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  • 1
    In: Cerebrovascular Diseases Extra, S. Karger AG, Vol. 4, No. 2 ( 2014-7-22), p. 156-164
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Gastrointestinal (GI) hemorrhage is a potentially serious complication of acute stroke, but its incidence appears to be decreasing. The aim of this study was to elucidate the etiology of GI bleeding and its impact on clinical outcomes in patients with acute ischemic stroke in recent years. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Using the database of the Fukuoka Stroke Registry, 6,529 patients with acute ischemic stroke registered between June 2007 and December 2012 were included in this study. We recorded clinical data including any previous history of peptic ulcer, prestroke drug history including the use of antiplatelets, anticoagulants, steroids and nonsteroidal anti-inflammatory drugs (NSAIDs), and poststroke treatment with suppressing gastric acidity. GI bleeding was defined as any episode of hematemesis or melena on admission or during hospitalization. The cause and origin of bleeding were diagnosed endoscopically. Logistic regression analysis was used to identify risk factors for GI bleeding and its influence on deteriorating neurologic function, death, and poor outcome. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 GI bleeding occurred in 89 patients (1.4%) under the condition that 66% of the total patients received acid-suppressing agents after admission. Multivariate analysis revealed that GI bleeding was associated with the absence of dyslipidemia (p = 0.03), a previous history of peptic ulcer (p 〈 0.001), and the severity of baseline neurologic deficit (p = 0.002) but not with antiplatelet drugs, anticoagulants, and NSAIDs. The source was the upper GI tract in 51% of the cases; causes included peptic ulceration (28%) and malignancies (12%), and other or unidentified causes accounted for 60%. GI bleeding mostly occurred within 1 week after stroke onset. Hemoglobin concentration fell by a median value of 2.5 g/dl in patients with GI bleeding. Among them, 28 patients underwent blood transfusion (31.5%). After adjustment for confounding factors, GI bleeding was independently associated with neurologic deterioration (OR 3.9, 95% CI 2.3-6.6, p 〈 0.001), in-hospital death (OR 6.1, 95% CI 3.1-12.1, p 〈 0.001), and poor outcome at 3 months (OR 6.8, 95% CI 3.7-12.7, p 〈 0.001). These associations were significant irrespective of whether patients underwent red blood cell transfusion. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 GI bleeding infrequently occurred in patients with acute ischemic stroke, which was mostly due to etiologies other than peptic ulcer. GI bleeding was associated with poor clinical outcomes including neurologic deterioration, in-hospital mortality, and poor functional outcome.
    Type of Medium: Online Resource
    ISSN: 1664-5456
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2014
    detail.hit.zdb_id: 2651613-5
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  • 2
    Online Resource
    Online Resource
    S. Karger AG ; 2010
    In:  Cerebrovascular Diseases Vol. 30, No. 6 ( 2010), p. 606-611
    In: Cerebrovascular Diseases, S. Karger AG, Vol. 30, No. 6 ( 2010), p. 606-611
    Abstract: 〈 i 〉 Background: 〈 /i 〉 The present study investigated the frequency and morphological characteristics of carotid mobile plaques and examined the relationship between carotid mobile plaques and recurrent strokes. 〈 i 〉 Methods: 〈 /i 〉 The study included 94 consecutive acute stroke patients with large-artery atherosclerosis associated with extracranial carotid stenosis. We investigated the presence of mobile plaques by carotid ultrasonography and classified patients into two groups (mobile group and non-mobile group). We compared backgrounds, MRI and ultrasonographic findings, neurological severity on admission and at discharge, and the rate of early recurrent stroke between both groups. 〈 i 〉 Results: 〈 /i 〉 Mobile plaques were detected in 12 patients (12.8%). There were four types of mobile plaques: (1) the jellyfish-type plaque, in which the fibrous cap fluctuated like a jellyfish; (2) the streaming-band-type plaque, in which the string attached to the plaque was swaying; (3) the mobile-thrombus-type plaque, in which a mobile mass was attached to the plaque surface, and (4) the fluctuating-ulcer-type plaque, which contained a mobile substance in the plaque ulcer. Although National Institutes of Health Stroke Scale (NIHSS) scores on admission were less severe in the mobile group than in the non-mobile group (median 1 vs. 4, respectively; p = 0.004), the rate of early recurrent stroke was significantly higher in the mobile group than in the non-mobile group (33.3 vs. 7.3%, respectively; p = 0.022). There were no significant differences in NIHSS scores at discharge between groups. 〈 i 〉 Conclusions: 〈 /i 〉 Morphologically, several types of mobile plaques were detected in consecutive patients with acute stroke associated with carotid stenosis. Mobile plaques are strongly associated with an early recurrence of stroke.
    Type of Medium: Online Resource
    ISSN: 1015-9770 , 1421-9786
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2010
    detail.hit.zdb_id: 1482069-9
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  • 3
    In: Cerebrovascular Diseases, S. Karger AG, Vol. 32, No. 2 ( 2011), p. 148-154
    Abstract: 〈 i 〉 Background and Purpose: 〈 /i 〉 The purpose of the present study was to clarify the difference in the infarct topography on diffusion-weighted image (DWI) and cardiac and aortic findings on transesophageal echocardiography (TEE) in stroke patients with different embolic sources. 〈 i 〉 Methods: 〈 /i 〉 We studied 270 consecutive patients with acute ischemic stroke who had DWI-documented cortical or subcortical infarcts without significant stenosis of the cerebral arteries. As embolic sources, cardiac diseases, right-to-left shunt diseases and an aortic arch atheroma ≧4.0 mm in thickness were identified using various diagnostic tools including TEE. 〈 i 〉 Results: 〈 /i 〉 Seventy-eight (29%) patients had multiple embolic sources. Large infarcts were common in patients in whom cardiac disease was the only embolic source and uncommon in patients in whom aortic atheroma was the only embolic source (p 〈 0.0001). Vertebrobasilar infarcts were relatively common in patients only having aortic atheromas. Atrial septal aneurysms were more common in patients with a right-to-left shunt than in those with a shunt plus other embolic sources (p = 0.0036). Unique characteristics of the arch atheroma (mobile plaque, extension to branches, or ulcer formation; p 〈 0.0001) as well as small or moderate-sized infarcts (p = 0.0004) were more common in patients with arch atheromas as the only embolic source than in those with atheromas plus other embolic sources. 〈 i 〉 Conclusions: 〈 /i 〉 Embolic stroke patients often have multiple embolic sources. The present study suggests the possibility that embolic stroke has unique clinical features depending on its source. DWI and TEE findings might be helpful in characterizing cardiogenic, paradoxical and aortogenic brain embolism.
    Type of Medium: Online Resource
    ISSN: 1015-9770 , 1421-9786
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
    detail.hit.zdb_id: 1482069-9
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  • 4
    Online Resource
    Online Resource
    S. Karger AG ; 2015
    In:  Blood Purification Vol. 40, No. 4 ( 2015), p. 337-343
    In: Blood Purification, S. Karger AG, Vol. 40, No. 4 ( 2015), p. 337-343
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Cardiorenal syndrome (CRS) in patients with end-stage kidney disease (ESKD) represents mainly cardiovascular disease (CVD) due to various complications associated with renal dysfunction—defined as type 4 CRS by Ronco et al.—because the effect of cardiac dysfunction on the kidneys does not need to be taken into consideration, unlike in non-dialysis dependent chronic kidney disease (CKD). 〈 b 〉 〈 i 〉 Summary: 〈 /i 〉 〈 /b 〉 Patients with ESKD are often in a state of chronic inflammation due to the upregulation of proinflammatory cytokines. Chronic inflammation leads to malnutrition and consequently to vascular endothelial dysfunction and vascular calcification, which is referred to as malnutrition-inflammation-atherosclerosis (MIA) syndrome and acts as a major risk factor for CVD. Anemia also plays a crucial role in CVD, and individuals with erythropoietin-resistant anemia have a particularly high risk of CVD. However, caution is emphasized because not only anemia itself, but also the overtreatment of anemia with erythropoiesis-stimulating agents aimed at elevating hemoglobin to ≥13 g/dl can also increase the risk of CVD. In CKD-mineral and bone disorder (CKD-MBD), phosphate load triggers the interactions between various factors such as calcium, parathyroid hormone, vitamin D, and fibroblast growth factor 23, promoting vascular calcification and thus becoming a risk factor for CVD. 〈 b 〉 〈 i 〉 Key Messages: 〈 /i 〉 〈 /b 〉 In addition to traditional atherosclerosis risk factors such as hypertension, diabetes, and dyslipidemia, the involvement of MIA syndrome, anemia, and CKD-MBD accompanying CKD have also become a focus for investigation as major players in CRS in patients with ESKD.
    Type of Medium: Online Resource
    ISSN: 0253-5068 , 1421-9735
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482025-0
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  • 5
    In: Case Reports in Nephrology and Dialysis, S. Karger AG, Vol. 9, No. 1 ( 2019-4-16), p. 25-32
    Abstract: Patients with anti-glomerular basement membrane (GBM) antibody glomerulonephritis typically exhibit rapidly progressive glomerulonephritis (RPGN). The renal outcome as well as the prognosis of this disease is worse than other forms of RPGN such as those from microscopic polyangiitis. Therefore, early therapeutic intervention is essential to improve its prognosis. One month before referral to our hospital, a 54-year-old female attended another hospital because of macrohematuria. At that time, she had proteinuria and macrohematuria with normal renal function, was negative for anti-GBM antibodies, and was diagnosed with chronic glomerulonephritis. A month later when she was admitted to our hospital, she showed renal insufficiency and was positive for anti-GBM antibodies. Immediately after recognizing the anti-GBM antibody status, plasma exchange and the first course of steroid pulse therapy was started. After 5 days of therapy, renal biopsy confirmed severe crescentic glomerulonephritis in which all the observed glomeruli were involved with cellular crescents. Despite this, she survived without end-stage renal disease after three courses of steroid pulse therapy and seven sessions of plasma exchange. This favorable outcome reflects the repeated analysis of anti-GBM antibodies within a very short period and the rapid therapeutic intervention in addition to the intensive immunosuppressive therapies.
    Type of Medium: Online Resource
    ISSN: 2296-9705
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2019
    detail.hit.zdb_id: 2809879-1
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  • 6
    In: Cerebrovascular Diseases, S. Karger AG, Vol. 25, No. 5 ( 2008), p. 417-422
    Abstract: 〈 i 〉 Background and Purpose: 〈 /i 〉 Lymphotoxin α (LTA), one of the tumor necrosis factor family proteins, is an important proinflammatory cytokine and appears to play a putative role in the inflammatory process of atherosclerosis. Recent genetic studies have suggested that variations in the gene encoding LTA, which affect its expression and biological function, may contribute to the development of vascular diseases. We conducted a case-control study to clarify the association of 〈 i 〉 LTA 〈 /i 〉 gene polymorphisms with ischemic stroke in a large Japanese population. 〈 i 〉 Methods: 〈 /i 〉 Genotyping for 〈 i 〉 LTA 〈 /i 〉 A252G and C804A polymorphisms was achieved by a rapid-cycle polymerase chain reaction and melting curve analysis using fluorescent probes in 1,044 incident cases of ischemic stroke recruited from the Fukuoka Stroke Registry and 1,044 age- and sex-matched control subjects recruited from the Hisayama Study. 〈 i 〉 Results: 〈 /i 〉 The overall distribution of allele and genotype for each polymorphism was similar between stroke patients and control subjects. The allele frequencies of 252G and 804A were slightly lower in stroke patients than in control subjects; however, conditional logistic regression analysis adjusted for potential risk factors found no association between the risk of ischemic stroke and either polymorphism. In terms of stroke subtype, we also found no association of these polymorphisms with any subtypes of ischemic stroke. 〈 i 〉 Conclusions: 〈 /i 〉 Neither the A252G nor C804A polymorphism of the 〈 i 〉 LTA 〈 /i 〉 gene was associated with stroke overall and any subtypes of ischemic stroke in the Japanese population.
    Type of Medium: Online Resource
    ISSN: 1015-9770 , 1421-9786
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2008
    detail.hit.zdb_id: 1482069-9
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  • 7
    In: Cerebrovascular Diseases, S. Karger AG, Vol. 42, No. 5-6 ( 2016), p. 395-403
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Statins have neuroprotective effects against ischemic stroke. However, associations between pre-stroke statin treatment and initial stroke severity and between the treatment and functional outcome remain controversial. This study aimed at determining these associations in ischemic stroke patients. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Among patients registered in the Fukuoka Stroke Registry from June 2007 to October 2014, 3,848 patients with ischemic stroke within 24 h of onset, who had been functionally independent before onset, were enrolled in this study. Ischemic stroke was classified as cardioembolic or non-cardioembolic infarction. Primary and secondary study outcomes were mild neurological symptoms defined as a National Institutes of Health Stroke Scale score of ≤4 on admission and favorable functional outcome defined as a modified Rankin Scale score of ≤2 at discharge, respectively. Multivariable logistic regression models were used to quantify associations between pre-stroke statin treatment and study outcomes. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Of all 3,848 participants, 697 (18.1%) were taking statins prior to the stroke. The frequency of mild neurological symptoms was significantly higher in patients with pre-stroke statin treatment (64.1%) than in those without the treatment (58.3%, p 〈 0.01). Multivariable analysis showed that pre-stroke statin treatment was significantly associated with mild neurological symptoms (OR 1.31; 95% CI 1.04-1.65; p 〈 0.01). Sensitivity analysis in patients with dyslipidemia (n = 1,998) also showed the same trend between pre-stroke statin treatment and mild neurological symptoms (multivariable-adjusted OR 1.26; 95% CI 0.99-1.62; p = 0.06). In contrast, the frequency of favorable functional outcome was not different between patients with (67.0%) and without (65.3%) the treatment (p = 0.40). Multivariable analysis also showed no significant association between pre-stroke statin treatment and favorable functional outcome (OR 1.21; 95% CI 0.91-1.60; p = 0.19). Continuation of statin treatment, however, was significantly associated with favorable functional outcome among patients with pre-stroke statin treatment (multivariable-adjusted OR 2.17; 95% CI 1.16-4.00; p = 0.02). 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Pre-stroke statin treatment in ischemic stroke patients was significantly associated with mild neurological symptoms within 24 h of onset. Pre-stroke statin treatment per se did not significantly influence the short-term functional outcome; however, continuation of statin treatment during the acute stage of stroke seems to relate with favorable functional outcome for patients with pre-stroke statin treatment.
    Type of Medium: Online Resource
    ISSN: 1015-9770 , 1421-9786
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2016
    detail.hit.zdb_id: 1482069-9
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  • 8
    Online Resource
    Online Resource
    S. Karger AG ; 2014
    In:  Case Reports in Neurology Vol. 6, No. 1 ( 2014-1-24), p. 23-27
    In: Case Reports in Neurology, S. Karger AG, Vol. 6, No. 1 ( 2014-1-24), p. 23-27
    Abstract: The mechanism of cerebral decompression sickness (DCS) is still unclear. We report 2 cases of breath-hold divers with cerebral DCS in whom magnetic resonance imaging (MRI) demonstrated distinctive characteristics. One case presented right hemiparesthesia, diplopia, and gait disturbance after breath-hold diving into the sea at a depth of 20 m. Brain MRI with fluid-attenuated inversion recovery (FLAIR) sequence revealed multiple hyperintense lesions in the right frontal lobe, bilateral thalamus, pons, and right cerebellar hemisphere. The second case presented visual and gait disturbance after repetitive breath-hold diving into the sea. FLAIR imaging showed hyperintense areas in the bilateral occipito-parietal lobes. In both cases, diffusion-weighted imaging and apparent diffusion coefficient mapping revealed hyperintense areas in the lesions identified by FLAIR. Moreover, follow-up MRI showed attenuation of the FLAIR signal abnormalities. These findings are suggestive of transient hyperpermeability in the microvasculature as a possible cause of cerebral DCS.
    Type of Medium: Online Resource
    ISSN: 1662-680X
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2014
    detail.hit.zdb_id: 2505302-4
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  • 9
    In: Journal of Vascular Research, S. Karger AG, Vol. 51, No. 6 ( 2014), p. 429-438
    Abstract: Background: Pericytes are multifunctional cells surrounding capillaries and postcapillary venules. In brain microvasculature, pericytes play a pivotal role under physiological and pathological conditions by producing reactive oxygen species (ROS). The aims of this study were to elucidate the source of ROS and its regulation in human brain pericytes. Methods: The expression of Nox enzymes in the cells was evaluated using RT-PCR and western blot. Superoxide production was determined by superoxide dismutase-inhibitable chemiluminescence. Silencing of Nox4 was performed using RNAi, and cell proliferation was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. Results: Nox4 was predominant among the Nox family in human brain pericytes. Membrane fractions of cells produced superoxide in the presence of NAD(P)H. Superoxide production was almost abolished with diphenileneiodonium, a Nox inhibitor; however, inhibitors of other possible superoxide-producing enzymes had no effect on NAD(P)H-dependent superoxide production. Pericytes expressed angiotensin II (Ang II) receptors, and Ang II upregulated Nox4 expression. Hypoxic conditions also increased the Nox4 expression. Silencing of Nox4 significantly reduced ROS production and attenuated cell proliferation. Conclusion: Our study showed that Nox4 is a major superoxide-producing enzyme and that its expression is regulated by Ang II and hypoxic stress in human brain pericytes. In addition, Nox4 may promote cell growth.
    Type of Medium: Online Resource
    ISSN: 1018-1172 , 1423-0135
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2014
    detail.hit.zdb_id: 1482726-8
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  • 10
    In: Digestion, S. Karger AG, Vol. 103, No. 4 ( 2022), p. 308-318
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 An association has been found between human-gut microbiota and various diseases (e.g., metabolic disease) by analyzing fecal or colonic microbiota. Despite the importance of the small intestinal microbiota, sampling difficulties prevent its full analysis. We investigated the composition and metagenomic functions of microbiota along the small intestine and compared them with the microbiota from feces and from other gastrointestinal (GI) sites. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Mucosal samples from the six GI sites (stomach, duodenum, distal jejunum, proximal ileum, terminal ileum, and rectum) were collected under balloon-assisted enteroscopy. Fecal samples were collected from all participants. The microbial structures and metagenomic functions of the small intestinal mucosal microbiota were compared with those from feces and other GI sites using 16S ribosomal RNA gene sequencing. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 We analyzed 133 samples from 29 participants. Microbial beta diversity analysis showed that the jejunum and ileum differed significantly from the lower GI tract and the feces ( 〈 i 〉 p 〈 /i 〉 & #x3c; 0.001). Jejunal and duodenal microbiotas formed similar clusters. Wide clusters spanning the upper and lower GI tracts were observed with the ileal microbiota, which differed significantly from the jejunal microbiota ( 〈 i 〉 p 〈 /i 〉 & #x3c; 0.001). 〈 i 〉 Veillonella 〈 /i 〉 and 〈 i 〉 Streptococcus 〈 /i 〉 were abundant in the jejunum but less so in the lower GI tract and feces. The metagenomic functions associated with nutrient metabolism differed significantly between the small intestine and the feces. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 The fact that the compositional structures of small intestinal microbiota differed from those of fecal and other GI microbiotas reveals that analyzing the small intestinal microbiota is necessary for association studies on metabolic diseases and gut microbiota.
    Type of Medium: Online Resource
    ISSN: 0012-2823 , 1421-9867
    RVK:
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2022
    detail.hit.zdb_id: 1482218-0
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