884 resultados para MATURITY
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Se estudian la influencia en el microclima de racimos (temperatura e iluminación) de tres sistemas de conducción en la variedad Syrah en una zona calida.
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Hepatocyte nuclear factor 4α (HNF4α) plays a critical role in regulating the expression of many genes essential for normal functioning of liver, gut, kidney, and pancreatic islets. A nonsense mutation (Q268X) in exon 7 of the HNF4α gene is responsible for an autosomal dominant, early-onset form of non-insulin-dependent diabetes mellitus (maturity-onset diabetes of the young; gene named MODY1). Although this mutation is predicted to delete 187 C-terminal amino acids of the HNF4α protein the molecular mechanism by which it causes diabetes is unknown. To address this, we first studied the functional properties of the MODY1 mutant protein. We show that it has lost its transcriptional transactivation activity, fails to dimerize and bind DNA, implying that the MODY1 phenotype is because of a loss of HNF4α function. The effect of loss of function on HNF4α target gene expression was investigated further in embryonic stem cells, which are amenable to genetic manipulation and can be induced to form visceral endoderm. Because the visceral endoderm shares many properties with the liver and pancreatic β-cells, including expression of genes for glucose transport and metabolism, it offers an ideal system to investigate HNF4-dependent gene regulation in glucose homeostasis. By exploiting this system we have identified several genes encoding components of the glucose-dependent insulin secretion pathway whose expression is dependent upon HNF4α. These include glucose transporter 2, and the glycolytic enzymes aldolase B and glyceraldehyde-3-phosphate dehydrogenase, and liver pyruvate kinase. In addition we have found that expression of the fatty acid binding proteins and cellular retinol binding protein also are down-regulated in the absence of HNF4α. These data provide direct evidence that HNF4α is critical for regulating glucose transport and glycolysis and in doing so is crucial for maintaining glucose homeostasis.
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Targeted gene disruption in the murine TOP3β gene-encoding DNA topoisomerase IIIβ was carried out. In contrast to the embryonic lethality of mutant mice lacking DNA topoisomerase IIIα, top3β−/− nulls are viable and grow to maturity with no apparent defects. Mice lacking DNA topoisomerase IIIβ have a shorter life expectancy than their wild-type littermates, however. The mean lifespan of the top3β−/− mice is about 15 months, whereas that of their wild-type littermates is longer than 2 years. Mortality of the top3β−/− nulls appears to correlate with lesions in multiple organs, including hypertrophy of the spleen and submandibular lymph nodes, glomerulonephritis, and perivascular infiltrates in various organs. Because the DNA topoisomerase III isozymes are likely to interact with helicases of the RecQ family, enzymes that include the determinants of human Bloom, Werner, and Rothmund–Thomson syndromes, the shortened lifespan of top3β−/− mice points to the possibility that the DNA topoisomerase III isozymes might be involved in the pathogenesis of progeroid syndromes caused by defective RecQ helicases.
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Among fruit-fly species of the genus Drosophila there is remarkable variation in sperm length, with some species producing gigantic sperm (e.g., > 10 times total male body length). These flies are also unusual in that males of some species exhibit a prolonged adult nonreproductive phase. We document sperm length, body size, and sex-specific ages of reproductive maturity for 42 species of Drosophila and, after controlling for phylogeny, test hypotheses to explain the variation in rates of sexual maturation. Results suggest that delayed male maturity is a cost of producing long sperm. A possible physiological mechanism to explain the observed relationship is discussed.
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Eating disorders present a significant physical and psychological problem with a prevalence rate of approximately six percent in the United States. Despite the extensive literature, identifying the consistent risk factors for predicting the course of treatment in eating disorders remains difficult. The present study explores the use of a standardized assessment, using the consistently validated Eating Disorder Inventory-III (EDI-3), in predicting treatment outcome. Specifically, the study investigates the particular scale of Maturity Fears (MF) on the EDI-3, hypothesizing that higher scores on the MF scale would predict lower rates of recovery and treatment completion. The participants were 52 eating disorder patients (19 AN, 18 BN, and 15 EDNOS), consecutively admitted to a five-month long intensive outpatient program (IOP). The participants completed an EDI-3 self-report at pre and post treatment, and their score on the MF scale did not show a significant predictive relationship to treatment completion or change in symptoms, as measured by the Eating Disorder Risk Composite (EDRC) scale on the EDI-3. This finding primarily suggests that maturity fears are not a significant predictive factor in an outpatient setting with adults, as compared to previous studies that found a relationship between maturity fears and treatment outcome, primarily with adolescent and inpatient populations.
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High maturity fears predict poor treatment outcomes in women with anorexia nervosa (AN). The purpose of this study was to determine if weight gain predicts decreases in maturity fears (MF) for AN patients. Fifty-six patients in an eating disorders partial hospitalization program were administered a series of psychological tests at intake and discharge. R2 values indicate that percent change in weight restoration will not accurately forecast the change in MF scores, although a positive trend was identified between the two variables. The weak predictive relationship suggests that weight restoration alone is not adequate to address the psychological components of AN.
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The construct of maturity is often discussed in the realm of adolescent development; however, relatively little research has been devoted to developing a comprehensive, reliable, and valid measure with which to assess it. The purpose of this study was to investigate the concurrent validity of the Montana Adolescent Maturity Assessment - III (MAMA-III), a proxy measure completed by clinicians regarding an adolescent's functioning, with the immaturity scale (IMM) of the MMPI-A. To provide more specified results, a factor analysis of the IMM was undertaken. Results yielded a low but significant correlation between the MAMA-III and the IMM, as well as significant convergent correlations between individual factors of the MAMA and IMM scales. Correlations among the MAMA-III factors, the IMM factors, and the ten clinical scales of the MMPI-A were also analyzed with the goal of better understanding what each measures. Implications are discussed regarding the clinical distinctions between the two measures, and the prospect of a more comprehensive understanding of the construct of maturity.
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Aim: Vascular disease such as cardiovascular and cerebrovascular diseases, or retinopathy, nephropathy and neuropathy are common in diabetes. Maturity - onset diabetes of the young (MODY) describes a clinically heterogeneous group of familial diabetes characterized by monogenic, autosomal dominant inheritance that generally results from beta cell dysfunction. This study aims to assess the presence of vascular complications on Portuguese patients with a clinical diagnosis of MODY.
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Mode of access: Internet.
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Mode of access: Internet.
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Includes bibliography.
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Reproduced from type-written copy.
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Mode of access: Internet.
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