrophoresis and immunoblotting. An inhibition study was also performed to investigate the reduction in platelet aggregation size and HMW vWF multimers caused by either mechanical shear or enzymatic (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13—ADAMTS13, the von Willebrand factor protease) mechanism under low and high shear conditions (360 and 10 000 s−1). We found that the average size of platelet aggregates formed under physiological shear rates of 360-3000 s−1 (200-300 μm2) was significantly larger compared to those sheared at >6000 s−1 (50-100 μm2). Furthermore, HMW vWF multimers were reduced with increased shear rates. The inhibition study revealed that the reduction in platelet aggregation size and HWM vWF multimers were mainly associated with ADAMTS13. In conclusion, the threshold of shear rate must not exceed >6000 s−1 in order to maintain the optimal size of platelet aggregates to “plug off” the injury site and stop bleeding. 相似文献
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98.
Masayuki Itoh Yuji Iwasaki Kohsaku Ohno Takehiko Inoue Masaharu Hayashi Shuichi Ito Tetsuo Matsuzaka Shuhei Ide Masataka Arima 《Brain & development》2014
Aim: We have never known any epidemiological study of Arima syndrome since it was first described in 1971. To investigate the number of Arima syndrome patients and clarify the clinical differences between Arima syndrome and Joubert syndrome, we performed the first nationwide survey of Arima syndrome, and herein report its results. Furthermore, we revised the diagnostic criteria for Arima syndrome. Methods: As a primary survey, we sent out self-administered questionnaires to most of the Japanese hospitals with a pediatric clinic, and facilities for persons with severe motor and intellectual disabilities, inquiring as to the number of patients having symptoms of Arima syndrome, including severe psychomotor delay, agenesis or hypoplasia of cerebellar vermis, renal dysfunction, visual dysfunction and with or without ptosis-like appearance. Next, as the second survey, we sent out detailed clinical questionnaires to the institutes having patients with two or more typical symptoms. Results: The response rate of the primary survey was 72.7% of hospitals with pediatric clinic, 63.5% of national hospitals and 66.7% of municipal and private facilities. The number of patients with 5 typical symptoms was 13 and that with 2–4 symptoms was 32. The response rate of the secondary survey was 52% (23 patients). After reviewing clinical features of 23 patients, we identified 7 Arima syndrome patients and 16 Joubert syndrome patients. Progressive renal dysfunction was noticed in all Arima syndrome patients, but in 33% of those with Joubert syndrome. Conclusion: It is sometimes difficult to distinguish Arima syndrome from Joubert syndrome. Some clinicians described a patient with Joubert syndrome and its complications of visual dysfunction and renal dysfunction, whose current diagnosis was Arima syndrome. Thus, the diagnosis of the two syndromes may be confused. Here, we revised the diagnostic criteria for Arima syndrome. 相似文献
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100.
Masataka Sugahara Akiko Goda Mitsuru Masaki Ayumi Nakabo Shohei Fujiwara Miho Fukui Kanako Itohara Shinichi Hirotan Kazuo Komamura Masaaki Kawabata-Lee Takeshi Tsujino Tohru Masuyama 《Journal of Echocardiography》2014,12(2):68-70
An 80-year-old man visited our hospital because of dyspnea on exertion from 6 months ago. Echo Doppler study showed severe calcification in the aortic valve with restricted movement and the sigmoid septum causing obstruction at the LV outflow tract (LVOT). Considering the aortic valve area (AVA) might have been inaccurately estimated, we carried out beta-blocker stress echocardiography. The transaortic pressure gradient and AVA were respectively calculated as 52 mmHg and 0.90 cm2 before propranolol administration and as 64 mmHg and 0.86 cm2 after propranolol administration. Thus, beta-blocker stress echocardiography may provide an accurate assessment of AS if the LVOT obstruction is concomitant. 相似文献