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Shibata, W.; Sohara, M.; Wu, R.; Kobayashi, K.; Yagi, S.; Yaguchi, K.; Iizuka, Y.; Iwasa, M.; Nakahata, H.; Yamaguchi, T.; Matsumoto, H.; Okada, M.; Taniguchi, K.; Hayashi, A.; Inazawa, S.; Inagaki, N.; Sasaki, T.; Koh, R.; Kinoshita, H.; Nishio, M.; Ogashiwa, T.; Ookawara, A.; Miyajima, E.; Oba, M.; Ohge, H.; Maeda, S.; Kimura, H.; Kunisaki, R. |
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Title |
Incidence and Outcomes of Central Venous Catheter-related Blood Stream Infection in Patients with Inflammatory Bowel Disease in Routine Clinical Practice Setting |
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Journal Article |
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Year |
2017 |
Publication |
Inflammatory Bowel Diseases |
Abbreviated Journal |
Inflamm Bowel Dis |
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Volume |
23 |
Issue  |
11 |
Pages |
2042-2047 |
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Abstract |
BACKGROUND: Patients with inflammatory bowel disease (IBD) occasionally require central venous catheter (CVC) placement to support a therapeutic plan. Given that CVC can predispose patients to infection, this investigation was undertaken to assess the incidence, risk factors, and outcomes of CVC-related blood stream infection (CRBSI) in patients with IBD during routine clinical practice. METHODS: Data were compiled using retrospective chart reviews of 1367 patients treated at our IBD center between 2007 and 2012 during routine clinical practice. Among the 1367 patients, 314 who had received CVC placements were included. Patients with positive blood culture were considered as “definite” CRBSI, whereas “possible” CRBSI was defined as patients in whom fever alleviated within 48 hours post-CVC without any other infection. Patients' demographic variables including age, body mass index, serum albumin, duration of CVC placement, use of antibiotics, medications for IBD, and perioperative status between CRBSI and non-CRBSI subgroups were compared by applying a multivariate Poisson logistic regression model. RESULTS: Among the 314 patients with CVC placement, there were 83 CRBSI cases (26.4%). The average time to the onset of CRBSI was 22.5 days (range 4-105 days). The jugular vein access was found to be the most serious risk of CRBSI (risk ratio 2.041 versus subclavian vein). All patients with CRBSI fully recovered. CONCLUSIONS: In this investigation, regardless of the patients' demographic features including immunosuppressive therapy, up to 30% of febrile IBD patients with CVC showed CRBSI. It is believed that CVC placement per se is a risk of CRBSI in patients with IBD. |
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*Inflammatory Bowel Disease Center, Yokohama City University Medical Centre, Yokohama, Japan;daggerDivision of Gastroenterology, Department of Medicine, Yokohama City University, Yokohama, Japan;double daggerSchool of Medicine, Yokohama City University, Yokohama, Japan; section signDepartment of Laboratory Medicine and Clinical Investigation, Yokohama City University Medical Centre, Yokohama, Japan; ||Department of Biostatistics and Epidemiology, Graduate School of Medicine, Yokohama City University, Yokohama, Japan; and paragraph signDepartment of Infectious Diseases, Hiroshima University Hospital, Japan |
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1078-0998 |
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PMID:29045261 |
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100389 |
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Sullivan, K.E.; Rojas, K.; Cerione, R.A.; Nakano, I.; Wilson, K.F. |
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Title |
The stem cell/cancer stem cell marker ALDH1A3 regulates the expression of the survival factor tissue transglutaminase, in mesenchymal glioma stem cells |
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Journal Article |
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Year |
2017 |
Publication |
Oncotarget |
Abbreviated Journal |
Oncotarget |
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Volume |
8 |
Issue |
14 |
Pages |
22325-22343 |
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Aldehyde Oxidoreductases/genetics/*metabolism; Biomarkers, Tumor/metabolism; Brain Neoplasms/genetics/*metabolism; Cell Line, Tumor; Cell Proliferation; Cell Survival; Dacarbazine/analogs & derivatives/pharmacology; GTP-Binding Proteins/genetics/*metabolism; Gene Expression Regulation, Neoplastic; Glioma/genetics/*metabolism; Humans; Mesenchymal Stromal Cells/*physiology; Neoplastic Stem Cells/*physiology; RNA, Small Interfering/genetics; Stem Cells/*physiology; Transglutaminases/genetics/*metabolism; Tretinoin/metabolism; Up-Regulation; aldehyde dehydrogenase; cancer stem cells; glioblastoma; retinoic acid; tissue transglutaminase |
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Tissue transglutaminase (tTG), a dual-function enzyme with GTP-binding and acyltransferase activities, has been implicated in the survival and chemotherapy resistance of aggressive cancer cells and cancer stem cells, including glioma stem cells (GSCs). Using a model system comprising two distinct subtypes of GSCs referred to as proneural (PN) and mesenchymal (MES), we find that the phenotypically aggressive and radiation therapy-resistant MES GSCs exclusively express tTG relative to PN GSCs. As such, the self-renewal, proliferation, and survival of these cells was sensitive to treatment with tTG inhibitors, with a benefit being observed when combined with the standard of care for high grade gliomas (i.e. radiation or temozolomide). Efforts to understand the molecular drivers of tTG expression in MES GSCs revealed an unexpected link between tTG and a common marker for stem cells and cancer stem cells, Aldehyde dehydrogenase 1A3 (ALDH1A3). ALDH1A3, as well as other members of the ALDH1 subfamily, can function in cells as a retinaldehyde dehydrogenase to generate retinoic acid (RA) from retinal. We show that the enzymatic activity of ALDH1A3 and its product, RA, are necessary for the observed expression of tTG in MES GSCs. Additionally, the ectopic expression of ALDH1A3 in PN GSCs is sufficient to induce the expression of tTG in these cells, further demonstrating a causal link between ALDH1A3 and tTG. Together, these findings ascribe a novel function for ALDH1A3 in an aggressive GSC phenotype via the up-regulation of tTG, and suggest the potential for a similar role by ALDH1 family members across cancer types. |
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Department of Molecular Medicine, Cornell University, Ithaca, NY, USA |
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1949-2553 |
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PMID:28423611 |
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Call Number |
ref @ user @ |
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96595 |
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Yan, H.; Romero-Lopez, M.; Benitez, L.I.; Di, K.; Frieboes, H.B.; Hughes, C.C.W.; Bota, D.A.; Lowengrub, J.S. |
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3D Mathematical Modeling of Glioblastoma Suggests That Transdifferentiated Vascular Endothelial Cells Mediate Resistance to Current Standard-of-Care Therapy |
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Journal Article |
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2017 |
Publication |
Cancer Research |
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Cancer Res |
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77 |
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15 |
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4171-4184 |
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Brain Neoplasms/*pathology; Cell Transdifferentiation/physiology; Endothelial Cells/*pathology; Glioblastoma/*pathology; Humans; *Models, Theoretical; Neoplastic Stem Cells/*pathology |
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Glioblastoma (GBM), the most aggressive brain tumor in human patients, is decidedly heterogeneous and highly vascularized. Glioma stem/initiating cells (GSC) are found to play a crucial role by increasing cancer aggressiveness and promoting resistance to therapy. Recently, cross-talk between GSC and vascular endothelial cells has been shown to significantly promote GSC self-renewal and tumor progression. Furthermore, GSC also transdifferentiate into bona fide vascular endothelial cells (GEC), which inherit mutations present in GSC and are resistant to traditional antiangiogenic therapies. Here we use three-dimensional mathematical modeling to investigate GBM progression and response to therapy. The model predicted that GSCs drive invasive fingering and that GEC spontaneously form a network within the hypoxic core, consistent with published experimental findings. Standard-of-care treatments using DNA-targeted therapy (radiation/chemo) together with antiangiogenic therapies reduced GBM tumor size but increased invasiveness. Anti-GEC treatments blocked the GEC support of GSCs and reduced tumor size but led to increased invasiveness. Anti-GSC therapies that promote differentiation or disturb the stem cell niche effectively reduced tumor invasiveness and size, but were ultimately limited in reducing tumor size because GECs maintain GSCs. Our study suggests that a combinatorial regimen targeting the vasculature, GSCs, and GECs, using drugs already approved by the FDA, can reduce both tumor size and invasiveness and could lead to tumor eradication. Cancer Res; 77(15); 4171-84. (c)2017 AACR. |
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Center for Complex Biological Systems, University of California, Irvine, California |
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0008-5472 |
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PMID:28536277 |
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96585 |
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Roy, A.; Attarha, S.; Weishaupt, H.; Edqvist, P.-H.; Swartling, F.J.; Bergqvist, M.; Siebzehnrubl, F.A.; Smits, A.; Ponten, F.; Tchougounova, E. |
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Serglycin as a potential biomarker for glioma: association of serglycin expression, extent of mast cell recruitment and glioblastoma progression |
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Journal Article |
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2017 |
Publication |
Oncotarget |
Abbreviated Journal |
Oncotarget |
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Volume |
8 |
Issue |
15 |
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24815-24827 |
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Cd44; Zeb1; glioma; mast cell; serglycin |
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Serglycin is an intracellular proteoglycan with a unique ability to adopt highly divergent structures by glycosylation with variable types of glycosaminoglycans (GAGs) when expressed by different cell types. Serglycin is overexpressed in aggressive cancers suggesting its protumorigenic role. In this study, we explored the expression of serglycin in human glioma and its correlation with survival and immune cell infiltration. We demonstrate that serglycin is expressed in glioma and that increased expression predicts poor survival of patients. Analysis of serglycin expression in a large cohort of low- and high-grade human glioma samples reveals that its expression is grade dependent and is positively correlated with mast cell (MC) infiltration. Moreover, serglycin expression in patient-derived glioma cells is significantly increased upon MC co-culture. This is also accompanied by increased expression of CXCL12, CXCL10, as well as markers of cancer progression, including CD44, ZEB1 and vimentin.In conclusion, these findings indicate the importance of infiltrating MCs in glioma by modulating signaling cascades involving serglycin, CD44 and ZEB1. The present investigation reveals serglycin as a potential prognostic marker for glioma and demonstrates an association with the extent of MC recruitment and glioma progression, uncovering potential future therapeutic opportunities for patients. |
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Uppsala University, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala, Sweden |
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1949-2553 |
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PMID:28445977 |
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96590 |
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Godin, K.M.; Chacon, V.; Barnoya, J.; Leatherdale, S.T. |
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The school environment and sugar-sweetened beverage consumption among Guatemalan adolescents |
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Journal Article |
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2017 |
Publication |
Public Health Nutrition |
Abbreviated Journal |
Public Health Nutr |
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20 |
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16 |
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2980-2987 |
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Latin America; Nutrition policy; School health; Sugar-sweetened beverages |
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OBJECTIVE: The current study sought to examine Guatemalan adolescents' consumption of sugar-sweetened beverages (SSB), identify which individual-level characteristics are associated with SSB consumption and describe school characteristics that may influence students' SSB consumption. DESIGN: Within this observational pilot study, a questionnaire was used to assess students' consumption of three varieties of SSB (soft drinks, energy drinks, sweetened coffees/teas), as well as a variety of sociodemographic and behavioural characteristics. We collected built environment data to examine aspects of the school food environment. We developed Poisson regression models for each SSB variety and used descriptive analyses to characterize the sample. SETTING: Guatemala City, Guatemala. SUBJECTS: Guatemalan adolescents (n 1042) from four (two public, two private) secondary schools. RESULTS: Built environment data revealed that students from the two public schools lacked access to water fountains/coolers. The SSB industry had a presence in the schools through advertisements, sponsored food kiosks and products available for sale. Common correlates of SSB consumption included school type, sedentary behaviour, frequency of purchasing lunch in the cafeteria, and frequency of purchasing snacks from vending machines in school and off school property. CONCLUSIONS: Guatemalan adolescents frequently consume SSB, which may be encouraged by aspects of the school environment. Schools represent a viable setting for equitable population health interventions designed to reduce SSB consumption, including increasing access to clean drinking-water, reducing access to SSB, restricting SSB marketing and greater enforcement of existing food policies. |
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1School of Public Health and Health Systems,University of Waterloo, 200 University Avenue West,Waterloo,ON,Canada,N2L 3G1 |
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1368-9800 |
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PMID:28803573 |
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97159 |
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