bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development and introduction of a pain score documentation chart in the acute oncology setting
Authors: CLARK Katherine , GREAVES Judi , SUNG Emily , GLARE Paul 
Published: June 2007

AbstractBackground:  Recommendations to improve cancer pain management include the introduction of routine and clearly visible documentation of pain scores. Whilst this practise has been adopted in many cancer and palliative care units, longitudinal evidence to support the view that the practise has provided improved analgesic outcomes for patients is limited. The aims of this study were threefold; (i) to collaboratively develop a locally acceptable pain documentation chart; (ii) to test this chart by comparing patient‐reported and nurse‐documented scores with pain scores collected by researchers using validated measures; and (iii) to examine whether or not pain scores and analgesia scores longitudinally improved over the study period.Methods:  Using a multidisciplinary approach, a pain score documentation chart was developed for use on an acute hospital's oncology ward. Prior to the chart's introduction, the brief pain inventory (BPI) was administered to 45 in‐patients. The patients were then asked to report on a regular basis their numeric pain scores, which were documented on the chart. At the time of discharge or after 7 days, the BPI was repeated. The pain chart scores and the BPI item, ‘average pain experienced in the preceding 24 h’ were correlated.Results:  The initial chart scores significantly correlated with the first BPI score (P = 0.001), and a similar relationship was found between scores collected at the end of the study period (P = 0.020). Analgesic scores improved, patients were satisfied with the approach taken to their analgesic management and the pain scores were charted with a similar frequency to vital signs (pulse, temperature, blood pressure).Conclusions:  Pain score charting is feasible and acceptable to patients and nursing staff in an acute hospital. Most importantly, this process has the potential to improve the analgesic outcomes of cancer patients.
Capecitabine and oral cyclophosphamide: A novel oral treatment combination for advanced cancer
Authors: FINDLAY Michael , SHARPLES Katrina , RILEY Greta A , SIMPSON Andrew , ACKLAND Stephen , HALL Katherine , ISAACS Richard , HUMM Gillian , MCKEAGE Mark J 
Published: June 2007

AbstractBackground:  This dose escalation study assessed feasibility of a totally oral chemotherapy regimen using cyclophosphamide and capecitabine. The rationale for this combination was based on the observation that preclinical models of cyclophosphamide up‐regulated tumor thymidine phosphorylase and increased the activation of capecitabine.Methods:  Eligible patients with advanced cancer were treated with oral cyclophosphamide and capecitabine on a 28‐day cycle. If no dose limiting toxicities (DLT) were encountered during the first two treatment cycles, the next patient group was assigned to the next highest dose level until the maximum tolerable dose (MTD) was determined.Results:  Twenty‐seven patients entered treatment. The majority of non‐DLT were grades 1 and 2. DLT experienced in the first 8‐week observation period were grade 3 diarrhea (one patient, level III) and grade 3 emesis (two patients, level V). MTD was observed at level 5, 1331 mg/m2/day capecitabine days 1–28 with 125 mg/m2/day cyclophosphamide days 1–14 of the 28‐day cycle. The recommended phase II dose is therefore 1331 mg/m2/day capecitabine with 100 mg/m2/day cyclophosphamide. The best response evaluation showed four partial responses (breast, colon, ovary and pancreas).Conclusion:  Cyclophosphamide and capecitabine can be combined at their full oral single agent dose with promising tolerability and activity.
Review of case reports of inadvertent intrathecal administration of vincristine: Recommendations to reduce occurrence
Authors: GILBAR Peter J , DOOLEY Michael J 
Published: June 2007

AbstractVincristine has been in clinical use for over 40 years with initial publication of the results from successful trials in 1962. Catastrophic neurotoxicity has been associated with the administration of vincristine directly into the cerebrospinal fluid (CSF). Since the first case in 1968 there have been numerous other instances, of which 23 have been reported in the literature. Of these cases 18 resulted in death. The most prominent damage on autopsy was generally in the spinal cord, brain stem and cerebellum, with severity tending to be greater in the neurons adjacent to the CSF. Fatalities appeared due to a progressive ascending myeloencephalopathy. Early recognition and immediate treatment with CSF drainage and intrathecal exchange appears to be the only intervention that has improved patient survival. The volume of injection, dose and time from the incident until the ventriculo‐lumbar washout appear critical, as these factors might contribute to the extent of drug distribution in the CNS. Although several antidotes for vincristine have been suggested, including folinic acid and glutamic acid, supportive evidence for their effectiveness is scant. Several recommendations regarding prevention of this catastrophic event have been proposed.
Treatment of massively bleeding patients: introducing real‐time monitoring, transfusion packages and thrombelastography (TEG®)
Authors: Johansson P. I. 
Published: June 2007

Background  Continued haemorrhage remains a major cause of mortality in massively transfused patients, many of whom develop coagulopathy. When reviewing transfusion practice for these patients at our hospital, more than 10% received a suboptimal transfusion therapy and survivors had a higher platelet count than non‐survivors. We therefore speculated whether the blood bank could improve its service and hence improve the outcome.Methods  The blood bank introduced monitoring the delivery of blood products and contacted the clinician provided there was an imbalance in the transfusion practice. For massively bleeding patients, transfusion packages, encompassing 5 red blood cells, 5 fresh frozen plasma and 2 platelet concentrates was introduced to improve haemostatic competence. The thrombelastograph (TEG) was implemented, aiding in the diagnosis and treatment of coagulopathy.Results The fraction of suboptimally transfused patients declined from > 10% to < 3%. The transfusion package administered intraoperatively to patients operated for a ruptured abdominal aortic aneurysm resulted in decreased postoperative transfusion requirements and improved 30‐day survival (66% vs. 44%) compared to controls. Only performing TEG in patients with a significant bleeding as judged by the anaesthetist reduces the number of analyses by ~85%, whereas those patients with coagulopathy remain identified. The TEG showed 97% predictability in identifying a surgical cause of bleeding in postoperative patients. Ten percent of the massively bleeding trauma patients had hyperfibrinolysis as the major cause of bleeding, whereas 45% were hypercoagulable.Conclusion  The initiatives from the blood bank has improved the transfusion practice and, hence, survival in massively transfused patients at our hospital.
The Analytical Method in Geomechanics
Authors: Selvadurai A. P. S. 
Published: June 2007

AbstractThis article presents an overview of the application of analytical methods in the theories of elasticity, poroelasticity, flow, and transport in porous media and plasticity to the solution of boundary value problems and initial boundary value problems of interest to geomechanics. The paper demonstrates the role of the analytical method in geomechanics in providing useful results that have practical importance, pedagogic value, and serve as benchmarking tools for calibrating computational methodologies that are ultimately used for solving more complex practical problems in geomechanics. There are 315 references cited in this article.
Acid reflux into the oesophagus does not influence exercise-induced airway narrowing in bronchial asthma
Authors: Ferrari M , Bonella F , Benini L , Ferrari P , De Iorio F , Testi R , Lo Cascio V 
Published: June 2007

Objectives:A few studies on small patient series have investigated the relationship between gastroesophageal reflux and bronchial responsiveness as expressed by exercise-induced bronchoconstriction (EIB), with non-conclusive results. The aim of this study was to evaluate whether the presence of acid in the oesophagus may influence EIB.Methods:45 patients with bronchial asthma underwent spirometry, exercise challenge on bicycle ergometer and 24 h oesophageal pH monitoring. Subjects with EIB (Forced expiratory volume in the first second (FEV1)) percentage decrease after exercise (ΔFEV1) ⩾15%, n  =  28) were retested after a 2 week treatment course with omeprazole 40 mg/daily. Exercise at baseline was performed at the same time as oesophageal pH monitoring.Results:In basal condition, there was no difference in FEV1, acid exposure time or number of refluxes measured during 24 h pH monitoring between patients with and without EIB. There was no relationship between spirometry results and ΔFEV1 on one hand, and parameters of gastroesophageal reflux on the other. Nine patients with EIB (31.0%) and six patients without EIB (37.5%) had one or more episodes of GER during exercise challenge, without significant differences between the two groups. After gastric acid inhibition by omeprazole, ΔFEV1 did not change significantly.Conclusions:The results indicate that acid in the oesophagus, or its short-term inhibition by proton pump inhibitors, has no influence on exercise-induced bronchoconstriction.
Genetic Variation in H2AFX Contributes to Risk of Non–Hodgkin Lymphoma
Authors: Novik Karen L. , Spinelli John J. , MacArthur Amy C. , Shumansky Karey , Sipahimalani Payal , Leach Stephen , Lai Agnes , Connors Joseph M. , Gascoyne Randy D. , Gallagher Richard P. , Brooks-Wilson Angela R. 
Published: June 2007

Abstract
Non–Hodgkin lymphoma (NHL) comprises a group of lymphoid tumors that have in common somatic translocations. H2AFX encodes a key histone involved in the detection of the DNA double-stranded breaks that can lead to translocations. H2afx is a dosage-dependent gene that protects against B-cell lymphomas in mice, making its human orthologue an ideal candidate gene for susceptibility to lymphoma. We did a population-based genetic association study of H2AFX variants in 487 NHL cases and 531 controls. Complete resequencing of the human H2AFX gene in 95 NHL cases was done to establish the spectrum of variation in affected individuals; this was followed by both direct and indirect tests for association at the level of individual single nucleotide polymorphisms (SNP) and as haplotypes. Homozygosity for the AA genotype of a SNP 417 bp upstream of the translational start of H2AFX is strongly associated [odds ratio (OR), 0.54; P = 0.001] with protection from NHL. We find a strong association of this SNP with the follicular lymphoma subtype of NHL (AA genotype: OR, 0.40; P = 0.004) and with mantle cell lymphoma (AA genotype: OR, 0.20; P = 0.01) that remains significant after adjustment for the false discovery rate, but not with diffuse large B-cell lymphoma. These data support the hypothesis that genetic variation in the H2AFX gene influences genetic susceptibility or resistance to some subtypes of NHL by contributing to the maintenance of genome stability. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1098–106)
Associations between Smoking, Polymorphisms in Polycyclic Aromatic Hydrocarbon (PAH) Metabolism and Conjugation Genes and PAH-DNA Adducts in Prostate Tumors Differ by Race
Authors: Nock Nora L. , Tang Deliang , Rundle Andrew , Neslund-Dudas Christine , Savera Adnan T. , Bock Cathryn H. , Monaghan Kristin G. , Koprowski Allison , Mitrache Nicoleta , Yang James J. , Rybicki Benjamin A. 
Published: June 2007

AbstractPolycyclic aromatic hydrocarbon (PAH)-DNA adducts may induce mutations that contribute to carcinogenesis. We evaluated potential associations between smoking and polymorphisms in PAH metabolism [CYP1A1 Ile462Val, CYP1B1 Ala119Ser and Leu432Val, microsomal epoxide hydrolase (mEH) Tyr113His and His139Arg, CYP3A4 A(−392)G] and conjugation [glutathione S-transferase (GST) M1 null deletion, GSTP1 Ile105Val] genes and PAH-DNA adduct levels (measured by immunohistochemistry) in tumor and nontumor prostate cells in 400 prostate cancer cases. Although no statistically significant associations were observed in the total sample, stratification by ethnicity revealed that Caucasian ever smokers compared with nonsmokers had higher adduct levels in tumor cells (mean staining intensity in absorbance units ± SE, 0.1748 ± 0.0052 versus 0.1507 ± 0.0070; P = 0.006), and Caucasians carrying two mEH 139Arg compared with two 139His alleles had lower adducts in tumor (0.1320 ± 0.0129 versus 0.1714 ± 0.0059; P = 0.006) and nontumor (0.1856 ± 0.0184 versus 0.2291 ± 0.0085; P = 0.03) cells. African Americans with two CYP1B1 432Val compared with two 432Ile alleles had lower adducts in tumor cells (0.1600 ± 0.0060 versus 0.1970 ± 0.0153; P = 0.03). After adjusting for smoking status, carrying the putative “high-risk” genotype combination, the faster metabolism of PAH-epoxides to PAH-diol-epoxides (CYP1B1 432Val/Val and mEH 139Arg/Arg) with lower PAH-diol-epoxide conjugation (GSTP1 105Ile/Ile), was associated with increased adducts only in Caucasian nontumor cells (0.2363 ± 0.0132 versus 0.1920 ± 0.0157; P= 0.05). We present evidence, for the first time in human prostate that the association between smoking and PAH-DNA adducts differs by race and is modified by common genetic variants. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1236–45)
Triallelic Single Nucleotide Polymorphisms and Genotyping Error in Genetic Epidemiology Studies:MDR1(ABCB1)G2677/T/Aas an Example
Authors: Hüebner Claudia , Petermann Ivonne , Browning Brian L. , Shelling Andrew N. , Ferguson Lynnette R. 
Published: June 2007

AbstractAccurate measurement of allele frequencies between population groups with differing sensitivities to disease is fundamental to genetic epidemiology. Genotyping errors can markedly influence the biological conclusions of a study. This issue may be especially important now there is increasing recognition of triallelic single nucleotide polymorphisms (SNPs) in the genome and their possible role in diseases like inflammatory bowel disease. For example, the MDR1 (ABCB1) SNP G2677/T/A was, like many other triallelic SNPs, originally described as diallelic. Here, we report a comprehensive analyses of estimated allele frequencies of this SNP in a set of 73 human DNA samples, comparing six commonly used genotyping methods (Applied Biosystems Taqman, Roche LightCycler melting analysis, allelic discrimination PCR, DNA sequencing, Sequenom, and RFLP) from the angle of their error potential. Only Sequenom and DNA sequencing provided accurate measurements, if we had not had prior knowledge of the triallelic nature of this SNP. The other tested methods (with the exception of LightCycler) failed to show any indication of the presence of the rare third A- allele in a diallelic assay. Although most of the errors were due to the inability to detect the third allele, all methods except Sequenom and sequencing produced errors for the detection of the two common alleles G and T (LightCycler, 6 errors; PCR, 4 errors; RFLP, 2 errors; Taqman, 1 error). There is considerable variability in the reported frequencies of the different alleles of the MDR1 G2677/T/A SNP, and the role of this SNP in the etiology of inflammatory bowel disease has been controversial. Our data emphasize the importance of choosing the appropriate method for SNP detection and lead us to suggest that part of the previously reported variation may reflect artifacts associated with the different genotyping methodologies used. The failure to recognize the triallic nature of a SNP may lead to underestimations of real genetic associations. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1185–92)
The Cigarette Controversy
Authors: Cummings K. Michael , Brown Anthony , O'Connor Richard 
Published: June 2007

AbstractThis study examines the history of the cigarette controversy using the tobacco documents as a roadmap to explore the following four questions: (a) What did tobacco companies know about the health risks of smoking and when did they know it? (b) What evidence is there that tobacco companies conspired to deliberately mislead the public about the health risks of smoking? (c) How were scientists involved in the cigarette controversy? (d) Have tobacco companies changed the way they do business since signing the 1998 Master Settlement Agreement? The tobacco companies knew and for most part accepted the evidence that cigarette smoking was a cause of cancer by the late 1950s. The documents also reveal that the tobacco companies helped manufacture the smoking controversy by funding scientific research that was intended to obfuscate and prolong the debate about smoking and health. Today, the tobacco companies acknowledge that smoking is a cause of disease, but they have not materially altered the way they do business. In our opinion, it is not sufficient for the tobacco industry to merely concede the obvious point that smoking is a cause of disease when it is evident that decades of misinformation has resulted in a public that is massively ignorant about the risks of smoking low-tar cigarettes, nicotine addiction, and secondhand smoke exposure. Public education efforts are still needed to correct these misperceptions along with government oversight to ensure that the industry is not permitted to mislead the public further. If the past 50 years have taught us anything, it is that the tobacco industry cannot be trusted to put the public's interest above their profits no matter what they say. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1070–6)
Intermediate Outcomes from Project MYTRI: Mobilizing Youth for Tobacco-Related Initiatives in India
Authors: Stigler Melissa H. , Perry Cheryl L. , Arora Monika , Shrivastav Radhika , Mathur Charu , Reddy K. Srinath 
Published: June 2007

Abstract
The purpose of this article is to present the intermediate results for Project MYTRI, a school-based, multiple component intervention designed to prevent and reduce many forms of tobacco use (chewing tobacco, cigarettes, and bidis) among youth in India. The intervention is based on effective models in the United States “translated” for use in this context. The intervention targets two cohorts of students who were in the 6th and 8th grade when the study started. Thirty-two schools in Delhi (north India) and Chennai (south India) were randomized to receive the intervention (n = 16) or serve as a delayed intervention control (n = 16). Students in these schools were surveyed before the intervention began and at an intermediate point, 1 year into this 2-year intervention (n = 8,369). A test of the changes in risk factors for tobacco use between the baseline and intermediate surveys revealed that, compared with the control, students in the intervention condition (a) had better knowledge about the health effects of tobacco (P &lt; 0.01); (b) believed that there were more negative social consequences to using tobacco (P = 0.04); (c) had fewer reasons to use tobacco (P &lt; 0.01); (d) had more reasons not to use tobacco (P = 0.03); (e) were less socially susceptible to chewing (P = 0.04) and smoking (P = 0.03) tobacco; (f) perceived fewer peers and adults around them smoked (P &lt; 0.01) or chewed (P &lt; 0.01) tobacco; (g) felt that tobacco use was not acceptable, especially among their peers (P &lt; 0.01); (h) were more confident in their ability to advocate for tobacco control (P = 0.03); (i) were more knowledgeable about tobacco control policies (P &lt; 0.01); and (j) supported these policies, too (P = 0.04). Fewer students in the intervention condition reported having intentions to smoke tobacco in the next year (P = 0.02) or chew tobacco when they reached college (P &lt; 0.01). No changes in actual tobacco use were observed at this stage of the study. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1050–6)
Association of COMT Val108/158Met Genotype with Smoking Cessation in a Nicotine Replacement Therapy Randomized Trial
Authors: Johnstone Elaine C. , Elliot Katherine M. , David Sean P. , Murphy Michael F.G. , Walton Robert T. , Munafò Marcus R. 
Published: June 2007

Abstract
We investigated the association of catechol O-methyltransferase (COMT) genotype with abstinence following a smoking cessation attempt among a large cohort of smokers who attempted to quit using either the nicotine transdermal patch or placebo and were followed up over an 8-year period following their initial cessation attempt. In addition, we examined the possible moderating influence of sex on any association. The genotype × treatment interaction effect at 12-week follow-up indicated a greater benefit of active nicotine replacement treatment compared with placebo on likelihood of abstinence in the COMT Met/Met genotype group (33% versus 12%), in comparison to the Met/Val + Val/Val group (22% versus 16%). Our results indicate that COMT genotype may moderate the effect of active transdermal nicotine patch compared with placebo, with reduced relative benefit of nicotine replacement therapy in individuals with Met/Val or Val/Val genotype. Our data follow an emerging pattern of results suggesting that genetic variation in the dopamine pathway may provide a future basis for tailored smoking cessation therapies, but indicate that different genes influencing various components of this pathway may have different effects on response to smoking cessation pharmacotherapy. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1065–9)
Supplemental and Dietary Vitamin E Intakes and Risk of Prostate Cancer in a Large Prospective Study
Authors: Wright Margaret E. , Weinstein Stephanie J. , Lawson Karla A. , Albanes Demetrius , Subar Amy F. , Dixon L. Beth , Mouw Traci , Schatzkin Arthur , Leitzmann Michael F. 
Published: June 2007

Abstract
Supplemental vitamin E (α-tocopherol) has been linked to lower prostate cancer incidence in one randomized trial and several, although not all, observational studies. The evidence regarding dietary intake of individual vitamin E isoforms and prostate cancer is limited and inconclusive, however. We prospectively examined the relations of supplemental vitamin E and dietary intakes of α-, β-, γ-, and δ- tocopherols to prostate cancer risk among 295,344 men, ages 50 to 71 years and cancer-free at enrollment in 1995 to 1996, in the NIH-AARP Diet and Health Study. At baseline, participants completed a questionnaire that captured information on diet, supplement use, and other factors. Proportional hazards models were used to estimate relative risks (RR) and 95% confidence intervals (95% CI) of prostate cancer. During 5 years of follow-up, 10,241 incident prostate cancers were identified. Supplemental vitamin E intake was not related to prostate cancer risk (for &gt;0-99, 100-199, 200-399, 400-799, and ≥800 IU/d versus never use: RR, 0.97, 0.89, 1.03, 0.99, and 0.97 (95% CI, 0.87-1.07) respectively; Ptrend = 0.90). However, dietary γ-tocopherol, the most commonly consumed form of vitamin E in the United States, was significantly inversely related to the risk of advanced prostate cancer (for highest versus lowest quintile: RR, 0.68; 95% CI, 0.56-0.84; Ptrend = 0.001). These results suggest that supplemental vitamin E does not protect against prostate cancer, but that increased consumption of γ-tocopherol from foods is associated with a reduced risk of clinically relevant disease. The potential benefit of γ-tocopherol for prostate cancer prevention deserves further attention. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1128–35)