Alaska-Washington Trade Profile: Waterborne Commerce

The overall purpose of this study was to establish a profile of Alaska-Washington waterborne movements, emphasizing commodity and port components that determine the needs of a physical distribution system. Specific objectives of the report are : 1. To determine Washington's share of the total Alaska-bound, waterborne traffic. 2. To present selected Washington-to-Alaska, waterborne movements by commodity and destination ports. 3. To present selected Alaska-to-Washington, waterborne movements by commodity and origination ports. 4. To determine implications of the trade profile with regard to future transportation and marketing needs. It should be noted that there are sizable noncommodity trade flows between the regions, i.e., labor, capital, and services that are not in this data base. This report contains only data on major commodity grouping and principal ports in Alaska. Additional information is on file at the Agricultural Experiment Station, University of Alaska, and at the Department of Agricultural Economics, Washington State University

IS IT FEASIBLE TO DEVELOP AN AGRIBUSINESS SELLING PRECISION FARMING SERVICES TO FARMERS?

With the introduction of Variable-Rate Technology, farmers have the capability to decrease input costs, increase output or both. Not all farmers can justify purchasing the equipment, therefore relying on agribusiness firms to provide precision farming services. This study was conducted to determine the feasibility of operating such an agribusiness.Agribusiness,

Targeting DNA repair pathways for cancer treatment: what's new?

Disruptions in DNA repair pathways predispose cells to accumulating DNA damage. A growing body of evidence indicates that tumors accumulate progressively more mutations in DNA repair proteins as cancers progress. DNA repair mechanisms greatly affect the response to cytotoxic treatments, so understanding those mechanisms and finding ways to turn dysregulated repair processes against themselves to induce tumor death is the goal of all DNA repair inhibition efforts. Inhibition may be direct or indirect. This burgeoning field of research is replete with promise and challenge, as more intricacies of each repair pathway are discovered. In an era of increasing concern about healthcare costs, use of DNA repair inhibitors can prove to be highly effective stewardship of R&D resources and patient expenses

Surface Gravities for 228 M, L, and T Dwarfs in the NIRSPEC Brown Dwarf Spectroscopic Survey

We combine 131 new medium-resolution (R~2000) J-band spectra of M, L, and T dwarfs from the Keck NIRSPEC Brown Dwarf Spectroscopic Survey (BDSS) with 97 previously published BDSS spectra to study surface-gravity-sensitive indices for 228 low-mass stars and brown dwarfs spanning spectral types M5-T9. Specifically, we use an established set of spectral indices to determine surface gravity classifications for all M6-L7 objects in our sample by measuring equivalent widths (EW) of the K I lines at 1.1692, 1.1778, 1.2529 um, and the 1.2 um FeHJ absorption index. Our results are consistent with previous surface gravity measurements, showing a distinct double peak - at ~L5 and T5 - in K I EW as a function of spectral type. We analyze K I EWs of 73 objects of known ages and find a linear trend between log(Age) and EW. From this relationship, we assign age ranges to the very low gravity, intermediate gravity, and field gravity designations for spectral types M6-L0. Interestingly, the ages probed by these designations remain broad, change with spectral type, and depend on the gravity sensitive index used. Gravity designations are useful indicators of the possibility of youth, but current datasets cannot be used to provide a precise age estimate.Comment: 33 pages, 13 figures, ApJ in pres

Exploiting the Ref-1-APE1 node in cancer signaling and other diseases: from bench to clinic

Reduction-oxidation factor 1-apurinic/apyrimidinic endonuclease (Ref-1/APE1) is a critical node in tumor cells, both as a redox regulator of transcription factor activation and as part of the DNA damage response. As a redox signaling protein, Ref-1/APE1 enhances the transcriptional activity of STAT3, HIF-1α, nuclear factor kappa B, and other transcription factors to promote growth, migration, and survival in tumor cells as well as inflammation and angiogenesis in the tumor microenvironment. Ref-1/APE1 is activated in a variety of cancers, including prostate, colon, pancreatic, ovarian, lung and leukemias, leading to increased aggressiveness. Transcription factors downstream of Ref-1/APE1 are key contributors to many cancers, and Ref-1/APE1 redox signaling inhibition slows growth and progression in a number of tumor types. Ref-1/APE1 inhibition is also highly effective when paired with other drugs, including standard-of-care therapies and therapies targeting pathways affected by Ref-1/APE1 redox signaling. Additionally, Ref-1/APE1 plays a role in a variety of other indications, such as retinopathy, inflammation, and neuropathy. In this review, we discuss the functional consequences of activation of the Ref-1/APE1 node in cancer and other diseases, as well as potential therapies targeting Ref-1/APE1 and related pathways in relevant diseases. APX3330, a novel oral anticancer agent and the first drug to target Ref-1/APE1 for cancer is entering clinical trials and will be explored in various cancers and other diseases bringing bench discoveries to the clinic

Targeting Ref-1/APE1 Pathway Inhibition in Pancreatic Cancer Using APX3330 for Clinical Trials

poster abstractPancreatic ductal adenocarcinoma is the 4th leading cause of cancer-related mortality in the US. Most patients present with advanced disease and ~95% die within five years, most surviving under six months. Targeted therapies offer modest improvement in survival, albeit at an increase in side effects and unwanted toxicities. Ref-1 regulates transcription factors involved in pancreatic cancer cell survival signaling due to its redox-coactivator activity, such as HIF-1α, NFκB, NRF2 and STAT3. High expression levels of Ref-1 indicate decreased survival in PDAC and other cancers. APX3330, a specific Ref-1 inhibitor, has been shown in multiple in vitro and in vivo pancreatic cancer models to be effective in reducing tumor growth and metastases. The safety and dose administration of APX3330 have been previously established, including toxicology, phase I, and phase II clinical evaluation in non-cancer patients in Japan (Eisai). We have partnered with ApeX Therapeutics to develop APX3330 for cancer treatment (phase I trial anticipated early 2016). We studied interactions of Ref-1, APX3330, convergent pathways; i.e. HIF-1α and STAT3, and downstream targets like CAIX. We performed in vivo studies demonstrating single and combination effects of APX3330 with Gemcitabine (Gem) showing significantly decreased tumor volume in the combination treatments. We also tested single and combination studies of APX3330 in an ex vivo 3-D tumor-stroma model system using patient derived tumor cells along with patient derived cancer-associated fibroblasts. We used the CAIX inhibitor SLC-0111 and JAK2 inhibitor, Ruxolitinib; both in clinical trials. In our system, APX3330 decreases the tumor area and intensity in a dose-dependent manner. The combination of APX3330 with Gem demonstrated an additive enhancement effect in the tumor, and APX3330 with SLC-0111/Ruxolitinib enhanced tumor killing. These data demonstrate APX3330 single agent efficacy in our 3D patient model and enhanced tumor killing when pathways regulated by Ref-1, HIF-1 and STAT3 are blocked

The Exemplar T8 Subdwarf Companion of Wolf 1130

We have discovered a wide separation (188.5") T8 subdwarf companion to the sdM1.5+WD binary Wolf 1130. Companionship of WISE J200520.38+542433.9 is verified through common proper motion over a ~3 year baseline. Wolf 1130 is located 15.83 +/- 0.96 parsecs from the Sun, placing the brown dwarf at a projected separation of ~3000 AU. Near-infrared colors and medium resolution (R~2000-4000) spectroscopy establish the uniqueness of this system as a high-gravity, low-metallicity benchmark. Although there are a number of low-metallicity T dwarfs in the literature, WISE J200520.38+542433.9 has the most extreme inferred metallicity to date with [Fe/H] = -0.64 +/- 0.17 based on Wolf 1130. Model comparisons to this exemplar late-type subdwarf support it having an old age, a low metallicity, and a small radius. However, the spectroscopic peculiarities of WISE J200520.38+542433.9 underscore the importance of developing the low-metallicity parameter space of the most current atmospheric models.Comment: Accepted to ApJ on 05 September 2013; 33 pages in preprint format, 8 figures, 3 table

Modeling Chronic Traumatic Encephalopathy: The Way Forward for Future Discovery

Despite the extensive media coverage associated with the diagnosis of chronic traumatic encephalopathy (CTE), our fundamental understanding of the disease pathophysiology remains in its infancy. Only recently have scientific laboratories and personnel begun to explore CTE pathophysiology through the use of preclinical models of neurotrauma. Some studies have shown the ability to recapitulate some aspects of CTE in rodent models, through the use of various neuropathologic, biochemical, and/or behavioral assays. Many questions related to CTE development however remain unanswered. These include the role of impact severity, the time interval between impacts, the age at which impacts occur, and the total number of impacts sustained. Other important variables such as the location of impacts, character of impacts, and effect of environment/lifestyle and genetics also warrant further study. In this work we attempt to address some of these questions by exploring work previously completed using single and repetitive injury paradigms. Despite some models producing some deficits similar to CTE symptoms, it is clear that further studies are required to understand the development of neuropathological and neurobehavioral features consistent with CTE-like features in rodents. Specifically, acute and chronic studies are needed that characterize the development of tau-based pathology