bluuebunny/crossref_metadata_2025_split huggingface dataset:
Localized superficial femoral vein thrombosis coupled with iatrogenic arteriovenous fistulas presenting as pulmonary emboli
Authors: De Santis F , Zywica M , Mani G , Martini G 
Published: September 2011

Introduction ‘Localized’ femoral vein thrombosis (FVT) is a relatively rare condition usually associated with traumas, external compression or iatrogenic etiologies and the consequence can be pulmonary embolism. Report This is the case of a 46-year-old woman who presented with pulmonary emboli secondary to ‘localized’ superficial FVT, coupled with post-puncture arteriovenous fistulas (AVFs), two days after trans-femoral vein radio-frequency cardiac ablation. After placing a temporary IVC-filter, the AVFs were sutured directly while the residual FVT was treated conservatively. Discussion Close local monitoring and adequate medical and surgical management are mandatory to avoid possible dangerous complications, also in apparently ‘low-risk’ iatrogenic AVFs.
Fibulin-1 Is a Marker for Arterial Extracellular Matrix Alterations in Type 2 Diabetes
Authors: Cangemi Claudia , Skov Vibe , Poulsen Michael Kjaer , Funder Jonas , Twal Waleed O , Gall Mari-Anne , Hjortdal Vibeke , Jespersen Marie Louise , Kruse Torben A , Aagard Jan , Parving Hans-Henrik , Knudsen Steen , Høilund-Carlsen Poul-Flemming , Rossing Peter , Henriksen Jan Erik , Argraves William Scott , Rasmussen Lars Melholt 
Published: September 2011

BACKGROUNDExtracellular matrix alterations are important elements in the arterial changes seen in diabetes, being associated with increased vascular stiffness and the development of cardiovascular diseases. However, no biomarkers for diabetes-related arterial changes have been defined.METHODSMammary artery specimens from 17 men with type 2 diabetes and 18 nondiabetic individuals were used for microarray expression profiling, quantitative real-time PCR, immunoassay, and immunohistochemical analyses. A derived candidate marker, fibulin-1, which is an elastin-associated matrix molecule, was measured immunochemically in plasma from (a) 70 patients scheduled for vascular surgery, (b) 305 patients with type 2 diabetes examined with carotid ultrasonography and echocardiography, and (c) 308 patients with type 2 diabetes, followed for 15 years.RESULTSThe most upregulated transcript in nonatherosclerotic arterial tissue from patients with type 2 diabetes encoded the extracellular matrix protein, fibulin-1. Higher concentrations of fibulin-1-protein were present in artery extracts from patients with diabetes than extracts from individuals without diabetes, and increased fibulin-1 immunostaining was apparent around the external elastic lamina of diabetic arteries. Patients with diabetes displayed increased plasma concentrations of fibulin-1 (P = 0.006). Plasma fibulin-1 concentrations correlated with hemoglobin A1c (P &lt; 0.001), arterial stiffness indices including pulse pressure (P &lt; 0.001), and carotid compliance (P = 0.004), as well as plasma N-terminal pro–B-type natriuretic peptide concentrations (P &lt; 0.001) and were predictive of 15-year mortality (P = 0.013).CONCLUSIONSFibulin-1 accumulates in the arterial wall and in plasma of patients with type 2 diabetes, and appears to be a factor associated with arterial extracellular matrix changes in type 2 diabetes.
The diagnostic accuracy of two human epididymis protein 4 (HE4) testing systems in combination with CA125 in the differential diagnosis of ovarian masses
Authors: Lenhard Miriam , Stieber Petra , Hertlein Linda , Kirschenhofer Angela , Fürst Sophie , Mayr Doris , Nagel Dorothea , Hofmann Karin , Krocker Katja , Burges Alexander 
Published: September 2011

AbstractCancer antigen 125 (CA125) is the best known single tumor marker for ovarian cancer (OC). We investigated whether the additional information of the human epididymis protein 4 (HE4) improves diagnostic accuracy.We retrospectively analyzed preoperative sera of 109 healthy women, 285 patients with benign ovarian masses (cystadenoma: n=78, leimyoma: n=66, endometriosis: n=52, functional ovarian cysts: n=79, other: n=10), 16 low malignant potential (LMP) ovarian tumors and 125 OC (stage I: 22, II: 15, III: 78, IV: 10). CA125 was analyzed using the ARCHITECT system, HE4 using the ARCHITECT(a) system and EIA(e) technology additionally.The lowest concentrations of CA125 and HE4 were observed in healthy individuals, followed by patients with benign adnexal masses and patients with LMP tumors and OC. The area under the curve (AUC) for the differential diagnosis of adnexal masses of CA125 alone was not significantly different to HE4 alone in premenopausal (CA125: 86.7, HE4(a): 82.6, HE4(e): 81.6% p>0.05) but significantly different in postmenopausal [CA125: 93.4 vs. HE4(a): 88.3 p=0.023 and vs. HE4(e): 87.8% p=0.012] patients. For stage I OC, HE4 as a single marker was superior to CA125, which was the best single marker in stage II-IV. The combination of CA125 and HE4 using risk of malignancy algorithm (ROMA) gained the highest sensitivity at 95% specificity for the differential diagnosis of adnexal masses [CA125: 70.9, HE4(a): 67.4, HE4(e): 66.0, ROMA(a): 76.6 and ROMA(e): 74.5%], especially in stage I OC [CA125: 27.3, HE4(a): 40.9, HE4(e): 40.9, ROMA(a): 45.5 and ROMA(e): 45.5%].CA125 is still the best single marker in the diagnosis of OC. HE4 alone and even more the combined analysis of CA125 and HE4 using ROMA improve the diagnostic accuracy of adnexal masses, especially in early OC.
Chemical characterization of polymerized products formed in the reactions of matairesinol and pinoresinol with the stable radical 2,2-diphenyl-1-picrylhydrazyl
Authors: Smeds Annika I. , Eklund Patrik C. , Monogioudi Evanthia , Willför Stefan M. 
Published: September 2011

AbstractPolymerization reactions of the lignans matairesinol and pinoresinol with the stable radical 2,2-diphenyl-1-picrylhydrazyl (DPPH) were studied. The reactions were rapid and almost quantitative. The molecular weight distribution (MWD) of the formed lignan dimers and polymers was determined by high-performance size-exclusion chromatography (HPSEC) combined with evaporative light-scattering detection (ELSD), and the compounds were characterized by HPLC-MS, pyrolysis-GC/MS, NMR, MALDI-ToF-MS, and GC-MS of the monomeric and dimeric units formed by KMnO4oxidation. The yield of high-MW polymers is higher for pinoresinol (69%) than for matairesinol (43%). According to the HPSEC-ELSD analyses, the MWD is also broader for the pinoresinol polymers. The latter seem to consist mainly of hepta-hexacontalignans (MW 2.5–21.4 kDa), whereas the matairesinol polymers are mainly penta-pentadecalignans (MW 1.8–5.3 kDa). The polymers seem to contain mainly unmodified lignan units linked by 5-5′ bonds.
Effect of ammonia addition to alkaline copper quaternary wood preservative solution on the distribution of copper complexes and leaching
Authors: Pankras Sedric , Cooper Paul A. 
Published: September 2011

Abstract
The effects of ammonia (NH3) addition to monoethanolamine (Mea)-based alkaline copper quaternary (ACQ) on the predicted distribution of cupric (Cu2+) species in solution and copper leaching from treated wood were investigated. Addition of ammonia in higher proportions reduced the amount of neutral copper-Mea complex at high pH and increased the amounts of divalent copper-NH3 complexes. At lower pH, the amounts of high-ligand copper-Mea complexes were reduced. These effects should promote better fixation and diminish copper leaching. However, ammonia addition also reduced the monovalent copper-Mea complex and the amount of copper fixed by precipitation at lower pH. This effect could, potentially, reduce fixation and leach resistance. Ammonia addition to the ACQ formulation from a Cu:Mea:NH3 ratio of 1:4:0 (normal Mea formulation, pH=9) to 1:4:2 (pH 10–10.2) and 1:4:4 (pH 10.4–10.5) did not significantly affect the amount of copper leached. However, a further increase in ammonia to 1:4:6 (pH 10.6–10.7) resulted in a significant reduction in copper leaching. At pH 9, an increase in the proportional amount of ammonia increased the amount of copper leached by reducing the amount of monovalent copper-Mea complex and increasing the divalent copper-NH3 complexes. Ammonia addition with a lower amount of Mea, 1:2.5:4 formulation (pH 10.5–10.7), significantly reduced copper leaching as a result of higher amounts of divalent copper-NH3 complexes adsorbed at higher pH (higher cation exchange capacity) without compromising the amount of copper precipitated at lower pH.
Structure of oak wood from the Swedish warship Vasa revealed by X-ray scattering and microtomography
Authors: Svedström Kirsi , Bjurhager Ingela , Kallonen Aki , Peura Marko , Serimaa Ritva 
Published: September 2011

Abstract
The degradation of oak wood of the historical warship Vasa was studied, focusing on cellular structure by X-ray microtomography (μCT) and on the nanostructure of the cell wall by wide- and small-angle X-ray scattering (WAXS, SAXS). Solid samples [polyethylene glycol (PEG)-, impregnated and PEG-extracted] were submitted to X-ray analysis and the results compared to those of recent oak. The cellular structure of the Vasa oak was surprisingly well preserved at the micrometer level, according to the μCT images. As revealed by WAXS, the fraction of crystalline cellulose was lower in the Vasa samples compared with recent oak, but the average length and width of cellulose crystallites (25±2 nm and 3.0±0.1 nm, respectively), and the mean microfibril angles (4–9°), showed no significant differences. Accordingly, the crystalline parts of cellulose microfibrils are well preserved in the Vasa oak. The SAXS results indicated a declined short-range order between the cellulose microfibrils and a higher porosity of the Vasa oak compared with recent oak, which may be explained by modification of the hemicellulose-lignin matrix.
Evidence that release of internal stress contributes to drying strains of wood
Authors: Clair Bruno 
Published: September 2011

AbstractWood shrinks during drying, with the departure of bond water. Along the fibre direction, the magnitude of this shrinkage is mainly governed by the orientation of cellulose microfibrils (MF) in the cell wall. However, tension wood has an unexpectedly high longitudinal shrinkage considering the fact that MFs are oriented nearly parallel to the cell direction. This effect is thought to be caused by the gel collapse of the G-layer; however, some species producing a tension wood without a G-layer also exhibit a higher longitudinal shrinkage than normal wood. The aim of this study is to analyse the contribution of maturation stresses to drying shrinkage. Longitudinal and tangential drying shrinkage of tension wood and normal wood were measured on two sets of matched chestnut wood samples. The first set was directly oven-dried, whereas on the second set, a hygrothermal treatment released the maturation stress before oven-drying. The analysis of the strains during each step of the procedure revealed that part of the drying shrinkage is caused by the release of internal stresses during the desorption process. Finally, a tentative schematic model is proposed, taking into account the cumulative contributions to longitudinal drying shrinkage.
Trisomic and Allelic Differences Influence Phenotypic Variability During Development of Down Syndrome Mice
Authors: Deitz Samantha L , Roper Randall J 
Published: September 2011

AbstractIndividuals with full or partial Trisomy 21 (Ts21) present with clinical features collectively referred to as Down syndrome (DS), although DS phenotypes vary in incidence and severity between individuals. Differing genetic and phenotypic content in individuals with DS as well as mouse models of DS facilitate the understanding of the correlation between specific genes and phenotypes associated with Ts21. The Ts1Rhr mouse model is trisomic for 33 genes (the “Down syndrome critical region” or DSCR) hypothesized to be responsible for many clinical DS features, including craniofacial dysmorphology with a small mandible. Experiments with Ts1Rhr mice showed that the DSCR was not sufficient to cause all DS phenotypes by identifying uncharacteristic craniofacial abnormalities not found in individuals with DS or other DS mouse models. We hypothesized that the origins of the larger, dysmorphic mandible observed in adult Ts1Rhr mice develop from larger embryonic craniofacial precursors. Because of phenotypic variability seen in subsequent studies with Ts1Rhr mice, we also hypothesized that genetic background differences would alter Ts1Rhr developmental phenotypes. Using Ts1Rhr offspring from two genetic backgrounds, we found differences in mandibular precursor volume as well as total embryonic volume and postnatal body size of Ts1Rhr and nontrisomic littermates. Additionally, we observed increased relative expression of Dyrk1a and differential expression of Ets2 on the basis of the genetic background in the Ts1Rhr mandibular precursor. Our results suggest that trisomic gene content and allelic differences in trisomic or nontrisomic genes influence variability in gene expression and developmental phenotypes associated with DS.
Experimental Designs for Robust Detection of Effects in Genome-Wide Case–Control Studies
Authors: Ball Roderick D 
Published: September 2011

Abstract
In genome-wide association studies hundreds of thousands of loci are scanned in thousands of cases and controls, with the goal of identifying genomic loci underpinning disease. This is a challenging statistical problem requiring strong evidence. Only a small proportion of the heritability of common diseases has so far been explained. This “dark matter of the genome” is a subject of much discussion. It is critical to have experimental design criteria that ensure that associations between genomic loci and phenotypes are robustly detected. To ensure associations are robustly detected we require good power (e.g., 0.8) and sufficiently strong evidence [i.e., a high Bayes factor (e.g., 106, meaning the data are 1 million times more likely if the association is real than if there is no association)] to overcome the low prior odds for any given marker in a genome scan to be associated with a causal locus. Power calculations are given for determining the sample sizes necessary to detect effects with the required power and Bayes factor for biallelic markers in linkage disequilibrium with causal loci in additive, dominant, and recessive genetic models. Significantly stronger evidence and larger sample sizes are required than indicated by traditional hypothesis tests and power calculations. Many reported putative effects are not robustly detected and many effects including some large moderately low-frequency effects may remain undetected. These results may explain the dark matter in the genome. The power calculations have been implemented in R and will be available in the R package ldDesign.
Drug-Sensitive DNA Polymerase δ Reveals a Role for Mismatch Repair in Checkpoint Activation in Yeast
Authors: Reha-Krantz Linda J , Siddique Md Shahjahan P , Murphy Kelly , Tam Andrea , O’Carroll Michelle , Lou Sam , Schultz Amy , Boone Charles 
Published: September 2011

Abstract
We have used a novel method to activate the DNA damage S-phase checkpoint response in Saccharomyces cerevisiae to slow lagging-strand DNA replication by exposing cells expressing a drug-sensitive DNA polymerase δ (L612M-DNA pol δ) to the inhibitory drug phosphonoacetic acid (PAA). PAA-treated pol3-L612M cells arrest as large-budded cells with a single nucleus in the bud neck. This arrest requires all of the components of the S-phase DNA damage checkpoint: Mec1, Rad9, the DNA damage clamp Ddc1-Rad17-Mec3, and the Rad24-dependent clamp loader, but does not depend on Mrc1, which acts as the signaling adapter for the replication checkpoint. In addition to the above components, a fully functional mismatch repair system, including Exo1, is required to activate the S-phase damage checkpoint and for cells to survive drug exposure. We propose that mismatch repair activity produces persisting single-stranded DNA gaps in PAA-treated pol3-L612M cells that are required to increase DNA damage above the threshold needed for checkpoint activation. Our studies have important implications for understanding how cells avoid inappropriate checkpoint activation because of normal discontinuities in lagging-strand replication and identify a role for mismatch repair in checkpoint activation that is needed to maintain genome integrity.
Emergent Neutrality in Adaptive Asexual Evolution
Authors: Schiffels Stephan , Szöllősi Gergely J , Mustonen Ville , Lässig Michael 
Published: September 2011

Abstract
In nonrecombining genomes, genetic linkage can be an important evolutionary force. Linkage generates interference interactions, by which simultaneously occurring mutations affect each other’s chance of fixation. Here, we develop a comprehensive model of adaptive evolution in linked genomes, which integrates interference interactions between multiple beneficial and deleterious mutations into a unified framework. By an approximate analytical solution, we predict the fixation rates of these mutations, as well as the probabilities of beneficial and deleterious alleles at fixed genomic sites. We find that interference interactions generate a regime of emergent neutrality: all genomic sites with selection coefficients smaller in magnitude than a characteristic threshold have nearly random fixed alleles, and both beneficial and deleterious mutations at these sites have nearly neutral fixation rates. We show that this dynamic limits not only the speed of adaptation, but also a population’s degree of adaptation in its current environment. We apply the model to different scenarios: stationary adaptation in a time-dependent environment and approach to equilibrium in a fixed environment. In both cases, the analytical predictions are in good agreement with numerical simulations. Our results suggest that interference can severely compromise biological functions in an adapting population, which sets viability limits on adaptive evolution under linkage.
The Maize High-Lysine Mutantopaque7Is Defective in an Acyl-CoA Synthetase-Like Protein
Authors: Miclaus Mihai , Wu Yongrui , Xu Jian-Hong , Dooner Hugo K , Messing Joachim 
Published: September 2011

AbstractMaize (Zea mays) has a large class of seed mutants with opaque or nonvitreous endosperms that could improve the nutritional quality of our food supply. The phenotype of some of them appears to be linked to the improper formation of protein bodies (PBs) where zein storage proteins are deposited. Although a number of genes affecting endosperm vitreousness have been isolated, it has been difficult to clone opaque7 (o7), mainly because of its low penetrance in many genetic backgrounds. The o7-reference (o7-ref) mutant arose spontaneously in a W22 inbred, but is poorly expressed in other lines. We report here the isolation of o7 with a combination of map-based cloning and transposon tagging. We first identified an o7 candidate gene by map-based cloning. The putative o7-ref allele has a 12-bp in-frame deletion of codons 350–353 in a 528-codon-long acyl-CoA synthetase-like gene (ACS). We then confirmed this candidate gene by generating another mutant allele from a transposon-tagging experiment using the Activator/Dissociation (Ac/Ds) system in a W22 background. The second allele, isolated from ∼1 million gametes, presented a 2-kb Ds insertion that resembles the single Ds component of double-Ds, McClintock’s original Dissociation element, at codon 496 of the ACS gene. PBs exhibited striking membrane invaginations in the o7-ref allele and a severe number reduction in the Ds-insertion mutant, respectively. We propose a model in which the ACS enzyme plays a key role in membrane biogenesis, by taking part in protein acylation, and that altered PBs render the seed nonvitreous.
Aberrant Accumulation of Undifferentiated Myeloid Cells in the Adipose Tissue of CCR2-Deficient Mice Delays Improvements in Insulin Sensitivity
Authors: Gutierrez Dario A. , Kennedy Arion , Orr Jeb S. , Anderson Emily K. , Webb Corey D. , Gerrald William K. , Hasty Alyssa H. 
Published: September 2011

OBJECTIVE
Mice with CCR2 deficiency are protected from insulin resistance but only after long periods of high-fat diet (HFD) feeding, despite the virtual absence of circulating inflammatory monocytes. We performed a time course study in mice with hematopoietic and global CCR2 deficiency to determine adipose tissue–specific mechanisms for the delayed impact of CCR2 deficiency on insulin resistance.

RESEARCH DESIGN AND METHODS
Mice with global or hematopoietic CCR2 deficiency (CCR2−/− and BM-CCR2−/−, respectively) and wild-type controls (CCR2+/+ and BM-CCR2+/+, respectively) were placed on an HFD for 6, 12, and 20 weeks. Adipose tissue myeloid populations, degree of inflammation, glucose tolerance, and insulin sensitivity were assessed.

RESULTS
Flow cytometry analysis showed that two different populations of F4/80+ myeloid cells (CD11bloF4/80lo and CD11bhiF4/80hi) accumulated in the adipose tissue of CCR2−/− and BM-CCR2−/− mice after 6 and 12 weeks of HFD feeding, whereas only the CD11bhiF4/80hi population was detected in the CCR2+/+ and BM-CCR2+/+ controls. After 20 weeks of HFD feeding, the CD11bloF4/80lo cells were no longer present in the adipose tissue of CCR2−/− mice, and only then were improvements in adipose tissue inflammation detected. Gene expression and histological analysis of the CD11bloF4/80lo cells indicated that they are a unique undifferentiated monocytic inflammatory population. The CD11bloF4/80lo cells are transiently found in wild-type mice, but CCR2 deficiency leads to the aberrant accumulation of these cells in adipose tissue.

CONCLUSIONS
The discovery of this novel adipose tissue monocytic cell population provides advances toward understanding the pleiotropic role of CCR2 in monocyte/macrophage accumulation and regulation of adipose tissue inflammation.