bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of osteoprotegerin (OPG), TNF related apoptosis inducing ligand (TRAIL), and receptor activator of nuclear factor κB ligand (RANKL) in human breast tumours
Authors: Van Poznak C , Cross S S , Saggese M , Hudis C , Panageas K S , Norton L , Coleman R E , Holen I 
Published: January 2006

Background:Osteoprotegerin (OPG) is involved in the regulation of bone turnover through binding to the receptor activator of nuclear factor κB ligand (RANKL), and has also been reported to be a potential survival factor for several different cell types. The survival effects are mediated through inhibition of the activity of tumour necrosis factor related apoptosis inducing ligand (TRAIL). Both breast and prostate cancer cells produce sufficient amounts of OPG to be protected against the effects of TRAIL in vitro.Aims:To investigate the spatial expression of OPG, RANKL, and TRAIL in non-neoplastic breast tissue and breast cancer, and its relation with oestrogen receptor (ER) expression.Methods:Forty breast cancers (20 ER+, 20 ER−) and five non-neoplastic breast tissue samples were stained with antibodies against OPG, RANKL, and TRAIL.Results:OPG was not expressed in non-neoplastic breast tissue except when colocalised with altered columnar epithelium. RANKL was expressed at the apical surface of luminal epithelial cells and TRAIL was expressed in myoepithelial cells. All three proteins were expressed in some breast cancers but showed no significant association with tumour type. OPG expression showed a significant positive correlation with ER expression (p = 0.011).Conclusions:This is the first published study of the spatial expression of OPG, RANKL, and TRAIL in breast tissue and breast cancer. The localisation of each protein was specific and they were not colocalised. This specificity may provide a useful marker of functional differentiation in breast cancer; for example, TRAIL expression as a marker of myoepithelial differentiation.
Focal interstitial CC chemokine receptor 7 (CCR7) expression in idiopathic interstitial pneumonia
Authors: Choi E S , Pierce E M , Jakubzick C , Carpenter K J , Kunkel S L , Evanoff H , Martinez F J , Flaherty K R , Moore B B , Toews G B , Colby T V , Kazerooni E A , Gross B H , Travis W D , Hogaboam C M 
Published: January 2006

Background/Aims:Idiopathic interstitial pneumonias (IIPs) are a diverse grouping of chronic pulmonary diseases characterised by varying degrees of pulmonary fibrosis. The triggers of the fibroproliferative process in IIP remain enigmatic but recent attention has been directed towards chemokine involvement in this process.Methods:The expression of two chemokine receptors, CCR7 and CXCR4, and their respective ligands, CCL19, CCL21, and CXCL12, were examined in surgical lung biopsies (SLBs) from patients with IIP. Transcript and protein expression of these receptors and their ligands was compared with that detected in histologically normal margin SLBs.Results:CCR7 and CXCR4 were detected by gene array and real time polymerase chain reaction analysis and CCR7, but not CXCR4, expression was significantly raised in usual interstitial pneumonia (UIP) relative to biopsies from patients diagnosed with non-specific interstitial pneumonia (NSIP) or respiratory bronchiolitis/interstitial lung disease (RBILD). CCR7 protein was expressed in interstitial areas of all upper and lower lobe UIP SLBs analysed. CCR7 expression was present in 50% of NSIP SLBs, and CCR7 was restricted to blood vessels and mononuclear cells in 75% of RBILD SLBs. Immune cell specific CXCR4 expression was seen in IIP and normal margin biopsies. CCR7 positive areas in UIP biopsies were concomitantly positive for CD45 (the leucocyte common antigen) but CCR7 positive areas in all IIP SLBs lacked the haemopoietic stem cell antigen CD34, collagen 1, and α smooth muscle actin.Conclusion:This molecular and immunohistochemical analysis showed that IIPs are associated with abnormal CCR7 transcript and protein expression.
Reassessment of a simple chemical method using DCIP for screening for haemoglobin E
Authors: Chapple L , Harris A , Phelan L , Bain B J 
Published: January 2006

Background:Haemoglobin E is a variant haemoglobin that can lead to considerable morbidity in compound heterozygous states with β thalassaemia. Therefore, its detection is important because it permits antenatal counselling. The parts of the world where haemoglobin E is prevalent are resource poor and detection can therefore be problematical. A simple visual test using 2,6-dichlorophenolindophenol (DCIP) has been developed in Thailand, but its use has not become widespread. This test has now become available in kit form.Aims/Methods:To evaluate the new DCIP test kit for the detection of haemoglobin E.Results:Seventeen of 18 samples from individuals with haemoglobin E gave positive results and one gave an equivocal result. False positive or equivocal results were seen in three of 21 individuals with other disorders of globin chain synthesis but were not seen in normal subjects.Conclusions:This study evaluated the sensitivity, specificity, and reproducibility of the kit and confirmed the usefulness of the DCIP test as a screening test for haemoglobin E. In countries with limited health resources, its use would reduce the number of samples requiring referral to a central laboratory for definitive tests.
Postmortem bacteriology: a re-evaluation: Table 1
Authors: Morris J A , Harrison L M , Partridge S M 
Published: January 2006

Aim:To assess the value of postmortem bacteriology in necropsy practice, with specific emphasis on bacterial invasion of blood and cerebrospinal fluid (CSF).Methods:A review of published articles on postmortem bacteriology. Studies were selected to cover the full range of necropsy practice including adults, the perinatal period, and infancy. The review covers over 5000 necropsies, mainly in adults, but including 1108 perinatal cases and 468 cases of sudden unexpected death in infancy. Data are available on 4992 blood cultures, 1168 specimens of CSF, and 743 cultures of spleen.Results:Studies in which careful precautions have been taken to reduce contamination show that approximately two thirds of blood cultures are negative, two in nine yield a single isolate, and one in nine have a mixed growth. The postmortem interval has only a small effect on the isolation rate. A pure growth of a known pathogen has a more than 50% likelihood of being found in association with genuine infection in adults and in the perinatal period.Conclusions:The main postmortem artefact is contamination, but this can be considerably reduced by careful technique. Agonal spread is less common than is often assumed. Postmortem translocation is not a problem if the body is appropriately stored. A pure growth of a pathogen in blood or CSF should be regarded as a possible contributing factor to death at all ages.
Myopericytoma: a unifying term for a spectrum of tumours that show overlapping features with myofibroma. A review of 14 cases
Authors: Dray M S , McCarthy S W , Palmer A A , Bonar S F , Stalley P D , Marjoniemi V , Millar E , Scolyer R A 
Published: January 2006

Background:Myopericytoma (MPC) is a recently proposed term to describe a group of tumours that originate from perivascular myoid cells and show a range of histological growth patterns. Only a small number of series describing MPC have been reported. MPC is frequently misdiagnosed as a sarcoma.Aims:To document the clinical and histopathological findings of a series of MPCs, to describe the range of growth patterns and morphological spectrum, and to compare MPC with myofibroma (MF).Patients/Methods:Fourteen patients with features of MPC and/or MF were identified from the archival files of the department of anatomical pathology, Royal Prince Alfred Hospital, Sydney, Australia.Results:There were six female and eight male patients. The mean and median patient ages were 37 and 35.5 years, respectively. The tumours were located in the skin, subcutis, or superficial soft tissues of the distal extremities (13 patients) or the head and neck region (one patient), and showed a spectrum of morphological appearances. They were divided into two groups based upon the predominant growth pattern corresponding to MPC (seven cases) and MF (seven cases). The feature most suggestive of MPC was the presence of a concentric perivascular arrangement of plump spindle shaped cells. The presence of a zonation/biphasic appearance was most characteristic of MF.Conclusions:MPC exhibits a spectrum of growth patterns that overlap with MF. Tumours can be designated as MPC or MF depending on the predominant growth pattern.
TGF-β1 increases proliferation of airway smooth muscle cells by phosphorylation of map kinases
Authors: Chen Gang , Khalil Nasreen 
Published: January 2006

AbstractBackgroundAirway remodeling in asthma is the result of increased expression of connective tissue proteins, airway smooth muscle cell (ASMC) hyperplasia and hypertrophy. TGF-β1 has been found to increase ASMC proliferation. The activation of mitogen-activated protein kinases (MAPKs), p38, ERK, and JNK, is critical to the signal transduction associated with cell proliferation. In the present study, we determined the role of phosphorylated MAPKs in TGF-β1 induced ASMC proliferation.MethodsConfluent and growth-arrested bovine ASMCs were treated with TGF-β1. Proliferation was measured by [3H]-thymidine incorporation and cell counting. Expressions of phosphorylated p38, ERK1/2, and JNK were determined by Western analysis.ResultsIn a concentration-dependent manner, TGF-β1 increased [3H]-thymidine incorporation and cell number of ASMCs. TGF-β1 also enhanced serum-induced ASMC proliferation. Although ASMCs cultured with TGF-β1 had a significant increase in phosphorylated p38, ERK1/2, and JNK, the maximal phosphorylation of each MAPK had a varied onset after incubation with TGF-β1. TGF-β1 induced DNA synthesis was inhibited by SB 203580 or PD 98059, selective inhibitors of p38 and MAP kinase kinase (MEK), respectively. Antibodies against EGF, FGF-2, IGF-I, and PDGF did not inhibit the TGF-β1 induced DNA synthesis.ConclusionOur data indicate that ASMCs proliferate in response to TGF-β1, which is mediated by phosphorylation of p38 and ERK1/2. These findings suggest that TGF-β1 which is expressed in airways of asthmatics may contribute to irreversible airway remodeling by enhancing ASMC proliferation.
Linkage analysis of alcohol dependence using both affected and discordant sib pairs
Authors: Shih Pei-Ying , Wang Tao , Xing Chao , Sinha Moumita , Song Yeunjoo , Elston Robert C 
Published: January 2006

Abstract
The basic idea of affected-sib-pair (ASP) linkage analysis is to test whether the inheritance pattern of a marker deviates from Mendelian expectation in a sample of ASPs. The test depends on an assumed Mendelian control distribution of the number of marker alleles shared identical by descent (IBD), i.e., 1/4, 1/2, and 1/4 for 2, 1, and 0 allele(s) IBD, respectively. However, Mendelian transmission may not always hold, for example because of inbreeding or meiotic drive at the marker or a nearby locus. A more robust and valid approach is to incorporate discordant-sib-pairs (DSPs) as controls to avoid possible false-positive results. To be robust to deviation from Mendelian transmission, here we analyzed Collaborative Study on the Genetics of Alcoholism data by modifying the ASP LOD score method to contrast the estimated distribution of the number of allele(s) shared IBD by ASPs with that by DSPs, instead of with the expected distribution under the Mendelian assumption. This strategy assesses the difference in IBD sharing between ASPs and the IBD sharing between DSPs. Further, it works better than the conventional LOD score ASP linkage method in these data in the sense of avoiding false-positive linkage evidence.
Linkage analysis of GAW14 simulated data: comparison of multimarker, multipoint, and conditional approaches
Authors: Barber Mathew J , Wheeler Eleanor , Cordell Heather J 
Published: January 2006

Abstract
The purposes of this study were 1) to examine the performance of a new multimarker regression approach for model-free linkage analysis in comparison to a conventional multipoint approach, and 2) to determine the whether a conditioning strategy would improve the performance of the conventional multipoint method when applied to data from two interacting loci. Linkage analysis of the Kofendrerd Personality Disorder phenotype to chromosomes 1 and 3 was performed in three populations for all 100 replicates of the Genetic Analysis Workshop 14 simulated data. Three approaches were used: a conventional multipoint analysis using the Zlr statistic as calculated in the program ALLEGRO; a conditioning approach in which the per-family contribution on one chromosome was weighted according to evidence for linkage on the other chromosome; and a novel multimarker regression approach. The multipoint and multimarker approaches were generally successful in localizing known susceptibility loci on chromosomes 1 and 3, and were found to give broadly similar results. No advantage was found with the per-family conditioning approach. The effect on power and type I error of different choices of weighting scheme (to account for different numbers of affected siblings) in the multimarker approach was examined.
Identifying genomic regions for fine-mapping using genome scan meta-analysis (GSMA) to identify the minimum regions of maximum significance (MRMS) across populations
Authors: Cooper Margaret E , Goldstein Toby H , Maher Brion S , Marazita Mary L 
Published: January 2006

Abstract
In order to detect linkage of the simulated complex disease Kofendrerd Personality Disorder across studies from multiple populations, we performed a genome scan meta-analysis (GSMA). Using the 7-cM microsatellite map, nonparametric multipoint linkage analyses were performed separately on each of the four simulated populations independently to determine p-values. The genome of each population was divided into 20-cM bin regions, and each bin was rank-ordered based on the most significant linkage p-value for that population in that region. The bin ranks were then averaged across all four studies to determine the most significant 20-cM regions over all studies. Statistical significance of the averaged bin ranks was determined from a normal distribution of randomly assigned rank averages. To narrow the region of interest for fine-mapping, the meta-analysis was repeated two additional times, with each of the 20-cM bins offset by 7 cM and 13 cM, respectively, creating regions of overlap with the original method. The 6–7 cM shared regions, where the highest averaged 20-cM bins from each of the three offsets overlap, designated the minimum region of maximum significance (MRMS). Application of the GSMA-MRMS method revealed genome wide significance (p-values refer to the average rank assigned to the bin) at regions including or adjacent to all of the simulated disease loci: chromosome 1 (p < 0.0001 for 160–167 cM, including D1), chromosome 3 (p-value < 0.0000001 for 287–294 cM, including D2), chromosome 5 (p-value < 0.001 for 0–7 cM, including D3), and chromosome 9 (p-value < 0.05 for 7–14 cM, the region adjacent to D4). This GSMA analysis approach demonstrates the power of linkage meta-analysis to detect multiple genes simultaneously for a complex disorder. The MRMS method enhances this powerful tool to focus on more localized regions of linkage.
Calculation of multipoint likelihoods using flanking marker data: a simulation study
Authors: George Andrew W , Mangin LaVonne A , Bartlett Christopher W , Logue Mark W , Segre Alberto M , Vieland Veronica J 
Published: January 2006

Abstract
The calculation of multipoint likelihoods is computationally challenging, with the exact calculation of multipoint probabilities only possible on small pedigrees with many markers or large pedigrees with few markers. This paper explores the utility of calculating multipoint likelihoods using data on markers flanking a hypothesized position of the trait locus. The calculation of such likelihoods is often feasible, even on large pedigrees with missing data and complex structures. Performance characteristics of the flanking marker procedure are assessed through the calculation of multipoint heterogeneity LOD scores on data simulated for Genetic Analysis Workshop 14 (GAW14). Analysis is restricted to data on the Aipotu population on chromosomes 1, 3, and 4, where chromosomes 1 and 3 are known to contain disease loci. The flanking marker procedure performs well, even when missing data and genotyping errors are introduced.
Modeling the effect of an associated single-nucleotide polymorphism in linkage studies
Authors: Houwing-Duistermaat Jeanine J , Uh Hae-Won , Lebrec Jeremie JP , Putter Hein , Hsu Li 
Published: January 2006

Abstract
For linkage analysis in affected sibling pairs, we propose a regression model to incorporate information from a disease-associated single-nucleotide polymorphism located under the linkage peak. This model can be used to study if the associated single-nucleotide polymorphism marker partly explains the original linkage peak. Two sources of information are used for performing this task, namely the genotypes of the parents and the genotypes of the siblings. We applied the methods to three significantly disease-associated single-nucleotide polymorphisms and five microsatellite markers at the end of chromosome 3 of replicate 1 of Aipotu population. Two out of five of the microsatellite markers showed a LOD score higher than 3. The question to be answered was whether one of the single-nucleotide polymorphisms partly explains these high LOD scores. We did not have the answers when we analyzed the data.
A gene-model-free method for linkage analysis of a disease-related-trait based on analysis of proband/sibling pairs
Authors: Sung Heejong , Finch Stephen J , Ye Kenny Q , Mendell Nancy R 
Published: January 2006

Abstract
In this paper we investigate the power of finding linkage to a disease locus through analysis of the disease-related traits. We propose two family-based gene-model-free linkage statistics. Both involve considering the distribution of the number of alleles identical by descent with the proband and comparing siblings with the disease-related trait to those without the disease-related-trait. The objective is to find linkages to disease-related traits that are pleiotropic for both the disease and the disease-related-traits. The power of these statistics is investigated for Kofendrerd Personality Disorder-related traits a (Joining/founding cults) and trait b (Fear/discomfort with strangers) of the simulated data. The answers were known prior to the execution of the reported analyses. We find that both tests have very high power when applied to the samples created by combining the data of the three cities for which we have nuclear family data.
Epidemiological geomatics in evaluation of mine risk education in Afghanistan: introducing population weighted raster maps
Authors: Andersson Neil , Mitchell Steven 
Published: January 2006

Abstract
Evaluation of mine risk education in Afghanistan used population weighted raster maps as an evaluation tool to assess mine education performance, coverage and costs. A stratified last-stage random cluster sample produced representative data on mine risk and exposure to education. Clusters were weighted by the population they represented, rather than the land area. A "friction surface" hooked the population weight into interpolation of cluster-specific indicators. The resulting population weighted raster contours offer a model of the population effects of landmine risks and risk education. Five indicator levels ordered the evidence from simple description of the population-weighted indicators (level 0), through risk analysis (levels 1–3) to modelling programme investment and local variations (level 4). Using graphic overlay techniques, it was possible to metamorphose the map, portraying the prediction of what might happen over time, based on the causality models developed in the epidemiological analysis. Based on a lattice of local site-specific predictions, each cluster being a small universe, the "average" prediction was immediately interpretable without losing the spatial complexity.
Report card on school snack food policies among the United States' largest school districts in 2004–2005: Room for improvement
Authors: Greves H Mollie , Rivara Frederick P 
Published: January 2006

Abstract

Background
Federal nutritional guidelines apply to school foods provided through the national school lunch and breakfast programs, but few federal regulations apply to other foods and drinks sold in schools (labeled "competitive foods"), which are often high in calories, fat and sugar. Competitive food policies among school districts are increasingly viewed as an important modifiable factor in the school nutrition environment, particularly to address rising rates of childhood overweight. Congress passed legislation in 2004 requiring all school districts to develop a Wellness Policy that includes nutrition guidelines for competitive foods starting in 2006–2007. In addition, the Institute of Medicine (IOM) recently published recommendations for schools to address childhood obesity.

Methods
Representatives of school districts with the largest student enrollment in each state and D.C. (N = 51) were interviewed in October-November 2004 about each school district's nutrition policies on "competitive foods." District policies were examined and compared to the Institute of Medicine's recommendations for schools to address childhood obesity. Information about state competitive food policies was accessed via the Internet, and through state and district contacts.

Results
The 51 districts accounted for 5.9 million students, representing 11% of US students. Nineteen of the 51 districts (39%) had competitive food policies beyond state or federal requirements. The majority of these district policies (79%) were adopted since 2002. School district policies varied in scope and requirements. Ten districts (53%) set different standards by grade level. Most district policies had criteria for food and beverage content (74%) and prohibited the sale of soda in all schools (63%); fewer policies restricted portion size of foods (53%) or beverages (47%). Restrictions more often applied to vending machines (95%), cafeteria à la carte (79%), and student stores (79%) than fundraising activities (47%). Most of the policies did not address more comprehensive approaches to the school nutrition environment, such as nutrition education (32%) or advertising to students (26%), nor did they include guidelines on physical education (11%). In addition, few policies addressed monitoring (32%) or consequences for non-compliance (11%). No policy restricted foods sold for after-school fundraising or required monitoring physical health indicators (e.g. BMI).

Conclusion
When compared to the Institute of Medicine's recommendations for schools' role in preventing obesity, none of the nutrition policies among each state's largest school district had addressed all the recommendations by 2004–2005. Nutritionists, nurses, pediatricians, parents, and others concerned about child health have an unprecedented opportunity to help shape and implement more comprehensive school district nutrition policies as part of the Congressional requirement for a "Wellness Policy" by 2006–2007.