bluuebunny/crossref_metadata_2025_split huggingface dataset:
A high–low model of daily stock price ranges
Authors: Cheung Yan‐Leung , Cheung Yin‐Wong , Wan Alan T. K. 
Published: September 2008

AbstractWe observe that daily highs and lows of stock prices do not diverge over time and, hence, adopt the cointegration concept and the related vector error correction model (VECM) to model the daily high, the daily low, and the associated daily range data. The in‐sample results attest to the importance of incorporating high–low interactions in modeling the range variable. In evaluating the out‐of‐sample forecast performance using both mean‐squared forecast error and direction of change criteria, it is found that the VECM‐based low and high forecasts offer some advantages over alternative forecasts. The VECM‐based range forecasts, on the other hand, do not always dominate—the forecast rankings depend on the choice of evaluation criterion and the variables being forecast. Copyright © 2008 John Wiley & Sons, Ltd.
NG2 cell response in the CNP‐EGFP mouse after contusive spinal cord injury
Authors: Lytle Judith M. , Chittajallu Ramesh , Wrathall Jean R. , Gallo Vittorio 
Published: September 2008

AbstractNG2+ cells in the adult CNS are a heterogeneous population. The extent to which the subpopulation of NG2+ cells that function as oligodendrocyte progenitor cells (OPCs) respond to spinal cord injury (SCI) and recapitulate their normal developmental progression remains unclear. We used the CNP‐EGFP mouse, in which oligodendrocyte lineage cells express EGFP, to study NG2+ cells in the normal and injured spinal cord. In white matter of uninjured mice, bipolar EGFP+NG2+ cells and multipolar EGFPnegNG2+ cells were identified. After SCI, EGFP+NG2+ cell proliferation in residual white matter peaked at 3 days post injury (DPI) rostral to the epicenter, while EGFPnegNG2+ cell proliferation peaked at 7 DPI at the epicenter. The expression of transcription factors, Olig2, Sox10, and Sox17, and the basic electrophysiological membrane parameters and potassium current phenotype of the EGFP+NG2+ population after injury were consistent with those of proliferative OPCs during development. EGFPnegNG2+ cells did not express transcription factors involved in oligodendrogenesis. EGFP+CC1+ oligodendrocytes at 6 weeks included cells that incorporated BrdU during the peak of EGFP+NG2+ cell proliferation. EGFPnegCC1+ oligodendrocytes were never observed. Treatment with glial growth factor 2 and fibroblast growth factor 2 enhanced oligodendrogenesis and increased the number of EGFPnegNG2+ cells. Therefore, based on EGFP and transcription factor expression, spatiotemporal proliferation patterns, and response to growth factors, two populations of NG2+ cells can be identified that react to SCI. The EGFP+NG2+ cells undergo cellular and physiological changes in response to SCI that are similar to those that occur in early postnatal NG2+ cells during developmental oligodendrogenesis. © 2008 Wiley‐Liss, Inc.
Addition of risperidone to sertraline improves sertraline‐resistant refractory depression without influencing plasma concentrations of sertraline and desmethylsertraline
Authors: Yoshimura Reiji , Umene‐Nakano Wakako , Ueda Nobuhisa , Ikenouchi‐Sugita Atsuko , Hori Hikaru , Nakamura Jun 
Published: September 2008

AbstractIn the present study, we examined the efficacy of risperidone addition on sertraline‐resistant depressed patients and the effects of risperidone on the metabolism of sertraline. Ten patients (M/F: 4/6, age: 54 ± 10 years) met the DSM‐IV criteria for major depressive disorder enrolled the study. Hamilton Dating Scale for Depression (HAM‐D) scores (mean ± SD) in all 10 patients significantly decreased from 19 ± 4 (before risperidone addition) to 11 ± 3 (4 weeks after risperidone addition). Plasma levels of sertraline and desmethylsertraline did not change after risperidone addition. Serum BDNF levels in responders to risperidone addition were changed from 8.1 ± 2.7 ng/ml (before risperidone addition) to 11.5 ± 0.9 ng/ml (4 weeks after risperidone addition); in contrast, those in nonresponders changed from 7.8 ± 2.2 ng/ml (before risperidone addition) to 7.9 ± 2.4 ng/ml (4 weeks after risperidone addition). These results suggest that the addition of risperidone to sertraline is effective and well tolerated for sertraline‐resistant depressive patients, which is accompanied with the increase in serum BDNF levels in responders to the risperidone addition, and the addition of risperidone to sertraline does not seem to influence sertraline metabolism. Copyright © 2008 John Wiley & Sons, Ltd.
Clinical implication of recurrent copy number alterations in hepatocellular carcinoma and putative oncogenes in recurrent gains on 1q
Authors: Kim Tae‐Min , Yim Seon‐Hee , Shin Seung‐Hun , Xu Hai‐Dong , Jung Yu‐Chae , Park Cheol‐Keun , Choi Jong‐Young , Park Won‐Sang , Kwon Mi‐Seon , Fiegler Heike , Carter Nigel P. , Rhyu Mun‐Gan , Chung Yeun‐Jun 
Published: September 2008

AbstractTo elucidate the pathogenesis of hepatocellular carcinoma (HCC) and develop useful prognosis predictors, it is necessary to identify biologically relevant genomic alterations in HCC. In our study, we defined recurrently altered regions (RARs) common to many cases of HCCs, which may contain tumor‐related genes, using whole‐genome array‐CGH and explored their associations with the clinicopathologic features. Gene set enrichment analysis was performed to investigate functional implication of RARs. On an average, 23.1% of the total probes were altered per case. Mean numbers of altered probes are significantly higher in high‐grade, bigger and microvascular invasion (MVI) positive tumors. In total, 32 RARs (14 gains and 18 losses) were defined and 4 most frequent RARs are gains in 1q21.1‐q32.1 (64.5%), 1q32.1‐q44 (59.2%), 8q11.21‐q24.3 (48.7%) and a loss in 17p13.3‐p12 (51.3%). Through focusing on RARs, we identified genes and functional pathways likely to be involved in hepatocarcinogenesis. Among genes in the recurrently gained regions on 1q, expression of KIF14 and TPM3 was significantly increased, suggesting their oncogenic potential in HCC. Some RARs showed the significant associations with the clinical features. Especially, the recurrent loss in 9p24.2‐p21.1 and gain in 8q11.21‐q24.3 are associated with the high tumor grade and MVI, respectively. Functional analysis showed that cytokine receptor binding and defense response to virus pathways are significantly enriched in high grade‐related RARs. Taken together, our results and the strategy of analysis will help to elucidate pathogenesis of HCC and to develop biomarkers for predicting behaviors of HCC. © 2008 Wiley‐Liss, Inc.
TP53 mutation signature supports involvement of aristolochic acid in the aetiology of endemic nephropathy‐associated tumours
Authors: Nedelko Tatiana , Arlt Volker M. , Phillips David H. , Hollstein Monica 
Published: September 2008

AbstractThe proposal has been put forward that the primary cause of Balkan endemic nephropathy (BEN) is exposure to food crops contaminated with seeds of Aristolochia spp, which contain high levels of aristolochic acids (AA). Recently, tumour DNA samples from patients with BEN were found to harbour principally A to T mutations in the TP53 tumour suppressor gene (Grollman et al., Proc Natl Acad Sci USA 2007;104:12129–34). Using a novel mutation assay in which we can induce and select mutations in human TP53 sequences in vitro by exposure of cultured cells to a mutagen, we found that A to T mutations were elicited by aristolochic acid at sites in TP53 rarely mutated in human cancers in general, but which were observed in the BEN patients. This concordance of specific mutations in patient tumours and aristolochic acid I‐exposed cultures supports the argument that AA has a direct role in the aetiology of BEN‐associated cancer. © 2008 Wiley‐Liss, Inc.
Stimulatory effects of CpG oligodeoxynucleotide on dendritic cell‐based immunotherapy of colon cancer in CEA/HLA‐A2 transgenic mice
Authors: Saha Asim , Bhattacharya‐Chatterjee Malaya , Foon Kenneth A. , Celis Esteban , Chatterjee Sunil K. 
Published: September 2008

AbstractImmunostimulatory DNA containing unmethylated cytosine‐guanine (CpG) motifs have been successfully used as adjuvants to enhance the immunity of vaccines designed to trigger antitumor T‐cell responses. We examined the effect of a CpG oligodeoxynucleotide (CpG ODN) for its ability to potentiate the activity of tumor antigen‐pulsed dendritic cells (DC) in a clinically relevant mouse model, which is transgenic for both carcinoembryonic antigen (CEA) and HLA‐A2 for the treatment of colon carcinoma in a therapeutic setting. The systemic administration of CpG ODN 1826 alone had modest effect on tumor growth when tumors were palpable and had no effect with larger tumor burden. However, coadministration of CpG ODN 1826 with the vaccine provided significant increase in tumor‐free survival compared with mice immunized with DC‐based vaccines alone. The DC/CpG combined vaccination strategy resulted in increased secretion of Th1 cytokines and HLA‐A2‐restricted CEA‐specific CTL responses were also enhanced. Both tumor regression and extended tumor‐free survival resulting from DC/CpG combination therapy required the participation of T cells. Tumor‐free mice were resistant to tumor rechallenge and immunity conferred by the vaccine was transferable in athymic nude mice. These results provide evidence that vaccination with antigen‐pulsed DC with CpG ODN as adjuvant can lead to effective tumor regression and long‐term survival in a murine model of colon carcinoma. © 2008 Wiley‐Liss, Inc.
Coeliac disease screening in children: assessment of a novel anti‐gliadin antibody assay
Authors: Leach Steven T. , Aurangzeb Brekhna , Day Andrew S. 
Published: September 2008

AbstractCoeliac disease (CD) screening has progressed rapidly with tissue transglutaminase (TTG), the screening tool of choice. However, TTG may be unreliable in young children and advances in CD etiology understanding have seen improvements in anti‐gliadin (AGA) assay technology. The aim of this study was to investigate the utility of an updated and refined AGA (Neogliadin) assay for CD screening in children with gastrointestinal symptoms. Children attending the Sydney Children's Hospital, Randwick, with gastrointestinal symptoms had sera collected and assayed by Neogliadin and commercial TTG assays in addition to the usual clinical work‐up. One hundred and fifteen children were recruited in which 32 were diagnosed with CD. AGA–IgA screening by Neogliadin showed improved sensitivity (83%) and specificity (91%) but did not eclipse the sensitivity (93%) and specificity (90%) of TTG–IgA screening. In the children diagnosed with CD, 7 were identified as younger than 5 years of age with 4/7 AGA–IgA positive, 5/7 AGA–IgG positive, and 6/7 TTG–IgA positive. The updated Neogliadin IgA assay does not improve on the accuracy achieved by TTG screening. TTG appears to be a suitable screening tool for children younger than 5 years of age although this preliminary finding requires confirmation. J. Clin. Lab. Anal. 22:327–333, 2008. © 2008 Wiley‐Liss, Inc.
Pleural fluid findings as prognostic factors for malignant pleural mesothelioma
Authors: Gonlugur Tanseli Efeoglu , Gonlugur Ugur 
Published: September 2008

AbstractThe aim of this study was to determine the prognostic value of pleural fluid glucose, lactate dehydrogenase (LDH), albumin, total protein, and total leukocyte levels in patients with malignant pleural mesothelioma. We retrospectively analyzed 71 consecutive patients (33 men and 38 women) who were referred to the department of chest diseases in a university hospital. Pleural fluid glucose levels, the ratio of pleural fluid to serum LDH>1.0, and total leukocyte count were significant predictors for the survival in univariate analysis. However, none of these variables emerged as statistically significant from the multivariate Cox model. In conclusion, our results showed that there is an inverse correlation between the intensity of inflammation and survival. J. Clin. Lab. Anal. 22:334–336, 2008. © 2008 Wiley‐Liss, Inc.
Three‐way comparison of methods for the measurement of the erythrocyte sedimentation rate
Authors: Mahlangu Johnny Ndoni , Davids Melony 
Published: September 2008

AbstractAn erythrocyte sedimentation rate (ESR) is a nonspecific sickness index, which is not diagnostic of any particular disease, but which when elevated may indicate the presence of inflammation, infection, rheumatologic disease, or neoplasm. Technological advances continue to evolve to make this old test to conform to requirements of a modern analytical laboratory. In this evaluation, two new semi‐automated ESR measuring systems, the HumaSed and ESR‐Auto Plus® (EAP), were compared with the Westergren method with regard to the accuracy and precision of ESR measurement, sample stability, and interference of various substances with the ESR assay. Samples from 125 patients were analyzed with the three methods and the results compared using linear regression and Bland–Altman plots. The mean ESR values of the HumaSed (32.10±4.86) and EAP (38.09±5.33) were comparable to that of the Westergren (31.54±4.94). The high correlation coefficients of 0.910–0.96 and the Bland–Altman scatter plots revealed good association and agreement between the three methods. Bias between the three methods was small and the imprecision was within acceptable limits. ESR analysis beyond 4 hr was found to be unacceptable owing to sample instability. There was bilirubin and lipid but not heparin interference in the two automated systems. Overall, two automated analyzers were found to be fast, reliable, standardized, simplified, and safe instruments with accuracy and precision for ESR measurement comparable to the Westergren. J. Clin. Lab. Anal. 22:346–352, 2008. © 2008 Wiley‐Liss, Inc.
Do intrinsic factor antibodies assays provide univocal answers in Biermer's disease?
Authors: Corcuff Jean‐Benoît , Morel Stéphanie , Georges Agnès , de Bosredon Karine , Bordenave Laurence 
Published: September 2008

AbstractThe objective of the study is to evaluate the concordance of four assays for antibodies against intrinsic factor (IF‐Ab). Sixty‐two sera were tested with one competitive automated and three manual noncompetitive assays. Thirty‐five percent patients had discordant results with at least one of the four assays. However, any method uncovered patients with proven Biermer's disease missed by the others assays. The observed discordance partly explains the poor sensitivity of IF‐Ab in studies using a single assay. J. Clin. Lab. Anal. 22:337–339, 2008. © 2008 Wiley‐Liss, Inc.
Improved diagnoses of autoimmune hepatitis using an anti‐actin ELISA
Authors: Aubert Vincent , Graf Pisler Isabelle , Spertini François 
Published: September 2008

AbstractThe presence of antismooth muscle antibodies is one of the diagnostic criteria of autoimmune hepatitis. We evaluated a new anti‐F‐actin ELISA test and compared it with indirect immunofluorescence assay (IIFA) for antismooth muscle antibodies (ASMA). Two hundred and nine serum samples (35 autoimmune hepatitis, 174 other hepatopathies and control sera) were tested by IIFA on mouse stomach kidney sections for ASMA and by the Quanta Lite Actin ELISA for anti‐F‐actin antibodies. ASMA were detected in 26 of 35 sera from autoimmune hepatitis (74%) as compared with 25 (71%) with anti‐actin antibodies, as well as in 25 of 49 (51%) samples from viral hepatitis as compared with 7 (14%) with anti‐actin antibodies. With regards to autoimmune hepatitis, though sensitivity (74.3 vs 71.4%) and negative predictive value (93.5 vs 93.9%) of ASMA and anti‐actin ELISA were comparable, anti‐actin ELISA was significantly better than ASMA IIFA in terms of specificity (89.7 vs 74.7%), and positive predictive value (58.1 vs 37.1%). Although frequently positive in HCV samples, a comparable sensitivity but better specificity makes the anti‐actin ELISA a useful tool in combination with ASMA IIFA for the screening and diagnosis of autoimmune hepatitis. J. Clin. Lab. Anal. 22:340–345, 2008. © 2008 Wiley‐Liss, Inc.
9‐Cis‐retinoic acid reduces ischemic brain injury in rodents via bone morphogenetic protein
Authors: Shen Hui , Luo Yu , Kuo Chi‐Chung , Deng Xiaolin , Chang Chen‐Fu , Harvey Brandon K. , Hoffer Barry J. , Wang Yun 
Published: September 2008

AbstractRetinoic acid (RA), a biologically active derivative of vitamin A, has protective effects against damage caused by H2O2 or oxygen‐glucose deprivation in mesangial and PC12 cells. In cultured human osteosarcoma cells, RA enhances the expression of bone morphogenetic protein‐7 (BMP7), a trophic factor that reduces ischemia‐ or neurotoxin‐mediated neurodegeneration in vivo. The purpose of this study is to examine whether RA reduces ischemic brain injury through a BMP7 mechanism. We found that intracerebroventricular administration of 9‐cis‐retinoic acid (9cRA) enhanced BMP7 mRNA expression, detected by RT‐PCR, in rat cerebral cortex at 24 hr after injection. Rats were also subjected to transient focal ischemia induced by ligation of the middle cerebral artery (MCA) at 1 day after 9cRA injection. Pretreatment with 9cRA increased locomotor activity and attenuated neurological deficits 2 days after MCA ligation. 9cRA also reduced cerebral infarction and TUNEL labeling. These protective responses were antagonized by the BMP antagonist noggin given 1 day after 9cRA injection. Taken together, our data suggest that 9cRA has protective effects against ischemia‐induced injury, and these effects involve BMPs. © 2008 Wiley‐Liss, Inc.
Increase in mitochondrial density within axons and supporting cells in response to demyelination in the Plp1 mouse model
Authors: Hogan Vanessa , White Kathryn , Edgar Julia , McGill Alison , Karim Saadia , McLaughlin Mark , Griffiths Ian , Turnbull Doug , Nichols Philip 
Published: September 2008

AbstractWe used the Plp1‐overexpressing transgenic mouse model to investigate whether progressive demyelination of axons results in adaptive changes involving mitochondria within the axons. These models have myelinated axons from birth but gradually lose myelin and develop axonal loss associated with progressive neurological disability analogous to patients with secondary progressive mulltiple sclerosis (SPMS). At 1 and 2 months, electron microscopy demonstrated a significant increase in intraaxonal mitochondrial density in the homozygous line 72 Plp1‐overexpressing mice compared with wild type (1.43 ± 0.31 vs. 0.84 ± 0.16 μm−3, P = 0.031; 1.66 ± 0.11 vs. 0.92 ± 0.43 μm−3, P = 0.02) and a significant increase at 1 and 4 months in the density of mitochondria in the surrounding cells in the same mice (1.86 ± 0.31 vs. 0.81 ± 0.30 μm−3, P = 0.006; 2.77 ± 0.44 vs. 1.37 ± 0.42 μm−3, P = 0.016). At both 1 and 4 months, COX histochemistry and time‐lapse histochemistry demonstrated a significant increase in mitochondrial activity and rate of mitochondrial activity in the homozygous Plp1‐overexpressing mouse optic nerve compared with the wild type (112.37 ± 11.9 vs. 136.89 ± 9.1 MeanD, P = 0.006; 128.02 ± 3.0 vs. 188.77 ± 9.7 MeanD P < 0.001; Rate –0.78 ± 0.25 vs. –0.58 ± 0.15 MeanD min−1, P < 0.001; –1.48 ± 0.15 vs. 0.51 ± 0.17 MeanD min−1, P < 0.001, respectively). We propose that adaptive changes involving mitochondria occur within CNS axons in Plp1‐overexpressing mice, which may be detrimental to long‐term viability. Analogous changes occurring in chronically demyelinated axons in MS lesions would be one mechanism increasing axonal vulnerability in SPMS. © 2008 Wiley‐Liss, Inc.
Proteomic identification of nitrated brain proteins in traumatic brain‐injured rats treated postinjury with gamma‐glutamylcysteine ethyl ester: Insights into the role of elevation of glutathione as a potential therapeutic strategy for traumatic brain injury
Authors: Reed Tanea T. , Owen Joshua , Pierce William M. , Sebastian Andrea , Sullivan Patrick G. , Butterfield D. Allan 
Published: September 2008

AbstractTraumatic brain injury (TBI) occurs suddenly and has damaging effects to the brain that are dependent on the severity of insult. Symptoms can be mild, moderate, or severe. Oxidative damage is associated with traumatic brain injury through reactive oxygen/nitrogen species production. One such species, peroxynitrite, is elevated in TBI brain tissue (Orihara et al. [ 2001] Forensic Sci. Int. 123:142–149; Deng et al. [ 2007] Exp. Neurol. 205:154–165). Peroxynitrite can react with carbon dioxide and decompose to produce NO2 and carbonate radicals, which in turn can lead to 3‐nitrotyrosine, an index of protein nitration. Gamma‐glutamylcysteine ethyl ester (GCEE) is an ethyl ester moiety of gamma‐glutamylcysteine, an agent that up‐regulates glutathione (GSH) production in brain (Drake et al. [ 2002] J. Neurosci. Res. 68:776–784). Many preclinical studies of TBI have employed pretreatment of animals with proposed beneficial agents prior to the injury itself. However, in the real world of TBI, treatment begins postinjury. Hence, insights into agents that improve outcome following injury are desperately needed. This study is one of the first to investigate a potential GSH‐based therapy for TBI postinjury. Protein carbonyls, an index of protein oxidation, were significantly elevated in brain of animals subjected to TBI. However, if, after TBI, GCEE was administered i.p., protein carbonyl levels were significantly reduced. Similarly, 3‐nitrotyrosine levels were elevated in brain following TBI but significantly decreased following TBI if GCEE was administered i.p. Redox proteomics analysis showed that several brain proteins were nitrated after TBI. However, if GCEE was given i.p. following TBI, many of these proteins were protected from nitration. The results are encouraging and are discussed with reference to potential therapeutic strategies for TBI involving elevated GSH. © 2008 Wiley‐Liss, Inc.
Organizational Psychology and poverty reduction: where supply meets demand
Authors: Carr Stuart C. , MacLachlan Malcolm , Reichman Walter , Klobas Jane , Berry Mary O'Neill , Furnham Adrian 
Published: September 2008

AbstractDeveloping a globally responsive Science‐Practitioner‐Humanist model (Lefkowitz, 2008) means articulating professional values (supply) and meeting global demand. The United Nations' Millennium Development Goals (MDGs) seek to halve human poverty by 2015 and how organizations respond to this constitutes a formidable demand on Organizational Psychology. A key process for delivering more effective aid is the Paris Declaration on Aid Effectiveness, which seeks collaborative contributions from a plethora of Organizations, including business organizations and professions like ours. We argue that a thoughtful articulation of what Organizational Psychology uniquely stands for, and can offer, is therefore needed. It is proposed that a key mechanism for addressing this challenge is a Task Force, whose functions will include the coordination of institutions within psychology, and linking them to those in development. We describe such a task force and outline its core mission (Reichman, Frese, Schein, Carr, MacLachlan, & Landy, 2008). Organizational Psychology's response to poverty reduction should meet Lefkowitz's criteria for developing a more humanist model of science and practice as the MDGs are inherently humanist and values‐based. Copyright © 2008 John Wiley & Sons, Ltd.