bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of roasting on oxidative and tocopherol stability of walnut oil during storage in the dark
Authors: Vaidya Bipin , Eun Jong‐Bang 
Published: November 2012

AbstractThe effect of roasting on the oxidative stability of oil from walnut (Juglans sinensis Dode) was investigated by observing changes in the characteristics of oils from unroasted and roasted kernels during storage in the dark at 60°C. Walnut kernels were roasted at 160°C for 15 min prior to oil extraction with the solvent, hexane. Roasting of kernels increased the peroxide value (POV) and conjugated dienoic acid (CDA) value of the oil. The rate of increase in the POV was significantly lower in roasted than in the unroasted walnut oil during storage at 60°C (1.90 vs. 1.06 and 4.45 vs. 3.55 meq/kg/day during induction period (IP) and post‐IP, respectively). Roasting of kernels significantly increased the IP of walnut oil from 0.89 to 3.39 days during storage. The total tocopherol content in roasted walnut oil was lower as compared to that in unroasted one (277.77 vs. 314.88 µg/g). However, the rate of degradation of total tocopherol during storage was lower in roasted walnut oil compared to unroasted one (1.18 vs. 2.17%/day), which showed that the tocopherol retention was higher in roasted walnut oil. These results indicate that roasting of kernels increased the oxidative and tocopherol stability of oil during storage in the dark.
One‐Pot Synthesis of Symmetrical Diaryl Trithiocarbonates through Copper‐Catalyzed Coupling of Aryl Compounds, Sodium Sulfide, and Carbon Disulfide
Authors: Gholinejad Mohammad 
Published: November 2012

AbstractIn this study, a protocol for the synthesis of symmetrical diaryl trithiocarbonates through the one‐pot copper‐catalyzed coupling reaction of sodium sulfide, carbon disulfide, and aryl compounds in DMF solution is presented. This method allows the synthesis of symmetrical diaryl trithiocarbonates without the use of highly toxic thiophosgene, and also, commercially available aryl halides were used instead of less available, toxic thiols.
Gold‐Catalyzed Mannich Addition Reactions of 1,3‐Dicarbonyl Compounds with N‐Protected Imines
Authors: Delgado‐Rebollo Manuela , Moreno Rocio , Fructos Manuel R. , Prieto Auxiliadora 
Published: November 2012

AbstractThe first (N‐heterocyclic carbene)AuI‐catalyzed Mannich addition reactions of N‐protected imines with different 1,3‐dicarbonyl compounds are described. IPrAuNTf2 was proven to be an efficient catalyst for the reactions of β‐keto esters and 1,3‐diketones with N‐sulfonylimines to afford the desired β‐amino carbonyl compounds in good yields under very mild conditions.
Sphingosine analogue drug FTY720 targets I2PP2A/SET and mediates lung tumour suppression via activation of PP2A‐RIPK1‐dependent necroptosis
Authors: Saddoughi Sahar A. , Gencer Salih , Peterson Yuri K. , Ward Katherine E. , Mukhopadhyay Archana , Oaks Joshua , Bielawski Jacek , Szulc Zdzislaw M. , Thomas Raquela J. , Selvam Shanmugam P. , Senkal Can E. , Garrett‐Mayer Elizabeth , De Palma Ryan M. , Fedarovich Dzmitry , Liu Angen , Habib Amyn A. , Stahelin Robert V. , Perrotti Danilo , Ogretmen Besim 
Published: November 2012

AbstractMechanisms that alter protein phosphatase 2A (PP2A)‐dependent lung tumour suppression via the I2PP2A/SET oncoprotein are unknown. We show here that the tumour suppressor ceramide binds I2PP2A/SET selectively in the nucleus and including its K209 and Y122 residues as determined by molecular modelling/simulations and site‐directed mutagenesis. Because I2PP2A/SET was found overexpressed, whereas ceramide was downregulated in lung tumours, a sphingolipid analogue drug, FTY720, was identified to mimick ceramide for binding and targeting I2PP2A/SET, leading to PP2A reactivation, lung cancer cell death, and tumour suppression in vivo. Accordingly, while molecular targeting of I2PP2A/SET by stable knockdown prevented further tumour suppression by FTY720, reconstitution of WT‐I2PP2A/SET expression restored this process. Mechanistically, targeting I2PP2A/SET by FTY720 mediated PP2A/RIPK1‐dependent programmed necrosis (necroptosis), but not by apoptosis. The RIPK1 inhibitor necrostatin and knockdown or genetic loss of RIPK1 prevented growth inhibition by FTY720. Expression of WT‐ or death‐domain‐deleted (DDD)‐RIPK1, but not the kinase‐domain‐deleted (KDD)‐RIPK1, restored FTY720‐mediated necroptosis in RIPK1−/− MEFs. Thus, these data suggest that targeting I2PP2A/SET by FTY720 suppresses lung tumour growth, at least in part, via PP2A activation and necroptosis mediated by the kinase domain of RIPK1.
Analysis of a meshless solver for high Reynolds number flow
Authors: Su Xinrong , Yamamoto Satoru , Nakahashi Kazuhiro 
Published: November 2012

SUMMARYIn this paper, the extension of an upwind least‐square based meshless solver to high Reynolds number flow is explored, and the properties of the meshless solver are analyzed both theoretically and numerically. Existing works have verified the meshless solver mostly with inviscid flows and low Reynolds number flows, and in this work, we are interested in the behavior of the meshless solver for high Reynolds number flow, especially in the near‐wall region. With both theoretical and numerical analysis, the effects of two parameters on the meshless solver are identified. The first one is the misalignment effect caused by the significantly skewed supporting points, and it is found that the meshless solver still yields accurate prediction. It is a very interesting property and is opposite to the median‐dual control volume based vertex‐centered finite volume method, which is known to give degraded result with stretched triangular/tetrahedral cells in the near‐wall region. The second parameter is the curvature, and according to theoretical analysis, it is found in the region with both large aspect ratio and curvature, and the streamwise residual is less affected; however, the wall‐normal counterpart suffers from accuracy degradation. In this paper, an improved method that uses a meshless solver for the streamwise residual and finite difference for wall‐normal residual is developed. This method is proved to be less sensitive to the curvature and provides improved accuracy. This work presents an understanding of the meshless solver for high Reynolds number flow computation, and the analysis in this paper is verified with a series of numerical experiments. Copyright © 2012 John Wiley & Sons, Ltd.
Antimitochondrial antibody heterogeneity and the xenobiotic etiology of primary biliary cirrhosis
Authors: Chen Richy C.Y. , Naiyanetr Phornnop , Shu Shang-An , Wang Jinjun , Yang Guo-Xiang , Kenny Thomas P. , Guggenheim Kathryn C. , Butler Jeffrey D. , Bowlus Christopher , Tao Mi-Hua , Kurth Mark J. , Ansari Aftab A. , Kaplan Marshall , Coppel Ross L. , Lleo Ana , Gershwin Eric M. , Leung Patrick S.C. 
Published: November 2012

Abstract

Antimitochondrial antibodies (AMAs) directed against the lipoyl domain of the E2 subunit of pyruvate dehydrogenase (PDC-E2) are detected in 95% of patients with primary biliary cirrhosis (PBC) and are present before the onset of clinical disease. The recent demonstration that AMAs recognize xenobiotic modified PDC-E2 with higher titers than native PDC-E2 raises the possibility that the earliest events involved in loss of tolerance are related to xenobiotic modification. We hypothesized that reactivity to such xenobiotics would be predominantly immunoglobulin M (IgM) and using sera from a large cohort of PBC patients and controls (n = 516), we examined in detail sera reactivity against either 6,8-bis(acetylthio) octanoic acid (SAc)-conjugated bovine serum albumin (BSA), recombinant PDC-E2 (rPDC-E2) or BSA alone. Further, we also defined the relative specificity to the SAc moiety using inhibition enzyme-linked immunosorbent assay (ELISA); SAc conjugate and rPDC-E2-specific affinity-purified antibodies were also examined for antigen specificity, isotype, and crossreactivity. Reactivity to SAc conjugates is predominantly IgM; such reactivity reflects a footprint of previous xenobiotic exposure. Indeed, this observation is supported by both direct binding, crossreactivity, and inhibition studies. In both early and late-stage PBC, the predominant Ig isotype to SAc is IgM, with titers higher with advanced stage disease. We also note that there was a higher level of IgM reactivity to SAc than to rPDC-E2 in early-stage versus late-stage PBC. Interestingly, this finding is particularly significant in light of the structural similarity between SAc and the reduced form of lipoic acid, a step which is similar to the normal physiological oxidation of lipoic acid.

Conclusion:

Specific modifications of the disulfide bond within the lipoic-acid-conjugated PDC-E2 moiety, i.e., by an electrophilic agent renders PDC-E2 immunogenic in a genetically susceptible host.
Availability of stage at diagnosis, cancer treatment delay and compliance with cancer guidelines as cancer registry indicators for cancer care in Europe: Results of EUROCHIP‐3 survey
Authors: Siesling Sabine , Kwast Annemiek , Gavin Anna , Baili Paolo , Otter Renee ,   EUROCHIP‐3 Workpackage 5
Published: November 2012

AbstractEUROCHIP (European Cancer Health Indicators Project) focuses on understanding inequalities in the cancer burden, care and survival by the indicators “stage at diagnosis,” “cancer treatment delay” and “compliance with cancer guidelines” as the most important indicators. Our study aims at providing insight in whether cancer registries collect well‐defined variables to determine these indicators in a comparative way. Eighty‐six general European population‐based cancer registries (PBCR) from 32 countries responded to the questionnaire, which was developed by EUROCHIP in collaboration with ENCR (European Network of Cancer Registries) and EUROCOURSE. Only 15% of all the PBCR in EU had all three indicators available. The indicator “stage at diagnosis” was gathered for at least one cancer site by 81% (using TNM in 39%). Variables for the indicator “cancer treatment delay” were collected by 37%. Availability of type of treatment (30%), surgery date (36%), starting date of radiotherapy (26%) and starting date of chemotherapy (23%) resulted in 15% of the PBCRs to be able to gather the indicator “compliance to guidelines”. Lack of data source access and qualified staff were the major reasons for not collecting all the variables. In conclusion, based on self‐reporting, a few of the participating PBCRs had data available which could be used for clinical audits, evaluation of cancer care projects, survival and for monitoring national cancer control strategies. Extra efforts should be made to improve this very efficient tool to compare cancer burden and the effects of the national cancer plans over Europe and to learn from each other.
Leukocyte telomere length‐related genetic variants in 1p34.2 and 14q21 loci contribute to the risk of esophageal squamous cell carcinoma
Authors: Shi Juan , Sun Fang , Peng Li , Li Bo , Liu Li , Zhou Changchun , Han Jianjun , Zhang Li , Zhou Liqing , Zhang Xiaojiao , Pu Honglei , Tong Lei , Yuan Qipeng , Song Xianrang , Yang Ming 
Published: November 2012

AbstractShort leukocyte telomere length has been associated with significantly increased risk of esophageal cancer. A previous genome‐wide association study demonstrated that four SNPs (rs398652 on 14q21, rs621559 on 1p34.2, rs6028466 on 20q11.22 and rs654128 on 6q22.1) were associated with leukocyte telomere length in Caucasians. However, the role of these genetic variants on esophageal squamous cell carcinoma (ESCC) susceptibility is still unknown. Therefore, we investigated whether these polymorphisms have impact on leukocyte telomere length and the risk of ESCC in Chinese. After measuring leukocyte telomere length of 550 healthy individuals, we observed that both rs621559 and rs398652 genetic variants are significantly associated with leukocyte telomere length. On the basis of analyzing 1550 ESCC patients and frequency‐matched 1620 controls from 4 medical centers in China, we found that 0.71‐fold decreased risk of ESCC is associated with the rs621559 AA genotype compared with the rs621559 GG genotype (p = 5.9 × 10−6). We also detected a moderately increased OR for ESCC that was associated with the 14q21 rs398652 G allele (p = 6.5 × 10−4). It has been shown that both rs621559 and rs398652 polymorphisms were significantly associated with ESCC risk in additive, recessive or dominant genetic models. Stratified analyses demonstrated that these associations were more pronounced in males. Our results highlight the complexity of genetic regulation of telomere length and further support the important role of telomere in carcinogenesis.
Genetic variation in bone morphogenetic proteins and breast cancer risk in hispanic and non‐hispanic white women: The breast cancer health disparities study
Authors: Slattery Martha L. , John Esther M. , Torres‐Mejia Gabriela , Herrick Jennifer S. , Giuliano Anna R. , Baumgartner Kathy B. , Hines Lisa M. , Wolff Roger K. 
Published: November 2012

AbstractBone morphogenetic proteins (BMP) are thought to be important in breast cancer promotion and progression. We evaluated genetic variation in BMP‐related genes and breast cancer risk among Hispanic (2,111 cases, 2,597 controls) and non‐Hispanic White (NHW) (1,481 cases, 1,586 controls) women who participated in the 4‐Corner's Breast Cancer Study, the Mexico Breast Cancer Study and the San Francisco Bay Area Breast Cancer Study. BMP genes and their receptors evaluated include ACVR1, AVCR2A, ACVR2B, ACVRL1, BMP1, BMP2, BMP4, BMP6, BMP7, BMPR1A, BMPR1B, BMPR2, MSTN and GDF10. Additionally, 104 ancestral informative markers were assessed to discriminate between European and native American ancestry. The importance of estrogen on BMP‐related associations was suggested through unique associations by menopausal status and estrogen (ER) and progesterone (PR) receptor status of tumors. After adjustment for multiple comparisons ACVR1 (8 SNPs) was modestly associated with ER+PR+ tumors [odds ratios (ORs) between 1.18 and 1.39 padj < 0.05]. ACVR1 (3 SNPs) and BMP4 (3 SNPs) were associated with ER+PR− tumors (ORs 0.59–2.07; padj < 0.05). BMPR2 was associated with ER−PR+ tumors (OR 4.20; 95% CI 1.62, 10.91; padj < 0.05) as was GDF10 (2 SNPs; ORs 3.62 and 3.85; padj < 0.05). After adjustment for multiple comparisons several SNPs remained associated with ER−PR− tumors (padj < 0.05) including ACVR1
BMP4 and GDF10 (ORs between 0.53 and 2.12). Differences in association also were observed by percentage of native ancestry and menopausal status. Results support the hypothesis that genetic variation in BMPs is associated with breast cancer in this admixed population.
RUNX family: Regulation and diversification of roles through interacting proteins
Authors: Chuang Linda Shyue Huey , Ito Kosei , Ito Yoshiaki 
Published: November 2012

AbstractThe Runt‐related transcription factors (RUNX) belong to an ancient family of metazoan genes involved in developmental processes. Through multiple protein‐interacting partners, RUNX proteins have been implicated in diverse signaling pathways and cellular processes. The frequent inactivation of RUNX genes in cancer indicates crucial roles for RUNX in tumor suppression. This review discusses the abilities of RUNX proteins, in particular RUNX3, to integrate oncogenic signals or environmental cues and to initiate appropriate tumor suppressive responses.
The involvement of the RET variant G691S in medullary thyroid carcinoma enlightened by a meta‐analysis study
Authors: Lantieri Francesca , Caroli Francesco , Ceccherini Isabella , Griseri Paola 
Published: November 2012

AbstractMedullary thyroid carcinoma (MTC) is a rare tumor, partially explained by mutations in the rearranged during transfection (RET) proto‐oncogene. The nonsynonymous RET polymorphism G691S has been reported as associated with MTC, but findings are discordant. We sought to clarify the role of G691S in MTCs through in silico analysis, genetic association in our patients and a meta‐analysis with extensive literature revision. Ninety‐three Italian patients were compared to 85 healthy individuals. Results were included in a meta‐analysis together with 11 case‐control association studies identified through PubMed, EMBASE and Web of Science, with a combined sample of 968 cases and 2,115 controls. No association of G691S with MTC was found in our sample; however, we observed an excess of homozygotes for the variant, significantly higher among females. The overall allelic association in the meta‐analysis was significant under the fixed‐effect model (odds ratio [OR] = 1.22 [95% confidence intervals: 1.06–1.39], p = 0.0049), but borderline under the random effect model (OR = 1.21 [0.99–1.46], p = 0.0575), with a moderate/high heterogeneity (I2 = 44.6%, p = 0.047). Under the recessive model of transmission, applied to the eight studies with available genotype frequencies, results were significant under both effect models (OR = 2.016 and OR = 2.022, p = 0.0004). No heterogeneity was anymore detectable. In silico analyses on G691S confirmed a change of the phosphorylation pattern that might account for the enhanced signaling transduction previously reported for G691S in several cancers, thus also explaining its overrepresentation in MTCs. The G691S variant allele does increase the risk for MTC, with a recessive mechanism of action, apparently more evident among females.
Restriction endonuclease‐mediated real‐time digestion‐PCR for somatic mutation detection
Authors: Zhao Jinyin , Xie Feifei , Zhong Wei , Wu Weili , Qu Shoufang , Gao Shangxian , Liu Licheng , Zhao Jing , Wang Mengzhao , Zhou Junyi , Jie Huang , Chen Weijun 
Published: November 2012

AbstractPCR is a powerful platform for clinical and diagnostic applications, but challenges remain in detecting somatic mutations, as mutant cells are often mixed with more numerous wild‐type cells at the tissue‐sample sites. Here, we describe a novel method that couples PCR with restriction endonuclease digestion (designated real‐time digestion‐PCR, or RTD‐PCR) in a one‐step reaction tube for detecting somatic mutations from a minority of cells. The PCR mixture contains a thermostable restriction enzyme that digests wild‐type alleles during the PCR program, allowing selective amplification of the mutant alleles. To validate this method, we used real‐time digestion‐PCR for the specific detection of the EGFR (epidermal growth factor receptor) treatment resistance‐inducing mutation, T790M, combining with three different platforms: Sanger sequencing, TaqMan probe PCR and Sequenom MassArray. From 78 clinical samples, seven T790M mutations were consistently detected on all three platforms, indicating that RTD‐PCR may be a useful clinical tool for analyzing the T790M point mutation.
Circulating 25‐hydroxyvitamin D, vitamin D‐binding protein and risk of prostate cancer
Authors: Weinstein Stephanie J. , Mondul Alison M. , Kopp William , Rager Helen , Virtamo Jarmo , Albanes Demetrius 
Published: November 2012

AbstractWe recently reported a significant positive association between 25‐hydroxyvitamin D [25(OH)D], the accepted biomarker of vitamin D status, and prostate cancer risk. To further elucidate this association, we examined the influence of vitamin D‐binding protein (DBP), the primary transporter of vitamin D compounds in the circulation. Prediagnostic serum concentrations of DBP were assayed for 950 cases and 964 matched controls with existing 25(OH)D measurements within the Alpha‐Tocopherol, Beta‐Carotene Cancer Prevention Study of Finnish men. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs), and statistical tests were two sided. Serum DBP modified the association between serum 25(OH)D and prostate cancer, with higher risk for elevated 25(OH)D levels observed primarily among men having DBP concentrations above the median (OR = 1.81, 95% CI: 1.18–2.79 for highest vs. lowest quintile, p‐trend = 0.001) compared to those with DBP below the median (OR = 1.22, 95% CI: 0.81–1.84, p‐trend 0.97; p‐interaction = 0.04). Serum DBP was not associated with prostate cancer risk overall (OR = 0.96, 95% CI: 0.70–1.33 for highest vs. lowest quintile); however, high serum DBP was associated with significantly decreased risk of prostate cancer in men with lower (<median) 25(OH)D concentrations (OR = 0.59, 95% CI: 0.38–0.90 for highest vs. lowest quintile, p‐trend = 0.003) and increased risk in men with higher 25(OH)D concentrations (OR = 1.47, 95% CI: 0.98–2.20, p‐trend 0.10, p‐interaction = 0.02). Our data suggest that the primary vitamin D carrier protein, DBP, modulates the impact of vitamin D status on prostate cancer.
Transcriptional and post‐transcriptional regulation of β‐secretase
Authors: Tamagno Elena , Guglielmotto M. , Monteleone D. , Vercelli A. , Tabaton M. 
Published: November 2012

AbstractAlzheimer's disease (AD) is a devastating neurodegenerative disorder that results in loss of memory and cognitive function, eventually leading to dementia. A key neuropathological event in AD is the cerebral accumulation of senile plaques formed by aggregates of amyloid‐β‐peptides (Aβ). Aβ results from two sequential endoproteolytic cleavages operated on the amyloid‐β precursor protein (AβPP), an integral membrane protein with a single‐membrane spanning domain, a large extracellular N‐terminus and a shorter, cytoplasmic C‐terminus. First, β‐secretase (BACE1) cleaves AβPP at the N‐terminal end of the Aβ sequence to produce a secreted form of AβPP, named sAβPP, and a C‐terminal membrane‐bound 99‐aminoacid fragment (C99). Then, γ‐secretase cleaves C99 within the transmembrane domain to release the Aβ peptides of different lengths, predominantly Aβ1‐40 and Aβ1‐42. © 2012 IUBMB IUBMB Life, 64(12): 943–950, 2012
Imaging of the DNA damage‐induced dynamics of nuclear proteins via nonlinear photoperturbation
Authors: Tomas Martin , Blumhardt Philipp , Deutzmann Anja , Schwarz Tobias , Kromm Dimitri , Leitenstorfer Alfred , Ferrando‐May Elisa 
Published: November 2012

AbstractUnderstanding the cellular response to DNA strand breaks is crucial to decipher the mechanisms maintaining the integrity of our genome. We present a novel method to visualize how the mobility of nuclear proteins changes in response to localized DNA damage. DNA strand breaks are induced via nonlinear excitation with femtosecond laser pulses at λ = 1050 nm in a 3D‐confined subnuclear volume. After a time delay of choice, protein mobility within this volume is analysed by two‐photon photoactivation of PA‐GFP fusion proteins at λ = 775 nm. By changing the position of the photoactivation spot with respect to the zone of lesion the influence of chromatin structure and of the distance from damage are investigated. As first applications we demonstrate a locally confined, time‐dependent mobility increase of histone H1.2, and a progressive retardation of the DNA repair factor XRCC1 at damaged sites. This assay can be used to map the response of nuclear proteins to DNA damage in time and space. (© 2013 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)