Glacial Processes and Their Relationship to Streamflow Flute Glacier, Alaska

Flute Glacier is located at the head of the South Fork of Eagle River, Alaska, about twenty air-miles east northeast of Anchorage. It is a small north-facing glacier, approximately two miles long and half a mile wide, situated in a deep glacial valley (see Figure 1). Elevations on the glacier range from 3,500 feet at the terminous to 5,800 feet at the top of the accumulation area. Water from Flute Glacier becomes the South Fork of Eagle River, draining about 32 square miles of area compared to a 192 square mile drainage basin for Eagle River. Limited discharge measurements made during October 1968 suggest that the South Fork contributes about 20% of the water flowing down Eagle River. Glacial meltwater forms an important percentage of the waters of the Eagle River system. Glaciers feeding the main Eagle River are large, complex and difficult to study. Flute Glacier, relatively small and of simple plan, was selected for study because of its small size and proximity to the metropolitan area of Anchorage. Water from the Eagle River system is presently included in the plans for future water supply for Anchorage. The Eagle River valley up to the 500 ft contour is a federal power reserve. The climate of the area surrounding Flute Glacier is alpine with cool temperatures and higher than average precipitation for the area. All the glacier is above treeline so no plant life is obvious. Mountain sheep inhabit the sharp alpine peaks surrounding the glacier.The work upon which this report is based was supported by funds (Project A-021- ALAS) provided by the United States Department of the Interior, Office of Water Resources Research, as authorized under the Water Resources Act of 1964 as amended

The Males Of Some Texan Ecitons

Integrative Biolog

On ℓ-adic representations for a space of noncongruence cuspforms

This paper is concerned with a compatible family of 4-dimensional ℓ-adic representations ρℓ of GQ := Gal(Q/Q) attached to the space of weight-3 cuspforms S3(Γ) on a noncongruence subgroup Γ ⊂ SL2(Z). For this representation we prove that: 1. It is automorphic: the L-function L(s,ρℓ∨) agrees with the L-function for an automorphic form for GL4(AQ), where ρℓ∨ is the dual of ρℓ. 2. For each prime p≥5 there is a basis hp = {hp+, hp-} of S3(Γ) whose expansion coefficients satisfy 3-term Atkin and Swinnerton-Dyer (ASD) relations, relative to the q-expansion coefficients of a newform f of level 432. The structure of this basis depends on the class of p modulo 12. The key point is that the representation ρℓ admits a quaternion multiplication structure in the sense of Atkin, Li, Liu, and Long

Double Bottom Line Progress Report: Assessing Social Impact in Double Bottom Line Ventures, Methods Catalog

Outlines methods for social entrepreneurs and their investors to define, measure and communicate social impact and return in early-stage ventures

Double Bottom Line Project Report: Assessing Social Impact in Double Bottom Line Ventures

This tool expresses costs and social impacts of an investment in monetary terms. Quantification is achieved according to one or more of three measures: NPV (the aggregate value of all costs, revenues and social impacts discounted), benefit-cost ratio (the discounted value of revenues and positive impacts divided by discounted value of costs and negative impacts) and internal rate of return (the net value of revenues plus impacts expressed as an annual percentage return on the total costs of the investment)

FSTL3 and its role in mediating fibrosis and hypertrophy in diet-induced obesity

Metabolic syndrome (MetS) is a conglomeration of several risk factors for cardiovascular disease, with obesity currently being one of the common causes of disability and death in the United States.1 Underlying the obesity, however, there is metabolic imbalance that could be exacerbating the issue of metabolic syndrome.2 Approximately 34% of adults over 20 years old matched the criteria for metabolic syndrome.3 The risk factors for cardiovascular disease (CVD) associated with metabolic syndrome can, over time, lead to severe CVDs, such as heart failure (HF).4 Metabolic syndrome can also lead to developing metabolic heart disease over time. Understanding the development of cardiac hypertrophy and fibrosis in diet-induced metabolic heart disease allow development of an early treatment of metabolic heart disease (MHD) and HF. This study looked at one potential mediator and its role in cardiac hypertrophy and fibrosis, follistatin-like 3 (FSTL3). FSTL3 is an extracellular antagonist of members of the TGF-β superfamily. The goal of our study was to determine the effect, if any, a knockout of FSTL3 would have on the development of cardiac hypertrophy and fibrosis after a high-fat, high-sucrose diet for five months. FSTL3 knockout mice were given a high-fat, high-sucrose (HFHS) diet for five months. These mice were then sacrificed and their hearts were analyzed for cardiac myocyte hypertrophy and interstitial fibrosis using histological methods. After five months on the HFHS diet, wild-type (WT) mice had cardiac hypertrophy. In FLRG KO mice the diet-induced cardiac hypertrophy was attenuated. WT HFHS-fed mice developed interstitial fibrosis, and FLRG KO HFHS developed more accentuated interstitial fibrosis than WT HFHS diet fed mice. This study is useful in suggesting that FTSL3 contributes to the pathogenesis of cardiac hypertrophy in MHD. FTSL3 may be a useful biomarker for cardiac hypertrophy in patients with suspected MHD, and may be a viable target for therapeutic interventions aimed at decreasing pathologic myocardial hypertrophy