California State University, Long Beach

About: California State University, Long Beach is a education organization based out in Long Beach, California, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 10036 authors who have published 13933 publications receiving 377394 citations. The organization is also known as: Cal State Long Beach & Long Beach State.

A History of Chile, 1808-2002

Abstract: A History of Chile chronicles the nation's political, social, and economic evolution from its independence until the early years of the Lagos regime. Employing primary and secondary materials, it explores the growth of Chile's agricultural economy, during which the large landed estates appeared; the nineteenth-century wheat and mining booms; the rise of the nitrate mines; their replacement by copper mining; and the diversification of the nation's economic base. This volume also traces Chile's political development from oligarchy to democracy, culminating in the election of Salvador Allende, his overthrow by a military dictatorship, and the return of popularly elected governments. Additionally, the volume examines Chile's social and intellectual history: the process of urbanization, the spread of education and public health, the diminution of poverty, the creation of a rich intellectual and literary tradition, the experiences of middle and lower classes and the development of Chile's unique culture.

Re-validation and shortening of the Functional Assessment of Anorexia/Cachexia Therapy (FAACT) questionnaire.

Abstract: Purpose: The original Functional Assessment of Anorexia/Cachexia Therapy (FAACT) was designed to measure general aspects of quality of life (QOL) as well as specific anorexia/cachexia-related concerns. Our primary purpose was to reduce the number of anorexia/cachexia subscale items in a manner that either retains or improves reliability, validity and precision. Methods: The FAACT was administered using an interactive computer program that allowed immediate entry of the data. A total of 213 patients were recruited. Results: A combined empirical and conceptual approach led to the reduction of the anorexia/cachexia subscale (A/CS) from 18 to 12 items. A 26-item trial outcome index (TOI) combining physical well-being (PWB), functional well-being (FWB), and the A/CS-12 was highly reliable and sensitive to change in performance status rating (PSR). We found that PWB, FWB, and A/CS-12 subscales performed differently. Specifically, PWB and FWB scores decreased in patients whose (PSR) worsened. However, although A/CS-12 scores were responsive to change in PSR over time, average A/CS-12 scores of all patients, even those whose PSR worsened, improved over the course of treatment. Conclusions: Elimination of six items from the anorexia/cachexia subscale of the FAACT was accomplished without loss of internal consistency or sensitivity to change in performance status. The A/CS-12 subscale provides unique, important information not captured by a generic chronic illness questionnaire.

The evolution of domain-general mechanisms in intelligence and learning.

Abstract: For both humans and animals, domain-general mechanisms are fallible but powerful tools for attaining evolutionary goals (e.g., resources) in uncertain, novel environments that were not recurrent features of the environment of evolutionary adaptedness. Domain-general mechanisms interact in complex ways with domain-specific, information-encapsulated modules, most importantly by manipulating information obtained from various modules in attempting to solve novel problems. Mechanisms of general intelligence, particularly the executive functions of working memory, underlie analogical reasoning as well as the decontextualization processes that are central to human thought. Although there is a variety of evolved, special purpose learning devices, learning is also characterized by domain-general mechanisms that are able to achieve evolutionary goals by making novel and serendipitous associations with environmental cues.

Estrogen Inhibits Cardiac Hypertrophy: Role of Estrogen Receptor-β to Inhibit Calcineurin

Abstract: Estrogen has been reported to prevent development of cardiac hypertrophy in female rodent models and in humans. However, the mechanisms of sex steroid action are incompletely understood. We determined the cellular effects by which 17-estradiol (E2) inhibits angiotensin II (AngII)-induced cardiac hypertrophy in vivo. Two weeks of angiotensin infusioninfemalemiceresultedinmarkedhypertrophyofthe left ventricle, exacerbated by the loss of ovarian steroid hormones from oophorectomy. Hypertrophy was 51% reversed by the administration of E2 (insertion of 0.1 mg/21-d-release tablets). The effects of E2 were mainly mediated by the estrogen receptor (ER) -isoform, because E2 had little effect in ERnull mice but comparably inhibited AngII-induced hypertrophy in wild-type or ER-null mice. AngII induced a switch of myosin heavy chain production from to , but this was inhibited by E2 via ER. AngII-induced ERK activation was also inhibited by E2 through the -receptor. E2 stimulated brain natriuretic peptide protein expression and substantially prevented ventricular interstitial cardiac fibrosis (collagen deposition) as induced by AngII. Importantly, E2 inhibited calcineurin activity that was stimulated by AngII, related to E2 stimulating the modulatory calcineurin-interacting protein (MCIP) 1 gene and protein expression. E2 acting mainly through ER mitigates the important signaling by AngII that produces cardiac hypertrophy and fibrosis in female mice. (Endocrinology 149: 3361–3369, 2008)