bluuebunny/crossref_metadata_2025_split huggingface dataset:
A method for accurate group difference detection by constraining the mixing coefficients in an ICA framework
Authors: Sui Jing , Adali Tülay , Pearlson Godfrey D. , Clark Vincent P. , Calhoun Vince D. 
Published: July 2009

AbstractIndependent component analysis (ICA) is a promising method that is increasingly used to analyze brain imaging data such as functional magnetic resonance imaging (fMRI), structural MRI, and electroencephalography and has also proved useful for group comparison, e.g., differentiating healthy controls from patients. An advantage of ICA is its ability to identify components that are mixed in an unknown manner. However, ICA is not necessarily robust and optimal in identifying between‐group effects, especially in highly noisy situations. Here, we propose a modified ICA framework for multigroup data analysis that incorporates prior information regarding group membership as a constraint into the mixing coefficients. Our approach, called coefficient‐constrained ICA (CC‐ICA), prioritizes identification of components that show a significant group difference. The performance of CC‐ICA via synthetic and hybrid data simulations is evaluated under different hypothesis testing assumptions and signal to noise ratios (SNRs). Group analysis is also conducted on real multitask fMRI data. Results show that CC‐ICA improves the estimation accuracy of the independent components greatly, especially those that have different patterns for different groups (e.g., patients vs. controls); In addition, it enhances the data extraction sensitivity to group differences by ranking components with P value or J‐divergence more consistently with the ground truth. The proposed algorithm performs quite well for both group‐difference detection and multitask fMRI data fusion, which may prove especially important for the identification of relevant disease biomarkers. Hum Brain Mapp 2009. © 2009 Wiley‐Liss, Inc.
Advanced time‐series analysis of MEG data as a method to explore olfactory function in healthy controls and Parkinson's disease patients
Authors: Boesveldt Sanne , Stam Cornelis J. , Knol Dirk L. , Verbunt Jeroen P.A. , Berendse Henk W. 
Published: July 2009

AbstractObjectives:To determine whether time‐series analysis of magnetoencephalography (MEG) data is a suitable method to study brain activity related to olfactory information processing, and to detect differences in odor‐induced brain activity between patients with Parkinson's disease (PD) and controls.Methods:Whole head 151‐channel MEG recordings were obtained in 21 controls and 20 patients with PD during a 10‐min olfactory stimulus paradigm, consisting of 10 alternating rest‐stimulus cycles (30 s each), using phenylethyl alcohol administered by means of a Burghart olfactometer. Relative spectral power and synchronization likelihood (SL; an unbiased measure of functional connectivity) were calculated for delta, theta, alpha1, alpha2, beta, and gamma frequency bands.Results:In controls, olfactory stimulation produced an increase in theta power and a decrease in beta power. In patients with PD, there was a decrease in alpha1 power. No significant interaction between group and condition was found for spectral power. SL analysis revealed a significantly different response to olfactory stimulation in patients with PD compared to controls. In controls, the odor stimulus induced a decrease in local beta band SL. The response in patients with PD involved a decrease in intrahemispheric alpha2 band SL.Conclusion:This is the first study to show that time‐series analysis of MEG data, including spectral power and SL, can be used to detect odor‐induced changes in brain activity. In addition, differences in odor‐induced brain activity were found between patients with PD and controls using analysis of SL, but not of spectral power. Hum Brain Mapp 2009. © 2009 Wiley‐Liss, Inc.
Test–retest reliability of fMRI verbal episodic memory paradigms in healthy older adults and in persons with mild cognitive impairment
Authors: Clément Francis , Belleville Sylvie 
Published: July 2009

AbstractThis study investigated test–retest functional magnetic resonance imaging (fMRI) reproducibility in 10 healthy older adults and in 10 mild cognitive impairment (MCI) persons using a two‐condition (encoding and retrieval) verbal episodic memory task as well as a two‐condition (with and without a motor response) phonological processing task. Reproducibility measures included an overlap ratio with four different thresholds, statistical comparisons of the condition contrasts across sessions (test–retest contrasts), ANCOVAs, and intraclass correlation (ICC) on selected regions of interests (ROIs). In all four conditions and for all reproducibility measures, MCI individuals showed fMRI test–retest reproducibility indices that were comparable to those of healthy older adults. At the group level, the comparison of the test–retest condition contrasts yielded very few differences in the areas and level of activation and those differences tended to show a slight reduction of activation in the second session. In addition, the results from the ANCOVAs showed that the fMRI signal measured at the group level does not vary significantly from one session to another. Overlap ratios, however, showed that the fMRI signal failed to produce a reliable pattern of significantly activated voxels across sessions. ICC analyses on selected ROIs indicated that there is high within‐subject variability, suggesting reduced reliability at the individual level. Overall, these findings indicate that MCI individuals show fMRI test–retest reproducibility comparable to those of healthy controls and hence that MCI do not alter fMRI reproducibility. Furthermore, they indicate that monitoring treatment effects is reliable when comparing groups but reduced when comparing single individuals. These results have precise implications for the design of longitudinal studies relying on fMRI measures in older adults. Hum Brain Mapp, 2009. © 2009 Wiley‐Liss, Inc.
Caring for mom and neglecting yourself? The health effects of caring for an elderly parent
Authors: Coe Norma B. , Van Houtven Courtney Harold 
Published: July 2009

AbstractWe examine the physical and mental health effects of providing care to an elderly mother on the adult child caregiver. We address the endogeneity of the selection in and out of caregiving using an instrumental variable approach, using the death of the care recipient and sibling characteristics. We also carefully control for baseline health and work status of the adult child. We explore flexible specifications, such as Arellano–Bond estimation techniques. Continued caregiving over time increases depressive symptoms and decreases self‐rated health for married women and married men. In addition, the increase in depressive symptoms is persistent for married women. While depressive symptoms for single men and women are not affected by continued caregiving, there is evidence of increased incidence of heart conditions for single men, and that these effects are persistent. Robustness checks indicate that these health changes can be directly attributable to caregiving behavior, and not due to a direct effect of the death of the mother. The initial onset of caregiving has modest immediate negative effects on depressive symptoms for married women and no immediate effects on physical health. Negative physical health effects emerge 2 years later, however, suggesting that there are delayed effects on health that would be missed with a short recall period. Initial caregiving does not affect health of married men. Published in 2009 by John Wiley & Sons, Ltd.
The impact of health on individual retirement plans: self‐reported versus diagnostic measures
Authors: Datta Gupta Nabanita , Larsen Mona 
Published: July 2009

AbstractWe reassess the impact of health on retirement plans of older workers using a unique survey‐register match‐up which allows comparing the retirement effects of potentially biased survey self‐reports of health to those of unbiased register‐based diagnostic measures. The aim is to investigate whether even for narrowly defined health measures a divergence exists in the impacts of health on retirement between self‐reported health and objective physician‐reported health. Our sample consists of older workers and retirees drawn from a Danish panel survey from 1997 and 2002, merged to longitudinal register data. Estimation of measurement error‐reduced and selection‐corrected pooled OLS and fixed effects models of retirement show that receiving a medical diagnosis is an important determinant of retirement planning for both men and women, in fact more important than economic factors. The type of diagnosis matters, however. For men, the largest reduction in planned retirement age occurs for a diagnosis of lung disease while for women it occurs for musculo‐skeletal disease. Except for cardiovascular disease, diagnosed disease is more influential in men's retirement planning than in women's. Our study provides evidence that men's self‐report of myalgia and back problems and women's self‐report of osteoarthritis possibly yield biased estimates of the impact on planned retirement age, and that this bias ranges between 1.5 and 2 years, suggesting that users of survey data should be wary of applying self‐reports of health conditions with diffuse symptoms to the study of labor market outcomes. On the other hand, self‐reported cardiovascular disease such as high blood pressure does not appear to bias the estimated impact on planned retirement. Copyright © 2009 John Wiley & Sons, Ltd.
Model‐based projections for deriving up‐to‐date cancer survival estimates: An international evaluation
Authors: Gondos Adam , Holleczek Bernd , Janssen‐Heijnen Maryska , Brewster David H. , Bray Freddie , Rosso Stefano , Hakulinen Timo , Brenner Hermann 
Published: July 2009

AbstractModel‐based projections were shown to be useful for deriving most up‐to‐date population‐based cancer survival estimates. However, the performance of these projections, which can be derived by various approaches, has only been evaluated in very few cancer patient populations. Using incidence and follow‐up data for 22 common cancers from 9 long‐standing population‐based cancer registries from diverse parts of Europe, we compared the performance of model‐based period and cohort analysis for predicting 5‐year relative survival of patients diagnosed in 1996–2000 against standard survival analysis approaches (cohort, complete and period analysis). Overall, model‐based predictions provided a best estimate of the later observed actual survival in 135 of 198 occasions, compared to 25, 18 and 33 occasions for cohort, complete and period analysis, respectively. Projections based on cohort and period type modeling performed essentially equally well on average, and their performance was better for more common cancers, in registries with larger population bases, and for cancers subjected to continuous clinical progress and/or ongoing screening efforts. Projections from model‐based analysis may contribute to improved timeliness of monitoring of concurrent trends in population‐based cancer survival in cancer registries operating in different populations and socioeconomic environments. © 2009 UICC
Consistent genomic alterations in carcinoma in situ of the urinary bladder confirm the presence of two major pathways in bladder cancer development
Authors: Zieger Karsten , Marcussen Niels , Borre Michael , Ørntoft Torben F. , Dyrskjøt Lars 
Published: July 2009

AbstractBladder cancer develops through different pathways, provisionally entitled “papillary” and “invasive.” Carcinoma in situ (CIS) is thought to be the precursor of invasive bladder cancer. However, little is known about chromosomal alterations of these clinically important lesions, and the relationship between chromosomal alterations and the different pathways. We laser‐microdissected 12 CIS and 4 dysplasia samples concomitant to invasive bladder cancer. We determined genome‐wide chromosome copy number changes and loss of heterozygosity (LOH) using Mapping 10K SNP microarrays. We further examined 48 high‐risk non‐muscle‐invasive bladder cancers using SNP microarrays to reveal characteristic changes correlated with the CIS‐phenotype. DNA copy‐number changes were further validated using QPCR in 77 independent tumor samples. CIS was found to be chromosomal unstable in 8 of 12 cases. Characteristic chromosomal changes were copy number gains of chromosomes 5p, 6p22.3, 10p15.1 and losses/LOH of chromosome 5q and 13q13‐q14. Tumor samples with these alterations were significantly associated with CIS. Using FGFR3 mutations as markers of the opposing papillary phenotype, we found 5p gains and FGFR3 mutations mutually exclusive. No FGFR3 mutations were found in 23 CIS and dysplasia samples. Based on this, we classified high‐risk non‐muscle‐invasive bladder tumors according to FGFR3 mutations and chromosomal changes into papillary and CIS‐type tumors with high correlation to CIS status (p = 0.001). Furthermore, we found significant correlation to the results of molecular classifiers based on gene‐expression. We concluded that chromosomal changes may be used to characterize different pathways in bladder cancer development. © 2009 UICC
The reduction of cell death and proliferation by p27Kip1 minimizes DNA damage in an experimental model of genotoxicity
Authors: Ranchal Isidora , González Raúl , Bello Rosario I. , Ferrín Gustavo , Hidalgo Ana B. , Linares Clara I. , Aguilar‐Melero Patricia , González‐Rubio Sandra , Barrera Pilar , Marchal Trinidad , Nakayama Keiichi I. , de la Mata Manuel , Muntané Jordi 
Published: July 2009

AbstractHepatocellular carcinoma (HCC) is the fifth most commonly occurring cancer worldwide. The expression of p27 has been related to reduced severity of tumor grade and recurrence of HCC. The study assessed the role of p27 on the cell proliferation and death, and DNA mutagenesis in experimental genotoxicity induced by aflatoxin B1 (AFB1) in cultured hepatocytes obtained from control and p27Kip1 deficient mice. The overexpression of p27 was assessed with wild type p27Kip1 expression vector in HepG2 cells. The expression of p27, p21 and p53 was assessed in well and poorly‐differentiated liver tumors. DNA damage and cell death induced by AFB1 were related to a reduction of p27 and p21 expression in cultured hepatocytes. AFB1‐induced nuclear phosphorylated (Ser 10) p27 degradation was related to a rise of nuclear KIST, Rsk‐1 and Rsk‐2 expression and cytoplasm phosphorylated (Thr 198) p27 expression. The overexpression of p27 reduced cell proliferation, cell death and DNA damage in AFB1‐treated hepatocytes. The enhanced survival of patients with well differentiated compared to poorly‐differentiated tumors was related to high expression of p27, p21 and p53 in liver sections. The study showed that the p27 reduced cell proliferation and death, as well as the accumulation of DNA damage in hepatocarcinogenesis. © 2009 UICC
Identification of modifier genes for cutaneous malignant melanoma in melanoma‐prone families with and without CDKN2A mutations
Authors: Yang Xiaohong Rose , Pfeiffer Ruth M. , Wheeler William , Yeager Meredith , Chanock Stephen , Tucker Margaret A. , Goldstein Alisa M. 
Published: July 2009

AbstractCDKN2A is a major susceptibility gene for cutaneous malignant melanoma (CMM), but the variable penetrance and clinical manifestations among mutation carriers suggest the existence of modifier factors. The goal of this study was to identify modifier genes for CMM in CMM‐prone families with or without CDKN2A mutations. We genotyped 537 individuals (107 CMM) from 28 families (19 CDKN2A+, 9 CDKN2A−) for 1,536 SNPs in 152 genes involved in DNA repair, apoptosis and immune response pathways. We used conditional logistic regression to account for family ascertainment and differences in disease prevalence among families. Pathway‐ and gene‐based permutation analyses were used to assess the risk of CMM associated with genes in the 5 pathways (DNA repair, apoptosis, TNF/NFκB, TH1:TH2 and other immune regulation). Our analyses identified some candidate genes such as FAS, BCL7A, CASP14, TRAF6, WRN, IL9, IL10RB, TNFSF8, TNFRSF9 and JAK3 that were associated with CMM risk (p < 0.01, gene‐based test). After correction for multiple comparisons, IL9 remained significant (Bonferroni p < 0.05). The effects of some genes were stronger in CDKN2A‐positive families (BCL7A and IL9), while some were stronger in CDKN2A‐negative families (BCL2L1). Our findings support the hypothesis that common genetic polymorphisms in DNA repair, apoptosis and immune response pathways may modify the risk of CMM in CMM‐prone families with or without CDKN2A mutations. Published 2009 UICC.
IGF2R polymorphisms and risk of esophageal and gastric adenocarcinomas
Authors: Hoyo Cathrine , Schildkraut Joellen M. , Murphy Susan K. , Chow Wong‐Ho , Vaughan Thomas L. , Risch Harvey , Marks Jeffrey R. , Jirtle Randy L. , Calingeart Brian , Mayne Susan , Fraumeni Joseph , Gammon Marilie D. 
Published: July 2009

AbstractThe mannose‐6‐phosphate/insulin‐like growth factor 2 receptor (M6P/IGF2R) encodes a protein that plays a critical role in tumor suppression, in part by modulating bioavailability of a potent mitogen, insulin‐like growth factor‐2 (IGF2). We tested the hypothesis that the common nonsynonymous genetic variants in M6P/IGF2R c.901C > G (Leu > Val) in exon 6 and c.5002G > A (Gly > Arg) in exon 34 are associated with risk of esophageal and gastric cancers. Study participants in this population‐based study comprise 197 controls and 182 cases, including 105 with esophageal‐gastric cardia adenocarcinoma (EGA), 57 with noncardia gastric adenocarcinoma and 20 with esophageal squamous (ES) cell carcinoma. Among white males, odds ratios (ORs) were elevated in relation to carrying at least 1 c.901C > G allele for EGA [OR = 1.9; 95% confidence intervals (CIs) = 1.0–3.6] and noncardia gastric cancer (OR = 2.5; 95% CI = 1.2–5.5), but not ES. Exploratory subgroup analyses suggested that associations between EGA and this variant were stronger among irregular or nonusers of nonsteroidal anti‐inflammatory drugs (NSAIDs) (OR = 2.3; 95% CI = 1.2–4.2) and cigarette smokers (OR = 2.1; 95% CI = 1.0–4.2). An association between carrying the c.5002G > A genotype and EGA was not evident. These findings suggest that nonsynonymous polymorphisms in M6P/IGF2R may contribute to the risks of EGA and noncardia adenocarcinomas. Larger studies are required to confirm these findings. © 2009 UICC
The novel tumor‐suppressor Mel‐18 in prostate cancer: Its functional polymorphism, expression and clinical significance
Authors: Wang Wei , Yuasa Takeshi , Tsuchiya Norihiko , Ma Zhiyong , Maita Shinya , Narita Shintaro , Kumazawa Teruaki , Inoue Takamitsu , Tsuruta Hiroshi , Horikawa Yohei , Saito Mitsuru , Hu Weilie , Ogawa Osamu , Habuchi Tomonori 
Published: July 2009

AbstractMel‐18 is a member of the polycomb group (PcG) proteins, which are chromatin regulatory factors and play important roles in development and oncogenesis. This study was designed to investigate the clinical and prognostic significance of Mel‐18 in patients with prostate cancer. A total of 539 native Japanese subjects consisting of 393 prostate cancer patients and 146 controls were enrolled in this study. Mel‐18 genotyping was analyzed using a PCR‐RFLP method and an automated sequencer using the GENESCAN software. Immunohistochemistry revealed that Mel‐18 expression was diminished in high grade and high stage prostate cancers. Moreover, patients with positive Mel‐18 expression had significantly longer PSA recurrence‐free survival than patients negative for Mel‐18 expression (p = 0.038). A Mel‐18 1805A/G SNP was located in the 3' untranslated region and was predicted to alter the secondary structure of the mRNA. Mel‐18 mRNA expression of the 1805A allele was clearly higher than expression of the 1805G allele by allele specific quantitative RT‐PCR. In multivariate analysis, a homozygous G allele genotype and negative Mel‐18 expression were independent risk factors predicting high PSA recurrence after radical prostatectomy, with HRs of 2.757 (p = 0.022) and 2.271 (p = 0.045), respectively. Moreover, the G allele was also an independent predictor of poor cancer‐specific survival with an HR of 4.658 (p = 0.019) for patients with stage D2 prostate cancer. This is the first study to provide important evidence demonstrating that Mel‐18 is a tumor suppressor and possible therapeutic target, as well as a diagnostic marker for poor prognosis in prostate cancer patients. © 2009 UICC
Response surface analysis of microwave‐assisted extraction of polysaccharides from cultured Cordyceps militaris
Authors: Song Jiang‐Feng , Li Da‐Jing , Liu Chun‐Quan 
Published: July 2009

AbstractBACKGROUND: Microwave‐assisted extraction was employed to extract polysaccharides from cultured Cordyceps militaris. The optimal conditions for polysaccharide extraction were determined by response surface methodology. Box–Behnken design was applied to evaluate the effects of three independent variables (microwave power, extraction time and ratio of solution to solid) on the polysaccharide yield of C. militaris.RESULTS: Correlation analysis of the mathematical‐regression model indicated that a quadratic polynomial model could be employed to optimize the microwave‐assisted extraction of polysaccharide. Response surface plots showed that microwave power, extraction time and ratio of solution to solid exhibited independent and interactive effects on the extraction of polysaccharide. The optimal conditions to obtain the highest polysaccharide yield of C. militaris were a microwave power of 744.8 W, an extraction time of 4.2 min and a ratio of solution to solid of 31.1 mL g−1.CONCLUSION: Under these optimal conditions, the experimental values agreed with the predicted values, using analysis of variance, indicating the goodness of fit of the model used and the success of response surface methodology for optimizing microwave‐assisted extraction of polysaccharide from C. militaris. Copyright © 2009 Society of Chemical Industry
Depletion of CD4+CD25+ T cells exacerbates experimental autoimmune encephalomyelitis induced by mouse, but not rat, antigens
Authors: Akirav Eitan M. , Bergman Cheryl M. , Hill Myriam , Ruddle Nancy H. 
Published: July 2009

AbstractA key question in the field of autoimmunity concerns the fact that experimental disease is generally induced more easily with closely related, but not completely identical, tissue‐restricted antigens. Here, the possibility that naturally occurring regulatory T cells (Tregs) for self‐antigens are more potent than those for related antigens was investigated. The self‐antigen specificity of naturally occurring Tregs was tested in experimental autoimmune encephalomyelitis (EAE) induced with mouse (self) or closely related (rat) myelin oligodendrocyte glycoproteins (MOGs). Surprisingly, Treg depletion increased EAE severity in mice immunized with mouse, but not rat, MOG. This increase was associated with increased T‐cell activation and infiltration of the central nervous system, as well as increased interleukin (IL)‐17 production and a higher ratio of interferon‐γ‐ to IL‐10‐producing cells. These data suggest that Tregs are specific for self‐antigen and do not “cross‐protect” against autoimmunity even when disease is induced with closely related foreign antigens. © 2009 Wiley‐Liss, Inc.