bluuebunny/crossref_metadata_2025_split huggingface dataset:
Construction of a stereotaxic DTI atlas with full diffusion tensor information for studying white matter maturation from childhood to adolescence using tractography‐based segmentations
Authors: Verhoeven Judith S. , Sage Caroline A. , Leemans Alexander , Van Hecke Wim , Callaert Dorothée , Peeters Ronald , De Cock Paul , Lagae Lieven , Sunaert Stefan 
Published: December 2009

AbstractReconstruction of white matter (WM) fiber tracts based on diffusion tensor imaging (DTI) is increasingly being used in clinical and research settings to study normal and pathological WM tissue as well as the maturation of this WM tissue. Such fiber tracking (FT) methodology, however, is highly dependent on the manual delineation of anatomical landmarks and the algorithm settings, often rendering the reproducibility and reliability questionable. Predefining these regions of interest on a fractional anisotropy (FA) atlas in standard space has already been shown to improve the reliability of FT results. In this paper, we constructed a new DTI atlas, which contains the complete diffusion tensor information in ICBM152 coordinates. From this high‐dimensional DTI atlas, and using robust FT protocols, we reconstructed a large number of WM tracts. Subsequently, we created tract masks from these fiber tract bundles and evaluated the atlas framework by comparing the reproducibility of the results obtained from our standardized tract masks with regions‐of‐interest labels from the conventional FA‐based WM atlas. Finally, we assessed laterality and age‐related WM changes in 42 normal subjects aged 0 to 18 years using these tractography‐derived tract segmentations. In agreement with previous literature, we observed an FA increase with age, which was mainly due to the decrease of perpendicular diffusivity. In addition, major functional pathways in the language, motor, and limbic system, showed a significant asymmetry in terms of the observed diffusion metrics. Hum Brain Mapp, 2010. © 2009 Wiley‐Liss, Inc.
Nonlinear relationship between emotional valence and brain activity: Evidence of separate negative and positive valence dimensions
Authors: Viinikainen Mikko , Jääskeläinen Iiro P. , Alexandrov Yuri , Balk Marja H. , Autti Taina , Sams Mikko 
Published: December 2009

AbstractEmotion plays a significant role in goal‐directed behavior, yet its neural basis is yet poorly understood. In several psychological models the cardinal dimensions that characterize the emotion space are considered to be valence and arousal. Here 3T functional magnetic resonance imaging (fMRI) was used to reveal brain areas that show valence‐ and arousal‐dependent blood oxygen level dependent (BOLD) signal responses. Seventeen healthy adults viewed pictures from the International Affective Picture System (IAPS) for brief 100 ms periods in a block design paradigm. In many brain regions BOLD signals correlated significantly positively with valence ratings of unpleasant pictures. Interestingly, partly in the same regions but also in several other regions BOLD signals correlated negatively with valence ratings of pleasant pictures. Therefore, there were several areas where the correlation across all pictures was of inverted U‐shape. Such correlations were found bilaterally in the dorsolateral prefrontal cortex (DLPFC), dorsomedial prefrontal cortex (DMPFC) extending to anterior cingulate cortex (ACC), and insula. Self‐rated arousal of those pictures which were evaluated to be unpleasant correlated with BOLD signal in the ACC, whereas for pleasant pictures arousal correlated positively with the BOLD signal strength in the right substantia innominata. We interpret our results to suggest a major division of brain mechanisms underlying affective behavior to those evaluating stimuli to be pleasant or unpleasant. This is consistent with the basic division of behavior to approach and withdrawal, where differentiation of hostile and hospitable stimuli is crucial. Hum Brain Mapp, 2010. © 2009 Wiley‐Liss, Inc.
Hippocampal damage produces retrograde but not anterograde amnesia for a cued location in a spontaneous exploratory task in rats
Authors: Travis Scott G. , Sparks Fraser T. , Arnold Tyrell , Lehmann Hugo , Sutherland Robert J. , Whishaw Ian Q. 
Published: December 2009

AbstractPerformance in several memory tasks is known to be unaffected by hippocampal damage sustained before learning, but is severely disrupted if the same damage occurs after learning. Memories for preferred locations, or home bases, in exploratory tasks can be formed by rats with hippocampal damage, but it is unknown if the memory for a home base survives hippocampal damage. To examine this question, for 30 min each day for five consecutive days, rats explored a circular open field containing one local cue. By Day 5 the rats preferentially went directly to that location, spent the majority of their time at that location, made rapid direct trips to that location when returning from an excursion and so demonstrated that the location was a home base. Memory for the cued location was examined after a 24 h or 14‐day interval with the cue removed. In Experiments 1 and 2, control rats and rats with prior N‐methyl‐D‐aspartic acid hippocampal lesions demonstrated memory of the home base location by making direct trips to that location. In Experiment 3, rats that had first explored the open field and cue and then received hippocampal lesions showed no memory for the cued location. The absence of anterograde impairment vs. the presence of retrograde impairment for memory of a spatial home base confirms a role for the hippocampus in the retention of spatial memory acquired during exploration. © 2009 Wiley‐Liss, Inc.
Epigenetic silencing of SFRP5 is related to malignant phenotype and chemoresistance of ovarian cancer through Wnt signaling pathway
Authors: Su Her‐Young , Lai Hung‐Cheng , Lin Ya‐Wen , Liu Chin‐Yun , Chen Chi‐Kuan , Chou Yu‐Ching , Lin Shin‐Ping , Lin Wen‐Chi , Lee Hsin‐Yi , Yu Mu‐Hsien 
Published: December 2009

AbstractOncogenic activation of the Wnt signaling pathway is common in cancers, but mutation of β‐catenin in ovarian cancer is rare. In addition to genetic events, epigenetic modification of secreted frizzled‐related protein (SFRP) family has been shown to be important in regulating Wnt signaling. Although high degree of homology is observed in the same family, different SFRPs may have opposing effects on the same process. We reported recently that a Wnt antagonist, SFRP5, is downregulated frequently through promoter hypermethylation and that this hypermethylation is associated with overall survival in ovarian cancer. The aim of this study was to analyze the function of SFRP5 in ovarian cancer. Functional assays including measuring cell proliferation, invasion, colony formation and xenograft were performed using ovarian cancer cell lines with overexpression of SFRP5 or a short hairpin RNA silencing. The methylation status of SFRP5 in relation to cisplatin resistance in ovarian cancer patients was analyzed. Restoration of the expression of SFRP5 attenuated Wnt signaling in ovarian cancer cells and suppressed cancer cell growth, invasion of cells and tumorigenicity in mice. These effects were independent of the canonical pathway. The expression of SFRP5 inhibited epithelial–mesenchymal transition (EMT). The restoration of SFRP5 downregulated AKT2 and sensitized ovarian cancer cells to chemotherapy. These effects are consistent with the poor response to platinum‐based chemotherapy in patients with methylation of SFRP5. Our data suggested that epigenetic silencing of SFRP5 leads to oncogenic activation of the Wnt pathway and contributes to ovarian cancer progression and chemoresistance through the TWIST‐mediated EMT and AKT2 signaling.
Fluid intake and the risk of bladder cancer: Results from the South and East China case‐control study on bladder cancer
Authors: Hemelt Marjolein , Hu Zhiquan , Zhong Zhaohui , Xie Li‐Ping , Wong Y.C. , Tam Po‐Chor , Cheng K.K. , Ye Zhangqun , Bi Xuecheng , Lu Qiang , Mao Yeqing , Zhong Wei‐de , Zeegers Maurice P. 
Published: December 2009

AbstractAlthough several studies have assessed the association between total fluid intake, specific drinks and bladder cancer, no firm conclusions can yet be drawn. Four hundred thirty two bladder cancer cases and 392 frequency matched hospital‐based controls recruited in the South and East of China between October 2005 and June 2008 were interviewed on their intake of 6 nonalcoholic and 3 alcoholic drinks. Age, sex, smoking and hospital‐adjusted odds ratios (OR) and 95 percent confidence intervals (95% CI) were calculated for all drinks and for total fluid intake using logistic regression. For 381 cases (81.9% men) and 371 controls (76.3% men), total fluid intake could be calculated. In men, an increase in total fluid intake was associated with a significantly decreased bladder cancer risk (OR 0.93, 95% CI: 0.88–0.99, per cup fluid consumed). Neither green nor black tea consumption was associated with bladder cancer. Daily consumption of milk significantly reduced the risk of bladder cancer by a half (OR 0.49, 95% CI: 0.32–0.76), which strengthens earlier suggestions that milk is probably associated with a decreased bladder cancer risk. Consumption of wine (OR 0.49, 95% CI: 0.34–0.70) and liquor/spirits (OR 0.65, 95% CI: 0.47–0.92) were associated with a significantly reduced risk. Consumption of water, fruit juice and beer appeared not associated with bladder cancer. There is no clear indication that the risks observed in this Chinese population are substantially different from those observed in Caucasian populations.
Down‐regulation of type I interferon receptor sensitizes bladder cancer cells to vesicular stomatitis virus‐induced cell death
Authors: Zhang Kai‐xin , Matsui Yoshiyuki , Hadaschik Boris A. , Lee Cleo , Jia William , Bell John C. , Fazli Ladan , So Alan I. , Rennie Paul S. 
Published: December 2009

AbstractThe intrinsic oncolytic specificity of vesicular stomatitis virus (VSV) is currently being exploited to develop alternative therapeutic strategies for bladder cancer and other cancers. Previously we reported that oncolytic VSV is a potent agent for intravesical treatment of high risk bladder cancer. We observed that VSV preferentially targeted bladder cancer cells resistant to type I interferon (IFN) treatment. The goal of the current study was to further elucidate the nature of the molecular defect of IFN signaling by which bladder cancer cells become susceptible to VSV infection. Using a tissue microarray composed of human bladder cancer cores, we observed that expression of type I IFN receptor (IFNAR) was decreased relative to normal bladder tissue. Advanced bladder cancers had even lower expression of IFNAR. We found that bladder cancer cells susceptible to VSV‐induced lysis had low expression of IFNAR as well. We hypothesized that down‐regulation of IFNAR in bladder cancer cells may be a molecular mechanism responsible for resistance to type I IFN treatment and sensitivity to VSV oncolysis. SiRNA knockdown of IFNAR indeed facilitated replication of VSV in cells previously resistant to VSV treatment. Blocking IFNAR with a neutralizing antibody showed a similar effect. Hence down‐regulation of IFNAR in bladder cancer may be one of the primary molecular mechanisms for clinical IFN resistance. However, this also facilitates VSV replication and oncolysis in high risk bladder cancers and provides a basis for selecting bladder cancer patients for IFN or oncolytic VSV therapy in future clinical trials.
Meta‐analysis: Reduced incidence of hepatocellular carcinoma in patients not responding to interferon therapy of chronic hepatitis C
Authors: Miyake Yasuhiro , Iwasaki Yoshiaki , Yamamoto Kazuhide 
Published: December 2009

AbstractInterferon treatment for chronic hepatitis C reduces the incidence of hepatocellular carcinoma (HCC) in sustained responders. However, estimation of the effect of interferon treatment on HCC development in nonresponders is yet to be fully implemented. We conducted a meta‐analysis of 3 randomized controlled trials and 6 prospective cohort studies, including 3,246 patients (1,922 patients received interferon treatment) to estimate the effect of single‐course interferon treatment on HCC development in patients with chronic hepatitis C. Single‐course interferon treatment prevented HCC development (RR 0.45; 95% CI 0.31–0.65). This preventive effect was shown even in nonresponders (RR 0.48; 95% CI 0.25–0.90). By subgroup analyses, single‐course interferon treatment reduced HCC incidence in cirrhotic patients (RR 0.49; 95% CI 0.29–0.84), patients with annual HCC incidence less than 3% in control group (RR 0.42; 95% CI 0.26–0.66) and patients with annual HCC incidence of 3% or more in control group (RR 0.46; 95% CI 0.26–0.83). Furthermore, HCC incidence was reduced in 3 studies with follow‐up period less than 5 years (RR 0.38; 95% CI 0.21–0.66) and in 6 studies with follow‐up period of 5 years or more (RR 0.46; 95% CI 0.28–0.76). In conclusion, single‐course interferon treatment was shown to prevent HCC development in chronic hepatitis C, even in nonresponders. This preventive effect may be speculated to be due to anti‐inflammatory effect on persistent necro‐inflammation and blocking progression of fibrosis in liver. Even if sustained virological response is not achieved, interferon may be worth administering in order to reduce HCC incidence in patients with chronic hepatitis C.
Naringenin and 17β‐estradiol coadministration prevents hormone‐induced human cancer cell growth
Authors: Bulzomi Pamela , Bolli Alessandro , Galluzzo Paola , Leone Stefano , Acconcia Filippo , Marino Maria 
Published: December 2009

AbstractFlavonoids have been described as health‐promoting, disease‐preventing dietary components.In vivoandin vitroexperiments also support a protective effect of flavonoids to reduce the incidence of certain hormone‐responsive cancers. In particular, our previous results indicate that the flavanone naringenin (Nar), decoupling estrogen receptor α (ERα) action mechanisms, drives cancer cells to apoptosis. Because these studies were conducted in the absence of the endogenous hormone 17β‐estradiol (E2), the physiological relevance of these findings is not clear. We investigate whether the antiproliferative Nar effect persists in the presence of physiological E2 concentration (i.e. 10 nM), using both ERα‐transfected (HeLa cells) and ERα‐containing (HepG2 cells) cancer cell lines. Ligand saturation experiments indicate that Nar decreases the binding of E2 to ERα without impairing the estrogen response element (ERE)‐driven reporter plasmid activity. In contrast, Nar stimulation prevents E2‐induced extracellular regulated kinases (ERK1/2) and AKT activation and still induces the activation of p38, the proapoptotic member of mitogen‐activating protein kinase (MAPK) family. As a consequence, Nar stimulation impedes the E2‐induced transcription of cyclin D1 promoter and reverts the E2‐induced cell proliferation, driving cancer cell to apoptosis. Thus, these results suggest that coexposure to this low‐affinity, low‐potency ligand for ERα specifically antagonizes the E2‐induced ERα‐dependent rapid signals by reducing the effect of the endogenous hormone in promoting cellular proliferation. As a whole, these data indicate that Nar is an excellent candidate as a chemopreventive agent in E2‐dependent cancers. © 2009 IUBMB IUBMB Life, 62(1):51–60, 2010
Surface characterization of commercial oral implants on the nanometer level
Authors: Svanborg Lory Melin , Andersson Martin , Wennerberg Ann 
Published: December 2009

AbstractLately, there has been a growing interest in how the presence of nanometer structures on a bone integrated implant surface influences the healing process. Recent in vitro studies have revealed an increased osteoblast response to different nanophase surfaces. Some commercial implant brands claim their implants have nanometer structures. However, at present, there are no studies where the nano topography of today's commercially available oral implants has been investigated. The aim of this study was to characterize commercial oral implants on the nanometer level and to investigate whether or not the nanometer surface roughness was correlated to the more well‐known micrometer roughness on the implants. Twelve different commercial screw‐shaped oral implants with various surface modifications were examined using scanning electron microscopy and a white light interferometer. The interferometer is suitable for detection of nanoscale roughness in the vertical dimension; however, limitation exists on the horizontal due to the wavelength of the light. A 1 × 1 μm Gaussian filter was found to be useful for identifying nm roughness with respect to height deviation. The results demonstrated that an implant that was smooth on the micrometer level was not necessarily smooth on the nanometer level. Different structures in the nanometer scale was found on some of the implants, indicating that to fully understand the relationship between the properties of an implant surface and its osseointegration behavior, a characterization at the nanometer scale might be relevant. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2010
Fatigue properties of superelastic Ti–Ni filaments and braided cables for bone fixation
Authors: Baril Y. , Brailovski V. 
Published: December 2009

AbstractThis work is focused on the fatigue properties of the braided hollow tubular cables for bone fixation made of superelastic Ti–Ni filaments. To evaluate the fatigue life of the cable and the impact of braiding on fatigue life, a comparative study was conducted on both the braided cable and the single filament. The results of strain‐controlled fatigue testing under variable mean and alternating strain conditions demonstrated that: (a) even though alternating strain is the most influent parameter, mean strain also has a significant impact on the fatigue life of both the filament and the braid; an improvement in the braided cable's fatigue life is observed under mean strains corresponding to the middle of the superelastic loop plateau; and (b) run‐out (105 cycles) is reached at 1% of alternating strain for the filament, and at 0.3% for the braided cable. It was proved that the negative impact of braiding on fatigue life is caused: (a) by friction‐induced damage of the braided filaments during cable manufacturing and (b) by locally occurring bending in the vicinity of the filaments' crossing, combined with the interfilament fretting during repetitive stretching of the braided cable. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2010
Healing of bone defects in the goat mandible, using COLLOSS® E and β‐tricalciumphosphate
Authors: Nienhuijs M. E. L. , Walboomers X. F. , Briest A. , Merkx M. A. W. , Stoelinga P. J. W. , Jansen J. A. 
Published: December 2009

AbstractCOLLOSS® E, an equine extracellular matrix product containing native transforming growth factor β1 and several bone morphogenetic proteins, has shown osteoinductive properties in ectopic sites. This study was set up to examine its properties in an orthotoptic site in conjunction with a β‐tricalciumphosphate (β‐TCP) scaffolding material. Thirty‐two 17‐mm circular defects in goat mandibles were filled with COLLOSS E, β‐TCP, COLLOSS E + β‐TCP, or left empty. After 9 weeks the results were quantified by micro‐computed tomography and histology. The empty defects contained the highest percentage of new bone (62%). The β‐TCP scaffold resulted in 38% (p = 0.0029), the mixture of β‐TCP/COLLOSS E resulted in 36% (p = 0.0057), while the use of COLLOSS E alone resulted in 55% (not significant p = 0.34). These results show that addition of TCP did not result in the expected synergy with regard to the healing of the defect and seemed even to inhibit the healing process. On the other hand, the addition of COLLOSS E induced the formation of small islands of new bone, not connected to the defect edges. This was not observed in the specimens not containing COLLOSS E (4.61% of bone formation centrally in the defect vs. 0.56%; p = 0.042). In conclusion, the results of the present study are somewhat unexpected in that the empty defects showed the most bone ingrowth; however, this ingrowth was always connected to the defect edges. In contrast, the application of COLLOSS E with or without β‐TCP induced bone formation in the center of the defects also. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2010
Repair of osteochondral defects with adipose stem cells and a dual growth factor‐releasing scaffold in rabbits
Authors: Im Gun‐Il , Lee Jin Ho 
Published: December 2009

AbstractThe purpose of this work was to evaluate the in vivo effectiveness of a TGF‐β2 and bone morphogenetic protein (BMP)‐7‐immobilized porous polycaprolactone (PCL)/F127 scaffold to enhance the healing of cartilage defect. An osteochondral defect was created on the patellar groove of the right distal femur of 12 rabbits and managed by one of the following methods: filling it with the scaffold only (Group I); the scaffold seeded with adipose stem cells (ASCs) (Group II); a TGF‐β2 and BMP‐7‐immobilized scaffold (Group III); and a TGF‐β2 and BMP‐7‐immobilized scaffold seeded with ASCs (Group IV). Each group had three rabbits. Nine weeks after the implantation, the implanted scaffolds were filled with yellowish, dense tissue, and had distinct margins with adjacent normal cartilage. The histological findings showed infiltration of foreign‐body giant cells and blood vessel, more prominently in Groups III and IV. The presence of growth factor significantly increased the ICRS Macroscopic Score (p = 0.045) while the presence of ASC did not. The ICRS Visual Histological Score was not significantly affected by the presence of either growth factors or ASCs, showing similar values in all groups. In conclusion, the use of TGF‐β2 and BMP‐7‐immobilized PCL/F127 scaffolds improved gross appearances of the osteochondral defects while not actually leading to better histological results and induced a greater degree of foreign body reaction. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2010
Chitosan‐coated poly(vinyl alcohol) nanofibers for wound dressings
Authors: Kang Yun Ok , Yoon In‐Soo , Lee So Young , Kim Dae‐Duk , Lee Seung Jin , Park Won Ho , Hudson Samuel M. 
Published: December 2009

AbstractA PVA nanofibrous matrix was prepared by electrospinning an aqueous 10 wt % PVA solution. The mean diameter of the PVA nanofibers electrospun from the PVA aqueous solution was 240 nm. The water resistance of the as‐spun PVA nanofibrous matrix was improved by physically crosslinking the PVA nanofibers by heat treatment at 150°C for 10 min, which were found to be the optimal heat treatment conditions determined from chemical and morphological considerations. In addition, the heat‐treated PVA (H‐PVA) nanofibrous matrix was coated with a chitosan solution to construct biomimetic nanofibrous wound dressings. The chitosan‐coated PVA (C‐PVA) nanofibrous matrix showed less hydrophilic and better tensile properties than the H‐PVA nanofibrous matrix. The effect of the chitosan coating on open wound healing in a mouse was examined. The C‐PVA and H‐PVA nanofibrous matrices showed faster wound healing than the control. The histological examination and mechanical stability revealed the C‐PVA nanofibrous matrix to be more effective as a wound‐healing accelerator in the early stages of wound healing than the H‐PVA nanofibrous matrix. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2010