bluuebunny/crossref_metadata_2025_split huggingface dataset:
Blood pressure control in haemodialysis patients: An audit
Authors: AL‐HILALI NABIEH , AL‐HUMOUD HANI , NINAN VADAKETHU T , NAMPOORY MANGALATHILLAM RN , JOHNY KAIVILAYIL V 
Published: April 2006

SUMMARY:Objective:  This audit was conducted to study the level of achievement of some criteria relevant to blood pressure control in haemodialysis patients and to evaluate if auditing process improves the quality of medical care given to these patients.Methods:  The records of all 105 patients on maintenance haemodialysis were included in the study. Five criteria relevant to blood pressure control were selected for auditing. The criteria were: predialysis blood pressure control <140/80, dry weight, dialysis adequacy, salt and water intake restriction, and patient education. The auditing process was conducted at two different times 6 months apart.Results:  The first data collected in the auditing process showed that there were only 40 patients (38%) with controlled predialysis blood pressure. In the second data collection the number of patients with controlled predialysis blood pressure had risen significantly to 78 (74.3%), P < 0.0001. The same improvement was achieved for dry weight 39 (37%) to 73 (69.5%) P < 0.0001, dialysis adequacy 38 (36.2%) to 75 (71.4%) P = 0.043, salt and water intake restriction 39 (37%) to 71 (67.6%) P = 0.045, and patient education 30 (28.6%) to 55 (52.4%) P < 0.0001.Conclusion:  Setting up audit cycles to evaluate achievement of required standard in relevant criteria contribute to better blood pressure control and leads to improvement in the care of patients on dialysis. Auditing can be an essential tool in identification of poorly controlled blood pressure, its cause and is useful in control of hypertension in the haemodialysis population.
Levels of RANKL and OPG in gingival crevicular fluid during orthodontic tooth movement and effect of compression force on releases from periodontal ligament cells in vitro
Authors: Nishijima Y , Yamaguchi M , Kojima T , Aihara N , Nakajima R , Kasai K 
Published: April 2006

Structured AbstractAuthors –  Nishijima Y, Yamaguchi M, Kojima T, Aihara N, Nakajima R, Kasai KObjective –  To determine the levels of the receptor activator of NFkB ligand (RANKL) and osteoprotegerin (OPG) in the gingival crevicular fluid (GCF) during orthodontic tooth movement. A second objective was to investigate the effect of compression force on RANKL and OPG production from human periodontal ligament (hPDL) cells.Design –  Ten adolescent patients were included. GCF was collected at the distal cervical margins of the experimental and control teeth 0, 1, 24, and 168 h after the retracting force was applied. Thisin vitro study was performed to examine the secretion of RANKL and OPG from hPDL cells following a compression force (0, 0.5, 1.0, 2.0, or 3.0 g/cm2 for 48 h). Enzyme‐linked immunosorbent assay (ELISA) kits were used to determine RANKL and OPG levels in the GCF and the conditioned medium.Results –  GCF levels of RANKL were significantly higher, and the levels of OPG significantly lower, in the experimental canines than in the control teeth at 24 h, but there were no such significant differences at 0, 1, or 168 h. In vitro study indicated that the compression force significantly increased the secretion of RANKL and decreased that of OPG in hPDL cells in a time‐ and force magnitude‐dependent manner. The compression‐stimulated secretion of RANKL increased approximately 16.7‐fold and that of OPG decreased 2.9‐fold, as compared with the control.Conclusions –  The results obtained suggest that the changes of amount of RANKL and OPG may be involved in bone resorption as a response to compression force.
Correlation of Hsp110 expression with caspase‐3 and ‐9 during apoptosis induced by in vivo embryonic exposition to retinoic acid or irradiation in early mouse craniofacial development
Authors: Gashegu J , Vanmuylder N , Philippson C , Choa‐Duterre M , Rooze M , Louryan S 
Published: April 2006

Structured AbstractAuthors –  Gashegu J, Vanmuylder N, Philippson C, Choa‐Duterre M, Rooze M, Louryan SObjective –  To analyze the expression and role of three proteins (HSP110, caspase‐3 and caspase‐9) during craniofacial development.Design –  Seven pregnant C57Bl/6J mice received, by force‐feeding at gestation day 9 (E9), 80 mg/kg of all‐trans retinoic acid mixed to sesame oil. Seven pregnant NMRI mice received two grays irradiation at the same gestation day. Control mice of both strains (seven mice for each strain) were not submitted to any treatment. Embryos were obtained at various stages after exposition (3, 6, 12 and 24 h), fixed, dehydrated and embedded. Coronal sections (5 μm) were made. Slide staining occurred alternatively using anti‐Hsp110, anti‐caspase‐3 and anti‐caspase‐9 immunohistochemistry.Results –  Expression of HSP110, caspase‐3 and caspase‐9 was found in cells of well‐known locations of programmed cell death. After retinoic acid exposure, expressions were increased especially in neural crest cells of mandibular and hyoid arches. Quantification of positive cells shows that caspase‐9 and Hsp110 were expressed before caspase‐3. After irradiation, the expression of the three proteins quickly increased with a maximum 3 h after irradiation. For all three models of apoptosis (physiological, retinoic‐induced and irradiation‐induced) HSP110 positive cells were more numerous than caspase‐3 positive cells. Caspase‐3 positive cells were more numerous than caspase‐9 positive cells especially in mesectodermal irradiation‐induced apoptotic cells.Conclusion –  The findings show a potential function of HSP110 in apoptosis during embryo development. Caspase‐3‐expressing cells are more numerous than cells expressing caspase‐9, especially irradiation‐induced apoptotic neural crest cells. This suggests that other caspases, still to be identified, may activate caspase‐3 in this model.
Clinically Relevant Chromosomally Encoded Multidrug Resistance Efflux Pumps in Bacteria
Authors: Piddock Laura J. V. 
Published: April 2006

SUMMARYEfflux pump genes and proteins are present in both antibiotic-susceptible and antibiotic-resistant bacteria. Pumps may be specific for one substrate or may transport a range of structurally dissimilar compounds (including antibiotics of multiple classes); such pumps can be associated with multiple drug (antibiotic) resistance (MDR). However, the clinical relevance of efflux-mediated resistance is species, drug, and infection dependent. This review focuses on chromosomally encoded pumps in bacteria that cause infections in humans. Recent structural data provide valuable insights into the mechanisms of drug transport. MDR efflux pumps contribute to antibiotic resistance in bacteria in several ways: (i) inherent resistance to an entire class of agents, (ii) inherent resistance to specific agents, and (iii) resistance conferred by overexpression of an efflux pump. Enhanced efflux can be mediated by mutations in (i) the local repressor gene, (ii) a global regulatory gene, (iii) the promoter region of the transporter gene, or (iv) insertion elements upstream of the transporter gene. Some data suggest that resistance nodulation division systems are important in pathogenicity and/or survival in a particular ecological niche. Inhibitors of various efflux pump systems have been described; typically these are plant alkaloids, but as yet no product has been marketed.
Raised troponin T and echocardiographic abnormalities after prolonged strenuous exercise—the Australian Ironman Triathlon
Authors: Tulloh L , Robinson D , Patel A , Ware A , Prendergast C , Sullivan D , Pressley L 
Published: April 2006

Background:There is concern about whether cardiac damage occurs as a result of prolonged strenuous exercise.Objective:To investigate whether competing in a triathlon is associated with cardiac damage based on a sustained increase in cardiac troponin T (cTnT), and whether such an increase correlates with echocardiographic changesMethods:cTnT and echocardiographic measurements were made in 38 participants in the 2001 Australian ironman triathlon. cTnT was measured the day before, immediately after, and the day following the race. Echocardiography was done the day before, immediately after, and two to six weeks later for measurement of ejection fraction, stroke volume, cardiac output, wall motion analysis, and global left ventricular function (LVF).Results:No subject had detectable cTnT in the pre-race sample. Following the race, 32 subjects (86.5%) had detectable levels of cTnT (>0.01 ng/ml), with six (16.2%) having >0.10 ng/ml. The day after the race, nine subjects (23.7%) still had detectable cTnT, with two recording a level >0.10 ng/ml. Previously described echocardiographic changes of “cardiac fatigue” were observed in the whole cohort. There was a modest but significant correlation between change in ejection fraction and peak cTnT level (p = 0.02,r = 0.39). Athletes with a post-race cTnT >0.10 ng/ml had a greater decrease in global LVF (p = 0.02) and a trend toward a greater fall in ejection fraction and stroke volume than athletes with cTnT levels <0.10 ng/ml. Cardiac output fell in the group with cTnT >0.10 ng/ml (p>0.05).Conclusions:Participation in ironman triathlon often resulted in persistently raised cTnT levels, and the troponin rise was associated with echocardiographic evidence of abnormal left ventricular function. The clinical significance and long term sequelae of such damage remains to be determined.
Circuits and Properties of Signal Transmission in the Retina
Authors: Witkovsky Paul , Stell William K. , Ishida Andrew T. 
Published: April 2006

This essay looks at the historical significance of three APS classic papers that are freely available online: Naka K-I and Nye PW. Role of horizontal cells in organization of the catfish retinal receptive field. J. Neurophysiol 34:785–801, 1971. Marmarelis PZ and Naka K-I. Nonlinear analysis and synthesis of receptive-field responses in the catfish retina. II. One-input white-noise analysis. J. Neurophysiol 36: 619–633, 1973. Naka K-I, Marmarelis PZ, and Chan RY. Morphological and functional identifications of catfish retinal neurons. III. Functional identification. J. Neurophysiol 38: 92–131, 1975.
Changes in Cancer Registry Coding for Lymphoma Subtypes: Reliability Over Time and Relevance for Surveillance and Study
Authors: Clarke Christina A. , Undurraga Dawn M. , Harasty Patricia J. , Glaser Sally L. , Morton Lindsay M. , Holly Elizabeth A. 
Published: April 2006

Abstract
Because lymphoma comprises numerous histologic subtypes, understanding the reasons for ongoing increases in its incidence requires surveillance and etiologic study of these subtypes. However, this research has been hindered by many coexisting classification schemes. The Revised European American classification of Lymphoid Neoplasms (REAL)/WHO system developed in 1994 and now used in clinical settings was not incorporated into the International Classification of Diseases-Oncology (ICD-O), used by cancer registries, until the release of the third edition (ICD-O-3) in 2001. Studies including patients diagnosed before 2001 may have codes from earlier ICD-O versions that must be converted to ICD-O-3 and have higher proportions of unclassified (e.g., lymphoma and not otherwise specified) cases. To better understand (a) the agreement of computer-converted ICD-O-3 codes to ICD-O-3 codes generated directly from diagnostic pathology reports and (b) the reproducibility of unclassified status, we reviewed a population-based series of diagnostic pathology reports for lymphoma patients diagnosed before (1988-1994; n = 1,493) and after (1998-2000; n = 1,527) the REAL/WHO scheme was introduced. Overall, computer- and coder-assigned ICD-O-3 codes agreed for 77% of patients in both groups and improved slightly (82%) when codes were grouped. The most common lymphoma subtypes, diffuse large B cell and follicular, had relatively good reliability (84-89%) throughout the study period. T-cell and natural killer cell lymphomas had worse agreement than B-cell lymphomas, even when grouped. Many (42-43%) lymphomas reported as unclassifiable could be assigned a subtype upon pathology report review. These findings suggest that the study of lymphoma subtypes could be improved by (a) use of more standardized terminology in pathology reports, (b) grouping individual ICD-O-3 codes to reduce misclassification bias, and (c) routine secondary editing of unclassified lymphomas by central cancer registries. (Cancer Epidemiol Biomarkers Prev 2006;15(4):630–8)
Assessment of DNA Damage in WBCs of Workers Occupationally Exposed to Fumes and Aerosols of Bitumen
Authors: Marczynski Boleslaw , Raulf-Heimsoth Monika , Preuss Ralf , Kappler Martin , Schott Klaus , Pesch Beate , Zoubek Gerd , Hahn Jens-Uwe , Mensing Thomas , Angerer Jürgen , Käfferlein Heiko U. , Brüning Thomas 
Published: April 2006

Abstract
We conducted a cross-shift study with 66 bitumen-exposed mastic asphalt workers and 49 construction workers without exposure to bitumen. Exposure was assessed using personal monitoring of airborne bitumen exposure, urinary 1-hydroxypyrene (1-OHP), and the sum of 1-, 2 + 9–,3-,4-hydroxyphenanthrene (OHPH). Genotoxic effects in WBC were determined with nonspecific DNA adduct levels of 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodGuo) and the formation of DNA strand breaks and alkali-labile sites. Concentration of fumes and aerosols of bitumen correlated significantly with the concentrations of 1-OHP and OHPH after shift (rs = 0.27; P = 0.03 and rs = 0.55; P &lt; 0.0001, respectively). Bitumen-exposed workers had more DNA strand breaks than the reference group (P &lt; 0.0001) at both time points and a significant correlation with 1-OHP and OHPH in the postshift urines (rs = 0.32; P = 0.001 and rs = 0.27; P = 0.004, respectively). Paradoxically, we measured higher levels of DNA strand breaks, although not significant, in both study groups before shift. 8-OxodGuo adduct levels did not correlate with DNA strand breaks. Further, 8-oxodGuo levels were associated neither with personal exposure to bitumen nor with urinary metabolite concentrations. Significantly more DNA adducts were observed after shift not only in bitumen-exposed workers but also in the reference group. Only low-exposed workers had significantly elevated 8-oxodGuo adduct levels before as well as after shift (P = 0.0002 and P = 0.02, respectively). Our results show that exposure to fumes and aerosols of bitumen may contribute to an increased DNA damage assessed with strand breaks. (Cancer Epidemiol Biomarkers Prev 2006;15(4):645–51)
Do Testicular Seminoma and Nonseminoma Share the Same Etiology? Evidence from an Age-Period-Cohort Analysis of Incidence Trends in Eight European Countries
Authors: Bray Freddie , Richiardi Lorenzo , Ekbom Anders , Forman David , Pukkala Eero , Cuninkova Martina , Møller Henrik 
Published: April 2006

AbstractThe incidence of the two main clinical subentities of testicular germ cell cancer (seminoma and nonseminoma) is increasing throughout Europe. Most studies have revealed little variation in risk factors between the two subtypes. This study compared generation-specific trends in eight European countries, hypothesizing that similar temporal pattern by birth cohort implied that seminoma and nonseminoma had a largely comparable etiology. The results are presented using the age-period-cohort model and the nonidentifiability problem highlighted by partitioning the age, period, and cohort effects in terms of their linear and curvature component parts, assuming a priori that cohort effects predominated. Despite uniform overall increases by calendar period, declining rates of nonseminoma but not pure seminoma were observed in the majority of countries during the 1990s. The subtype trends were, however, largely analogous on a birth cohort scale. Notable observations were a decline in rates of both subtypes among recent birth cohorts in Switzerland and a short-term wartime effect in several countries, involving an attenuation of increasing risk of both subtypes in men born in 1940 to 1945. Departures from the steady increases in testicular cancer over time were likely to occur for nonseminomas some years ahead of seminoma on a period scale. The importance of birth cohort coincided with the view that given a short time interval of susceptibility to exposures earlier in life and a biologically constant time to diagnosis, all temporal changes in rate-limiting exposures should appear as generational effects. Trends in seminoma and nonseminoma conform to largely the same temporal patterns on this scale, implying that they share important etiologic factors. (Cancer Epidemiol Biomarkers Prev 2006;15(4):652–8)
GSTP1 Genetic Polymorphism Is Associated with a Higher Risk of DNA Damage in Pesticide-Exposed Fruit Growers
Authors: Liu Yi-Jie , Huang Pei-Lin , Chang Yu-Fen , Chen Yen-Hui , Chiou Yu-Hu , Xu Zong-Lin , Wong Ruey-Hong 
Published: April 2006

Abstract
Pesticide exposure is associated with various neoplastic diseases and congenital malformations. Animal studies also indicated that pesticides may be metabolized by cytochrome P450 3A5 (CYP3A5) enzymes, paraoxonases (PON1 and PON2), or glutathione S-transferases (GSTM1, GSTT1, and GSTP1). However, little is known about the genotoxicity of pesticides in people with various genetic polymorphisms of human CYP3A5, PON1, PON2, GSTM1, GSTT1, and GSTP1. Thus, this study was designed to investigate whether various metabolic genotypes are more susceptible to DNA damage in pesticide-exposed fruit growers. Using the Comet assay, the extent of DNA damage was evaluated in the peripheral blood of 91 fruit growers who experienced pesticide exposure and 106 unexposed controls. Questionnaires were administered to obtain demographic data, cigarette smoking habits, medical, and occupational histories. The genotypes for CYP3A5, PON1, PON2, GSTM1, GSTT1, and GSTP1 genes were identified by PCR. The results showed that subjects experiencing high or low pesticide exposure had a significantly greater DNA tail moment (DAN damage) than did controls. The multiple regression model also revealed that age (P &lt; 0.01), high pesticide exposure (P &lt; 0.01), low pesticide-exposure (P &lt; 0.01), and CYP3A5 (P = 0.04) and GSTP1 (P = 0.02) genotypes were significantly associated with an increased DNA tail moment. Further analysis of environmental and genetic interactions revealed a significant interaction for GSTP1 genotypes to influence DNA tail moment for the high pesticide exposure group. These results suggest that individuals with susceptible metabolic GSTP1 genotypes may experience an increased risk of DNA damage elicited by pesticide exposure. (Cancer Epidemiol Biomarkers Prev 2006;15(4):659–66)
OGG1Polymorphisms and Breast Cancer Risk
Authors: Rossner Pavel , Terry Mary Beth , Gammon Marilie D. , Zhang Fang Fang , Teitelbaum Susan L. , Eng Sybil M. , Sagiv Sharon K. , Gaudet Mia M. , Neugut Alfred I. , Santella Regina M. 
Published: April 2006

AbstractThe role of oxidative stress in breast cancer risk is still unclear. OGG1 encodes an 8-oxoguanine DNA glycosylase/AP lyase that catalyzes the removal of 8-oxodeoxyguanosine from DNA. 8-Oxodeoxyguanosine, the most abundant lesion generated by oxidative stress, is highly mutagenic. Environmental sources of oxidative stress, such as alcohol consumption, cigarette smoking, high body mass index (BMI), and low fruits and vegetables intake, may modify the association of genetic polymorphisms with breast cancer risk. We investigated the association between three genetic polymorphisms in OGG1 (Ser326Cys, 7143A/G, and 11657A/G) and breast cancer risk among 1,058 cases and 1,102 controls participating in the Long Island Breast Cancer Study Project. No associations were observed between individual OGG1 polymorphisms, haplotypes, or diplotypes and breast cancer. The association between having at least one variant allele and breast cancer risk was stronger among moderate alcohol drinkers for Ser326Cys [odds ratio (OR), 1.82; 95% confidence interval (95% CI), 1.06-3.10] relative to nondrinkers with the wild-type genotype and among those with higher BMI for 7143A/G (OR, 1.47; 95% CI, 1.10-1.96) and for 11657A/G (OR, 1.41; 95% CI, 1.05-1.88), relative to women with BMI &lt; 25 kg/m2 and the wild-type genotype. However, the patterns were not seen for all three single nucleotide polymorphisms (SNP) nor were there any clear allele dose associations; only one interaction was statistically significant, assuming a multiplicative model (11657A/G, Pinteraction = 0.04). In summary, although we found some differences between the three OGG1 SNPs and breast cancer risk among moderate alcohol drinkers and women with higher BMI, replication of these results is needed to rule out spurious findings. In addition, data on functionality of these polymorphisms are crucial to understand if these modest differences are important. (Cancer Epidemiol Biomarkers Prev 2006;15(4):811–5)
Pancreatic Cancer Genetic Epidemiology Consortium
Authors: Petersen Gloria M. , de Andrade Mariza , Goggins Michael , Hruban Ralph H. , Bondy Melissa , Korczak Jeannette F. , Gallinger Steven , Lynch Henry T. , Syngal Sapna , Rabe Kari G. , Seminara Daniela , Klein Alison P. 
Published: April 2006

AbstractWe have organized the Pancreatic Cancer Genetic Epidemiology (PACGENE) Consortium to identify susceptibility genes in familial pancreatic cancer (FPC). The Consortium comprises seven data collection centers, a statistical genetics core, and a pathology/archival genotyping core. We recruit kindreds containing two or more affected blood relatives ascertained through incident pancreatic adenocarcinoma cases, physician referrals, and/or through Internet recruitment. Accrual to a database containing core clinical, demographic, lifestyle, and family history information from questionnaires is ongoing, along with biospecimen collection. To date, 13,147 patients have been screened for family history, of whom 476 (50% male) probands and 1,912 of their adult (99% unaffected) relatives have been enrolled. Of these, 379 kindreds meet criteria for FPC, having at least two first-degree relatives with pancreatic cancer. Cumulative incidence curves using available age of diagnosis (onset) among and affected relatives were compared with those for incident pancreatic cancer cases reported to 13 U.S. Surveillance Epidemiology and End Results (SEER) sites from 1973 to 2000 (N = 72,700). The mean age ± SD at diagnosis among 466 PACGENE probands and 670 affected relatives was 64.1 ± 11.8 and was 65.4 ± 11.6 for the subset of 369 FPC probands and 429 relatives. Both samples were significantly younger than the mean age at diagnosis in the SEER population (70.0 ± 12.1 years; differences in curves versus SEER, P &lt; 0.001). Age at diagnosis (excluding probands) in FPC kindreds does not decrease with increasing number of affected individuals. In our sample, younger age at diagnosis was observed whether we grouped probands by recruitment sites that predominantly recruited through high-risk referrals, or through screening all pancreatic cancer patients for family history. Linkage studies are ongoing. The PACGENE Consortium will be a valuable family-based resource that will greatly enhance genetic epidemiology research in pancreatic cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(4):704–10)