Automated online preconcentration system for the determination of trace amounts of lead using Pb-selective resin and inductively coupled plasma-atomic emission spectrometry

An automated sequential-injection online preconcentration system was developed for the determination of lead by inductively coupled plasma - atomic emission spectrometry (ICP-AES). The preconcentration of lead was performed with a minicolumn containing a lead-selective resin, Analig Pb-01, which was installed between a selection and a switching valve. In an acidic condition ( pH 1), lead could be adsorbed on the resin. The concentrated lead was afterward eluted with 25 mu L of 0.06 M nitrilotriacetic acid (NTA) solution ( pH 9) and was subsequently transported into the nebulizer of ICP-AES for quantification. The selectivity of the resin toward lead was examined using a solution containing a mixture of 61 elements. When a sample volume of 5 mL was used, the quantitative collection of lead ( &#62;= 97%) was achieved, along with an enrichment factor of 19, a sampling frequency of 12 samples hr(-1), a detection limit of 70 pg mL(-1), and a lowest quantification limit of 100 pg mL(-1). The linear dynamic range was 0.1 to 5 ng mL(-1), and the relative standard deviation (n = 9) was 0.5% at a 5 ng mL(-1) Pb level. The detection limit of 30 pg mL(-1) and lowest quantification limit of 50 pg mL(-1) could be achieved when 10 mL of sample volume was used. The accuracy of the proposed method was validated by determining lead in the standard reference material of river water (SLRS-4), and its applicability to the determination of lead in environmental river water samples was demonstrated.</p

Confidence Elicitation And Anchoring In The Respondent-Generated Intervals (RGI) Protocol

The Respondent-Generated Intervals protocol (RGI) has been used to have respondents recall the answer to a factual question by giving not only a point estimate but also bounds within which they feel it is almost certain that the true value of the quantity being reported upon falls. The RGI protocol is elaborated in this article with the goal of improving the accuracy of the estimators by introducing cueing mechanisms to direct confident (and thus presumably accurate) respondents to give shorter intervals and less confident (and thus presumably less accurate) respondents to give longer ones

Magnetic resonance angiography signal intensity as a marker of hemodynamic impairment in intracranial arterial stenosis.

BackgroundIntracranial arterial stenosis (ICAS) is the predominant cause of ischemic stroke and transient ischemic attack in Asia. Change of signal intensities (SI) across an ICAS on magnetic resonance angiography (MRA) may reflect its hemodynamic severity.MethodsIn-patients with a symptomatic single ICAS detected on 3D time-of-flight MRA were recruited from 2 hospitals. Baseline and 1-year follow-up data were collected. Signal intensity ratio (SIR) [ =  (mean post-stenotic SI -mean background SI)/(mean pre-stenotic SI - mean background SI)] was evaluated on baseline MRA to represent change of SIs across an ICAS. Acute infarct volume was measured on baseline diffusion-weighted images (DWI). Relationships between SIR and baseline characteristics as well as 1y outcomes were evaluated.ResultsThirty-six subjects (86.1% males, mean age 55.0) were recruited. Overall, mean SIR was 0.84±0.23. Mean SIRs were not significantly different between the 23 (63.9%) anatomically severe stenoses and the 13 (36.1%) anatomically moderate stenoses (0.80±0.23 versus 0.92±0.21, p = 0.126). SIR was significantly, linearly and negatively correlated to acute infarct volume on DWI (Spearman correlation coefficient -0.471, p = 0.011). Two patients (5.6%) had recurrent ischemic strokes at 1y, not related to SIR values.ConclusionsChange of signal intensities across an ICAS on MRA may reflect its hemodynamic and functional severity. Future studies are warranted to further verify the relationships between this index and prognosis of patients with symptomatic ICAS

Kinetic Approaches to Understanding the Mechanisms of Fidelity of the Herpes Simplex Virus Type 1 DNA Polymerase

We discuss how the results of presteady-state and steady-state kinetic analysis of the polymerizing and excision activities of herpes simplex virus type 1 (HSV-1) DNA polymerase have led to a better understanding of the mechanisms controlling fidelity of this important model replication polymerase. Despite a poorer misincorporation frequency compared to other replicative polymerases with intrinsic 3′ to 5′ exonuclease (exo) activity, HSV-1 DNA replication fidelity is enhanced by a high kinetic barrier to extending a primer/template containing a mismatch or abasic lesion and by the dynamic ability of the polymerase to switch the primer terminus between the exo and polymerizing active sites. The HSV-1 polymerase with a catalytically inactivated exo activity possesses reduced rates of primer switching and fails to support productive replication, suggesting a novel means to target polymerase for replication inhibition

Disrupted CXCR2 Signaling in Oligodendroglia Lineage Cells Enhances Myelin Repair in a Viral Model of Multiple Sclerosis.

CXCR2 is a chemokine receptor expressed on oligodendroglia that has been implicated in the pathogenesis of neuroinflammatory demyelinating diseases as well as enhancement of the migration, proliferation, and myelin production by oligodendroglia. Using an inducible proteolipid protein (Plp) promoter-driven Cre-loxP recombination system, we were able to assess how timed ablation of Cxcr2 in oligodendroglia affected disease following intracranial infection with the neurotropic JHM strain of mouse hepatitis virus (JHMV). Generation of Plp-Cre-ER(T)::Cxcr2flox/flox transgenic mice (termed Cxcr2-CKO mice) allows for Cxcr2 to be silenced in oligodendrocytes in adult mice following treatment with tamoxifen. Ablation of oligodendroglia Cxcr2 did not influence clinical severity in response to intracranial infection with JHMV. Infiltration of activated T cells or myeloid cells into the central nervous system (CNS) was not affected, nor was the ability to control viral infection. In addition, the severity of demyelination was similar between tamoxifen-treated mice and vehicle-treated controls. Notably, deletion of Cxcr2 resulted in increased remyelination, as assessed by g-ratio (the ratio of the inner axonal diameter to the total outer fiber diameter) calculation, compared to that in vehicle-treated control mice. Collectively, our findings argue that CXCR2 signaling in oligodendroglia is dispensable with regard to contributing to neuroinflammation, but its deletion enhances remyelination in a preclinical model of the human demyelinating disease multiple sclerosis (MS).IMPORTANCE Signaling through the chemokine receptor CXCR2 in oligodendroglia is important for developmental myelination in rodents, while chemical inhibition or nonspecific genetic deletion of CXCR2 appears to augment myelin repair in animal models of the human demyelinating disease multiple sclerosis (MS). To better understand the biology of CXCR2 signaling on oligodendroglia, we generated transgenic mice in which Cxcr2 is selectively ablated in oligodendroglia upon treatment with tamoxifen. Using a viral model of neuroinflammation and demyelination, we demonstrate that genetic silencing of CXCR2 on oligodendroglia did not affect clinical disease, neuroinflammation, or demyelination, yet there was increased remyelination. These findings support and extend previous findings suggesting that targeting CXCR2 may offer a therapeutic avenue for enhancing remyelination in patients with demyelinating diseases

Directing mesenchymal stem cells to bone to augment bone formation and increase bone mass.

Aging reduces the number of mesenchymal stem cells (MSCs) that can differentiate into osteoblasts in the bone marrow, which leads to impairment of osteogenesis. However, if MSCs could be directed toward osteogenic differentiation, they could be a viable therapeutic option for bone regeneration. We have developed a method to direct MSCs to the bone surface by attaching a synthetic high-affinity and specific peptidomimetic ligand (LLP2A) against integrin α4β1 on the MSC surface to a bisphosphonate (alendronate, Ale) that has a high affinity for bone. LLP2A-Ale induced MSC migration and osteogenic differentiation in vitro. A single intravenous injection of LLP2A-Ale increased trabecular bone formation and bone mass in both xenotransplantation studies and in immunocompetent mice. Additionally, LLP2A-Ale prevented trabecular bone loss after peak bone acquisition was achieved or as a result of estrogen deficiency. These results provide proof of principle that LLP2A-Ale can direct MSCs to the bone to form new bone and increase bone strength

TRA-901: OPTIMIZING THE LOCATION OF ROAD WEATHER INFORMATION SYSTEMS (RWIS) STATIONS – A SAMPLING DESIGN OPTIMIZATION APPROACH

This study presents an innovative approach to the design of a road weather information monitoring system (RWIS) that optimally combines spatial data on weather-related road surface conditions with data on traffic volume over a state-wide road network. The optimization method minimizes the spatially averaged ordinary kriging variance of hazardous road surface condition (HRSC) frequencies. Since it is desired that an RWIS should also be located at high traffic demand areas, road class data is implemented in the optimization process. Spatial simulated annealing (SSA) is used to search for the optimal RWIS network design by iteratively examining each possible location and accepting designs that ameliorate a weighted sum of average kriging variance and road class detection capability. This novel approach is applied in the optimization of Minnesota RWIS network to illustrate the distinct features of the proposed method, assess the effectiveness of the current location setting, and recommend new additional stations locations. The findings of the study suggest that the method introduced in this study is useful for determining the optimal RWIS station locations and placing a few in addition to the existing stations by incorporating key elements being considered in practice

Sterilization of lung matrices by supercritical carbon dioxide

Lung engineering is a potential alternative to transplantation for patients with end-stage pulmonary failure. Two challenges critical to the successful development of an engineered lung developed from a decellularized scaffold include (i) the suppression of resident infectious bioburden in the lung matrix, and (ii) the ability to sterilize decellularized tissues while preserving the essential biological and mechanical features intact. To date, the majority of lungs are sterilized using high concentrations of peracetic acid (PAA) resulting in extracellular matrix (ECM) depletion. These mechanically altered tissues have little to no storage potential. In this study, we report a sterilizing technique using supercritical carbon dioxide (ScCO(2)) that can achieve a sterility assurance level 10(−6) in decellularized lung matrix. The effects of ScCO(2) treatment on the histological, mechanical, and biochemical properties of the sterile decellularized lung were evaluated and compared with those of freshly decellularized lung matrix and with PAA-treated acellular lung. Exposure of the decellularized tissue to ScCO(2) did not significantly alter tissue architecture, ECM content or organization (glycosaminoglycans, elastin, collagen, and laminin), observations of cell engraftment, or mechanical integrity of the tissue. Furthermore, these attributes of lung matrix did not change after 6 months in sterile buffer following sterilization with ScCO(2), indicating that ScCO(2) produces a matrix that is stable during storage. The current study's results indicate that ScCO(2) can be used to sterilize acellular lung tissue while simultaneously preserving key biological components required for the function of the scaffold for regenerative medicine purposes