bluuebunny/crossref_metadata_2025_split huggingface dataset:
Response of Juvenile Rainbow Trout to Turbulence Produced by Prismatoidal Shapes
Authors: Smith David L. , Brannon Ernest L. , Odeh Mufeed 
Published: May 2005

AbstractWater velocity is a common measure of habitat suitability for salmonids. It is often noted that salmonid focal positions occur in low‐velocity areas adjacent to high‐velocity ones. Such locations are associated with increased turbulence. Turbulence in the stream regions typically occupied by salmonids is produced by flow separation around large objects such as rocks or on the riverbed. Turbulence has also been shown to increase the energetic cost of swimming for salmonids. Despite the link between cover and turbulence, no measurements of turbulence at the focal positions of juvenile salmonids have been reported in the literature. We measured turbulence at the focal positions of juvenile rainbow trout Oncorhynchus mykiss in a laboratory flume and found that those focal positions were characterized by low turbulence levels across a range of average velocities. Fish occupied highly turbulent locations if excessive average velocities were present. Eddy size, measured as the autocorrelation function of the velocity time series at a point, did not result in obvious correlations with focal position establishment, but it was correlated with turbulence levels. Turbulence provided some additional discriminatory resolution, allowing differentiation of potential focal positions of equal average velocities but different turbulence levels. Thus, accounting for turbulence levels may allow more accurate prediction of focal positions.
Passive scalar transport in polymer drag‐reduced turbulent channel flow
Authors: Gupta V. K. , Sureshkumar R. , Khomami B. 
Published: May 2005

AbstractPassive scalar transport in turbulent channel flow of viscoelastic dilute polymer solutions exhibiting drag reduction (DR) is studied using direct numerical simulations for DR values up to 74.0%. DR is accompanied by the stabilization of low‐speed streaks in the buffer layer that are primarily responsible for the streamwise heat transport. Moreover, as DR increases, the Reynolds stress and the root mean square fluctuations in the wall‐normal and spanwise velocity components decrease. Thus, as DR is increased, streamwise heat flux increases, whereas both wall‐normal and spanwise heat fluxes decrease. Consequently, for large DR values, the flow acts as a highly efficient heat pump. The turbulent Prandtl number, defined as the ratio of the eddy diffusivities of momentum to heat, increases from its Newtonian limit of unity to a value that exceeds the molecular Prandtl number for DR = 74.0%. This experimentally well documented phenomenon is predicted using first‐principle simulations for the first time in this work. © 2005 American Institute of Chemical Engineers AIChE J, 2005
Schimke‐immuno‐osseous dysplasia: New mutation with weak genotype–phenotype correlation in siblings
Authors: Lücke Thomas , Billing Heiko , Sloan Emily A. , Boerkoel Cornelius F. , Franke Doris , Zimmering Miriam , Ehrich Jochen H.H. , Das Anibh M. 
Published: May 2005

AbstractSchimke‐immuno‐osseous dysplasia (SIOD) is a multisystem disorder with the following consistent clinical features: spondyloepiphyseal dysplasia with disproportional growth deficiency, nephrotic syndrome with focal and segmental glomerulosclerosis, and defective cellular immunity. Transitory ischemic attacks due to vaso‐occlusive processes are complications in some patients with severe SIOD. Recently, mutations of SMARCAL1, which encodes a putative chromatin remodelling protein, have been associated with SIOD. Patients with milder disease were observed to harbor a missense mutation on each allele, whereas patients with a severe form of the disease were predicted to have at least one allele with a nonsense, frameshift or splicing mutation. We report two brothers who are both compound heterozygous for the mutations 836 T > C and 2542 G > T detected in exons 4 and 17, respectively. We demonstrate the lack of genotype–phenotype correlation in these patients as one brother shows some features of the severe form while the other does not. Neither clinical nor molecular findings can fully predict the clinical course of SIOD. © 2005 Wiley‐Liss, Inc.
Sequence of abnormal dendritic spine development in primary somatosensory cortex of a mouse model of the fragile X mental retardation syndrome
Authors: Galvez Roberto , Greenough William T. 
Published: May 2005

AbstractAnatomical analyses of occipital and temporal cortex of patients with fragile X mental retardation syndrome (FXS) and in a mouse model of the syndrome (FraX mice) compared to controls have suggested that the fragile X mental retardation protein (FMRP) is important for normal spine structural maturation and pruning. However, a recent analysis of spine properties in somatosensory cortex of young FraX mice has suggested that this region may not exhibit spine abnormalities. While spine abnormalities were present 1 week after birth in somatosensory cortex, by 4 weeks almost all spine abnormalities had disappeared, suggesting that adult spine abnormalities observed in other cortical regions may not persist post‐developmentally in somatosensory cortex. To resolve this discrepancy we examined spine properties in somatosensory cortex of young (day 25) and adult (day 73–76) FraX compared to wild‐type (WT) mice. Spine properties in young FraX and WT mice did not consistently differ from each other, consistent with the recent analysis of developing somatosensory cortex. However, adult FraX mice exhibited increased spine density, longer spines, more spines with an immature‐appearing structure, fewer shorter spines, and fewer spines with a mature structure, a pattern consistent with prior analyses from other adult cortical brain regions in humans and mice. These findings (1) support the previous report of the absence of major spine abnormalities in the fourth postnatal week, (2) demonstrate normal spine development in WT mice, (3) demonstrate abnormal spine development after the fourth postnatal week in FraX mice, and (4) demonstrate spine abnormalities in somatosensory cortex of adult FraX compared to adult WT mice. In doing so, these findings resolve a potential conflict in the literature and more thoroughly describe the role of FMRP in spine development. © 2005 Wiley‐Liss, Inc.
Salivary gland epithelial cell exosomes: A source of autoantigenic ribonucleoproteins
Authors: Kapsogeorgou Efstathia K. , Abu‐Helu Rasmi F. , Moutsopoulos Haralampos M. , Manoussakis Menelaos N. 
Published: May 2005

AbstractObjectiveExosomes are membrane vesicles of endosomal origin that are distinct from apoptotic bodies and are thought to represent an acellular mechanism for antigen transfer to classic antigen‐presenting cells, as well as for direct antigen presentation with the capacity to induce immune response or tolerance. Nevertheless, it is not known whether exosomes are involved in the induction or regulation of immune responses against intracellular autoantigens that characterize autoimmune diseases. Exosomes have been shown to be secreted by several types of cells, whereas studies of non‐neoplastic epithelial cells are lacking. This study was undertaken to investigate the capacity of non‐neoplastic salivary gland epithelial cells (SGECs) to release exosomes, and to determine whether epithelial exosomes contain RNPs, which are major autoantigens in systemic rheumatic diseases.MethodsExosomes were isolated by ultracentrifugation from culture supernatants of 26 non‐neoplastic SGEC lines established from patients with various rheumatic disorders. They were analyzed by electron microscopy, immunoblotting, or immunoprecipitation.ResultsAll SGEC lines were found to release comparable and significant amounts of exosomes. Similar to other cell systems, exosome secretion was constitutive and was unrelated to activation or apoptotic processes. SGEC‐derived exosomes were found to contain the autoantigenic Ro/SSA, La/SSB, and Sm RNPs, as well as epithelial‐specific cytokeratins.ConclusionSGECs constitutively secrete exosomes that contain the major autoantigens Ro/SSA, La/SSB, and Sm. This mechanism may represent a pathway whereby intracellular autoantigens are presented to the immune system with an immunogenic or tolerogenic outcome.
Involvement of p38 MAPK in the up‐regulation of tissue factor on endothelial cells by antiphospholipid antibodies
Authors: Vega‐Ostertag Mariano , Casper Katherine , Swerlick Robert , Ferrara Dardo , Harris E. Nigel , Pierangeli Silvia S. 
Published: May 2005

AbstractObjectiveTo study the intracellular mechanism involved in the up‐regulation of tissue factor (TF) on endothelial cells (ECs) by antiphospholipid antibodies (aPL), we examined the effects of aPL on the transcription, expression, and function of TF, the expression of interleukin‐6 (IL‐6) and IL‐8, the induction of inducible nitric oxide synthase (iNOS), and the phosphorylation of p38 MAPK on human umbilical vein ECs (HUVECs).MethodsCultured HUVECs were treated with IgG aPL (from patients with antiphospholipid syndrome [APS]) or with control IgG (from normal human serum). Phorbol myristate acetate (PMA) and bacterial lipopolysaccharide (LPS) were used as positive controls. TF expression was determined on the surface of HUVECs using an enzyme‐linked immunosorbent assay (ELISA). TF activity was determined with the use of a chromogenic assay in cell lysates, and TF messenger RNA (mRNA) was determined by real‐time quantitative polymerase chain reaction. Phosphorylation of p38 MAPK and induction of iNOS were determined by Western blotting, and levels of IL‐6 and IL‐8 were determined by ELISA.ResultsPMA, LPS, and aPL significantly increased the expression of TF compared with controls. This up‐regulation was significantly inhibited by SB203580 (a specific inhibitor of p38 MAPK) and by MG132 (a specific inhibitor of NF‐κB). TF activity was significantly increased by treatment with IgG aPL and this effect was also inhibited by SB203580. Incubation of HUVECs with aPL increased TF mRNA 2–15‐fold; these effects were abrogated by SB203580. IgG aPL induced significant phosphorylation of p38 MAPK and produced iNOS on HUVECs in a time‐dependent manner. Treatment with IgG aPL also induced increased expression of IL‐6 and IL‐8 on HUVECs.ConclusionOur data show that aPL induces significant increases in TF transcription, function, and expression, in IL‐6 and IL‐8 up‐regulation, and in iNOS expression on HUVECs and that these processes involve phosphorylation of p38 MAPK and activation of NF‐κB. Understanding intracellular events in aPL‐mediated EC activation may help in designing new targeted therapies for thrombosis in APS.
Knee height, knee pain, and knee osteoarthritis: The Beijing Osteoarthritis Study
Authors: Hunter David J. , Niu Jingbo , Zhang Yuqing , Nevitt Michael C. , Xu Ling , Lui Li‐Yung , Yu Wei , Aliabadi Piran , Buchanan Thomas S. , Felson David T. 
Published: May 2005

AbstractObjectiveFew risk factors for knee osteoarthritis (OA) are appreciated, and the discordance between symptoms and the severity of structural disease has not been explained. Knee height contributes to moments around the knee. The longer the leg, the more torque is present. Although this would suggest that having long legs would be related to the occurrence of knee OA and pain, this issue has not been studied. Our aim was to explore the association between knee height, knee pain, and knee OA.MethodsWe recruited a random sample of Beijing residents ages 60 years and older. Subjects answered questions about joint symptoms, and radiographs of their knees were obtained. A knee joint with a Kellgren/Lawrence grade of ≥2 was defined as having radiographic OA. Patellofemoral OA was defined as being present when grade ≥1 osteophytes or grade ≥1 joint space narrowing was observed on skyline views of the patella or anterior femur. Subjects were considered to have symptomatic OA when both radiographic OA and self‐reported pain were present in the same joint. Knee height was measured on the right leg using a sliding broad‐blade caliper; the subject was seated, and the subject's feet were bare. We used logistic regression analyses to assess whether knee height was associated with prevalent radiographic and symptomatic OA. We then assessed whether knee height was associated with knee symptoms independently of structural change.ResultsA total of 1,006 men (mean ± SD age 68.4 ± 6.4 years) and 1,500 women (mean ± SD age 67.5 ± 6.1 years) participated in this study. Higher knee height was associated with an increasing prevalence of both radiographic and symptomatic OA, especially among women. For radiographic OA, the magnitude of association was similar for the patellofemoral and tibiofemoral compartments. Among women with knee pain, higher knee height was associated with more severe knee pain (P = 0.0004 for the highest quartile versus the lowest quartile of knee height) independently of the severity of radiographic OA.ConclusionKnee height is associated with prevalent radiographic and symptomatic knee OA. It may also play an important role in knee symptoms. This study highlights the importance of mechanical forces in the determination of OA and knee symptoms.
Autoantibodies to a 140‐kd polypeptide, CADM‐140, in Japanese patients with clinically amyopathic dermatomyositis
Authors: Sato Shinji , Hirakata Michito , Kuwana Masataka , Suwa Akira , Inada Shinichi , Mimori Tsuneyo , Nishikawa Takeji , Oddis Chester V. , Ikeda Yasuo 
Published: May 2005

AbstractObjectiveTo identify novel autoantibodies specific for dermatomyositis (DM), especially those specific for clinically amyopathic DM (C‐ADM).MethodsAutoantibodies were analyzed by immunoprecipitation in 298 serum samples from patients with various connective tissue diseases (CTDs) or idiopathic pulmonary fibrosis (IPF). Antigen specificity of the sera was further examined by immunoblotting and indirect immunofluorescence (IF). The disease specificity and clinical features associated with the antibody of interest were determined.ResultsEight sera recognized a polypeptide of ∼140 kd (CADM‐140 autoantigen) by immunoprecipitation and immunoblotting. Immunoreactivity was detected in the cytoplasm, and indirect IF revealed a granular or reticular pattern. Anti–CADM‐140 antibodies were detected in 8 of 42 patients with DM, but not in patients with other CTDs or IPF. Interestingly, all 8 patients with anti–CADM‐140 antibodies had C‐ADM. Among 42 patients with DM, those with anti–CADM‐140 autoantibodies had significantly more rapidly progressive interstitial lung disease (ILD) when compared with patients without anti–CADM‐140 autoantibodies (50% versus 6%; P = 0.008).ConclusionThese results indicate that the presence of anti–CADM‐140 autoantibodies may be a novel marker for C‐ADM. Further attention should be directed to the detection of rapidly progressive ILD in those patients with anti–CADM‐140 autoantibodies.
Systemic lupus erythematosus in three ethnic groups: XVI. Association of hydroxychloroquine use with reduced risk of damage accrual
Authors: Fessler Barri J. , Alarcón Graciela S. , McGwin Gerald , Roseman Jeffrey , Bastian Holly M. , Friedman Alan W. , Baethge Bruce A. , Vilá Luis , Reveille John D. ,   for the LUMINA Study Group
Published: May 2005

AbstractObjectiveTo examine whether hydroxychloroquine (HCQ) usage is associated with a reduced risk of damage accrual in patients with systemic lupus erythematosus (SLE).MethodsPatients (n = 518) meeting the American College of Rheumatology criteria for diagnosis of SLE and with ≤5 years disease duration at study entry were followed up annually. Socioeconomic, demographic, clinical, and serologic manifestations as well as disease activity (by the Systemic Lupus Activity Measure [SLAM]) and damage (by the Systemic Lupus International Collaborating Clinics damage index [SDI]) were measured. Propensity scores were calculated to adjust for confounding factors affecting treatment assignment. A Cox proportional hazards model was used to compare the risk of developing new damage according to HCQ use at enrollment into the study.ResultsFifty‐six percent of the patients were treated with HCQ at the time of study enrollment. Patients who were not treated with HCQ on enrollment had higher SLAM and SDI scores than patients who were treated. Untreated patients were significantly more likely to have major organ involvement such as renal disease (P < 0.0001) or central nervous system disease (P < 0.0025). Results of unadjusted analysis suggested that treated patients were less likely to accrue damage (hazard ratio [HR] 0.68). With adjustment for differences in treatment assignment, HCQ usage was still associated with a reduced risk of developing new damage, with an HR of 0.68 (95% confidence interval [95% CI] 0.53–0.93) (P = 0.014). With adjustment for differences in treatment assignment, HCQ usage was still associated with a reduced risk of developing new damage (HR 0.73 [95% CI 0.52–1.00]) (P = 0.05). However, patients receiving HCQ who had no damage at study entry had a statistically significant decrease in the risk of damage accrual (HR 0.55 [95% CI 0.34–0.87]) (P = 0.0111), whereas those receiving HCQ who had damage at study entry did not (HR 1.106 [95% CI 0.70–1.74]) (P = 0.6630).ConclusionThese findings indicate that, after adjustment for propensity to receive HCQ, HCQ usage is independently associated with a reduced risk of damage accrual in SLE patients who had not yet accrued damage at the time of treatment initiation.
Teratogen update: Lead and pregnancy
Authors: Bellinger David C. 
Published: May 2005

AbstractThis review focuses on the impacts of lead exposure on reproductive health and outcomes. High levels of paternal lead exposure (>40 μg/dl or >25 μg/dl for a period of years) appear to reduce fertility and to increase the risks of spontaneous abortion and reduced fetal growth (preterm delivery, low birth weight). Maternal blood lead levels of approximately 10 μg/dl have been linked to increased risks of pregnancy hypertension, spontaneous abortion, and reduced offspring neurobehavioral development. Somewhat higher maternal lead levels have been linked to reduced fetal growth. Some studies suggest a link between increased parental lead exposure and congenital malformations, although considerable uncertainty remains regarding the specific malformations and the dose‐response relationships. Common methodological weaknesses of studies include potential exposure misclassifications due to the frequent unavailability of exposure biomarker measurements at biologically appropriate times and uncertainty regarding the best exposure biomarker(s) for the various outcomes. A special concern with regard to the pregnant woman is the possibility that a fetus might be exposed to lead mobilized from bone stores as a result of pregnancy‐related metabolic changes, making fetal lead exposure the result of exposure to exogenous lead during pregnancy and exposure to endogenous lead accumulated by the woman prior to pregnancy. By reducing bone resorption, increased calcium intake during the second half of pregnancy might reduce the mobilization of lead from bone compartments, even at low blood lead levels. Subgroups of women who incurred substantial exposures to lead prior to pregnancy should be considered to be at increased risk. Birth Defects Research (Part A), 2005. © 2005 Wiley‐Liss, Inc.
2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) inhibition of coronary vasculogenesis is mediated, in part, by reduced responsiveness to endogenous angiogenic stimuli, including vascular endothelial growth factor A (VEGF‐A)
Authors: Ivnitski‐Steele Irena D. , Friggens Megan , Chavez Miquella , Walker Mary K. 
Published: May 2005

AbstractBACKGROUND2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin (TCDD) exposure prior to chick embryo incubation (GD 0) induces dilated cardiomyopathy, and reduces myocardial hypoxia, vascular endothelial growth factor A (VEGF‐A) expression, and coronary vascularization. We investigated whether reduced coronary vascularization 1) occurs in the absence of changes in cardiac morphology and 2) is associated with altered secretion of VEGF‐A and/or an antivasculogenic factor.METHODSChicken eggs were treated with control (corn oil) or TCDD (0.075–0.3 pmol of TCDD/gm) on GD 5. In vivo cardiac morphology and artery number were determined on GD 10, while in vitro vascular outgrowth and VEGF‐A secretion were determined from cardiac explants on GD 6. Effects of recombinant VEGF‐A (rcVEGF‐A), soluble flt‐1 (sFlt‐1) receptor plus rcVEGF‐A, and control conditioned media were assessed in TCDD explants, while effects of TCDD‐conditioned media was assessed in control explants.RESULTSTCDD reduced coronary artery number in vivo by 53 ± 8% and induced a dose‐related reduction in tube outgrowth in vitro, but had no effect on cardiac morphology. All TCDD doses reduced explant VEGF‐A secretion equally (43 ± 3%), compared to control. sFlt‐1 blocked outgrowth in control cultures and blocked rcVEGF‐A–mediated rescue of outgrowth in TCDD explants. Control conditioned media partially rescued outgrowth from TCDD explants, while conditioned media from TCDD explants had no effect on controls.CONCLUSIONSTCDD inhibition of coronary vascularization can occur in the absence of changes in cardiac morphology and is associated with reduced VEGF‐A secretion but not an antivasculogenic factor. Since control media only partly rescues TCDD's inhibitory effect, we suggest that TCDD‐exposed endothelial cells are less responsive to vasculogenic stimuli. Birth Defects Research (Part A), 2005. © 2005 Wiley‐Liss, Inc.
Transseptal technique of percutaneous PFO closure results in persistent interatrial shunting
Authors: Tande Aaron J. , Knickelbine Thomas , Chavez Ivan , Mooney Michael R. , Poulose Anil , Harris Kevin M. 
Published: May 2005

AbstractOur goal was to review the effectiveness of the transseptal and tunnel techniques of patent foramen ovale (PFO) closure. Percutaneous PFO closure is an increasingly common treatment for prevention of paradoxical embolism and is typically performed by passing the device through the defect tunnel itself. The transseptal technique, in which the septum primum is punctured to create a hole through which the device is passed, has been proposed for patients with long‐tunnel PFO. From May 2001 to December 2003, 120 patients underwent PFO closure at our institution and were included in this analysis. Defect closure was assessed by transesophageal echocardiography (TEE) with bubble study. Clinical follow‐up data were obtained by clinic visits or standardized telephone interviews. Device closure was successfully completed in all patients, with 12 (10%) undergoing transseptal closure and 108 (90%) undergoing tunnel closure. Immediately following the procedure, complete closure occurred in 6 of 12 (50%) of the transseptal group and 88 of 108 (81.5%) of the tunnel group (P = 0.0120). Of the 89 patients (74.2%) who returned for 6‐month TEE, complete closure was demonstrated in 4 out of 10 (40%) of the transseptal group and 58 out of 79 (73.4%) of the tunnel group (P = 0.0303). There have been four transient ischemic attacks during a mean follow‐up of 11 months. The transseptal technique of PFO closure results in a higher proportion of patients with persistent interatrial shunting when compared with the tunnel technique. Whether this is due to a difference in technique, device, or patient anatomy is unclear. © 2005 Wiley‐Liss, Inc.