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  • 1
    Online Resource
    Online Resource
    S. Karger AG ; 1995
    In:  Urologia Internationalis Vol. 54, No. 2 ( 1995), p. 104-106
    In: Urologia Internationalis, S. Karger AG, Vol. 54, No. 2 ( 1995), p. 104-106
    Type of Medium: Online Resource
    ISSN: 1423-0399 , 0042-1138
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1995
    detail.hit.zdb_id: 1464417-4
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  • 2
    In: Urologia Internationalis, S. Karger AG, Vol. 70, No. 4 ( 2003), p. 297-302
    Abstract: 〈 i 〉 Introduction: 〈 /i 〉 Micrometastasis before radical prostatectomy (RP) is considered to be related to the biochemical failure after surgery in patients with prostate cancer. To predict the biochemical failure, we evaluated microvascular (lymphatic/vascular) invasion and other pathological findings as prognostic factors for biochemical failure after RP. 〈 i 〉 Materials and Methods: 〈 /i 〉 Eighty-two men who underwent RPs and received neither preoperative nor postoperative adjuvant therapy were analyzed. Pathological findings of each patient were carefully reviewed to determine pathological factors predicting biochemical failure. The influence of pathological findings on the biochemical failure was evaluated. 〈 i 〉 Results: 〈 /i 〉 The overall biochemically assessed disease-free survival rate was 55.7% at 3 years. By univariate analysis, Gleason sum, capsular penetration, and microvascular invasion were significantly associated with the rate of biochemical failure. Microvascular invasion was strongly correlated with Gleason sum, capsular penetration, surgical margin, perineural invasion, and pathological stage. By multivariate analysis, Gleason sum, capsular penetration, and microvascular invasion were independent predictors of biochemical failure. 〈 i 〉 Conclusion: 〈 /i 〉 This study suggests that in addition to Gleason grade and capsular penetration, microvascular invasion is one of independent prognostic factors in patients with prostate cancer treated with RPs.
    Type of Medium: Online Resource
    ISSN: 0042-1138 , 1423-0399
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2003
    detail.hit.zdb_id: 1464417-4
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  • 3
    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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  • 4
    Online Resource
    Online Resource
    S. Karger AG ; 2000
    In:  ORL Vol. 62, No. 3 ( 2000), p. 170-172
    In: ORL, S. Karger AG, Vol. 62, No. 3 ( 2000), p. 170-172
    Abstract: A 46-year-old Japanese male was referred to a local hospital because of a firm, nontender mass on his neck. On physical examination, the tumor was soft, well demarcated, 3 × 2 cm in size and located in the submucosal region. It was entirely separate from the vertebrae. The resected tumor was shown to be a lipoma with focal ossification. Ossifying lipomas are rare, and the cases which are independent of bone even more so. A literature review revealed that ossifying lipoma independent of bone tissue has been reported in only 8 cases, and, interestingly, all of them occurred in the head and neck region.
    Type of Medium: Online Resource
    ISSN: 0301-1569 , 1423-0275
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2000
    detail.hit.zdb_id: 1483533-2
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  • 5
    In: Digestion, S. Karger AG
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 Length of stay (LOS) in hospital affects cost, patient quality of life, and hospital management; however, existing gastrointestinal bleeding models applicable at hospital admission have not focused on LOS. We aimed to construct a predictive model for LOS in acute lower gastrointestinal bleeding (ALGIB). 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We retrospectively analyzed the records of 8,547 patients emergently hospitalized for ALGIB at 49 hospitals (the CODE BLUE-J Study). A predictive model for prolonged hospital stay was developed using the baseline characteristics of 7,107 patients and externally validated in 1,440 patients. Furthermore, a multivariate analysis assessed the impact of additional variables during hospitalization on LOS. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Focusing on baseline characteristics, a predictive model for prolonged hospital stay was developed, the LONG-HOSP score, which consisted of low body mass index, laboratory data, old age, nondrinker status, nonsteroidal anti-inflammatory drug use, facility with ≥800 beds, heart rate, oral antithrombotic agent use, symptoms, systolic blood pressure, performance status, and past medical history. The score showed relatively high performance in predicting prolonged hospital stay and high hospitalization costs (area under the curve: 0.70 and 0.73 for derivation, respectively, and 0.66 and 0.71 for external validation, respectively). Next, we focused on in-hospital management. Diagnosis of colitis or colorectal cancer, rebleeding, and the need for blood transfusion, interventional radiology, and surgery prolonged LOS, regardless of the LONG-HOSP score. By contrast, early colonoscopy and endoscopic treatment shortened LOS. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 At hospital admission for ALGIB, our novel predictive model stratified patients by their risk of prolonged hospital stay. During hospitalization, early colonoscopy and endoscopic treatment shortened LOS.
    Type of Medium: Online Resource
    ISSN: 0012-2823 , 1421-9867
    RVK:
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2023
    detail.hit.zdb_id: 1482218-0
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  • 6
    In: Oncology, S. Karger AG, Vol. 55, No. Suppl. 1 ( 1998), p. 35-44
    Abstract: The role of estrogen and estrogen-related growth factors in the mechanism of hormone dependency of endometrial adenocarcinoma cells was investigated. The proliferation of hormone-responsive human endometrial adenocarcinoma cells (Ishikawa cells), which possess both estrogen and progesterone receptors, was optimally stimulated by 10 n 〈 i 〉 M 〈 /i 〉 estradiol. Both transforming growth factor (TGF)-α and epidermal growth factor (EGF), added to the culture media, stimulated the proliferation of Ishikawa cells in a dose-dependent manner. Anti-TGF-α antibody completely eliminated the stimulatory effects of TGF-α. Anti-EGF receptor antibody inhibited the proliferation of these cells. The production of TGF-α into culture media was 5–40 pg/10 cells/24 h in 9 human endometrial adenocarcinoma cells. Ten nanomoles of estradiol increased the TGF-α production of Ishikawa cells by approximately 2.5-fold of the control level. In contrast, the production of TGF-α in hormone-unresponsive HEC-50 cels was not influenced by estradiol. C-erbB-2 oncoprotein expression of human endometrial adenocarcinoma cells, detected by both immunocytochemical staining and Western blot analysis, was associated with the tumor grade of the original tumor tissues. Ten nanomoles of estradiol clearly increased the c-erbB-2 oncoprotein levels at an optimal incubation period of 72 h, whereas estradiol did not affect the expression in HEC-50 cells.
    Type of Medium: Online Resource
    ISSN: 0030-2414 , 1423-0232
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 1998
    detail.hit.zdb_id: 1483096-6
    detail.hit.zdb_id: 250101-6
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  • 7
    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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  • 8
    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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  • 9
    In: Cerebrovascular Diseases, S. Karger AG, Vol. 43, No. 1-2 ( 2017), p. 82-89
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Dementia and stroke are major causes of disability in the elderly. However, the association between pre-stroke dementia and functional outcome after stoke remains unresolved. We aimed to determine this association in patients with acute ischemic stroke. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Among patients registered in the Fukuoka Stroke Registry from June 2007 to May 2015, 4,237 patients with ischemic stroke within 24 h of onset, who were functionally independent before the onset, were enrolled in this study. Pre-stroke dementia was defined as any type of dementia that was present prior to the index stroke. Primary and secondary study outcomes were poor functional outcome (modified Rankin Scale 3-6) at 3 months after the stroke onset and neurological deterioration (≥2-point increases on the National Institutes of Health Stroke Scale score during hospitalization), respectively. For propensity score (PS)-matched cohort study to control confounding variables for pre-stroke dementia, 318 pairs of patients with and without pre-stroke dementia were also selected on the basis of 1:1 matching. Multivariable logistic regression models and conditional logistic regression analysis were used to quantify associations between pre-stroke dementia and study outcomes. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Of all 4,237 participants, 347 (8.2%) had pre-stroke dementia. The frequencies of neurological deterioration and poor functional outcome were significantly higher in patients with pre-stroke dementia than in those without pre-stroke dementia (neurological deterioration, 16.1 vs. 7.1%, 〈 i 〉 p 〈 /i 〉 〈 0.01; poor functional outcome, 63.7 vs. 27.1%, 〈 i 〉 p 〈 /i 〉 〈 0.01). Multivariable analysis showed that pre-stroke dementia was significantly associated with neurological deterioration (OR 1.67; 95% CI 1.14-2.41; 〈 i 〉 p 〈 /i 〉 〈 0.01) and poor functional outcome (OR 2.91; 95% CI 2.17-3.91; 〈 i 〉 p 〈 /i 〉 〈 0.01). In the PS-matched cohort study, the same trends were observed between the pre-stroke dementia and neurological deterioration (OR 2.60; 95% CI 1.17-5.78; 〈 i 〉 p 〈 /i 〉 〈 0.01) and between the dementia and poor functional outcome (OR 3.62; 95% CI 1.89-6.95; 〈 i 〉 p 〈 /i 〉 〈 0.01). 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Pre-stroke dementia was significantly associated with higher risks for poor functional outcome at 3 months after stroke onset as well as for neurological deterioration during hospitalization in patients with acute ischemic stroke.
    Type of Medium: Online Resource
    ISSN: 1015-9770 , 1421-9786
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482069-9
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  • 10
    In: Cerebrovascular Diseases, S. Karger AG, Vol. 31, No. 5 ( 2011), p. 477-484
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Cigarette smoking is an established risk factor for stroke and coronary heart disease (CHD) in Western countries. However, it is uncertain whether or not smoking raises the risk of stroke in Japanese. We examined the influence of smoking on the development of stroke and CHD and the effects of interactions between smoking and hypercholesterolemia on these outcomes in a general Japanese population. 〈 i 〉 Methods: 〈 /i 〉 A total of 2,421 community-dwelling Japanese individuals, aged 40–79 years, with no history of cardiovascular disease, were followed up for 14 years. 〈 i 〉 Results: 〈 /i 〉 During the follow-up, 194 total stroke and 112 CHD events occurred. Compared with never smokers, the multivariate-adjusted hazard ratios for the occurrence of total stroke were 1.53 (95% confidence interval = 0.90–2.61) in former smokers, 1.90 (1.18–3.06) in current light smokers ( 〈 20 cigarettes/day) and 2.01 (1.11–3.65) in current heavy smokers (≧20 cigarettes/day). The multivariate-adjusted hazard ratios for the development of CHD were 1.10 (0.56–2.15), 1.88 (1.02–3.47) and 2.31 (1.17–4.57), respectively. In regard to stroke subtypes, current smoking was an independently significant risk factor for ischemic stroke and subarachnoid hemorrhage. Furthermore, the combination of smoking and hypercholesterolemia synergistically increased the risks of total stroke and CHD (all p for interaction 〈 0.05). 〈 i 〉 Conclusion: 〈 /i 〉 Our findings suggest that smoking raises the risks of ischemic stroke, subarachnoid hemorrhage and CHD occurrence in the Japanese population, and that this effect is strengthened by hypercholesterolemia.
    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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