400 research outputs found

    Genetic and environmental causes of variation in basal levels of blood cells

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    Mesonic Form Factors

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    We have started a program to compute the electromagnetic form factors of mesons. We discuss the techniques used to compute the pion form factor and present preliminary results computed with domain wall valence fermions on MILC asqtad lattices, as well as Wilson fermions on quenched lattices. These methods can easily be extended to rho-to-gamma-pi transition form factors.Comment: 7 pages, 6 figures, Workshop on Lattice Hadron Physics 2003 (LHP2003

    Comparison of stainless and mild steel welding fumes in generation of reactive oxygen species

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    <p>Abstract</p> <p>Background</p> <p>Welding fumes consist of a wide range of complex metal oxide particles which can be deposited in all regions of the respiratory tract. The welding aerosol is not homogeneous and is generated mostly from the electrode/wire. Over 390,000 welders were reported in the U.S. in 2008 while over 1 million full-time welders were working worldwide. Many health effects are presently under investigation from exposure to welding fumes. Welding fume pulmonary effects have been associated with bronchitis, metal fume fever, cancer and functional changes in the lung. Our investigation focused on the generation of free radicals and reactive oxygen species from stainless and mild steel welding fumes generated by a gas metal arc robotic welder. An inhalation exposure chamber located at NIOSH was used to collect the welding fume particles.</p> <p>Results</p> <p>Our results show that hydroxyl radicals (<sup>.</sup>OH) were generated from reactions with H<sub>2</sub>O<sub>2 </sub>and after exposure to cells. Catalase reduced the generation of <b><sup>.</sup></b>OH from exposed cells indicating the involvement of H<sub>2</sub>O<sub>2</sub>. The welding fume suspension also showed the ability to cause lipid peroxidation, effect O<sub>2 </sub>consumption, induce H<sub>2</sub>O<sub>2 </sub>generation in cells, and cause DNA damage.</p> <p>Conclusion</p> <p>Increase in oxidative damage observed in the cellular exposures correlated well with <b><sup>.</sup></b>OH generation in size and type of welding fumes, indicating the influence of metal type and transition state on radical production as well as associated damage. Our results demonstrate that both types of welding fumes are able to generate ROS and ROS-related damage over a range of particle sizes; however, the stainless steel fumes consistently showed a significantly higher reactivity and radical generation capacity. The chemical composition of the steel had a significant impact on the ROS generation capacity with the stainless steel containing Cr and Ni causing more damage than the mild steel. Our results suggest that welding fumes may cause acute lung injury. Since type of fume generated, particle size, and elapsed time after generation of the welding exposure are significant factors in radical generation and particle deposition these factors should be considered when developing protective strategies.</p

    Nanoparticle inhalation augments particle-dependent systemic microvascular dysfunction

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    <p>Abstract</p> <p>Background</p> <p>We have shown that pulmonary exposure to fine particulate matter (PM) impairs endothelium dependent dilation in systemic arterioles. Ultrafine PM has been suggested to be inherently more toxic by virtue of its increased surface area. The purpose of this study was to determine if ultrafine PM (or nanoparticle) inhalation produces greater microvascular dysfunction than fine PM. Rats were exposed to fine or ultrafine TiO<sub>2 </sub>aerosols (primary particle diameters of ~1 ΞΌm and ~21 nm, respectively) at concentrations which do not alter bronchoalveolar lavage markers of pulmonary inflammation or lung damage.</p> <p>Results</p> <p>By histopathologic evaluation, no significant inflammatory changes were seen in the lung. However, particle-containing macrophages were frequently seen in intimate contact with the alveolar wall. The spinotrapezius muscle was prepared for in vivo microscopy 24 hours after inhalation exposures. Intraluminal infusion of the Ca<sup>2+ </sup>ionophore A23187 was used to evaluate endothelium-dependent arteriolar dilation. In control rats, A23187 infusion produced dose-dependent arteriolar dilations. In rats exposed to fine TiO<sub>2</sub>, A23187 infusion elicited vasodilations that were blunted in proportion to pulmonary particle deposition. In rats exposed to ultrafine TiO<sub>2</sub>, A23187 infusion produced arteriolar constrictions or significantly impaired vasodilator responses as compared to the responses observed in control rats or those exposed to a similar pulmonary load of fine particles.</p> <p>Conclusion</p> <p>These observations suggest that at equivalent pulmonary loads, as compared to fine TiO<sub>2</sub>, ultrafine TiO<sub>2 </sub>inhalation produces greater remote microvascular dysfunction.</p

    Near-Infrared Survey and Photometric Redshifts in the Extended GOODS-North field

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    We present deep JJ and HH-band images in the extended Great Observatories Origins Deep Survey-North (GOODS-N) field covering an area of 0.22 deg2\rm{deg}^{2}. The observations were taken using WIRCam on the 3.6-m Canada France Hawaii Telescope (CFHT). Together with the reprocessed KsK_{\rm s}-band image, the 5Οƒ5\sigma limiting AB magnitudes (in 2" diameter apertures) are 24.7, 24.2, and 24.4 AB mag in the JJ, HH, and KsK_{\rm s} bands, respectively. We also release a multi-band photometry and photometric redshift catalog containing 93598 sources. For non-X-ray sources, we obtained a photometric redshift accuracy ΟƒNMAD=0.036\sigma_{\mathrm{NMAD}}=0.036 with an outlier fraction Ξ·=7.3%\eta = 7.3\%. For X-ray sources, which are mainly active galactic nuclei (AGNs), we cross-matched our catalog with the updated 2M-CDFN X-ray catalog from Xue et al. (2016) and found that 658 out of 683 X-ray sources have counterparts. GALEXGALEX UV data are included in the photometric redshift computation for the X-ray sources to give ΟƒNMAD=0.040\sigma_{\mathrm{NMAD}} = 0.040 with Ξ·=10.5%\eta=10.5\%. Our approach yields more accurate photometric redshift estimates compared to previous works in this field. In particular, by adopting AGN-galaxy hybrid templates, our approach delivers photometric redshifts for the X-ray counterparts with fewer outliers compared to the 3D-HST catalog, which fit these sources with galaxy-only templates

    Familial keratoconus with cataract: Linkage to the long arm of chromosome 15 and exclusion of candidate genes

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    PURPOSE. Keratoconus and cataract are common causes of visual morbidity. Both conditions show genetic predisposition. The purpose of this study was to map the disease locus in a large three-generation family affected by combined early-onset autosomal dominant anterior polar cataract and clinically severe keratoconus. Uniquely, in this family both disorders were present and fully penetrant in those affected. METHODS. Thirty members of the family were examined clinically on two occasions, at an interval of 5 years, to establish their phenotypes and determine the progression of the disease. Genomic DNA was extracted from blood samples of 16 affected and 14 unaffected individuals, and typed with more than 350 highly polymorphic microsatellite loci in a genome-wide linkage screen. Markers were amplified by PCR with fluorescently labeled primers and sized with an automated DNA analyser before calculation of lod scores. After linkage was established, several positional candidate genes were assessed by PCR-based DNA sequencing. RESULTS. The locus for keratoconus with cataract was mapped to a 6.5-Mb region of the long arm of chromosome 15, at 22.33-24.2 between CYP11A and D15S211. The positional and functional candidate genes CTSH, CRABP1, IREB2, and RAS-GRF1 were excluded as the cause of keratoconus with cataract in this family. CONCLUSIONS. This is the first report of a family with autosomal dominant inheritance of keratoconus in association with cataract. The causative gene maps to the long arm of chromosome 15 but has not yet been identified. (Invest Ophthalmol Vis Sci

    Impairment of Coronary Arteriolar Endothelium-Dependent Dilation after Multi-Walled Carbon Nanotube Inhalation: A Time-Course Study

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    Engineered nanomaterials have been developed for widespread applications due to many highly unique and desirable characteristics. The purpose of this study was to assess pulmonary inflammation and subepicardial arteriolar reactivity in response to multi-walled carbon nanotube (MWCNT) inhalation and evaluate the time course of vascular alterations. Rats were exposed to MWCNT aerosols producing pulmonary deposition. Pulmonary inflammation via bronchoalveolar lavage and MWCNT translocation from the lungs to systemic organs was evident 24 h post-inhalation. Coronary arterioles were evaluated 24–168 h post-exposure to determine microvascular response to changes in transmural pressure, endothelium-dependent and -independent reactivity. Myogenic responsiveness, vascular smooth muscle reactivity to nitric oxide, and Ξ±-adrenergic responses all remained intact. However, a severe impact on endothelium-dependent dilation was observed within 24 h after MWCNT inhalation, a condition which improved, but did not fully return to control after 168 h. In conclusion, results indicate that MWCNT inhalation not only leads to pulmonary inflammation and cytotoxicity at low lung burdens, but also a low level of particle translocation to systemic organs. MWCNT inhalation also leads to impairments of endothelium-dependent dilation in the coronary microcirculation within 24 h, a condition which does not fully dissipate within 168 h. The innovations within the field of nanotechnology, while exciting and novel, can only reach their full potential if toxicity is first properly assessed

    Watershed Classification Predicts Streamflow Regime and Organic Carbon Dynamics in the Northeast Pacific Coastal Temperate Rainforest

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    Watershed classification has long been a key tool in the hydrological sciences, but few studies have been extended to biogeochemistry. We developed a combined hydro-biogeochemical classification for watersheds draining to the coastal margin of the Northeast Pacific coastal temperate rainforest (1,443,062 km2), including 2,695 small coastal rivers (SCR) and 10 large continental watersheds. We used cluster analysis to group SCR watersheds into 12 types, based on watershed properties. The most important variables for distinguishing SCR watershed types were evapotranspiration, slope, snowfall, and total precipitation. We used both streamflow and dissolved organic carbon (DOC) measurements from rivers (n = 104 and 90 watersheds respectively) to validate the classification. Watershed types corresponded with broad differences in streamflow regime, mean annual runoff, DOC seasonality, and mean DOC concentration. These links between watershed type and river conditions enabled the first region-wide empirical characterization of river hydrobiogeochemistry at the land-sea margin, spanning extensive ungauged and unsampled areas. We found very high annual runoff (mean > 3,000 mm, n = 10) in three watershed types totaling 59,024 km2 and ranging from heavily glacierized mountain watersheds with high flow in summer to a rain-fed mountain watershed type with high flow in fall-winter. DOC hotspots (mean > 4 mg Lβˆ’1, n = 14) were found in three other watershed types (48,557 km2) with perhumid rainforest climates and less-mountainous topography. We described four patterns of DOC seasonality linked to watershed hydrology, with fall-flushing being widespread. Hydro-biogeochemical watershed classification may be useful for other complex regions with sparse observation networks.Author Contributions: Conceptualization: Ian J. W. Giesbrecht, Suzanne E. Tank, Gordon W. Frazer, Eran Hood, David E. Butman, David V. D’Amore, Allison Bidlack, Ken P. Lertzman Data curation: Ian J. W. Giesbrecht, Santiago G. Gonzalez Arriola, David Hutchinson Formal analysis: Ian J. W. Giesbrecht, Gordon W. Frazer, Santiago G. Gonzalez ArriolaYe
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