bluuebunny/crossref_metadata_2025 huggingface dataset:
Saturated Hydraulic Conductivity of Semiarid Soils: Combined Effects of Salinity, Sodicity, and Rate of Wetting
Authors: Levy G. J. , Goldstein D. , Mamedov A. I.
Published: May 2005

Combined effects of soil conditions (wetting rate), soil sodicity, and salinity on soil saturated hydraulic conductivity (HC) have not been studied systematically and were the objective of our study. We examined the effects of (i) exchangeable sodium percentage (ESP, 1–20) and fast wetting (50 mm h−1) and leaching with distilled water on the HC of 60 Israeli soils (7–70% clay); and (ii) wetting rate (2 or 50 mm h−1), ESP and water salinity (distilled water or saline water, 2 dS m−1) on the HC of 16 selected samples. Results of the first experiment showed that (i) steady state HC of medium‐ and fine‐textured soils was lower than 2 cm h−1 already for nonsodic soils, and (ii) the adverse impact of sodicity on the HC strongly depended on soil texture. The second experiment revealed that in the loamy sand rate of wetting had no effect on the HC beyond that of sodicity and salinity. In the loam, sandy clay and clay soils a significant triple interaction among water quality, wetting rate and ESP in their effect on HC existed. In the absence of electrolytes, the impact of fast wetting (slaking) and swelling on the HC was most notable, mainly at the intermediate sodicity levels (ESP = 5–10). Use of saline water significantly reduced the impact of fast wetting and swelling on the HC. Our results suggested that combined effects of salinity, wetting rate, and sodicity on the HC were complex and should thus be considered simultaneously when estimating soil HC.
Effects of Sediment Deposition on Fine Root Dynamics in Riparian Forests
Authors: Cavalcanti Guadalupe G. , Lockaby B. Graeme
Published: May 2005

One of the most important functions of riparian zones is their ability to improve water quality by trapping sediment leaving agricultural fields and other disturbed areas. However, few data exist quantifying the impacts of sediment deposition from anthropogenic disturbance on belowground processes within these ecosystems. This study was conducted at Ft. Benning, GA, where disturbance caused by military training has generated a range of sedimentation levels in riparian forests near ephemeral streams. Nine ephemeral streams, exhibiting different levels of sediment deposition, were selected for study. Two paired treatment plots (upper and lower) were established along each catchment to represent potentially disturbed and control conditions, respectively. On highly and moderately disturbed catchments, upper plots had received varying rates of sediment from erosion along unpaved roads. Biomass, turnover, productivity, and nutrient contents of fine roots were compared within and across catchments. Temporal fluctuations in biomass of live and dead fine roots were observed for both treatments in the three disturbance categories, except for upper plots of highly disturbed catchments, where biomass remained fairly low and constant throughout the study. Fine root productivity declined sharply with sediment rates as low as 0.3 cm yr−1Nutrient contents of live and dead fine roots followed a similar trend to that of root biomass. These data suggest that fine root dynamics may be affected by sediment deposition rates commonly occurring in some wetland forests, and the water filtration function performed by these ecosystems may be at risk.
Strength Properties and Organic Carbon of Soils in the North Appalachian Region
Authors: Blanco-Canqui H. , Lal R. , Owens L. B. , Post W. M. , Izaurralde R. C.
Published: May 2005

Soil strength influenced by management and soil properties controls plant growth, root development, and soil‐moisture relations. The impact of textural and structural parameters on soil strength is moderated by soil organic C (SOC) concentration. Therefore, the objectives of this study were to assess differences in soil strength and SOC concentration in watersheds under long‐term (>15 yr) management practices in the North Appalachian region on a predominantly Typic Hapludults on undulating slopes (>6% slope). Seven watersheds without field replication under moldboard plow (MP), chisel plow, disk with beef cattle manure (DiskM), no‐till with beef cattle manure (NTm), no‐till with no beef cattle manure (NTnm), pasture, and forest were studied. Cone index (CI), shear strength, bulk density (ρb), volumetric moisture content (θv), and SOC concentration were determined at the summit, backslope, and footslope landscape positions at the 0‐ to 10‐, 10‐ to 20‐, and 20‐ to 30‐cm depths. The SOC concentration was slightly higher at the footslope than at the summit position in the cultivated watersheds. The ρbwas lower at the footslope than at the summit in NTm (1.22 vs. 1.42 Mg m−3) and chisel (1.34 vs. 1.47 Mg m−3) treatments. Forest had the lowest CI (0.19 MPa), shear strength (6.11 kPa), and ρb(0.93 Mg m−3) and the highest SOC concentration (62.7 g kg−1), whereas MP had the highest CI (0.67 MPa), shear strength (25.5 kPa), ρb(1.44 Mg m−3), and the lowest SOC concentration (13.6 g kg−1) in the 0‐ to 10‐cm depth (P< 0.01). The SOC concentration in NTm was 1.7 times higher than that in NTnm, and both no‐till treatments had lower ρb(<1.21 Mg m−3) than MP (1.44 Mg m−3) at 0‐ to 10‐cm depth (P< 0.01). Manuring decreased both CI and shear strength, but increased SOC concentration. The ρb, θv, and SOC concentration were potential predictors of CI; whereas ρband SOC concentration were of shear strength (r2> 0.42;P< 0.01). Results show that landscape positions had small effect, but management, particularly manuring, had large and significant effects on soil strength and SOC concentration.
Estimating Root Plus Rhizosphere Contributions to Soil Respiration in Annual Croplands
Authors: Raich James W. , Mora German
Published: May 2005

Although soil respiration represents an important C transfer from terrestrial ecosystems to the atmosphere, the effects of environmental and biological factors on soil respiration rates are not adequately understood. This is due primarily to the variety of processes that produce CO2 within the soil. Thus, separating the main CO2–producing processes is needed to improve our understanding of soil C cycling and dynamics. Here, we describe and test a model that estimates soil CO2 emissions derived from anabolic and catabolic processes, representing organic matter decomposition and root + rhizosphere respiration, respectively. Our model is based on the exponential response of organic matter decomposition with respect to temperature, and it requires only measurements of total soil CO2 emissions and soil temperature as inputs. To test the model, we relied on published measurements of soil respiration rates and soil temperatures in a maize (Zea mays L.) field in Ottawa, Canada, and on independent estimations of soil and root contributions for this field made on the basis of stable‐C isotope measurements of soil‐derived CO2 Model‐based and isotope estimations correlated significantly (r2 = 0.91, P < 10−9) on a daily basis. Model‐based estimations for root + rhizosphere respiration rates for the entire growing season totaled 145 g C m−2 or 27% of CO2 emissions, and those based on C isotopes totaled 158 g C m−2 or 30% of the total emissions. The excellent correspondence between model‐based and isotope‐based estimations suggests that this relatively simple model can be used to distinguish root from soil contributions to soil CO2 emissions in temperate‐zone, annual croplands free of significant water stress.
Passive scalar transport in polymer drag‐reduced turbulent channel flow
Authors: Gupta V. K. , Sureshkumar R. , Khomami B.
Published: May 2005

Passive 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

Schimke‐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

Anatomical 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

Objective

Exosomes 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.

Methods

Exosomes 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.

Results

All 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.

Conclusion

SGECs 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

Objective

To 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).

Methods

Cultured 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.

Results

PMA, 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.

Conclusion

Our 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

Objective

Few 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.

Methods

We 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.

Results

A 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.

Conclusion

Knee 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

Objective

To identify novel autoantibodies specific for dermatomyositis (DM), especially those specific for clinically amyopathic DM (C‐ADM).

Methods

Autoantibodies 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.

Results

Eight 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).

Conclusion

These 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

Objective

To examine whether hydroxychloroquine (HCQ) usage is associated with a reduced risk of damage accrual in patients with systemic lupus erythematosus (SLE).

Methods

Patients (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.

Results

Fifty‐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).

Conclusion

These 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

This 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

BACKGROUND

2,3,7,8‐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.

METHODS

Chicken 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.

RESULTS

TCDD 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.

CONCLUSIONS

TCDD 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

Our 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.
Effect of Zn⋅⋅⋅Zn Separation on the Hydrolytic Activity of Model Dizinc Phosphodiesterases
Authors: Bauer‐Siebenlist Bernhard , Meyer Franc , Farkas Etelka , Vidovic Denis , Dechert Sebastian
Published: May 2005

From the study of highly preorganized model systems, experimental support has been obtained for a possible functional role of the Zn–(H)O⋅⋅⋅HO(H)–Zn motif in oligozinc hydrolases. The mechanistic relevance of such an array, which may be described as a hydrated form of a pseudo‐terminal Zn‐bound hydroxide, has recently been supported by DFT calculations on various metallohydrolase active sites. In the present targeted approach, the Zn⋅⋅⋅Zn distance in two related dizinc complexes has been controlled through the use of multifunctional pyrazolate‐based ligand scaffolds, giving either a tightly bridged Zn–O(H)–Zn or a more loosely bridged Zn–(H)O⋅⋅⋅HO(H)–Zn species in the solid state. Zn‐bound water has been found to exhibit comparable acidity irrespective of whether the resulting hydroxide is supported by strong hydrogen‐bonding in the O2H3 moiety or is in a bridging position between two zinc ions, indicating that water does not necessarily have to adopt a bridging position in order for its pKa to be sufficiently lowered so as to provide a Zn‐bound hydroxide at physiological pH. Comparative reactivity studies on the cleavage of bis(4‐nitrophenyl)phosphate (BNPP) mediated by the two dizinc complexes have revealed that the system with the larger Zn⋅⋅⋅Zn separation is hydrolytically more potent, both in the hydrolysis and the transesterification of BNPP. The extent of active site inhibition by the reaction products has also been found to be governed by the Zn⋅⋅⋅Zn distance, since phosphate diester coordination in a bridging mode within the clamp of two zinc ions is only favored for Zn⋅⋅⋅Zn distances well above 4 Å. Different binding affinities are rationalized in terms of the structural characteristics of the product‐inhibited complexes for the two different ligand scaffolds, with dimethyl phosphate found as a bridging ligand within the bimetallic pocket.
Structurally Diverse Second‐Generation [2.2]Paracyclophane Ketimines with Planar and Central Chirality: Syntheses, Structural Determination, and Evaluation for Asymmetric Catalysis
Authors: Lauterwasser Frank , Nieger Martin , Mansikkamäki Heidi , Nättinen Kalle , Bräse Stefan
Published: May 2005

A set of 20 novel [2.2]paracyclophane ketimines with planar and central chirality has been synthesized from enantiomerically pure and racemic 5‐acyl‐4‐hydroxy[2.2]paracyclophane and α‐branched chiral amines. Their X‐ray structures were determined to elucidate the three‐dimensional structures and the absolute configuration. The ketimines were used as catalysts in the asymmetric 1,2‐addition reactions of diethylzinc with substituted benzaldehydes to furnish chiral alcohols in up to 95 % ee.
Radiotherapy alone or combined with surgery for salivary gland carcinoma
Authors: Mendenhall William M. , Morris Christopher G. , Amdur Robert J. , Werning John W. , Villaret Douglas B.
Published: May 2005

BACKGROUND

The authors analyzed the outcomes of patients treated with radiotherapy (RT) alone or combined with surgery for carcinoma of the salivary glands.

METHODS

Between October 1964 and June 2003, 224 previously untreated patients were treated with curative intent with RT alone (n= 64) or combined with surgery (n= 160) at the University of Florida College of Medicine (Gainesville, FL). The median follow‐up period was 5.0 years (range, 0.4–31.6 years).

RESULTS

The 10‐year local control rate was 75%. Multivariate analysis of local control revealed that T classification (P< 0.0001) and treatment group (P< 0.0001) impacted this end point. Patients treated with surgery and adjuvant RT had improved local control compared with patients treated with RT alone. The 10‐year locoregional control rate was 68%. Multivariate analysis of locoregional control revealed that overall stage (P< 0.0001) and treatment group (P= 0.0002) significantly influenced this end point. The 10‐year distant metastasis‐free survival rate was 68%. Multivariate analysis of distant metastasis‐free survival revealed that overall stage (P< 0.0001) significantly influenced this end point. The 10‐year cause‐specific and overall survival rates were 57% and 44%, respectively. Multivariate analysis of cause‐specific survival revealed that overall stage (P< 0.0001) significantly impacted this end point. Twenty‐three patients (10%) experienced severe complications.

CONCLUSIONS

A substantial proportion of patients with salivary gland carcinoma were cured with surgery combined with adjuvant RT. RT alone was used for patients with unresectable tumors and cured approximately 20% of those with advanced‐stage disease. The probability of cure was influenced by the extent of disease and treatment group. Cancer 2005. © 2005 American Cancer Society.
Recurrent central neurocytomas
Authors: Bertalanffy Alexander , Roessler Karl , Koperek Oskar , Gelpi Ellen , Prayer Daniela , Knosp Engelbert
Published: May 2005

BACKGROUND

Since the first description of Central neurocytomas (CNs) as a benign tumor entity in 1982, there has been great enthusiasm regarding the benign course and the curative surgical approach to this disease. The current study was performed to investigate the frequency of disease recurrence during long‐term follow‐up.

METHODS

A retrospective analysis of the medical files with emphasis on clinicoradiologic findings and histologic and immunohistochemical features was performed.

RESULTS

Between 1985–2003. surgical resection was performed in 14 patients with CNs ages 16–43 years (7 were female and 7 were male). Two patients (14%) died postoperatively and one patient had a malignant disease course (7%). In the remaining 11 patients, one patient with an incompletely resected CN had disease progression after 37 months but at the time of last follow‐up had had stable disease for 10 years. In addition, the authors reported 5 patients with disease recurrence occurring at a median of 67 months after surgery (range, 51–79 months after surgery), all of which occurred after complete surgical resection was performed. The observation period for the remaining 5 patients was short (median of 34 months [range, 5–44 months]). Extensive histologic and immunohistochemical workup did not identify any significant prognostic parameters. The MIB‐1 proliferation index ranged from 0.8–11% (median of 4.6%), but was reported to be 46.8% in the malignant transformed tumor. All patients with disease recurrence responded well to different forms of focal radiation therapy (gamma knife radiosurgery in three patients and interstitial irradiation in one patient) and for one patient with a recently detected recurrence, gamma knife radiosurgery was planned.

CONCLUSIONS

CNs appear to have a higher tendency to recur during long‐term follow‐up than previously reported, even after complete resection. Therefore, periodic neuroradiologic follow‐up examinations should be considered mandatory in all patients, even after several years. Cancer 2005. © 2005 American Cancer Society.
Generating neuronal diversity in the Drosophila central nervous system: A view from the ganglion mother cells
Authors: Karcavich Rachel E.
Published: May 2005

The original article to which this Erratum refers was published in Developmental Dynamics 232:609–616Developmental Dynamics(2005) 232(3) 609–616
DNA damage in leukocytes of workers occupationally exposed to arsenic in copper smelters
Authors: Palus Jadwiga , Lewinska Dobroslawa , Dziubaltowska Elzbieta , Stepnik Maciej , Beck Jens , Rydzynski Konrad , Nilsson Robert
Published: May 2005

Inorganic arsenic (i‐As) is a known human carcinogen; however, humans continue to be exposed to i‐As in drinking water and in certain occupational settings. In this study, we used the Comet assay to evaluate DNA damage in the somatic cells of workers from three Polish copper smelters who were occupationally exposed to i‐As. Blood samples were collected from 72 male workers and 83 unexposed male controls and used for the detection of DNA damage, oxidative DNA damage, and DNA damage after a 3‐hr incubation in culture. Urine samples were collected to assess the level of exposure. The mean concentration of arsenic metabolites in urine [the sum of arsenite (AsIII), arsenate (AsV), monomethylarsenate (MMA) and dimethylarsenate (DMA)] and the concentrations of DMA (the main metabolite in urine) were higher in workers than in controls, but the differences were not statistically significant. By contrast, the level of DNA damage, expressed as the median tail moment, was significantly higher in the leukocytes of workers than in the controls. Comet assays conducted with formamidopyrimidine glycosylase (FPG) digestion to detect oxidative DNA damage indicated that oxidative lesions were present in leukocytes from both the exposed and control groups, but the levels of damage were significantly higher among the workers. Incubation of the cells in culture resulted in a significant reduction in the levels of DNA damage, especially among leukocytes from the workers, suggesting that the DNA damage was subject to repair. Our findings indicate that copper smelter workers have increased levels of DNA damage in somatic cells, suggesting a potential health risk for the workers. Although i‐As was present in air samples from the smelters and in urine samples from workers, no clear association could be made between i‐As exposure and the DNA damage. Environ. Mol. Mutagen., 2005. © 2005 Wiley‐Liss, Inc.
Genotoxicity of drinking water disinfectants in plant bioassays
Authors: Monarca Silvano , Feretti Donatella , Zani Claudia , Rizzoni Marco , Casarella Silvia , Gustavino Bianca
Published: May 2005

The genotoxicity of two widely used drinking water disinfectants, sodium hypochlorite (NaClO) and chlorine dioxide (ClO2), and a new disinfectant, peracetic acid (PAA, CH3‐CO‐COOH), was evaluated in three short‐term plant tests: (1) induction of anaphase chromosome aberrations in the root cells of Allium cepa, (2) micronucleus induction in the root cells of Vicia faba, and (3) micronucleus induction in Tradescantia pollen cells. The study was carried out in the laboratory by directly exposing the plants to several concentrations of the disinfectants in redistilled water at unadjusted (acid) and adjusted (neutral) pHs. Both 0.1 and 0.2 mg/l NaClO induced chromosome aberrations in the Allium cepa test at acid pH, but concentrations up to 0.5 mg/l of all the disinfectants were negative at neutral pH. Concentrations ranging from 0.1 to 0.5 mg/l NaClO, ClO2, and PAA induced micronuclei in Vicia faba at acid pH, while 1–2 mg/l NaClO and ClO2 and 0.5–2 mg/l PAA gave positive responses at neutral pH. Most of concentrations of ClO2 produced positive responses in the Tradescantia micronucleus test. In general, the highest levels of genotoxicity were observed under acid conditions; at acid pH, significant effects were induced by low concentrations of ClO2 and PAA. Since the test concentrations of disinfectants are typical of those encountered in the biocidal treatment of tap water and similar concentrations are consumed daily by a large number of people, the genotoxicity of these compounds may constitute a significant public health concern. Environ. Mol. Mutagen., 2005. © 2005 Wiley‐Liss, Inc.
A weighted cohort approach for analysing factors modifying disease risks in carriers of high‐risk susceptibility genes
Authors: Antoniou Antonis C. , Goldgar David E. , Andrieu Nadine , Chang‐Claude Jenny , Brohet Richard , Rookus Matti A. , Easton Douglas F.
Published: May 2005

The authors propose a novel approach to evaluate the effects of risk factors on disease risks in carriers of high‐penetrance alleles in disease susceptibility genes. Most studies to date have utilised data collected on carriers identified through ongoing genetic testing programs. The advantage of this approach is that it allows relatively large numbers of affected and unaffected carriers to be identified rapidly. However, genetic testing is targeted at individuals with a strong family history of disease, so that the selection of carriers is not random with respect to disease status. Risk factors are often analysed by standard cohort analysis methods, but these can be biased in retrospective studies if subjects are selected on the basis of phenotype. To overcome this problem, a weighted cohort approach is proposed, under which individuals are weighted according to certain sampling probabilities in order to mimic a true cohort. The method is illustrated by analyses of data from the International BRCA1/2 Carrier Cohort Study (IBCCS). Simulations demonstrate that the method gives rate ratio estimates that are close to unbiased provided that the absolute disease risks are well estimated. The power to detect associations is, however, reduced compared with an unweighted approach. Genet. Epidemiol. © 2005 Wiley‐Liss, Inc.
A review of the possible relevance of inositol and the phosphatidylinositol second messenger system (PI‐cycle) to psychiatric disorders—focus on magnetic resonance spectroscopy (MRS) studies
Authors: Kim Hyeonjin , McGrath Brent M. , Silverstone Peter H.
Published: May 2005

Myo‐inositol is an important part of the phosphatidylinositol second messenger system (PI‐cycle). Abnormalities in nerve cell myo‐inositol levels and/or PI‐cycle regulation has been suggested as being involved in the pathophysiology and/or treatment of many psychiatric disorders including bipolar disorder, major depressive disorder, panic disorder, obsessive‐compulsive disorder, eating disorders and schizophrenia. This review examines the metabolism and biochemical importance of myo‐inositol and the PI‐cycle. It relates this to the current in vivo evidence for myo‐inositol and PI‐cycle involvement in these psychiatric disorders, particularly focusing upon the magnetic resonance spectroscopy (MRS) findings in patient studies to date. From this review it is concluded that while the evidence suggests probable relevance to the pathophysiology and/or treatment of bipolar disorder, there is much less support for a significant role for the PI‐cycle or myo‐inositol in any other psychiatric disorder. More definitive investigation is required before PI‐cycle dysfunction can be considered specific to bipolar disorder. Copyright © 2005 John Wiley & Sons, Ltd.
Role of smoking in global and regional cancer epidemiology: Current patterns and data needs
Authors: Ezzati Majid , Henley S. Jane , Lopez Alan D. , Thun Michael J.
Published: May 2005

Although smoking is widely recognized as a major cause of cancer, there is little information on how it contributes to the global and regional burden of cancers in combination with other risk factors that affect background cancer mortality patterns. We used data from the American Cancer Society's Cancer Prevention Study II (CPS‐II) and the WHO and IARC cancer mortality databases to estimate deaths from 8 clusters of site‐specific cancers caused by smoking, for 14 epidemiologic subregions of the world, by age and sex. We used lung cancer mortality as an indirect marker for accumulated smoking hazard. CPS‐II hazards were adjusted for important covariates. In the year 2000, an estimated 1.42 (95% CI 1.27–1.57) million cancer deaths in the world, 21% of total global cancer deaths, were caused by smoking. Of these, 1.18 million deaths were among men and 0.24 million among women; 625,000 (95% CI 485,000–749,000) smoking‐caused cancer deaths occurred in the developing world and 794,000 (95% CI 749,000–840,000) in industrialized regions. Lung cancer accounted for 60% of smoking‐attributable cancer mortality, followed by cancers of the upper aerodigestive tract (20%). Based on available data, more than one in every 5 cancer deaths in the world in the year 2000 were caused by smoking, making it possibly the single largest preventable cause of cancer mortality. There was significant variability across regions in the role of smoking as a cause of the different site‐specific cancers. This variability illustrates the importance of coupling research and surveillance of smoking with that for other risk factors for more effective cancer prevention. © 2005 Wiley‐Liss, Inc.
Overexpression of regucalcin suppresses cell death and apoptosis in cloned rat hepatoma H4‐II‐E cells induced by insulin or insulin‐like growth factor‐I
Authors: Fukaya Yuko , Yamaguchi Masayoshi
Published: May 2005

The role of regucalcin, a regulatory protein in intracellular signaling pathway, in cell death was investigated by using the cloned rat hepatoma H4‐II‐E cells overexpressing regucalcin. The hepatoma cells (wild‐type) and stable regucalcin/pCXN2 transfectants were cultured for 72 h in a medium containing 10% fetal bovine serum (FBS) to obtain subconfluent monolayers. After culture for 72 h, cells were further cultured for 24–72 h in a medium containing either vehicle, insulin (10−8 or 10−7M) or insulin‐like growth factor‐I (IGF‐I; 10−9 or 10−8M) in the absence of FBS. The number of wild‐type cells was significantly decreased by culture for 24, 48, or 72 h in the presence of insulin (10−8 or 10−7M) or IGF‐I (10−9 or 10−8M). Agarose gel electrophoresis showed the presence of low‐molecular‐weight deoxyribonucleic acid (DNA) fragments of adherent wild‐type cells cultured with insulin or IGF‐I. The effect of insulin or IGF‐I in stimulating cell death and DNA fragmentation in hepatoma cells (wild‐type) was significantly prevented in transfectants overexpressing regucalcin. Meanwhile, epinephrine (10−6 or 10−5M) or transforming growth factor‐β1 (10−13 or 10−12M) did not cause cell death of hepatoma cells. Insulin‐induced decrease in the number of wild‐type cells was significantly prevented by culture with caspase‐3 inhibitor (10−8M), although the effect of IGF‐I was not inhibited. The effect of insulin or IGF‐I in inducing the death of hepatoma cells (wild‐type) was significantly prevented in the presence of N ω‐nitro‐l‐arginine methylester (NAME), an inhibitor of nitric oxide synthase. Genistein (10−6M), an inhibitor of protein tyrosine kinase, or vanadate (10−5M), an inhibitor of protein tyrosine phosphatase, caused a significant decrease in the number of hepatoma cells (wild‐type). The effect of insulin in inducing the death of wild‐type cells was not seen in the presence of genistein or vanadate. The effect of IGF‐I on the death of wild‐type cells was observed in the presence of genistein or vanadate. The effect of genistein on cell death was significantly prevented in transfectants. Such effect was not seen with vanadate. This study demonstrates that insulin or IGF‐I stimulates cell death and apoptosis in the hepatoma cells, and that overexpression of regucalcin has a suppressive effect on cell death induced by insulin or IGF‐I that is mediated through different signaling pathway. © 2005 Wiley‐Liss, Inc.