Adaptive capacity in ecosystems.

Understanding the adaptive capacity of ecosystems to cope with change is crucial to management. However, unclear and often confusing definitions of adaptive capacity make application of this concept difficult. In this paper, we revisit definitions of adaptive capacity and operationalize the concept. We define adaptive capacity as the latent potential of an ecosystem to alter resilience in response to change. We present testable hypotheses to evaluate complementary attributes of adaptive capacity that may help further clarify the components and relevance of the concept. Adaptive sampling, inference and modeling can reduce key uncertainties incrementally over time and increase learning about adaptive capacity. Such improvements are needed because uncertainty about global change and its effect on the capacity of ecosystems to adapt to social and ecological change is high.

Enhancing quantitative approaches for assessing community resilience.

Scholars from many different intellectual disciplines have attempted to measure, estimate, or quantify resilience. However, there is growing concern that lack of clarity on the operationalization of the concept will limit its application. In this paper, we discuss the theory, research development and quantitative approaches in ecological and community resilience. Upon noting the lack of methods that quantify the complexities of the linked human and natural aspects of community resilience, we identify several promising approaches within the ecological resilience tradition that may be useful in filling these gaps. Further, we discuss the challenges for consolidating these approaches into a more integrated perspective for managing social-ecological systems.

Oral administration of the nitric oxide biosynthesis inhibitor, N-nitro-L-arginine methyl ester (L-NAME), causes hypertension, but not glucose intolerance or insulin resistance, in rats.

While essential hypertension may be characterized by insulin resistance, it is unclear which defect is primary. We therefore compared normotensive Sprague-Dawley male rats who drank N-nitro-L-arginine methyl ester (L-NAME, 1 mg/mL in distilled water), with control rats who drank distilled water. Blood pressure was measured noninvasively, weight was controlled by dietary restriction, and glucose tolerance was assessed via oral glucose tolerance tests (OGTT). Blood pressure rose by the second day of L-NAME treatment, and remained elevated throughout the study, in contrast to the rats drinking water (P < .001). Weight rose similarly in both groups. OGTT were performed after 2 weeks of L-NAME. Serum glucose and insulin responses, assessed by two-way ANOVA, were similar in the two groups (P = NS). In summary, L-NAME administration resulted in hypertension, but not a deterioration in glucose tolerance in diet-controlled Sprague-Dawley rats. We conclude that the insulin resistance of some hypertensive states is not the result of hypertension per se, or increased vasoconstriction, such as might result from inhibition of endogenous nitric oxide synthesis, but rather indicates a fundamental metabolic disorder.

Glucose tolerance and blood pressure are improved in the spontaneously hypertensive rat by ethyl-2-(6-(4-chlorophenoxy)-hexyl)oxirane-2-carboxylate (etomoxir), an inhibitor of fatty acid oxidation.

We have demonstrated that glucose tolerance and insulin action are impaired in the spontaneously hypertensive rat (SHR), and that free fatty acids are elevated. Etomoxir, an inhibitor of fatty acid oxidation, has been shown to improve hyperglycemia in diabetic rats. We therefore performed oral glucose tolerance tests in SHR to assess glucose tolerance and insulin action in response to etomoxir. Because of the proposed relation between insulin action and hypertension, we examined the effect of etomoxir on blood pressure. Thirteen-week-old male SHR were randomized into two groups. Food was withdrawn at 8 AM and at 11 AM, animals received etomoxir (50 mg/kg) or control vehicle by gavage. Oral glucose tolerance tests were started at 1 PM. In other studies, 21-week-old male SHR were randomized into two groups. Animals were treated by gavage with etomoxir (50 mg/kg) or control vehicle, and blood pressure was measured noninvasively before and after treatment. Two weeks later, these experiments were repeated, but the treatments were reversed. In etomoxir-treated rats, the glucose response was significantly lower, whereas the insulin response was not significantly different. The combination of lowered glucose response, in the face of an unchanged insulin response, suggests an improvement in insulin action. However, fasting free fatty acids were higher, as was the free fatty acid response following etomoxir treatment. There was a dramatic decrease in blood pressure following etomoxir, with significant differences at 1.25, 3, 4.5, and 21 h after dosing. In summary, etomoxir treatment improved glucose tolerance and insulin action in SHR, whereas free fatty acid values were higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Alternative splicing of the HOX 2.2 homeobox gene in human hematopoietic cells and murine embryonic and adult tissues.

The HOX 2.2 homeobox gene is expressed in human hematopoietic cell lines with erythroid features (W.-F. Shen, et al, Proc. Natl. Acad. Sci. 86, 8536-8540, 1989). Both human and murine Hox 2.2 genes contain a single 1 kb intron which interrupts the sequence encoding the proposed homeobox protein. Four human erythroleukemia cell lines express the spliced, homeobox-coding transcript as the major form of message, and variable low amounts of unspliced HOX 2.2 mRNAs. Murine embryonic tissues and adult kidney and uterus contain approximately equal amounts of transcripts containing this intron and mRNAs from which the intron has been excised. The spliced transcript encodes a 224 amino acid homeobox protein, while the unspliced transcript would potentially encode a 140 residue protein containing the same N-terminal sequence but lacking the homeodomain.