Language：Japanese   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/STROKEAHA.119.027230

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1083/jcb.201807178

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.brainres.2019.05.020

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.neuroscience.2018.11.046

Language：Japanese   Publishing type：Research paper (scientific journal)  

Pericytes are mural cells embedded in the basal membrane surrounding endothelial cells in capillary and small vessels (from precapillary arterioles to postcapillary venules). They exist with a high coverage ratio to endothelial cells in the brain and play crucial roles in the formation and maintenance of the blood-brain barrier and the control of blood flow through a close interaction with endothelial cells. Thus, intactness of pericyte is absolutely needed for neuronal/ brain functions. Ageing, life-style diseases, hypoperfusion/ischemia, drugs, and genetic factors can primarily cause pericyte dysfunctions, thereby leading to the development or progression of various brain disorders, including cerebrovascular diseases. Because pericytes also play an important role in tissue repair after brain injuries, they have received much attention as a therapeutic target even from the standpoint of functional recovery.

DOI： 10.5692/clinicalneurol.cn-001357

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1038/s41588-018-0058-3

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.brainres.2015.11.003

Language：English  

Language：Japanese  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/01.STR.0000163111.05825.0b

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/01.CIR.0000105680.92873.70

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1073/pnas.0735712100

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1038/88591

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1074/jbc.274.47.33644

Language：English   Publisher：Scientific Reports  

Smoking has detrimental effects on the cardiovascular system; however, some studies have reported better clinical outcomes after thrombolysis for ischemic stroke in smokers than in nonsmokers, a phenomenon known as the smoking paradox. Therefore, this study aimed to examine the smoking paradox in patients with ischemic stroke receiving reperfusion therapy. Data were collected from a multicenter hospital-based acute stroke registry in Fukuoka, Japan. The 1148 study patients were categorized into current and noncurrent smokers. The association between smoking and clinical outcomes, including neurological improvement (≥ 4-point decrease in the National Institutes of Health Stroke Scale during hospitalization or 0 points at discharge) and good functional outcomes (modified Rankin Scale score of 0–2) at 3 months, was evaluated using logistic regression analysis and propensity score-matched analysis. Among the participants, 231 (20.1%) were current smokers. The odds ratios (ORs) of favorable outcomes after adjusting for potential confounders were not significantly increased in current smokers (OR 0.85, 95% confidence interval [CI] 0.60–1.22 for neurological improvement; OR 0.95, 95% CI 0.65–1.38 for good functional outcome). No significant association was found in the propensity score-matched cohorts. Smoking cessation is strongly recommended since current smoking was not associated with better outcomes after reperfusion therapy.

DOI： 10.1038/s41598-024-59508-3

Web of Science

Scopus

PubMed

Language：English   Publisher：PLoS ONE  

Background It is unclear whether abdominal adiposity has an additional effect on post-stroke outcomes. This study aimed to determine whether waist circumference (WC) is independently associated with clinical outcomes after acute ischemic stroke. Methods We enrolled patients with acute ischemic stroke from a multicenter hospital-based stroke registry in Fukuoka, Japan. We measured WC on admission and categorized patients into four groups (Q1–Q4) according to the quartiles in females and males. The clinical outcomes were poor functional outcome (modified Rankin scale score 2–6) and death from any cause. Logistic regression analysis was performed to estimate the odds ratio and 95% confidence interval of the outcomes of interest after adjusting for potential confounding factors, including body mass index (BMI). Results A total of 11,989 patients (70.3±12.2 years, females: 36.1%) were included in the analysis. The risk of poor functional outcome significantly decreased for Q2–Q4 (vs. Q1) at discharge and Q2–Q3 (vs. Q1) at 3 months, even after adjusting for potential confounders, including BMI. In contrast, adjustment of BMI eliminated the significant association between WC and all-cause death at discharge and 3 months. The association between high WC and favorable functional outcome was not affected by fasting insulin levels or homeostatic model assessment for insulin resistance and was only found in patients without diabetes (P = 0.02 for heterogeneity). Conclusions These findings suggest that abdominal adiposity has an additional impact on post-stroke functional outcome, independent of body weight and insulin action.

DOI： 10.1371/journal.pone.0296833

Web of Science

Scopus

PubMed

Language：English  

DOI： 10.2196/46840

PubMed

Language：English   Publishing type：Research paper (scientific journal)  

DOI： doi.org/10.1371/journal.pone.0296833

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1371/journal.pone.0296639

Web of Science

Scopus

PubMed

Language：English   Publisher：Japan Atherosclerosis Society  

<p>There are still many patients suffering from ischemic stroke and related disabilities worldwide. To develop a treatment that promotes functional recovery after acute ischemic stroke, we need to elucidate endogenous tissue repair mechanisms. The concept of a neurovascular unit (NVU) indicates the importance of a complex orchestration of cell–cell interactions and their microenvironment in the physiology and pathophysiology of various central nervous system diseases, particularly ischemic stroke. In this concept, microvascular pericytes play a crucial role in regulating the blood–brain barrier integrity, cerebral blood flow (CBF), and vascular stability. Recent evidence suggests that pericytes are also involved in the tissue repair leading to functional recovery following acute ischemic stroke through the interaction with other cell types constituting the NVU; pericytes may organize CBF recovery, macrophage-mediated clearance of myelin debris, intrainfarct fibrosis, and periinfarct astrogliosis and remyelination. In this review, we will discuss the physiological and pathophysiological functions of pericytes, their involvement in the molecular mechanisms underlying tissue repair and functional recovery after ischemic stroke, and a therapeutic strategy to promote endogenous regeneration.</p>

DOI： 10.5551/jat.rv22007

Web of Science

Scopus

PubMed

CiNii Research

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1159/000526940

Web of Science

Scopus

PubMed

Language：Japanese   Publisher：(一社)日本神経学会  

症例は41歳女性.40歳時に右中大脳動脈領域の塞栓源不明脳塞栓症の既往があり,植込み型心電図記録計の留置とダビガトラン内服が開始となった.41歳時に再び構音障害と左片麻痺が出現した.頭部MRI拡散強調画像で右放線冠の急性期脳梗塞とMRAで右中大脳動脈M2分枝閉塞を認めた.頸動脈エコーでは右頸動脈球部に可動性プラーク様構造物を認め,頸動脈3次元CTangiographyでは同部後面から突出する構造物を呈し,carotid webと診断した.待機的に頸動脈内膜剥離術を施行し,病理学的に線維筋性異形成による血管形態異常であることを確認した.(著者抄録)

Language：English   Publisher：Journal of Stroke and Cerebrovascular Diseases  

The case study speculates that the antiphospholipid antibodies acquired during the follow-up period of carotid artery stenting may cause late stent thrombosis that is resistant to direct oral anticoagulants. A 73-year-old man was hospitalized with complaints of weakness in the right lower extremity. The patient had undergone carotid artery stenting for symptomatic stenosis of the left internal carotid artery 6 years prior and had received antiplatelet therapy with clopidogrel 75 mg/day. As the patient had developed atrial fibrillation without stent stenosis at the age of 70 years, anticoagulation therapy with rivaroxaban15 mg/day was initiated while discontinuing clopidogrel. On admission, diffusion weighted imaging (DWI) revealed acute brain infarcts in the territory of the left middle cerebral artery. Contrast-enhanced computed tomography and cerebral angiography exposed severe stenosis in the left carotid artery accompanied by a filling defect caused by a floating thrombus. Laboratory examination revealed the presence of three types of antiphospholipid antibodies, with marked prolongation of activated partial thromboplastin time (APTT). Replacement of rivaroxaban with warfarin eliminated the thrombus without recurrent stroke. In conclusion, late stent thrombosis may be associated with antiphospholipid antibodies acquired during the follow-up period of carotid artery stenting.

DOI： 10.1016/j.jstrokecerebrovasdis.2023.107143

Web of Science

Scopus

PubMed

Language：English   Publisher：PLoS ONE  

Background The association between clinical outcomes in ischemic stroke patients and decreases in serum uric acid levels, which often occur during the acute phase, remains unknown. Herein, we aimed to investigate the association using a large-scale, multicenter stroke registry. Methods We analyzed 4,621 acute ischemic stroke patients enrolled in the Fukuoka Stroke Registry between June 2007 and September 2019 whose uric acid levels were measured at least twice during hospitalization (including on admission). The study outcomes were poor functional outcome (modified Rankin Scale score ≥3) and functional dependence (modified Rankin Scale score 3–5) at 3 months after stroke onset. Changes in uric acid levels after admission were evaluated using a decrease rate that was classified into 4 sex-specific grades ranging from G1 (no change/increase after admission) to G4 (most decreased). Multivariable logistic regression analyses were used to assess the associations between decreases in uric acid levels and the outcomes. Results The frequencies of the poor functional outcome and functional dependence were lowest in G1 and highest in G4. The odds ratios (95% confidence intervals) of G4 were significantly higher for poor functional outcome (2.66 [2.05–3.44]) and functional dependence (2.61 [2.00–3.42]) when compared with G1 after adjusting for confounding factors. We observed no heterogeneity in results for subgroups categorized according to age, sex, stroke subtype, neurological severity, chronic kidney disease, or uric acid level on admission. Conclusions Decreases in serum uric acid levels were independently associated with unfavorable outcomes after acute ischemic stroke.

DOI： 10.1371/journal.pone.0287721

Web of Science

Scopus

PubMed

Language：Japanese   Publishing type：Research paper (scientific journal)  

DOI： doi.org/10.1371/journal.pone.0287721

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publisher：Stroke  

Background: It remains unclear how chronic kidney disease and its underlying pathological conditions, kidney dysfunction, and kidney damage, are associated with cardiovascular outcomes. This study aimed to determine whether kidney dysfunction (ie, decreased estimated glomerular filtration rate), kidney damage (ie, proteinuria), or both are associated with the long-term outcomes after ischemic stroke. Methods: A total of 12 576 patients (mean age, 73.0±12.6 years; 41.3% women) with ischemic stroke who were registered in a hospital-based multicenter registry, Fukuoka Stroke Registry, between June 2007 and September 2019, were prospectively followed up after stroke onset. Kidney function was assessed by estimated glomerular filtration rate and categorized into G1: ≥60 mL/(min·1.73 m2), G2: 45-59 mL/(min·1.73 m2), and G3: <45 mL/(min·1.73 m2). Kidney damage was evaluated by proteinuria using a urine dipstick test and classified into P1: -, P2: ±/1+, and P3: ≥2+. Hazard ratios and 95% CI for events of interest were estimated by a Cox proportional hazards model. Long-term outcomes included recurrence of stroke and all-cause death. Results: During the median follow-up of 4.3 years (interquartile range, 2.1-7.3 years), 2481 patients had recurrent stroke (48.0/1000 patient-years) and 4032 patients died (67.3/1000 patient-years). Chronic kidney disease was independently associated with increased risks of stroke recurrence and all-cause death even after adjustment for multiple confounding factors, including traditional cardiovascular risk factors. Both estimated glomerular filtration rate and proteinuria were independently associated with increased risks of stroke recurrence (multivariable-adjusted hazard ratio [95% CI], G3: 1.22 [1.09-1.37] versus G1, P3: 1.25 [1.07-1.46] versus P1) and death (G3: 1.45 [1.33-1.57] versus G1, P3: 1.62 [1.45-1.81] versus P1). In subgroup analyses, effect modifications were found in the association of proteinuria with death by age and stroke subtype. Conclusions: Kidney dysfunction and kidney damage were independently, but differently, associated with increased risks of recurrent stroke and all-cause death.

DOI： 10.1161/STROKEAHA.122.040958

Web of Science

Scopus

PubMed

Language：English   Publisher：Journal of Cerebral Blood Flow and Metabolism  

Post-stroke intra-infarct repair promotes peri-infarct neural reorganization leading to functional recovery. Herein, we examined the remodeling of extracellular matrix proteins (ECM) that constitute the intact basal membrane after permanent middle cerebral artery occlusion (pMCAO) in mice. Among ECM, collagen type IV remained localized on small vessel walls surrounding CD31-positive endothelial cells within infarct areas. Fibronectin was gradually deposited from peri-infarct areas to the ischemic core, in parallel with the accumulation of PDGFRβ-positive cells. Cultured PDGFRβ-positive pericytes produced fibronectin, which was enhanced by the treatment with PDGF-BB. Intra-infarct deposition of fibronectin was significantly attenuated in pericyte-deficient Pdgfrb+/− mice. Phagocytic activity of macrophages against myelin debris was significantly enhanced on fibronectin-coated dishes. In contrast, laminin α2, produced by GFAP- and aquaporin 4-positive astrocytes, accumulated strongly in the boundary of peri-infarct areas. Pericyte-conditioned medium increased the expression of laminin α2 in cultured astrocytes, partly through TGFβ1. Laminin α2 increased the differentiation of oligodendrocyte precursor cells into oligodendrocytes and the expression of myelin-associated proteins. Peri-infarct deposition of laminin α2 was significantly reduced in Pdgfrb+/− mice, with attenuated oligodendrogenesis in peri-infarct areas. Collectively, intra-infarct PDGFRβ-positive cells may orchestrate post-stroke remodeling of key ECM that create optimal environments promoting clearance of myelin debris and peri-infarct oligodendrogenesis.

DOI： 10.1177/0271678X221145092

Web of Science

Scopus

PubMed

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1038/s41598-023-35894-y

Web of Science

Scopus

PubMed

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jns.2023.120589

Web of Science

Scopus

PubMed

Language：English   Publisher：GLIA  

NOX4 is a major reactive oxygen species-producing enzyme that modulates cell stress responses. We here examined the effect of Nox4 deletion on demyelination–remyelination, the most common pathological change in the brain. We used a model of cuprizone (CPZ)-associated demyelination–remyelination in wild-type and Nox4-deficient (Nox4−/−) mice. While the CPZ-induced demyelination in the corpus callosum after 4 weeks of CPZ intoxication was slightly less pronounced in Nox4−/− mice than that in wild-type mice, remyelination following CPZ withdrawal was significantly enhanced in Nox4−/− mice with an increased accumulation of IBA1-positive microglia/macrophages in the demyelinating corpus callosum. Consistently, locomotor function, as assessed by the beam walking test, was significantly better during the remyelination phase in Nox4−/− mice. Nox4 deletion did not affect autonomous growth of primary-culture oligodendrocyte precursor cells. Although Nox4 expression was higher in cultured macrophages than in microglia, Nox4−/− microglia and macrophages both showed enhanced phagocytic capacity of myelin debris and produced increased amounts of trophic factors upon phagocytosis. The expression of trophic factors was higher, in parallel with the accumulation of IBA1-positive cells, in the corpus callosum in Nox4−/− mice than that in wild-type mice. Nox4 deletion suppressed phagocytosis-induced increase in mitochondrial membrane potential, enhancing phagocytic capacity of macrophages. Treatment with culture medium of Nox4−/− macrophages engulfing myelin debris, but not that of Nox4−/− astrocytes, enhanced cell growth and expression of myelin-associated proteins in cultured oligodendrocyte precursor cells. Collectively, Nox4 deletion promoted remyelination after CPZ-induced demyelination by enhancing microglia/macrophage-mediated clearance of myelin debris and the production of trophic factors leading to oligodendrogenesis.

DOI： 10.1002/glia.24292

Web of Science

Scopus

PubMed

Language：English   Publisher：Cerebrovascular Diseases  

Background: Little is known about the association between poststroke cognitive impairment (PSCI) and functional outcome in the acute care phase of ischemic stroke and the influence of the clinical condition of acute stroke on this association. We examined this issue, taking into account stroke-related factors, in a hospital-based prospective study of patients with acute ischemic stroke. The same analysis was also performed after subsequent rehabilitation to investigate whether the association observed in the acute care phase persisted after that. For comparison, the same analysis was performed for pre-stroke dementia (PreSD). Methods: We included in the study a total of 923 patients with acute ischemic stroke who were admitted to a hospital from 2012 to 2020 in Japan. Cognitive function was assessed using the Mini-Mental State Examination and Raven's Colored Progressive Matrices test at an average of 6.3 days after stroke onset. The subjects were divided into three groups with normal cognition, PSCI, and PreSD. Study outcome was a poor functional outcome, defined as a modified Rankin Scale score of ≥3 at the end of acute care (median 21 days after admission). Among total subjects, 460 were also assessed for poor functional outcome after rehabilitation (median 77 days after admission). A logistic regression model was applied in this study. Results: Patients with PSCI and PreSD had higher median National Institute of Health Stroke Scale scores than those with normal cognition (median [IQR]: 3 [2-6], 4 [2-12], and 2 [1-4], respectively). The age- and sex-adjusted cumulative incidence of poor functional outcome was significantly higher in patients with PSCI and PreSD than in those with normal cognition in the acute care and rehabilitation phases. In the acute care phase, these associations remained significant after adjustment for stroke-related factors and other confounders (multivariable-adjusted odds ratio [95% CI] for PSCI vs. normal cognition: 3.28 [2.07-5.20]; for PreSD: 2.39 [1.40-4.08]). Similar results were observed in the rehabilitation phase (for PSCI: 2.48 [1.31-4.70]; for PreSD: 3.92 [1.94-7.92]). Conclusions: Our findings suggest that PSCI, as well as PreSD, is possibly associated with the development of poor functional outcome in the acute care phase of ischemic stroke, and this association continues thereafter.

DOI： 10.1159/000524839

Web of Science

Scopus

PubMed

Language：Japanese   Publisher：Societas Neurologica Japonica  

<p>We present a case of a 41-year-old female presenting with recurrence of ischemic stroke on subtherapeutic doses of dabigatran. She had a history of embolic stroke of undetermined sources at the age of 40, and underwent implantable cardiac monitor implantation and had started dabigatran. One year after the first ischemic stroke, she presented with sudden dysarthria and left hemiparesis and was admitted to our hospital. An MRI of the head revealed acute cerebral infarction in the right corona radiata, and an MR angiography revealed right M2 occlusion. Cervical 3D-CTA revealed a protruding structure on the posterior wall of the carotid artery bulb, which was diagnosed as carotid web. She underwent carotid endarterectomy, and the specimen was pathologically confirmed to be vascular malformation due to fibromuscular dysplasia.</p>

DOI： 10.5692/clinicalneurol.cn-001872

Scopus

PubMed

CiNii Research

Language：English   Publisher：Japan Atherosclerosis Society  

<p> <b>Aim:</b> Secular trends in the risk of recurrent stroke have been reported in several epidemiological studies worldwide, but this issue has not been investigated in general Japanese populations. We examined the trends in the 5-year risk of recurrent stroke over a half century using community-based prospective data in Japan.</p><p><b>Methods:</b> We established 4 cohort studies in 1961, 1974, 1988, and 2002. To examine the risk of recurrent stroke, participants who developed stroke during a 10-year follow-up period in each cohort were followed-up for 5 years from the date of first onset. A total of 154 (first sub-cohort: 1961-1971), 144 (second sub-cohort: 1974-1984), 172 (third sub-cohort: 1988-1998), and 146 (fourth sub-cohort: 2002-2012) participants from each cohort were enrolled in the present study. The 5-year cumulative risk of recurrent stroke was compared among the sub-cohorts using the Kaplan-Meier method and the age- and sex-adjusted Cox proportional hazards model.</p><p><b>Results:</b> The risks of recurrent stroke after any stroke and ischemic stroke decreased significantly from the first to the third sub-cohort, but they did not clearly change from the third to the fourth sub-cohort. The risk of recurrent stroke after hemorrhagic stroke decreased mainly from the first to the second sub-cohort and there was no apparent decrease from the second to the fourth sub-cohort. These trends were substantially unchanged after adjusting for age and sex.</p><p><b>Conclusions:</b> In the Japanese community, the risk of recurrent stroke decreased mainly from the 1960s to 1990s, but there was no apparent decrease in recent years.</p>

DOI： 10.5551/jat.63344

Web of Science

Scopus

PubMed

CiNii Research

Language：English   Publisher：(一社)日本動脈硬化学会  

一般日本人集団の前向き追跡データを用いて、再発性脳卒中の5年リスクにみられる傾向を半世紀にわたり検討した。福岡県久山町の住民を対象に、1961年から続けられている久山町研究のデータを利用した。1961年(154名)、1974年(144名)、1988年(172名)、2002年(146名)を起点とする四つのコホートを設定し、脳卒中発症患者を起点から10年間追跡したデータを用いて再発性脳卒中リスクを調査した。全種類の脳卒中および虚血性脳卒中を発症した後の再発性脳卒中リスクは、一番目(1961年)のコホートから三番目のコホートにかけて有意に低下していたが、三番目から四番目のコホートでは明瞭な変化は示されなかった。出血性脳卒中後の同リスクは主として一番目から二番目のコホートにかけて低下しており、二番目から四番目まででは明らかな低下はみられなかった。こうした傾向は年齢・性別で調整しても実質的に不変であった。

Language：English   Publisher：Nature  

Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.

DOI： 10.1038/s41586-022-05165-3

Web of Science

Scopus

PubMed

Language：English   Publisher：Neurology: Genetics  

Background and Objective The objective of this case report was to identify a second-hit gene that may promote Moyamoya disease (MMD)–like vascular formation in an individual having the RNF213 p.R4810K variant. Methods We performed magnetic resonance imaging and genetic analyses of RNF213 and FLNA in a 21-year-old woman, who showed Ehlers-Danlos–like symptoms and developed a first-ever unprovoked seizure, and of her healthy parents. Results We identified bilateral periventricular nodular heterotopia (PNH) as the cause of seizures and MMD-like vascular formation in the patient. The patient had the RNF213 p.R4810K variant. Exome analysis identified c.4868delG in the X-linked FLNA gene encoding filamin A p.G1623V fs*41, which could explain PNH and Ehlers-Danlos–like symptoms. Her mother had the same FLNA variant and had asymptomatic bilateral PNH, whereas her father had the RNF213 variant and had normal cerebrovascular structure. Discussion The family study suggested that the FLNA variant promoted MMD-like vascular formation in a patient having the RNF213 variant, while the RNF213 variant amplified the phenotypic changes elicited by the FLNA abnormality. Collectively, we identified a gene abnormality in filamin A, a target of RNF213-mediated proteasomal degradation, that may promote MMD-like vascular formation as a possible second-hit gene in individuals having the RNF213 p.R4810K variant.

DOI： 10.1212/NXG.0000000000200017

Web of Science

Scopus

PubMed

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1038/s42003-022-03605-4

Web of Science

Scopus

PubMed

Language：English   Publisher：PLoS ONE  

Background Very few comparative studies have focused on the differences in the causes of ischemic stroke between young adults and non-young adults. This study was performed to determine what causes of ischemic stroke are more important in young adults than in non-young adults using a large-scale multicenter hospital-based stroke registry in Fukuoka, Japan. Methods and results We investigated data on 15,860 consecutive patients aged ≥18 years with acute ischemic stroke (mean age: 73.5 ± 12.4 years, 58.2% men) who were hospitalized between 2007 and 2019. In total, 779 patients were categorized as young adults (≤50 years of age). Although vascular risk factors, including hypertension, diabetes mellitus, and dyslipidemia, were less frequent in young adults than in non-young adults, the prevalence of diabetes mellitus and dyslipidemia in young adults aged >40 years were comparable to those of non-young adults. Lifestyle-related risk factors such as smoking, drinking, and obesity were more frequent in young adults than in non-young adults. As young adults became older, the proportions of cardioembolism and stroke of other determined etiologies decreased, but those of large-artery atherosclerosis and small-vessel occlusion increased. Some embolic sources (high-risk sources: arterial myxoma, dilated cardiomyopathy, and intracardiac thrombus; medium-risk sources: atrial septal defect, nonbacterial thrombotic endocarditis, patent foramen ovale, and left ventricular hypokinesis) and uncommon causes (vascular diseases: reversible cerebral vasoconstriction syndrome, moyamoya disease, other vascular causes, arterial dissection, and cerebral venous thrombosis; hematologic diseases: antiphospholipid syndrome and protein S deficiency) were more prevalent in young adults than in non-young adults, and these trends decreased with age. Conclusions Certain embolic sources and uncommon causes may be etiologically important causes of ischemic stroke in young adults. However, the contribution of conventional vascular risk factors and lifestyle-related risk factors is not negligible with advancing age, even in young adults.

DOI： 10.1371/journal.pone.0268481

Scopus

PubMed

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publisher：Hypertension Research  

DOI： 10.1038/s41440-022-00907-2

Web of Science

Scopus

PubMed

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publisher：Journal of Stroke and Cerebrovascular Diseases  

We report a case of a 59-year-old man with human immunodeficiency virus (HIV)/ acquired immunodeficiency syndrome (AIDS) who developed multiple small-vessel strokes during the immune reconstitution phase. The patient had been diagnosed with HIV/AIDS with a low CD4 count and high viral load and started combinational antiretroviral therapy (cART) with raltegravir, emtricitabine, and tenofovir alafenamide fumarate seven months before the admission. He was admitted to our hospital with complaints of mild dysarthria and left-sided hemiparesis, but lacking consciousness/cognitive disturbances. Diffusion-weighted images (DWI) revealed multiple areas of hyperintensity in the anterior circulation system of the brain. Because we identified decreased activity of protein S through extensive examinations, we treated him initially with intravenous infusion of heparin sodium and aspirin; however, DWI detected multiple progressive small-vessel strokes after that. We considered that the immune reconstitution accounted for the small-vessel vasculopathy/vasculitis, leading to ischemic stroke. Therefore, we initiated oral administration of prednisolone, which successfully prevented stroke recurrence. This report describes a case of multiple small-vessel strokes following cART for AIDS during the immune reconstitution phase, effectively treated with steroids, which may often go undiagnosed due to their relatively mild symptoms.

DOI： 10.1016/j.jstrokecerebrovasdis.2022.106409

Web of Science

Scopus

PubMed

Publisher：医歯薬出版  

DOI： 10.32118/ayu280101020

CiNii Research

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publisher：Stroke  

Background and Purpose: This study aimed to determine whether variability of day-by-day blood pressure (BP) during the subacute stage of acute ischemic stroke is predictive of long-term stroke recurrence. Methods: We analyzed 7665 patients (mean±SD age: 72.9±13.1 years; women: 42.4%) hospitalized for first-ever ischemic stroke in 7 stroke centers in Fukuoka, Japan, from June 2007 to November 2018. BP was measured daily during the subacute stage (4-10 days after onset). Its mean and coefficient of variation (CV) values were calculated and divided into 4 groups according to the quartiles of these BP parameters. Patients were prospectively followed up for recurrent stroke or all-cause death. The cumulative event rate was calculated with the Kaplan-Meier method. We estimated the hazard ratios and 95% confidence intervals of the events of interest after adjusting for potential confounders and mean BP values using Cox proportional hazards models. The Fine-Gray model was also used to account for the competing risk of death. Results: With a mean (±SD) follow-up duration of 3.9±3.2 years, the rates of recurrent stroke and all-cause death were 3.9 and 9.9 per 100 patient-years, respectively. The cumulative event rates of recurrent stroke and all-cause death increased with increasing CVs of systolic BP and diastolic BP. The systolic BP CV was significantly associated with an increased risk of recurrent stroke after adjusting for multiple confounders and mean BP (hazard ratio [95% CI] for fourth quartile versus first quartile, 1.26 [1.05-1.50]); the risk of recurrent stroke also increased with an increasing systolic BP CV for nonfatal strokes (1.26 [1.05-1.51]) and when death was regarded as a competing risk (1.21 [1.02-1.45]). Similar associations were observed for the diastolic BP CV. Conclusions: Day-by-day variability of BP during the subacute stage of acute ischemic stroke was associated with an increased long-term risk of recurrent stroke.

DOI： 10.1161/STROKEAHA.120.033751

Web of Science

Scopus

PubMed

Language：English   Publisher：Case Reports in Neurology  

A 63-year-old woman under treatment of autoimmune hepatitis presented with headache, memory loss, and somnolence. Three months before admission, the patient experienced liver inflammation relapse after prednisolone (PSL) cessation. Consequently, PSL was resumed and then tapered. Cerebrospinal fluid (CSF) examination showed lymphocytic pleocytosis with remarkably reduced glucose and elevated angiotensin-converting enzyme and soluble interleukin-2 receptor levels. Magnetic resonance imaging (MRI) revealed prominent bilateral periventricular white-matter lesions, hydrocephalus, ischemic stroke with gadolinium enhancement of frontoparietal and basilar meninges on contrast-enhanced fluid-attenuated inversion recovery. Magnetic resonance angiography (MRA) showed narrowing of the bilateral middle cerebral arteries. Based on these findings, we diagnosed the patient with neurosarcoidosis. Re-increment of PSL improved the neurological symptoms, CSF findings, and abnormalities found on MRI and MRA. This case suggests that neurosarcoidosis may occur as a complication of some autoimmune diseases during immunotherapy administration.

DOI： 10.1159/000526223

Web of Science

Scopus

PubMed

CiNii Research

CiNii Research

CiNii Research

CiNii Research

CiNii Research

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1097/MD.0000000000024145

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1038/s41598-020-71326-x

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jns.2020.116791

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jstrokecerebrovasdis.2019.104597

Language：English   Publishing type：Research paper (scientific journal)  

Background: Angiotensin II (Ang II) can cause hypertension and tissue impairment via AGTR1 (Ang II receptor type 1), particularly in renal proximal tubule cells, and can cause DNA damage in renal cells via nicotinamide adenine dinucleotide phosphate oxidase. BubR1 (budding uninhibited by benzimidazole-related 1) is a multifaceted kinase that functions as a mitotic checkpoint. BubR1 expression can be induced by Ang II in smooth muscle cells in vitro, but the relationship between systemic BubR1 expression and the Ang II response is unclear. Methods and Results: Twenty 24-week-old male BubR1 low-expression mice (BubR1^L/L mice) and age-matched BubR1^+/+ mice were used in this study. We investigated how Ang II stimulation affects BubR1^L/L mice. The elevated systolic blood pressure caused by Ang II stimulation in BubR1^+/+ mice was significantly attenuated in BubR1^L/L mice. Additionally, an attenuated level of Ang II–induced perivascular fibrosis was observed in the kidneys of BubR1^L/L mice. Immunohistochemistry revealed that the overexpression of AGTR1 induced by Ang II stimulation was repressed in BubR1^L/L mice. We evaluated AGTR1 and Nox-4 (nicotinamide adenine dinucleotide phosphate oxidase-4) levels to determine the role of BubR1 in the Ang II response. Results from in vitro assays of renal proximal tubule cells suggest that treatment with small interfering RNA targeting BubR1 suppressed Ang II-induced overexpression of AGTR1. Similarly, the upregulation in Nox4 and Jun N-terminal kinase induced by Ang II administration was repressed by treatment with small interfering RNA targeting BubR1. Conclusions: Ang II–induced hypertension is caused by AGTR1 overexpression in the kidneys via the upregulation of BubR1 and Nox4.

DOI： 10.1161/JAHA.118.011911

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1093/jnen/nlz079

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jstrokecerebrovasdis.2019.06.028

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jstrokecerebrovasdis.2019.02.020

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1212/CPJ.0000000000000608

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1161/CIRCULATIONAHA.118.038439

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1159/000502713

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jstrokecerebrovasdis.2018.06.007

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1177/1747493018765263

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.ensci.2018.08.003

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1001/jamanetworkopen.2018.2953

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jstrokecerebrovasdis.2018.02.053

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1212/CPJ.0000000000000464

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1186/s12883-017-1001-4

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：Japanese   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.yjmcc.2016.01.020

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.yjmcc.2015.11.013

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1016/j.jacc.2015.05.058

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Publishing type：Research paper (scientific journal)  

Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1006/bbrc.2001.5629

Language：Japanese   Book type：Scholarly book

Language：Japanese   Book type：Scholarly book

Language：Japanese   Book type：Scholarly book

Language：Japanese   Book type：General book, introductory book for general audience

Event date： 2015.5

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：新潟   Country：Japan  

Event date： 2012.3

Presentation type：Oral presentation (general)  

Country：Japan  

Event date： 2012.2

Presentation type：Oral presentation (general)  

Venue：New Orleans   Country：United States  

Event date： 2012.2

Presentation type：Oral presentation (general)  

Country：United States  

Event date： 2011.2

Venue：LA   Country：United States  

Event date： 2010.6

Presentation type：Oral presentation (general)  

Country：Switzerland  

Gordon Research Conference on Nox family NADPH oxidases 2010

Other Link： http://www.grc.org/programs.aspx?year=2010&program=nox

Event date： 2007.11

Country：United States  

Other Link： http://www.med.kyushu-u.ac.jp/stroke/PDF/Katz%20issue.pdf

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：大阪   Country：Japan  

Event date： 2024.3

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：横浜   Country：Japan  

Event date： 2023.11

Language：English   Presentation type：Oral presentation (general)  

Country：United States  

Event date： 2023.11

Language：English   Presentation type：Oral presentation (general)  

Country：United States  

Event date： 2023.10

Language：Japanese   Presentation type：Public lecture, seminar, tutorial, course, or other speech  

Venue：横浜   Country：Japan  

Event date： 2023.3

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：横浜   Country：Japan  

Event date： 2022.10

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：山梨   Country：Japan  

Event date： 2022.7

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：久留米   Country：Japan  

Event date： 2022.3

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：大阪   Country：Japan  

Event date： 2021.11

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：福岡   Country：Japan  

Event date： 2021.10

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：東京   Country：Japan  

Event date： 2021.10

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：沖縄   Country：Japan  

Event date： 2021.10

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：新潟   Country：Japan  

Event date： 2021.3

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：福岡   Country：Japan  

Event date： 2020.8

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：横浜   Country：Japan  

Event date： 2020.7

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：名古屋   Country：Japan  

Event date： 2019.11

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：横浜   Country：Japan  

Event date： 2019.6

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：久留米   Country：Japan  

Event date： 2019.3

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：横浜   Country：Japan  

Event date： 2019.3

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：横浜   Country：Japan  

Event date： 2018.7

Language：Japanese   Presentation type：Public lecture, seminar, tutorial, course, or other speech  

Venue：東京   Country：Japan  

Event date： 2018.6

Language：Japanese   Presentation type：Public lecture, seminar, tutorial, course, or other speech  

Venue：東京   Country：Japan  

Event date： 2018.6

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：東京   Country：Japan  

Event date： 2018.5

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：札幌   Country：Japan  

Event date： 2018.3

Language：English   Presentation type：Symposium, workshop panel (public)  

Venue：高松   Country：Japan  

Event date： 2017.12

Language：English   Presentation type：Symposium, workshop panel (public)  

Country：Japan  

Event date： 2017.11

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：大阪   Country：Japan  

Event date： 2017.10

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：愛媛   Country：Japan  

Event date： 2017.6

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：福岡   Country：Japan  

Event date： 2017.6

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：福岡   Country：Japan  

Event date： 2017.3

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：浜松   Country：Japan  

Event date： 2017.3

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Country：Japan  

Event date： 2012.10

Language：English   Presentation type：Oral presentation (general)  

Country：United States  

Event date： 2011.2

Country：United States  

Event date： 2011.2

Country：United States  

Event date： 2010.5

Country：Japan  

Event date： 2010.4

Venue：岩手   Country：Japan  

Event date： 2009.11 - 2010.11

Venue：大阪   Country：Japan  

Event date： 2009.5

Venue：仙台   Country：Japan  

Event date： 2009.3

Venue：島根   Country：Japan  

Language：Japanese   Presentation type：Oral presentation (invited, special)  

Country：Japan  

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Country：Japan  

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：東京   Country：Japan  

Language：English   Presentation type：Symposium, workshop panel (public)  

Country：United States  

Language：Japanese   Presentation type：Symposium, workshop panel (public)  

Venue：岡山   Country：Japan  

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：京都   Country：Japan  

Language：Japanese  

Venue：広島   Country：Japan  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：English  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：Japanese  

Language：English  

Language：Japanese  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Other Link： http://www.jstage.jst.go.jp/article/circj/75/8/75_1791/_article

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publisher：(株)メディカ出版  

Language：English   Publisher：eNeurologicalSci  

DOI： 10.1016/j.ensci.2023.100492

Scopus

PubMed

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publisher：(株)日本臨床社  

Language：English   Publisher：(一社)日本動脈硬化学会  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publisher：大道学館出版部  

Language：English   Publisher：Nature  

In the version of this article initially published, the name of the PRECISE4Q Consortium was misspelled as “PRECISEQ” and has now been amended in the HTML and PDF versions of the article. Further, data in the first column of Supplementary Table 55 were mistakenly shifted and have been corrected in the file accompanying the HTML version of the article.

DOI： 10.1038/s41586-022-05492-5

Scopus

PubMed

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publisher：(株)中外医学社  

Language：Japanese   Publisher：(有)科学評論社  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publisher：Nature Publishing Group  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publisher：医歯薬出版(株)  

脳機能遂行の中心をなすのは神経細胞である。しかし、脳の中には神経細胞のみならずアストロサイト、オリゴデンドロサイト、ミクログリア、など種々のグリア細胞が存在する。正常に神経細胞を機能させるためには、これらグリア細胞による構造的かつ機能的サポートが不可欠である。加えて、神経細胞の近傍にはかならず内皮細胞およびペリサイトによって形成される血液脳関門を有した毛細血管が存在し、需要に応じた適切な血流供給を行っている。脳機能の生理ならびに病理を考える際には、神経細胞のみに着目することなく、これをサポートする神経系および血管系すべての細胞をひとつの単位-neurovascular unit(NVU)-として捉える必要がある。この概念は、傷害発生後の機能回復を考えるうえでも重要である。本稿では、脳梗塞発症前から発症後機能回復に至るまでの過程において、NVUを構成する細胞群がどのように相互作用し危機的状況に対応しようとするのか、私見を含めて概説してみたい。(著者抄録)

Language：Japanese   Publisher：(株)日本臨床社  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publisher：(株)日本臨床社  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Peer review 

Number of peer-reviewed articles in foreign language journals：26

Proceedings of International Conference Number of peer-reviewed papers：30

Proceedings of domestic conference Number of peer-reviewed papers：46

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Peer review 

Number of peer-reviewed articles in foreign language journals：23

Proceedings of International Conference Number of peer-reviewed papers：30

Proceedings of domestic conference Number of peer-reviewed papers：60

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Peer review 

Number of peer-reviewed articles in foreign language journals：20

Proceedings of International Conference Number of peer-reviewed papers：20

Proceedings of domestic conference Number of peer-reviewed papers：56

Type：Academic society, research group, etc. 

Type：Peer review 

Number of peer-reviewed articles in foreign language journals：29

Proceedings of domestic conference Number of peer-reviewed papers：48

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Peer review 

Number of peer-reviewed articles in foreign language journals：20

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Peer review 

Number of peer-reviewed articles in foreign language journals：24

Type：Scientific advice/Review 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Peer review 

Number of peer-reviewed articles in foreign language journals：24

Proceedings of International Conference Number of peer-reviewed papers：20

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Academic society, research group, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Number of participants：100

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Type：Competition, symposium, etc. 

Number of participants：100

Type：Competition, symposium, etc. 

Number of participants：80

Type：Academic society, research group, etc. 

Type：Competition, symposium, etc. 

Audience： General,　Scientific,　Company,　Civic organization,　Governmental agency

Type：Lecture

Audience： General,　Scientific,　Company,　Civic organization,　Governmental agency

Type：Lecture

Audience： General,　Scientific,　Company,　Civic organization,　Governmental agency

Type：Lecture