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  • 1
    Language: English
    In: Journal of Japanese Society of Gastroenterology, 2017, Vol.114, Suppl. l-1, pp.240-240
    ISSN: 0446-6586
    Source: Medical*Online (Meteo, Inc.)
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  • 2
    Language: English
    In: PLoS ONE, 01 January 2015, Vol.10(7), p.e0133731
    Description: Stenotrophomonas maltophilia is an important nosocomial bacterial pathogen, as is Pseudomonas aeruginosa. Differentiation of these bacteria as bacteremic agents is critical in the clinical setting and to define a therapeutic strategy; however, the associated factors and prognosis for S. maltophilia bacteremia have not been fully evaluated to adequately characterize these factors. We first conducted a matched case-control study to clarify these questions. A total of 30 case patients with S. maltophilia bacteremia were compared with 30 control patients with P. aeruginosa bacteremia between January 2005 and August 2014, according to matching criteria based on underlying disease, age, and gender. The 30-day mortality rate for the case patients (53.3%) was significantly higher than that of the control group (30.0%) (P = 0.047, using the log-rank test). Conditional logistic regression analysis showed that the predisposing factors specific for the detection of S. maltophilia bacteremia were indwelling artificial products other than a central venous catheter, ICU stay, and previous use of anti-MRSA drugs. The high severity of illness was associated with mortality in both case and control patients. Interestingly, inappropriate antimicrobial treatment was an additional independent risk factor for mortality in only the case patients with S. maltophilia bacteremia (odds ratio = 13.64, P = 0.048). Monotherapy with fluoroquinolones inactive against the S. maltophilia isolates was mainly responsible for the inappropriate treatment. These results suggest that more precise prediction and more appropriate treatment might improve the prognosis of patients with S. maltophilia bacteremia.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 3
    Language: English
    In: PLoS ONE, 2011, Vol.6(3), p.e18059
    Description: Aberrant zinc (Zn) homeostasis is associated with abnormal control of mammalian growth, although the molecular mechanisms of Zn's roles in regulating systemic growth remain to be clarified. Here we report that the cell membrane-localized Zn transporter SLC39A14 controls G-protein coupled receptor (GPCR)-mediated signaling. Mice lacking Slc39a14 ( Slc39a14 -KO mice) exhibit growth retardation and impaired gluconeogenesis, which are attributable to disrupted GPCR signaling in the growth plate, pituitary gland, and liver. The decreased signaling is a consequence of the reduced basal level of cyclic adenosine monophosphate (cAMP) caused by increased phosphodiesterase (PDE) activity in Slc39a14 -KO cells. We conclude that SLC39A14 facilitates GPCR-mediated cAMP-CREB signaling by suppressing the basal PDE activity, and that this is one mechanism for Zn's involvement in systemic growth processes. Our data highlight SLC39A14 as an important novel player in GPCR-mediated signaling. In addition, the Slc39a14 -KO mice may be useful for studying the GPCR-associated regulation of mammalian systemic growth.
    Keywords: Research Article ; Biology ; Medicine ; Diabetes And Endocrinology ; Molecular Biology ; Physiology ; Developmental Biology
    E-ISSN: 1932-6203
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  • 4
    In: PLoS ONE, 2013, Vol.8(1)
    Description: Background Our unit adopted the single administration of cefepime as the initial treatment for febrile episodes in neutropenic patients with hematological malignancies. However, recently, cefepime-resistant gram-negative bacteremia, including those with extended-spectrum β-lactamase (ESBL)-producers, was frequently observed in these patients. Therefore, we instituted a rotation of primary antibiotics for febrile neutropenic patients in an attempt to control antibiotic resistance. Methods This prospective trial was performed from August 2008 through March 2011 at our unit. After a pre-intervention period, in which cefepime was used as the initial agent for febrile neutropenia, 4 primary antibiotics, namely, piperacillin-tazobactam, ciprofloxacin, meropenem, and cefepime, were rotated at 1-month intervals over 20 months. Blood and surveillance cultures were conducted for febrile episodes, in order to assess the etiology, the resistance pattern (particularly to cefepime), and the prognosis. Results In this trial, 219 patients were registered. A 65.9% reduction in the use of cefepime occurred after the antibiotic rotation. In the surveillance stool cultures, the detection rate of cefepime-resistant gram-negative isolates, of which ESBL-producers were predominant, declined significantly after the intervention (8.5 vs 0.9 episodes per 1000 patient days before and after intervention respectively, P 〈0.01). Interestingly, ESBL-related bacteremia was not detected after the initiation of the trial (1.7 vs 0.0 episodes per 1000 patient days before and after intervention respectively, P 〈0.01). Infection-related mortality was comparable between the 2 periods. Conclusions We implemented a monthly rotation of primary antibiotics for febrile neutropenic patients. An antibiotic heterogeneity strategy, mainly performed as a cycling regimen, would be useful for controlling antimicrobial resistance among patients treated for febrile neutropenia.
    Keywords: Research Article ; Biology ; Medicine
    E-ISSN: 1932-6203
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  • 5
    Language: English
    In: PLoS ONE, 01 January 2014, Vol.9(1), p.e85210
    Description: BACKGROUND: Fluoroquinolone prophylaxis in patients with neutropenia and hematological malignancies is said to be effective on febrile netropenia (FN)-related infection and mortality; however, the emergence of antibiotic resistance has become a concern. Ciprofloxacin and levofloxacin prophylaxis are most commonly recommended. A significant increase in the rate of quinolone-resistant Escherichia coli in fecal flora has been reported following ciprofloxacin prophylaxis. The acquisition of quinolone-resistant E. coli after levofloxacin use has not been evaluated. METHODS: We prospectively examined the incidence of quinolone-resistant E. coli isolates recovered from stool cultures before and after levofloxacin prophylaxis in patients with neutropenia from August 2011 to May 2013. Some patients received chemotherapy multiple times. RESULTS: In this trial, 68 patients were registered. Levofloxacin-resistant E. coli isolates were detected from 11 and 13 of all patients before and after the prophylaxis, respectively. However, this was not statistically significant (P = 0.65). Multiple prophylaxis for sequential chemotherapy did not induce additional quinolone resistance among E. coli isolates. Interestingly, quinolone-resistant E. coli, most of which were extended-spectrum β-lactamase (ESBL) producers, were already detected in approximately 20% of all patients before the initiation of prophylaxis. FN-related bacteremia developed in 2 patients, accompanied by a good prognosis. CONCLUSIONS: Levofloxacin prophylaxis for neutropenia did not result in a significant acquisition of quinolone-resistant E. coli. However, we detected previous colonization of quinolone-resistant E. coli before prophylaxis, which possibly reflects the spread of ESBL. The epidemic spread of resistant E. coli as a local factor may influence strategies toward the use of quinolone prophylaxis.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 6
    Language: English
    In: Journal of Japanese Society of Gastroenterology, 2017, Vol.114, Suppl. l-1, pp.240-240
    ISSN: 0446-6586
    Source: Medical*Online-E (Meteo, Inc.)
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  • 7
    Language: English
    In: Journal of Gastroenterology, 2011, Vol.46(Supplement 1), pp.29-38
    Description: Autoimmune liver diseases (ALDs) represent a wide spectrum of chronic inflammatory diseases that are characterized by an immune-mediated attack against either hepatocytes (in the case of autoimmune hepatitis types 1 and 2, AIH-1, 2) or cholangiocytes (in primary biliary cirrhosis, PBC). PBC is considered a model autoimmune disease due to the homogeneity of patients, the high specificity of antimitochondrial antibodies (AMAs), and the specificity of biliary epithelial cell (BEC) destruction. It ensues from a multi-lineage loss of tolerance to the E2 component of the pyruvate dehydrogenase complex (PDC-E2). One of the major unanswered questions in the pathogenesis of PBC is the specificity of small intrahepatic bile duct attack while PDC-E2 is present in mitochondria of nucleated cells. Recent findings suggest that the apoptosis of BECs may be of considerable importance for understanding PBC, and that they are more than simply an innocent victim of an immune attack. Rather, they attract immune attack by virtue of the unique biochemical mechanisms by which they handle PDC-E2. The role of apoptotic cells in AIH is not well defined, but advances in the study of autoreactive T cells stem mostly from AIH type 2, where the main autoantigen (CYP2D6) is known, enabling the characterization of antigen-specific immune responses. This review article is intended to provide a critical overview of current evidence on tissue specificity in ALDs, as well as the characteristics of the relevant epitopes and apotopes and their biological and clinical significance.
    Keywords: Autoimmunity ; Biliary epithelial cell ; Hepatocyte ; Apotope
    ISSN: 0944-1174
    E-ISSN: 1435-5922
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  • 8
    Language: English
    In: Digestive Diseases and Sciences, 2013, Vol.58(10), pp.3037-3043
    Description: Byline: Kenichi Harada (1), Yuko Kakuda (1), Minoru Nakamura (2), Shinji Shimoda (3), Yasuni Nakanuma (1) Keywords: Primary biliary cirrhosis; gp210; Fractalkine; Pathology; Cholangitis Abstract: Background Primary biliary cirrhosis (PBC), characterized by cholangitis and loss of intrahepatic small bile ducts, predominantly affects middle-aged females. We have reported that fractalkine expression associated with chronic inflammation is observed in the damaged bile ducts and periductal vessels of PBC patients, which is closely associated with chronic cholangitis. Aims We investigated the association between serum fractalkine levels and clinicopathological findings in PBC patients. Methods Liver biopsy specimens before ursodeoxycholic acid treatment and serum samples at the time of liver biopsy and 1 and 2 years after treatment were obtained from 68 PBC patients (M/F = 14/54). Serum fractalkine levels were measured by enzyme-linked immunosorbent assay, and their association with clinicopathological findings (liver function data, autoantibodies, cholangitis activity, hepatitis activity, fibrosis, bile duct loss, and orcein-positive granules) was analyzed. Results Serum fractalkine levels were in the range of 0.1--33.2 ng/ml (average, 3.2 ng/ml). They were increased in PBC patients with high degrees of cholangitis activity, a mild degree of hepatitis activity, fibrosis, orcein-positive granules, and early stages. In cases with high serum fractalkine levels, those who exhibited good biochemical responses to treatment mostly showed improved serum fractalkine levels after treatment. Conclusion Serum fractalkine levels of PBC patients were high in cases with marked cholangitis activity at early stages. In addition, they closely correlated with the effect of therapy, indicating that fractalkine plays a role in the pathogenesis of initial cholangitis in early stage PBC and consequent chronic cholangitis. Thus, our results suggest that fractalkine is a good candidate for molecular-targeted treatment. Author Affiliation: (1) Department of Human Pathology, Kanazawa University Graduate School of Medicine, Kanazawa, 920-8640, Japan (2) Department of Hepatology, Clinical Research Center, National Hospital Organization (NHO), Nagasaki Medical Center, Nagasaki University Graduate School of Biomedical Sciences, Omura, Japan (3) Department of Medicine and Biosystemic Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan Article History: Registration Date: 29/05/2013 Received Date: 04/01/2013 Accepted Date: 29/05/2013 Online Date: 14/06/2013
    Keywords: Primary biliary cirrhosis ; gp210 ; Fractalkine ; Pathology ; Cholangitis
    ISSN: 0163-2116
    E-ISSN: 1573-2568
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  • 9
    In: Transplantation Journal, 2013, Vol.95(6), pp.e38-e42
    Keywords: Adult–Therapeutic Use ; Aged–Therapy ; Antiviral Agents–Virology ; Female–Chemistry ; Hepatitis C–Therapeutic Use ; Humans–Methods ; Interferon Alpha-2–Chemistry ; Interferon-Alpha–Therapeutic Use ; Liver Transplantation–Pharmacology ; Living Donors–Pharmacology ; Male–Pharmacology ; Middle Aged–Pharmacology ; Recombinant Proteins–Pharmacology ; Recurrence–Pharmacology ; Ribavirin–Pharmacology ; Treatment Outcome–Pharmacology ; Antiviral Agents ; Interferon Alpha-2 ; Interferon-Alpha ; Recombinant Proteins ; Ribavirin;
    ISSN: 0041-1337
    E-ISSN: 15346080
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  • 10
    Language: Japanese
    In: 日本臨床免疫学会会誌, 2012, Vol.35(6), pp.455-462
    Description:   PBCは組織学的に小胆管の破壊をきたす慢性非化膿性破壊性胆管炎に特徴づけられる.しかし,PBCの成因は何か,なぜ女性優位であるのか,なぜ胆管が選択的に障害されるかなど未だ謎は多い.感染微生物あるいは化学物質xenobiotics等の刺激が,遺伝素因を有する個体においてPBC発症の誘因となることが想定される.胆管上皮細胞の組織障害は自己免疫反応により生じると考えられているが,病初期においては,自然免疫の活性化が鍵を握っている.胆管上皮細胞はToll様受容体(TLR)を含めて自然免疫システムを有し,PBCにおいてはPAMPsに対する過剰反応が胆管障害の原因とされる.胆管は,NK細胞を含む免疫細胞の遊走にあずかるフラクタルカイン(CX3CL1)と周囲環境をTh1シフトするいくつかのケモカインを産生し,ターゲットとなる胆管上皮細胞は,ケモカインによる誘導で浸潤した免疫細胞によって自己免疫反応を増強する.胆管周囲に集まる浸潤細胞の中でも,単球とNK細胞の役割は異なり,TLR4リガンドで刺激されたNK細胞は,TLR 3リガンドで刺激された単球によって産生されたインターフェロンαの存在のもと,自己胆管上皮細胞を破壊する.このような新らたに得られる知見で,PBC発症の不思議も明らかにされつつある.〈br〉
    Description:   Primary biliary cirrhosis (PBC) is histologically characterized by chronic nonsuppurative destructive cholangitis (CNSDC) associated with destruction of small bile ducts. The pathogenesis of PBC, predominance of female, or the reason why biliary duct is selectively involved, however, remains unknown. Infectious or non-infectious noxious insults such as xenobiotic chemicals may precipitate in the individual having a genetic background of PBC. Activation of innate immune response seems to be a key event in early PBC, leading to the autoimmune injury of small intrahepatic bile duct. Biliary epithelial cells possess an innate immune system consisting of the Toll-like receptor (TLR) family and recognize pathogen-associated molecular patterns (PAMPs). In PBC, dysregulated biliary innate immunity, namely hyper-responsiveness to PAMPs, is associated with the pathogenesis of cholangiopathy. Moreover, the targeted biliary epithelial cells (BEC) may play an active role in the perpetuation of autoimmunity by attracting immune cells via chemokine secretion. Biliary innate immune responses induce the production of two chemokines, CX3CL1 (fractalkine) and several Th1 shift chemokines, causing the migration of inflammatory cells including NK cells. TLR 4 ligand-stimulated NK cells destroy autologous BECs in the presence of interferon alpha (IFN-α) synthesized by TLR 3 ligand-stimulated monocytes. These findings give new insights in the pathogenesis of this mysterious disease, PBC.〈br〉
    Keywords: Primary Biliary Cirrhosis ; Cholangitis ; Pathogenesis ; Innate Immunity ; Fractalkine
    ISSN: 0911-4300
    E-ISSN: 13497413
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