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排序方式: 共有9861条查询结果,搜索用时 78 毫秒
1.
Tomoe Koizumi PhD Yodo Sugishita MD PhD Yuki Suzuki-Takahashi MD PhD Kazuko Nara MA Tomoko Miyagawa MA Misako Nakajima MA Kouhei Sugimoto MD PhD Manabu Futamura MD PhD Tatsuro Furui MD PhD Yasushi Takai MD PhD Hiroshi Matsumoto MD PhD Hideko Yamauchi MD Shinji Ohno MD PhD Akemi Kataoka MD PhD Kiyotaka Kawai MD PhD Eisuke Fukuma MD PhD Hiroko Nogi MD PhD Koichiro Tsugawa MD PhD Nao Suzuki MD PhD 《Cancer》2023,129(16):2568-2580
2.
Tetsuo Yamaguchi Daisuke Ueshima Makoto Utsunomiya Akihiro Matsui Toru Miyazaki Masaaki Matsumoto Tsukasa Shimura Naotaka Murata Yasushi Komatsu Kazuki Tobita Yo Fujimoto Takahide Kodama Kenji Suzuki Hitoshi Anzai Kentaro Jujo Michiaki Higashitani 《Journal of cardiology》2021,77(2):109-115
BackgroundMalnutrition measured by the geriatric nutritional risk index (GNRI) was reported to be associated with poor prognosis for patients with peripheral artery disease (PAD). However, the optimal cut-off value of preprocedural GNRI for critical limb ischemia (CLI) and intermittent claudication (IC) is unknown. We aimed to determine its optimal cut-off value for CLI or IC patients requiring endovascular revascularization.MethodsWe explored data of 2246 patients (CLI: n = 1061, IC: n = 1185) registered in the Tokyo-taMA peripheral vascular intervention research COmraDE (TOMA-CODE) registry, which prospectively enrolled consecutive PAD patients who underwent endovascular revascularization in 34 hospitals in Japan from August 2014 to August 2016. The optimal cut-off values of GNRI were assessed by the survival classification and regression tree (CART) analyses, and the survival curve analyses for major adverse cardiovascular and limb events (MACLEs) were performed for these cut-off values.ResultsIn addition to the first cut-off value of 96.2 in CLI and 85.6 in IC, the survival CART provided an additional cut-off value of 78.2 in CLI and 106.0 in IC for further risk stratification. The survival curve was significantly stratified by the GNRI-based malnutrition status in both CLI [high risk: 47.7% (51/107), moderate: 30.1% (118/392), and low: 10.2% (53/520), log–rank p < 0.001] and IC [high risk: 14.3% (7/49), moderate: 4.5% (29/646), and low: 0.5% (2/407), log–rank p < 0.001]. The multivariate Cox-proportional hazard analysis showed that a higher GNRI was significantly associated with a better outcome in both CLI [hazard ratio (HR) per 1-point increase: 0.97, 95% CI: 0.96–0.98, p < 0.001] and IC (HR: 0.94, 95% CI: 0.91–0.97, p < 0.001).ConclusionsPreprocedural nutritional status significantly stratified future events in patients with PAD. Given that the optimal cut-off value of GNRI in CLI was almost 10-points lower than that of IC, using a disease-specific cut-off value is important for risk stratification. 相似文献
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Yasushi Sawayama Hidehiro Itonaga Takuya Fukushima Nobuaki Nakano Hiroshi Fujiwara Atae Utsunomiya Takahiro Fukuda Toshihiro Miyamoto Tetsuya Eto Kaname Miyashita Hirohisa Nakamae Masao Ogata Atsushi Yamanoha Yasuhiko Miyazaki Junya Kanda Yoshiko Atsuta Koji Kato ATL Working Group of the Japan Society for Hematopoietic Cell Transplantation 《American journal of hematology》2019,94(5):E143-E146
6.
Yasushi Yamasaki Keita Harada Shumpei Yamamoto Eriko Yasutomi Shotaro Okanoue Mami Hirai Shohei Oka Yuka Obayashi Hiroyuki Sakae Kenta Hamada Toshihiro Inokuchi Hideaki Kinugasa Yuusaku Sugihara Masahiro Takahara Takehiro Tanaka Sakiko Hiraoka Yoshiro Kawahara Hiroyuki Okada 《Digestive endoscopy》2020,32(5):791-800
7.
ObjectivesWe sought to evaluate whether the cutaneous silent period (CSP) could be an electrophysiological indicator reflective of the effects of therapy for Parkinson's disease (PD), including anti-PD medications or deep brain stimulation (DBS).Material and MethodsWe recorded the CSP in 43 patients with PD prior to and following the administration of medication during a pre-DBS evaluation (30 cases) and the “on” and “off” states of subthalamic nucleus DBS (13 cases). The CSP was elicited from the abductor pollicis brevis muscle by an electrical stimulation of the index finger that was 2, 4, and 15 times stronger than the sensory threshold (ST). We measured changes in latencies, including the onset, duration, and end of CSP, and waveform scores from 0 to 3. The correlation between the CSP score and unified PD rating score part III (UPDRS-III) also was assessed.ResultsThe onset latency and duration of CSP were significantly different between high- (15ST) and low-strength stimulations (2ST and 4ST). However, there were no significant latency changes (onset, duration, end of CSP) before and after receiving medication, or during the on and off state of the DBS. Anti-PD medications substantially increased the CSP waveform score only in the 4ST state. However, the waveform score significantly increased in all stimuli states during the DBS-on state. Both medication and the DBS-on state decreased the UPDRS-III. Nevertheless, there was no statistically significant correlation between the UPDRS-III and CSP waveform scores.ConclusionDifferent onset latencies and the duration of CSP between low- and high-strength stimuli support the hypotheses proposing two different reflex pathways. Despite being independent from the UPDRS-III, the CSP may be an electrophysiological indicator reflective of the changes in inhibitory activity to the spinal α-motoneuron in response to anti-PD medications and DBS. 相似文献
8.
Yasushi Iwasaki 《Neuropathology》2020,40(5):436-449
This review considers whether the Braak hypothesis on protein propagation could account for prion disease, particularly Creutzfeldt–Jakob disease (CJD). In CJD, we can speculate on the pathological onset region to some degree in reference to the clinical symptoms and magnetic resonance imaging findings. Although relating the Braak hypothesis to prion disease is not straightforward, the following could be proposed based on experimental and previously reported case observations. Pathogenic abnormal prion protein (PrP) deposition in the central nervous system (CNS) probably begins several months or years before clinical symptom onset, signifying the potentiality of a preclinical stage, similar to α-synuclein deposition in Parkinson's disease (PD) and amyloid-β/tau deposition in Alzheimer's disease (AD). Unlike in PD and AD, the initial clinical symptoms of CJD vary by case, and thus the onset lesions must also be various and multiple in the CNS. Based on the pathological findings, particularly of PrP deposition extensively observed in the CNS gray matter of autopsy cases, it could be speculated that in the early disease stage, including the preclinical stage, abnormal PrP spreads from the onset region without directionality or hierarchy. Because each CNS region shows either vulnerability to or resistance against PrP deposition and pathological progression in prion disease, the lesion distribution shows system degeneration. Although pathologically combined cases of type 1 and type 2 PrP patterns are often recognized, type 1 and type 2 PrP patterns must never shift toward each other during the disease course; in other words, the original type of PrP deposition in each region presumably remains unchanged in each case. According to the several observations and corresponding speculations, there are at least partial similarities between prion disease and protein propagation, as explained by the Braak hypothesis, in terms of pathological lesion progression, but several noted contradictions preclude the hypothesis from comprehensively accounting for prion disease. 相似文献
9.
Akio Akagi Yasushi Iwasaki Akihiro Yamamoto Hiroshi Matsuura Toshimasa Ikeda Maya Mimuro Yuichi Riku Hiroaki Miyahara Tetsuyuki Kitamoto Mari Yoshida 《Neuropathology》2020,40(4):399-406
We report a case of early-phase sporadic Creutzfeldt–Jakob disease (sCJD) complicated by intracerebral hemorrhage (ICH), classified as MM1 + 2C-type based on autopsy. A 61-year-old Japanese man presented to our hospital with speaking difficulties including repeated usage of the same words. He was hospitalized on the seventh day after symptom onset, and diffusion-weighted images on magnetic resonance imaging showed hyperintense regions in the frontal cortex and caudate nucleus. On the 11th day after symptom onset, head computed tomography revealed ICH in the right occipital and parietal lobes. Routine laboratory evaluations and angiography revealed no cause of ICH. Myoclonus of the extremities and drowsiness were observed on the 15th day after symptom onset. He reached the state of akinetic mutism approximately two months after symptom onset. The cerebrospinal fluid test revealed positive real-time quaking-induced conversion and 14-3-3 protein. Electroencephalography revealed periodic sharp wave complexes. A clinical diagnosis of probable Creutzfeldt–Jakob disease was made according to the diagnostic criteria. After a relapse of pneumonia, he passed away on the 103rd day after symptom onset. Postmortem examination revealed ICH in the right posterior cingulate gyrus. No pathological change that might have caused ICH was obtained. Although the effect of sCJD on the onset of ICH is undeniable, the cause of ICH was unknown. Prion protein immunohistochemistry revealed the following results: (1) weak synaptic-type deposits in the tissue rarefacted by ICH; (2) synaptic-type deposits in the cerebral cortex, which showed fine vacuoles; and (3) perivacuolar-type deposits in the inferior temporal gyrus and lingual gyrus, which showed frequent large confluent vacuoles. Although it could be considered MM1-type sCJD clinically, this case was neuropathologically diagnosed as having MM1 + 2C-type sCJD. It was shown that ICH may occur in early-phase sCJD. To improve sCJD prognosis, treatment of complications and careful follow up are important. Furthermore, pathological diagnosis is indispensable for sCJD type diagnosis. 相似文献