Lake Whatcom Watershed Land Acquisition Project: environmental impact assessment

The purpose of this report is to reexamine and reevaluate the environmental impacts of the Lake Whatcom Watershed Land Acquisition Ordinance, (Ordinance 2000-09-058) which was passed by the City of Bellingham in the fall of 2000. The ordinance placed a $6.00 fee on the monthly drinking water bill of customers

Induced magnetism in transition metal intercalated graphitic systems

We investigate the structure, chemical bonding, electronic properties, and magnetic behavior of a three-dimensional graphitic network in aba and aaa stacking with intercalated transition metal atoms (Mn, Fe, Co, Ni, and Cu). Using density functional theory, we find induced spin-polarization of the C atoms both when the graphene sheets are aba stacked (forming graphite) and aaa stacked (resembling bi-layer graphene). The magnetic moment induced by Mn, Fe, and Co turns out to vary from 1.38 {\mu}B to 4.10 {\mu}B, whereas intercalation of Ni and Cu does not lead to a magnetic state. The selective induction of spin-polarization can be utilized in spintronic and nanoelectronic applications.Comment: 13 pages, 3 figures, 1 tabl

Drawing Trees with Perfect Angular Resolution and Polynomial Area

We study methods for drawing trees with perfect angular resolution, i.e., with angles at each node v equal to 2{\pi}/d(v). We show: 1. Any unordered tree has a crossing-free straight-line drawing with perfect angular resolution and polynomial area. 2. There are ordered trees that require exponential area for any crossing-free straight-line drawing having perfect angular resolution. 3. Any ordered tree has a crossing-free Lombardi-style drawing (where each edge is represented by a circular arc) with perfect angular resolution and polynomial area. Thus, our results explore what is achievable with straight-line drawings and what more is achievable with Lombardi-style drawings, with respect to drawings of trees with perfect angular resolution.Comment: 30 pages, 17 figure

Paradoxical roles of antioxidant enzymes:Basic mechanisms and health implications

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated from aerobic metabolism, as a result of accidental electron leakage as well as regulated enzymatic processes. Because ROS/RNS can induce oxidative injury and act in redox signaling, enzymes metabolizing them will inherently promote either health or disease, depending on the physiological context. It is thus misleading to consider conventionally called antioxidant enzymes to be largely, if not exclusively, health protective. Because such a notion is nonetheless common, we herein attempt to rationalize why this simplistic view should be avoided. First we give an updated summary of physiological phenotypes triggered in mouse models of overexpression or knockout of major antioxidant enzymes. Subsequently, we focus on a series of striking cases that demonstrate “paradoxical” outcomes, i.e., increased fitness upon deletion of antioxidant enzymes or disease triggered by their overexpression. We elaborate mechanisms by which these phenotypes are mediated via chemical, biological, and metabolic interactions of the antioxidant enzymes with their substrates, downstream events, and cellular context. Furthermore, we propose that novel treatments of antioxidant enzyme-related human diseases may be enabled by deliberate targeting of dual roles of the pertaining enzymes. We also discuss the potential of “antioxidant” nutrients and phytochemicals, via regulating the expression or function of antioxidant enzymes, in preventing, treating, or aggravating chronic diseases. We conclude that “paradoxical” roles of antioxidant enzymes in physiology, health, and disease derive from sophisticated molecular mechanisms of redox biology and metabolic homeostasis. Simply viewing antioxidant enzymes as always being beneficial is not only conceptually misleading but also clinically hazardous if such notions underpin medical treatment protocols based on modulation of redox pathways

The use of carboxymethylcellulose gel to increase non-viral gene transfer in mouse airways

We have assessed whether viscoelastic gels known to inhibit mucociliary clearance can increase lipid-mediated gene transfer. Methylcellulose or carboxymethylcellulose (0.25 to 1.5%) were mixed with complexes of the cationic lipid GL67A and plasmids encoding luciferase and perfused onto the nasal epithelium of mice. Survival after perfusion with 1% CMC or1% MC was 90 and 100%, respectively. In contrast 1.5% CMC was uniformly lethal likely due to the viscous solution blocking the airways. Perfusion with 0.5% CMC containing lipid/DNA complexes reproducibly increased gene expression by approximately 3-fold (n= 16, p<0.05). Given this benefit, likely related to increased duration of contact, we also assessed the effect of prolonging contact time of the liposome/DNA complexes by delivering our standard 80 μg DNA dose over either approximately 22 or 60 min of perfusion. This independently increased gene transfer by 6-fold (n=8, p<0.05) and could be further enhanced by the addition of 0.5% CMC, leading to an overall 25-fold enhancement (n=8, p<0.001) in gene expression. As a result of these interventions CFTR transgene mRNA transgene levels were increased several logs above background. Interestingly, this did not lead to correction of the ion transport defects in the nasal epithelium of cystic fibrosis mice nor for immunohistochemical quantification of CFTR expression. To assess if 0.5% CMC also increased gene transfer in the mouse lung, we used whole body nebulisation chambers. CMC was nebulised for 1 hr immediately before, or simultaneously with GL67A/pCIKLux. The former did not increase gene transfer, whereas co-administration significantly increased gene transfer by 4-fold (p<0.0001, n=18). This study suggests that contact time of non-viral gene transfer agents is a key factor for gene delivery, and suggests two methods which may be translatable for use in man

On the Connection Between Momentum Cutoff and Operator Cutoff Regularizations

Operator cutoff regularization based on the original Schwinger's proper-time formalism is examined. By constructing a regulating smearing function for the proper-time integration, we show how this regularization scheme simulates the usual momentum cutoff prescription yet preserves gauge symmetry even in the presence of the cutoff scales. Similarity between the operator cutoff regularization and the method of higher (covariant) derivatives is also observed. The invariant nature of the operator cutoff regularization makes it a promising tool for exploring the renormalization group flow of gauge theories in the spirit of Wilson-Kadanoff blocking transformation.Comment: 28 pages in plain TeX, no figures. revised and expande

Increased serum levels of interleukin-6 and von Willenbrand Factor in early phase of acute coronary syndrome in a young and multiethnic Malaysian population

Objective Interleukin-6 (IL6; proinflammatory marker), von Willebrand Factor (vWF; endothelial dysfunction marker) and P-selectin ( platelet activation marker), may play important roles in defining the pathogenesis of vulnerable plaques in acute coronary syndrome (ACS). This study aims to investigate the expression and relationship of these markers in early phases of ACS in a young and multiethnic Malaysian population. Design Peripheral whole blood mRNA, and serum levels of IL6, vWF and P-selectin were measured in 22 patients with ACS, and in 28 controls with angiographically significant coronary artery disease without previous ACS events. Venous blood from ACS patients was obtained within 1 h of hospital admission. Results No significant differences of IL6, vWF and P-selectin mRNA levels between ACS and controls were seen. ACS patients had significantly higher serum levels of IL6 and vWF ( p<0.001), compared with controls. P-selectin correlated with IL6 (r=0.697, p=0.003) and vWF (r=0.497, p=0.05) at mRNA levels, indicating a possible association between these three indices of ACS pathogenesis. Conclusions Increased serum levels of IL6 and vWF suggest that inflammation and endothelial dysfunction may play a prominent role in the pathogenesis of the disease during the early phase of ACS