Tribal Corridor Management Planning: Model, Case Study, and Guide for Caltrans District 1, Research Report 10-01

In Northern California, tribal governments and personnel of the California Department of Transportation (Caltrans) District 1, have applied innovative context-sensitive solutions to meet a variety of transportation challenges along state highways that traverse tribal lands. This report describes and discusses the efforts under way and offer suggestions for continuing and extending these initiatives through the development of Tribal Corridor Management Plans (TCMPs). The methods employed in this project are multidisciplinary and include: (1) content analysis of existing corridor management plans; (2) literature review to identify “best practices;” (3) participant observation; (4) interviews with local stakeholders; (5) focus group interviews with Caltrans personnel; and (6) landscape analysis. This study’s authors conclude that Caltrans District 1 staff and tribal governments share common goals for highway operations; however, progress —while significant—has been somewhat hampered by geographic and administrative challenges. It is recommended that Caltrans and the tribes seek early and frequent communication and collaboration to overcome these obstacles. Further, they identify several examples of non-standard design elements that could be incorporated into highway improvements to enhance local sense of place among both residents and travelers. A preliminary TCMP for the segment of State Route 96 that lies within the boundaries of the Hoopa Valley Indian Reservation is presented as an example. Beyond its role as a guide for initiating tribal corridor projects within Caltrans District 1, the report should prove instructive for any efforts to enhance sense of place within transportation byways, particularly in Native communities

Effects of Hurricane Katrina on the Mammalian and Vegetative Communities of the Barrier Islands of Mississippi

The barrier islands of the gulf coast of the U.S. have been shaped and changed by hurricanes for centuries. These storms can alter the vegetation of the barrier islands by redistributing sediments, scouring off vegetation, physical damage to the plants, and by salt stress following the storm. Hurricanes also alter the mammal communities of the barrier islands through direct mortality and by altering vegetative communities. It is important to understand how the vegetation of barrier islands recovers after major hurricanes because the vegetation provides the structure that maintains and builds these islands. Following the landfall of Hurricane Katrina in August of 2005, I studied the changes in the herbaceous ground cover and the density of woody plants in Gulf Islands National Seashore in Mississippi from the winter of 2005 to the summer of 2007. Growth from existing plants and seed banks quickly revegetated the islands after the storm. The amount of live ground cover increased and bare ground decreased on each island and in every vegetation type. Most woody plant species also showed a net increase in density, with the exception of pine (Pinus elliottii) and Florida rosemary (Ceratiola ericoides). The regeneration of woody species and the uniform increase in the live ground cover seemed to indicate that the vegetation of the islands was not irreversibly impacted. I also studied the changes in the composition of mammal populations in Gulf Islands National Seashore from the winter of 2005 to the summer of 2007. Prior to the storm 11 terrestrial mammal species were recorded in studies of the barrier islands. In the 2 years following Hurricane Katrina, I recorded only 1 of the 7 species on Cat Island, 5 of the 9 species on Horn Island and 2 species each on East Ship, West Ship, and Petit Bois Islands (which previously had 4, 4, and 2 each). Populations of mammals that used multiple vegetation types (raccoons [Procyon lotor], nutria [Myocastor coypus], and eastern cottontail [Sylvilagus floridanus]) seemed to show more tolerance to hurricane disturbance than more specialized species (black rat [Rattus rattus], marsh rice rat [Oryzomys palustris]). I also recorded at least one colonization event by river otter (Lutra canadensis), a species not recently recorded on the islands. This research serves as a baseline for future comparison following similar storms

Activation Energy of Metastable Amorphous Ge2Sb2Te5 from Room Temperature to Melt

Resistivity of metastable amorphous Ge2Sb2Te5 (GST) measured at device level show an exponential decline with temperature matching with the steady-state thin-film resistivity measured at 858 K (melting temperature). This suggests that the free carrier activation mechanisms form a continuum in a large temperature scale (300 K - 858 K) and the metastable amorphous phase can be treated as a super-cooled liquid. The effective activation energy calculated using the resistivity versus temperature data follow a parabolic behavior, with a room temperature value of 333 meV, peaking to ~377 meV at ~465 K and reaching zero at ~930 K, using a reference activation energy of 111 meV (3kBT/2) at melt. Amorphous GST is expected to behave as a p-type semiconductor at Tmelt ~ 858 K and transitions from the semiconducting-liquid phase to the metallic-liquid phase at ~ 930 K at equilibrium. The simultaneous Seebeck (S) and resistivity versus temperature measurements of amorphous-fcc mixed-phase GST thin-films show linear S-T trends that meet S = 0 at 0 K, consistent with degenerate semiconductors, and the dS/dT and room temperature activation energy show a linear correlation. The single-crystal fcc is calculated to have dS/dT = 0.153 {\mu}V/K for an activation energy of zero and a Fermi level 0.16 eV below the valance band edge.Comment: 5 pages, 5 figure

Pharmacologic inhibition of S-nitrosoglutathione reductase protects against experimental asthma in BALB/c mice through attenuation of both bronchoconstriction and inflammation

BACKGROUND: S-nitrosoglutathione (GSNO) serves as a reservoir for nitric oxide (NO) and thus is a key homeostatic regulator of airway smooth muscle tone and inflammation. Decreased levels of GSNO in the lungs of asthmatics have been attributed to increased GSNO catabolism via GSNO reductase (GSNOR) leading to loss of GSNO- and NO- mediated bronchodilatory and anti-inflammatory actions. GSNOR inhibition with the novel small molecule, N6022, was explored as a therapeutic approach in an experimental model of asthma. METHODS: Female BALB/c mice were sensitized and subsequently challenged with ovalbumin (OVA). Efficacy was determined by measuring both airway hyper-responsiveness (AHR) upon methacholine (MCh) challenge using whole body plethysmography and pulmonary eosinophilia by quantifying the numbers of these cells in the bronchoalveolar lavage fluid (BALF). Several other potential biomarkers of GSNOR inhibition were measured including levels of nitrite, cyclic guanosine monophosphate (cGMP), and inflammatory cytokines, as well as DNA binding activity of nuclear factor kappa B (NFκB). The dose response, onset of action, and duration of action of a single intravenous dose of N6022 given from 30 min to 48 h prior to MCh challenge were determined and compared to effects in mice not sensitized to OVA. The direct effect of N6022 on airway smooth muscle tone also was assessed in isolated rat tracheal rings. RESULTS: N6022 attenuated AHR (ED(50) of 0.015 ± 0.002 mg/kg; Mean ± SEM) and eosinophilia. Effects were observed from 30 min to 48 h after treatment and were comparable to those achieved with three inhaled doses of ipratropium plus albuterol used as the positive control. N6022 increased BALF nitrite and plasma cGMP, while restoring BALF and plasma inflammatory markers toward baseline values. N6022 treatment also attenuated the OVA-induced increase in NFκB activation. In rat tracheal rings, N6022 decreased contractile responses to MCh. CONCLUSIONS: The significant bronchodilatory and anti-inflammatory actions of N6022 in the airways are consistent with restoration of GSNO levels through GSNOR inhibition. GSNOR inhibition may offer a therapeutic approach for the treatment of asthma and other inflammatory lung diseases. N6022 is currently being evaluated in clinical trials for the treatment of inflammatory lung disease

HTLV-1 Tax Mediated Downregulation of miRNAs Associated with Chromatin Remodeling Factors in T Cells with Stably Integrated Viral Promoter

RNA interference (RNAi) is a natural cellular mechanism to silence gene expression and is predominantly mediated by microRNAs (miRNAs) that target messenger RNA. Viruses can manipulate the cellular processes necessary for their replication by targeting the host RNAi machinery. This study explores the effect of human T-cell leukemia virus type 1 (HTLV-1) transactivating protein Tax on the RNAi pathway in the context of a chromosomally integrated viral long terminal repeat (LTR) using a CD4+ T-cell line, Jurkat. Transcription factor profiling of the HTLV-1 LTR stably integrated T-cell clone transfected with Tax demonstrates increased activation of substrates and factors associated with chromatin remodeling complexes. Using a miRNA microarray and bioinformatics experimental approach, Tax was also shown to downregulate the expression of miRNAs associated with the translational regulation of factors required for chromatin remodeling. These observations were validated with selected miRNAs and an HTLV-1 infected T cells line, MT-2. miR-149 and miR-873 were found to be capable of directly targeting p300 and p/CAF, chromatin remodeling factors known to play critical role in HTLV-1 pathogenesis. Overall, these results are first in line establishing HTLV-1/Tax-miRNA-chromatin concept and open new avenues toward understanding retroviral latency and/or replication in a given cell type

Identification of the Allosteric Regulatory Site of Insulysin

Background: Insulin degrading enzyme (IDE) is responsible for the metabolism of insulin and plays a role in clearance of the Ab peptide associated with Alzheimer's disease. Unlike most proteolytic enzymes, IDE, which consists of four structurally related domains and exists primarily as a dimer, exhibits allosteric kinetics, being activated by both small substrate peptides and polyphosphates such as ATP.Principal Findings: the crystal structure of a catalytically compromised mutant of IDE has electron density for peptide ligands bound at the active site in domain 1 and a distal site in domain 2. Mutating residues in the distal site eliminates allosteric kinetics and activation by a small peptide, as well as greatly reducing activation by ATP, demonstrating that this site plays a key role in allostery. Comparison of the peptide bound IDE structure (using a low activity E111F IDE mutant) with unliganded wild type IDE shows a change in the interface between two halves of the clamshell-like molecule, which may enhance enzyme activity by altering the equilibrium between closed and open conformations. in addition, changes in the dimer interface suggest a basis for communication between subunits.Conclusions/Significance: Our findings indicate that a region remote from the active site mediates allosteric activation of insulysin by peptides. Activation may involve a small conformational change that weakens the interface between two halves of the enzyme.United States Public Health ServicesUniv Kentucky, Dept Mol & Cellular Biochem, Lexington, KY 40536 USAUniv Kentucky, Struct Biol Ctr, Lexington, KY USAUniversidade Federal de São Paulo, Dept Biophys, Escola Paulista Med, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biophys, Escola Paulista Med, São Paulo, BrazilUnited States Public Health Services: NS38041United States Public Health Services: DA02243United States Public Health Services: DA016176United States Public Health Services: P20 RR20171United States Public Health Services: T32 DA016176Web of Scienc