Search

Weather and climate extremes profoundly affect society and the environment, resulting in the loss of life, property, and habitat. The extremes discussed herein are causally related: extratropical storms account for the majority of extreme winds during the cold season, and extreme waves are largely driven by extreme winds. For assessment purposes, extremes are defined based on meteorological principles rather than physical destructiveness. Nevertheless, each of these extremes can result in substantial societal impacts. Estimates of extratropical storm activity primarily derive from two sources: atmospheric reanalyses and pressure-based indices. Reanalysis products have the advantage of uniform space and time fields on which to locate pressure minima or vorticity maxima, facilitating the identification of storm tracks. In contrast, pressure-based indices have the advantage of being directly computed from in situ observations, which often extend further back in time than most reanalyses.

INTRODUCTIONNative Americans have been subjected to colonial domination by European nations for five centuries, resulting in a radical destabilization of their sociocultural and economic systems, a general deterioration of health, and rapid depopulation. The resulting effects of cultural differences and conflicts, learned dependency, poverty, and feelings of powerlessness and low self-regard have impacted dramatically the health and quality of Native life. American Indians in the United States today are facing major health and social problems such as diabetes, substance abuse, poor nutrition, obesity, vehicular accidents, and suicides. Alcohol abuse, for example, is implicated in four of the ten leading causes of death among Native Americans. Entire communities are crippled by health problems, which ultimately feed into a cycle of despair, cultural dislocation, and lack of self-sufficiency.This article explores how participants in a self-empowerment program have understood and translated the training into self-sufficiency both at the personal and community levels. In analyzing this process we will listen to the participants’ voices, the words and the meanings they give to what they have learned from the program, and what enabled them to do something for themselves and others.

Two case studies are presented to compare and contrast the challenges encountered when attempting to conduct participatory evaluations (P-Es) with tribal programs that represented two extremes of collaboration between the programs and evaluators. In one case, the P-E was successful because the principals were invested in the program, whereas in the second case, the absence of a shared program vision hampered the ability to adequately evaluate the program. The authors contend that governmental funding agencies have responsibilities to ensure that their expectations are appropriate, the proposed program is feasible, and that technical assistance should be provided before the grant is written, not after it has been funded. (Contains 3 notes.)

Hepatic glucagon action increases in response to accelerated metabolic demands and is associated with increased whole body substrate availability, including circulating lipids. The hypothesis that increases in hepatic glucagon action stimulate AMP-activated protein kinase (AMPK) signaling and peroxisome proliferator-activated receptor-[alpha] (PPAR[alpha] and fibroblast growth factor 21 (FGF21) expression in a manner modulated by fatty acids was tested in vivo. Wild-type ([gcgr.sup.+/+]) and glucagon receptor-null ([gcgr.sup.-/-]) littermate mice were studied using an 18-h fast, exercise, and hyperglucagonemic-euglycemic clamps plus or minus increased circulating lipids. Fasting and exercise in [gcgr.sup.+/+], but not [gcgr.sup.-/-] mice, increased hepatic phosphorylated AMPK[alpha] at threonine 172 ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]) and PPAR[alpha] and FGF21 mRNA. Clamp results in [gcgr.sup.+/+] mice demonstrate that hyperlipidemia does not independently impact or modify glucagon-stimulated increases in hepatic AMP/ATP, [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII], or PPAR[alpha] and FGF21 mRNA. It blunted glucagon-stimulated acetyl-CoA carboxylase phosphorylation, a downstream target of AMPK, and accentuated PPAR[alpha] and FGF21 expression. All effects were absent in [gcgr.sup.-/-] mice. These findings demonstrate that glucagon exerts a critical regulatory role in liver to stimulate pathways linked to lipid metabolism in vivo and shows for the first time that effects of glucagon on PPARa and FGF21 expression are amplified by a physiological increase in circulating lipids. adenosine 5'-monophosphate-activated protein kinase; peroxisome proliferator-activated receptor-[alpha]; fibroblast growth factor 21 doi: 10.1152/ajpendo.00263.2010.

Endothelial nitric oxide synthase (eNOS) is associated with a number of physiological functions involved in the regulation of metabolism; however, the functional role of eNOS is poorly understood. We tested the hypothesis that eNOS is critical to muscle cell signaling and fuel usage during exercise in vivo, using 16-wk-old catheterized (carotid artery and jugular vein) C57BL/6J mice with wild-type (WT), partial (+/-), or no expression (-/-) of eNOS. Quantitative reductions in eNOS expression (~40%) elicited many of the phenotypic effects observed in [enos.sup.-/-] mice under fasted, sedentary conditions, with expression of oxidative phosphorylation complexes I to V and ATP levels being decreased, and total NOS activity and [Ca.sup.2+]/CaM kinase II [Thr.sup.286] phosphorylation being increased in skeletal muscle. Despite these alterations, exercise tolerance was markedly impaired in [enos.sup.-/-] mice during an acute 30-min bout of exercise. An eNOS-dependent effect was observed with regard to AMP-activated protein kinase signaling and muscle perfusion. Muscle glucose and long-chain fatty acid uptake, and hepatic and skeletal muscle glycogenolysis during the exercise bout was markedly accelerated in [enos.sup.-/-] mice compared with [enos.sup.+/-] and WT mice. Correspondingly, [enos.sup.-/-] mice exhibited hypoglycemia during exercise. Thus, the ablation of eNOS alters a number of physiological processes that result in impaired exercise capacity in vivo. The finding that a partial reduction in eNOS expression is sufficient to induce many of the changes associated with ablation of eNOS has implications for chronic metabolic diseases, such as obesity and insulin resistance, which are associated with reduced eNOS expression. mitochondria; oxidative phosphorylation; blood flow doi: 10.1152/ajpregu.00004.2009.