bluuebunny/crossref_metadata_2025_split huggingface dataset:
Using free text information to explore how and when GPs code a diagnosis of ovarian cancer: an observational study using primary care records of patients with ovarian cancer
Authors: Tate A Rosemary , Martin Alexander G R , Ali Aishath , Cassell Jackie A 
Published: March 2011

BackgroundPrimary care databases provide a unique resource for healthcare research, but most researchers currently use only the Read codes for their studies, ignoring information in the free text, which is much harder to access.ObjectivesTo investigate how much information on ovarian cancer diagnosis is ‘hidden’ in the free text and the time lag between a diagnosis being described in the text or in a hospital letter and the patient being given a Read code for that diagnosis.DesignAnonymised free text records from the General Practice Research Database of 344 women with a Read code indicating ovarian cancer between 1 June 2002 and 31 May 2007 were used to compare the date at which the diagnosis was first coded with the date at which the diagnosis was recorded in the free text. Free text relating to a diagnosis was identified (a) from the date of coded diagnosis and (b) by searching for words relating to the ovary.Results90% of cases had information relating to their ovary in the free text. 45% had text indicating a definite diagnosis of ovarian cancer. 22% had text confirming a diagnosis before the coded date; 10% over 4 weeks previously. Four patients did not have ovarian cancer and 10% had only ambiguous or suspected diagnoses associated with the ovarian cancer code.ConclusionsThere was a vast amount of extra information relating to diagnoses in the free text. Although in most cases text confirmed the coded diagnosis, it also showed that in some cases GPs do not code a definite diagnosis on the date that it is confirmed. For diseases which rely on hospital consultants for diagnosis, free text (particularly letters) is invaluable for accurate dating of diagnosis and referrals and also for identifying misclassified cases.
Uses and misuses of the STROBE statement: bibliographic study
Authors: da Costa Bruno R , Cevallos Myriam , Altman Douglas G , Rutjes Anne W S , Egger Matthias 
Published: March 2011

ObjectivesAppropriate reporting is central to the application of findings from research to clinical practice. The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) recommendations consist of a checklist of 22 items that provide guidance on the reporting of cohort, case–control and cross-sectional studies, in order to facilitate critical appraisal and interpretation of results. STROBE was published in October 2007 in several journals includingThe Lancet,BMJ,Annals of Internal MedicineandPLoS Medicine. Within the framework of the revision of the STROBE recommendations, the authors examined the context and circumstances in which the STROBE statement was used in the past.DesignThe authors searched the Web of Science database in August 2010 for articles which cited STROBE and examined a random sample of 100 articles using a standardised, piloted data extraction form. The use of STROBE in observational studies and systematic reviews (including meta-analyses) was classified as appropriate or inappropriate. The use of STROBE to guide the reporting of observational studies was considered appropriate. Inappropriate uses included the use of STROBE as a tool to assess the methodological quality of studies or as a guideline on how to design and conduct studies.ResultsThe authors identified 640 articles that cited STROBE. In the random sample of 100 articles, about half were observational studies (32%) or systematic reviews (19%). Comments, editorials and letters accounted for 15%, methodological articles for 8%, and recommendations and narrative reviews for 26% of articles. Of the 32 observational studies, 26 (81%) made appropriate use of STROBE, and three uses (10%) were considered inappropriate. Among 19 systematic reviews, 10 (53%) used STROBE inappropriately as a tool to assess study quality.ConclusionsThe STROBE reporting recommendations are frequently used inappropriately in systematic reviews and meta-analyses as an instrument to assess the methodological quality of observational studies.
A possible association between a dysfunctional skin barrier (filaggrin null-mutation status) and diabetes: a cross-sectional study
Authors: Thyssen Jacob P , Linneberg Allan , Carlsen Berit C , Johansen Jeanne D , Engkilde Kåre , Hansen Torben , Pociot Flemming , Pedersen Oluf , Meldgaard Michael , Szecsi Pal B , Stender Steen , Menné Torkil 
Published: March 2011

BackgroundFilaggrin proteins are located in the skin and prevent epidermal water loss and impede the entry of micro-organisms, allergens and chemicals. Filaggrin null mutations are strongly associated with ichthyosis vulgaris and atopic dermatitis.ObjectiveThe authors aimed to investigate the association between filaggrin null mutations, atopic dermatitis and diabetes.DesignA random sample of 3335 adults from the general population in Denmark was filaggrin-genotyped for R501X and 2282del4 null-mutations and questioned about atopic dermatitis and diabetes. Furthermore, two independent study populations of patients with type 1 (n=104) or 2 (n=774) diabetes were genotyped.ResultsIn a crude data analysis, a positive association was detected between the filaggrin null genotype and, respectively, subjects from the general population who reported diabetes (p=0.04) and patients with established type 2 diabetes (p=0.073). Adjustment for age and gender resulted in significant associations for patients with type 2 diabetes (p=0.048) and subjects with self-reported diabetes (p=0.032).ConclusionsAdult Danes with a filaggrin null genotype had a significantly increased prevalence of self-reported diabetes. This finding was replicated when an independent sample of Danish patients with established type 2 diabetes was compared with control subjects from the general population.
Socio-economic differences in long-term psychiatric work disability: prospective cohort study of onset, recovery and recurrence
Authors: Virtanen Marianna , Kawachi Ichiro , Oksanen Tuula , Salo Paula , Tuisku Katinka , Pulkki-Råback Laura , Pentti Jaana , Elovainio Marko , Vahtera Jussi , Kivimäki Mika 
Published: March 2011

ObjectivesTo examine the associations between socio-economic position (SEP) and the onset of psychiatric work disability, return to work and recurrence of disability.MethodsProspective observational cohort study (1997–2005) including register data on 141 917 public-sector employees in Finland. Information on International Classification of Diseases, 10th Revision diagnosis-specific psychiatric work disability (≥90 days) was obtained from national registers.ResultsDuring a mean follow-up of 6.3 years, 3938 (2.8%) participants experienced long-term psychiatric work disability. Of these, 2418 (61%) returned to work, and a further 743 (31%) experienced a recurrent episode. SEP was inversely associated with onset of disability owing to depressive disorders, anxiety disorders, personality disorders, schizophrenia and substance-use disorders. No association was found between SEP and disability owing to bipolar disorders or reaction to severe stress and adjustment disorders. High SEP was associated with a greater likelihood of a return to work following depressive disorders, personality disorders, schizophrenia and substance-use disorders, but not bipolar disorders, anxiety disorders or reaction to severe stress and adjustment disorders. Low SEP predicted recurrent episodes of work disability.ConclusionsHigh SEP is associated with lower onset of work disability owing to mental disorders, as well as return to work and lower rates of recurrence. However, the socio-economic advantage is diagnosis-specific. SEP predicted neither the onset and recovery from disability owing to bipolar disorders and reaction to severe stress and adjustment disorders, nor recovery from disability owing to anxiety disorders. SEP should be taken into account in the attempts to reduce long-term work disability owing to mental disorders.
Trends in mesothelioma mortality rates in South Africa: 1995–2007
Authors: Kielkowski D , Nelson G , Bello B , Kgalamono S , Phillips J I 
Published: March 2011

ObjectiveIn 1984, South Africa had one of the highest mesothelioma rates in the world. The objective of this analysis was to calculate mesothelioma mortality rates in the South African population from 1995 to 2007.MethodsAnnual mortality data and midyear population estimates were used to compute mortality rates by age group and gender for each year. The WHO World Standard Population was used as the reference population to calculate age-adjusted rates. Poisson regression models were used to test for trends.ResultsIn total, 2509 deaths due to mesothelioma were identified in the study period: 1920 in men and 588 in women. There were no significant trends in mesothelioma mortality rates: age-adjusted mortality rates fluctuated from 11 to 16 and from 3 to 5 per million per year for men and women, respectively.ConclusionThese mortality rates are much lower than expected, given the historical production and use of, and high exposure to, asbestos in South Africa. Possible reasons for this are discussed, including the effect of HIV which has been instrumental in reducing the life expectancy of South Africans in the last two decades. Asbestos-exposed individuals may not live long enough to develop mesothelioma. Competing causes of death need to be taken into account when constructing models to predict mesothelioma mortality rates.
The impact of a local smoke-free air law on wagering at an off-track betting facility in Indiana
Authors: Macy Jonathan T , Hernandez Erika L 
Published: March 2011

ObjectiveThis study measured the impact of a local smoke-free air law on wagering at an off-track betting (OTB) facility in Indiana.MethodsRegression analysis was used to compare the trend in per capita amount wagered at an OTB location that went smoke-free to the trend in per capita amount wagered at two comparison OTB locations that continued to permit smoking. Unemployment rate was included as a covariate.ResultsDuring the study period, there was a decreasing trend in the per capita amount wagered at each of the three OTB locations. There was no significant change in the trend for the location that went smoke free or for the locations where smoking has continued.ConclusionsThere is no economic reason to exclude OTB facilities from smoke-free legislation.
An Implicit Iteration Method for Variational Inequalities over the Set of Common Fixed Points for a Finite Family of Nonexpansive Mappings in Hilbert Spaces
Authors: Buong Nguyen , Quynh Anh NguyenThi 
Published: March 2011

AbstractWe introduce a new implicit iteration method for finding a solution for a variational inequality involving Lipschitz continuous and strongly monotone mapping over the set of common fixed points for a finite family of nonexpansive mappings on Hilbert spaces.
Existence Result of Generalized Vector Quasiequilibrium Problems in Locally "Equation missing" -Convex Spaces
Authors: Plubtieng Somyot , Sitthithakerngkiet Kanokwan 
Published: March 2011

AbstractThis paper deals with the generalized strong vector quasiequilibrium problems without convexity in locally "Equation missing"-convex spaces. Using the Kakutani-Fan-Glicksberg fixed point theorem for upper semicontinuous set-valued mapping with nonempty closed acyclic values, the existence theorems for them are established. Moreover, we also discuss the closedness of strong solution set for the generalized strong vector quasiequilibrium problems.
Therapeutic Targeting of PELP1 Prevents Ovarian Cancer Growth and Metastasis
Authors: Chakravarty Dimple , Roy Sudipa Saha , Babu Challa Ram , Dandamudi Rajasekhar , Curiel Tyler J. , Vivas-Mejia Pablo , Lopez-Berestein Gabriel , Sood Anil K. , Vadlamudi Ratna K. 
Published: March 2011

Abstract
Purpose: Ovarian cancer remains a major threat to women's health, partly due to difficulty in early diagnosis and development of metastases. A critical need exists to identify novel targets that curb the progression and metastasis of ovarian cancer. In this study, we examined whether the nuclear receptor coregulator PELP1 (proline-, glutamic acid-, leucine-rich protein-1) contributes to progression and metastatic potential of ovarian cancer cells and determined whether blocking of the PELP1 signaling axis had a therapeutic effect.
Experimental Design: Ovarian cancer cells stably expressing PELP1-shRNA (short hairpin RNA) were established. Fluorescent microscopy, Boyden chamber, invasion assays, wound healing, and zymography assays were performed to examine the role of PELP1 in metastasis. Expression analysis of the model cells was conducted using tumor metastasis microarray to identify PELP1 Target genes. Therapeutic potential of PELP1-siRNA in vivo was determined using a nanoliposomal formulation of PELP1-siRNA-DOPC (1,2-dioleoyl-sn-glycero-3-phosphatidylcholine) administered systemically in a xenograft model.
Results: PELP1 knockdown caused cytoskeletal defects and significantly affected the migratory potential of ovarian cancer cells. Microarray analysis revealed that PELP1 affected the expression of selective genes involved in metastasis including Myc, MTA1, MMP2, and MMP9. Zymography analysis confirmed that PELP1 knockdown caused a decrease in the activation of matrix metalloproteases (MMP) 2 and MMP9. Compared with control siRNA-DOPC–treated mice, animals injected with PELP1-siRNA-DOPC had 54% fewer metastatic tumor nodules, exhibited a 51% reduction in tumor growth and an 84% reduction in ascites volume.
Conclusion: The results suggest that PELP1 signaling axis is a potential druggable target and liposomal PELP1-siRNA-DOPC could be used as a novel drug to prevent or treat ovarian metastasis. Clin Cancer Res; 17(8); 2250–9. ©2011 AACR.
Brain-Derived Neurotrophic Factor Promotes Tumorigenesis via Induction of Neovascularization: Implication in Hepatocellular Carcinoma
Authors: Lam Chi-Tat , Yang Zhen-Fan , Lau Chi-Keung , Tam Ka-Ho , Fan Sheung-Tat , Poon Ronnie T.P. 
Published: March 2011

AbstractPurpose: Brain-derived neurotrophic factor (BDNF) has emerged as a novel angiogenic factor, and yet its impact on tumorigenesis is unclear. This study aimed at investigating the roles of BDNF in angiogenesis and tumor development.Experimental Design: BDNF was overexpressed in a mouse endothelial cell (EC) line by stable transfection, and angiogenic properties of the transfectants were assessed. Microarray analysis was employed to explore the molecular pathways. The impact of modulating BDNF levels in two mouse EC lines on tumorigenic potential of a transformed mouse liver cell line was evaluated by an in vivo cotransplantation model. BDNF and tropomyosin receptor kinase B (TrkB) protein levels were determined in 50 pairs of human hepatocellular carcinoma (HCC) tissues by Western blotting and immunohistochemistry. Survival analysis was carried out to determine their clinical significance.Results: Overexpression of BDNF could promote EC proliferation, migration, invasion, and survival. Microarray and molecular studies showed that RhoA, caspase-9, caspase-3, growth arrest specific 6, and VEGF could mediate BDNF/TrkB-induced angiogenesis. The cotransplantation experiment showed that high BDNF-expressing ECs could facilitate tumor angiogenesis and growth, whereas knockdown of BDNF by short hairpin RNAs impaired such effects. Furthermore, examination on human HCC tissues revealed upregulation of BDNF and TrkB protein levels in 46.0% and 33.3% of the cases studied, respectively. Immunohistochemistry disclosed strong BDNF reactivity in both tumor and endothelial cells. High TrkB expression was associated with shorter overall survival.Conclusions: BDNF/TrkB system was crucial for tumor angiogenesis and growth, which may represent a potential target for antiangiogenic therapy in HCC. Clin Cancer Res; 17(10); 3123–33. ©2011 AACR.
Vorinostat Increases Expression of Functional Norepinephrine Transporter in Neuroblastoma In Vitro and In Vivo Model Systems
Authors: More Swati S. , Itsara Melissa , Yang Xiaodong , Geier Ethan G. , Tadano Michelle K. , Seo Youngho , VanBrocklin Henry F. , Weiss William A. , Mueller Sabine , Haas-Kogan Daphne A. , DuBois Steven G. , Matthay Katherine K. , Giacomini Kathleen M. 
Published: March 2011

Abstract
Purpose: Histone deacetylase (HDAC) inhibition causes transcriptional activation or repression of several genes that in turn can influence the biodistribution of other chemotherapeutic agents. Here, we hypothesize that the combination of vorinostat, a HDAC inhibitor, with 131I-meta-iodobenzylguanidine (MIBG) would lead to preferential accumulation of the latter in neuroblastoma (NB) tumors via increased expression of the human norepinephrine transporter (NET).
Experimental Design: In vitro and in vivo experiments examined the effect of vorinostat on the expression of NET, an uptake transporter for 131I-MIBG. Human NB cell lines (Kelly and SH-SY-5Y) and NB1691-luc mouse xenografts were employed. The upregulated NET protein was characterized for its effect on 123I-MIBG biodistribution.
Results: Preincubation of NB cell lines, Kelly, and SH-SY-5Y, with vorinostat caused dose-dependent increases in NET mRNA and protein levels. Accompanying this was a corresponding dose-dependent increase in MIBG uptake in NB cell lines. Four- and 2.5-fold increases were observed in Kelly and SH-SY-5Y cells, respectively, pretreated with vorinostat in comparison to untreated cells. Similarly, NB xenografts, created by intravenous tail vein injection of NB1691-luc, and harvested from nude mice livers treated with vorinostat (150 mg/kg i.p.) showed substantial increases in NET protein expression. Maximal effect of vorinostat pretreatment in NB xenografts on 123I-MIBG biodistribution was observed in tumors that exhibited enhanced uptake in vorinostat-treated [0.062 ± 0.011 μCi/(mg tissue-dose injected)] vs. -untreated mice [0.022 ± 0.003 μCi/(mg tissue-dose injected); P &lt; 0.05].
Conclusions: The results of our study provide preclinical evidence that vorinostat treatment can enhance NB therapy with 131I-MIBG. Clin Cancer Res; 17(8); 2339–49. ©2011 AACR.
Aspirin and Low-Dose Nitric Oxide–Donating Aspirin Increase Life Span in a Lynch Syndrome Mouse Model
Authors: Mcilhatton Michael A. , Tyler Jessica , Kerepesi Laura A. , Bocker-Edmonston Tina , Kucherlapati Melanie H. , Edelmann Winfried , Kucherlapati Raju , Kopelovich Levy , Fishel Richard 
Published: March 2011

Abstract
Nonsteroidal anti–inflammatory drugs (NSAID) appear to be effective cancer chemopreventives. Previous cellular studies showed that aspirin (acetylsalicylic acid: ASA) and nitric oxide–donating ASA (NO-ASA) suppressed microsatellite instability (MSI) in mismatch repair (MMR)-deficient cells linked to the common cancer predisposition syndrome hereditary nonpolyposis colorectal cancer or Lynch syndrome (LS/HNPCC), at doses 300- to 3,000-fold less than ASA. Using a mouse model that develops MMR-deficient intestinal tumors that appear pathologically identical to LS/HNPCC, we show that ASA (400 mg/kg) and low-dose NO-ASA (72 mg/kg) increased life span by 18% to 21%. We also note a trend where ASA treatment resulted in intestinal tumors with reduced high MSI (H-MSI) and increased low MSI (L-MSI) as defined by the Bethesda Criteria. Low-dose NO-ASA had a minimal effect on MSI status. In contrast to previous studies, high-dose NO-ASA (720/1,500 mg/kg) treatments increased tumor burden, decreased life span, and exacerbated MSI uniquely in the LS/HNPCC mouse model. These results suggest that MMR-deficient tissues/mice may be specifically sensitive to intrinsic pharmacokinetic features of this drug. It is likely that long-term treatment with ASA may represent a chemopreventive option for LS/HNPCC patients. Moreover, as low-dose NO-ASA shows equivalent life span increase at 10-fold lower doses than ASA, it may have the potential to significantly reduce the gastropathy associated with long-term ASA treatment. Cancer Prev Res; 4(5); 684–93. ©2011 AACR.
Effects of anti-factor VIII inhibitor antibodies on factor VIIa/tissue factor-catalysed activation and inactivation of factor VIII
Authors: Yada Koji , Ogiwara Kenichi , Shibata Masaru , Shima Midori , Nogami Keiji 
Published: March 2011

SummaryFactor (F)VIIa/tissue factor (TF) rapidly activates FVIII activity by proteolysis at Arg372 and Arg740, and subsequently inactivates FVIIIa activity by proteolysis at Arg336, although this activation is weaker than that by thrombin. The effects of anti-FVIII inhibitor antibodies on these reactions remain unknown, however. In this study, 13 of anti-FVIII inhibitor antibodies recognising the A2 or C2 domain were prepared. None of them, irrespective of epitope specificity, significantly affected FVIIa/TFcatalysed FVIII activation in one-stage clotting assays. Anti-A2 and anti-C2 type 2 antibodies had little effect on the inactivation phase. Anti-C2 type 1 antibodies, however, modulated inactivation by 40–60% of that seen with control IgG, suggesting that the activity of FVIIIa generated by FVIIa/TF persisted in the presence of this specific type of inhibitor. SDS-PAGE analysis demonstrated that all antibodies had little effect on FVIIa/TF-catalyzed proteolysis at Arg372 and Arg740. Anti-C2 type 1, however, significantly delayed cleavage at Arg336 in dose-dependent manners. Neither anti-A2 nor anti-C2 type 2 affected this reaction, and the findings were consistent with the results of the functional assays. In addition, anti-C2 monoclonal antibodies with type 1 and 2 demonstrated similar patterns of reaction as the anti-C2 polyclonal antibodies in FVIIa/TF-mediated FVIII mechanisms. We demonstrated that FVIIa/TF activated FVIII even in the presence of anti-FVIII antibodies, but inactivation patterns appeared to depend on inhibitor type. It could be important to determine the characteristic of these inhibitor antibodies for prediction of their effects on FVIIa-related FVIII reactions, and the results could have significant therapeutic implications.Note: An account of this work was presented at the 51st annual meeting of the American Society of Hematology, 2009, New Orleans, LA, USA. This work was supported by grants for MEXT KAKENHI 21591370 in Japan and Bayer Hemophilia Award program.
Incidence and Predictors of Myocardial Infarction After Transient Ischemic Attack
Authors: Burns Joseph D. , Rabinstein Alejandro A. , Roger Veronique L. , Stead Latha G. , Christianson Teresa J.H. , Killian Jill M. , Brown Robert D. 
Published: March 2011

Background and Purpose—
Coronary artery disease is the leading cause of death after TIA. Reliable estimates of the risk of MI after TIA, however, are lacking.

Methods—
Our purpose was to determine the incidence of and risk factors for MI after TIA. We cross-referenced preexisting incidence cohorts from the Rochester Epidemiology Project for TIA (1985–1994) and MI (1979–2006) to identify all community residents with incident MI after incident TIA. Incidence of MI after TIA was determined using Kaplan–Meier life-table methods. This was compared to the age-, sex-, and period-specific MI incidences in the general population. Proportional hazards regression analysis was used to examine associations between clinical variables and the occurrence of MI after TIA.

Results—
Average annual incidence of MI after TIA was 0.95%. Relative risk for incident MI in the TIA cohort compared to the general population was 2.09 (95% CI, 1.52–2.81). This was highest in patients younger than 60 years old (relative risk, 15.1; 95% CI, 4.11–38.6). Increasing age (hazard ratio, 1.51 per 10 years; 95% CI, 1.14–2.01), male sex (hazard ratio, 2.19; 95% CI, 1.18–4.06), and the use of lipid-lowering therapy at the time of TIA (hazard ratio, 3.10; 95% CI, 1.20–8.00) were independent risk factors for MI after TIA.

Conclusions—
Average annual incidence of MI after TIA is ≈1%, approximately double that of the general population. The relative risk increase is especially high in patients younger than 60 years old. These data are useful for identifying subgroups of patients with TIA at highest risk for subsequent MI.