927 resultados para POPULATION CONTROL
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Dissection of the primary and secondary response to an influenza A virus established that the liver contains a substantial population of CD8+ T cells specific for the immunodominant epitope formed by H-2Db and the influenza virus nucleoprotein peptide fragment NP366–374 (DbNP366). The numbers of CD8+ DbNP366+ cells in the liver reflected the magnitude of the inflammatory process in the pneumonic lung, though replication of this influenza virus is limited to the respiratory tract. Analysis of surface phenotypes indicated that the liver CD8+ DbNP366+ cells tended to be more “activated” than the set recovered from lymphoid tissue but generally less so than those from the lung. The distinguishing characteristic of the lymphocytes from the liver was that the prevalence of the CD8+ DbNP366+ set was always much higher than the percentage of CD8+ T cells that could be induced to synthesize interferon γ after short-term, in vitro stimulation with the NP366–374 peptide, whereas these values were generally comparable for virus-specific CD8+ T cells recovered from other tissue sites. Also, the numbers of apoptotic CD8+ T cells were higher in the liver. The results overall are consistent with the idea that antigen-specific CD8+ T cells are destroyed in the liver during the control and resolution phases of this viral infection, though this destruction is not necessarily an immediate process.
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We have found suppressor T cells that inhibit the proliferative response of naive CD4+ T cells in T cell receptor (TCR) Vβ8.1 transgenic mice rendered tolerant in vivo by inoculation of Mls-1a-positive cells. This suppression was mediated by CD4+ T cells but not by CD8+ T cells or double-negative (DN) cells, and splenic CD4+ T cells from tolerant mice displayed a greater suppression than lymph node CD4+ T cells. Cell contact was required for efficient suppression, and known inhibitory cytokines such as IL-4, IL-10, and transforming growth factor β were not involved. Suppressor T cells inhibited IL-2 production by naive CD4+ T cells, and the addition of exogenous IL-2 diminished the suppressed activity while having little activity on tolerant T cells. Suppression was abolished by the elimination of CD25+ T cells in the tolerant CD4+ T cell subset. CD25+CD4+ T cells suppressed the proliferative response of the residual fraction of the nonanergic population, namely, 6C10+CD4+ T cells still present in the tolerant mice. However, 6C10−CD4+ T cells still had reduced reactivity to Mls-1a even after CD25+CD4+ T cells were removed and exogenous IL-2 was added. Suppressor cells appear to affect only residual nonanergic cells in situ, thereby facilitating the maintenance of the unresponsive state in vivo. These data provide a framework for understanding suppressor T cells and explain the difficulties and variables in defining their activity in other systems, because suppressor T cells apparently control only a small population of nonanergic cells in the periphery and may be viewed as a homeostatic mechanism.
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An analysis of Y-chromosomal haplotypes in several European populations reveals an almost monomorphic pattern in the Finns, whereas Y-chromosomal diversity is significantly higher in other populations. Furthermore, analyses of nucleotide positions in the mitochondrial control region that evolve slowly show a decrease in genetic diversity in Finns. Thus, relatively few men and women have contributed the genetic lineages that today survive in the Finnish population. This is likely to have caused the so-called "Finnish disease heritage"-i.e., the occurrence of several genetic diseases in the Finnish population that are rare elsewhere. A preliminary analysis of the mitochondrial mutations that have accumulated subsequent to the bottleneck suggests that it occurred about 4000 years ago, presumably when populations using agriculture and animal husbandry arrived in Finland.
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The role of heritable, population-wide cell damage in neoplastic development was studied in the 28 L subline of NIH 3T3 cells. These cells differ from the 17(3c) subline used previously for such studies in their lower frequency of "spontaneous" transformation at high population density and their greater capacity to produce large, dense transformed foci. Three cultures of the 28 L subline of NIH 3T3 cells were held under the constraint of confluence for 5 wk (5 wk 1 degree assay) and then assayed twice in succession (2 degrees and 3 degrees assays) for transformed foci and saturation density. After the 2 degrees assay, the cells were also passaged at low density to determine their exponential growth rates and cloned to determine the size and morphological features of the colonies. Concurrent measurements were made in each case with control cells that had been kept only in frequent low-density passages and cells that had been kept at confluence for only 2 wk (2 wk 1 degree). Two of the three cultures transferred from the 2 degrees assay of the 5 wk 1 degree cultures produced light transformed foci, and the third produced dense foci. The light focus-forming cultures grew to twice the control saturation density in their 2 degrees assay and 6-8 times the control density in the 3 degrees assay; saturation densities for the dense focus formers were about 10 times the control values in both assays. All three of the cultures transferred from the 2 degrees assay of the 5 wk 1 degree cultures multiplied at lower rates than controls at low densities, but the dense focus formers multiplied faster than the light focus formers. The reduced rates of multiplication of the light focus formers persisted for > 50 generations of exponential multiplication at low densities. Isolated colonies formed from single cells of the light focus formers were of a lower population density than controls; colonies formed by the dense focus formers were slightly denser than the controls but occupied only half the area. A much higher proportion of the colonies from the 5 wk 1 degree cultures than the controls consisted of giant cells or mixtures of giant and normal-appearing cells. The results reinforce the previous conclusion that the early increases in saturation density and light focus formation are associated with, and perhaps caused by, heritable, population-wide damage to cells that is essentially epigenetic in nature. The more advanced transformation characterized by large increases in saturation density and dense focus formation could have originated from rare genetic changes, such as chromosome rearrangements, known to occur at an elevated frequency in cells destabilized by antecedent cellular damage.
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Introducción: En España, cerca del 14% de la población es diabética y el 95% corresponde a DM2. Un pobre control glucémico provoca un aumento de la morbilidad y mortalidad. Tres son los pilares en el tratamiento de la DM2: la dieta, la medicación y el ejercicio físico, sin embargo, el potencial de la prescripción de entrenamiento físico no ha sido totalmente explotado. Objetivo: Analizar el efecto de las distintas modalidades de ejercicio físico (AE, RT, Combo, INT) en el control glucémico en pacientes con diabetes mellitus tipo 2. Métodos: La búsqueda bibliográfica se realizó en 3 bases de datos electrónicas (Pubmed, Scopus y Proquest), incluyendo publicaciones desde enero de 2011 hasta mayo de 2014, que realizaran la intervención con AE, RT, Combo o INT, y que midieran la glucemia a través de la glucosa capilar, CGMS o HbA1c. Resultados: Del total de 386 artículos encontrados, 14 cumplieron los criterios de inclusión. Estos artículos fueron clasificados atendiendo a la modalidad de ejercicio físico de la intervención (AE, RT, Combo, INT), y en función de si analizaban el control glucémico como consecuencia del entrenamiento a largo plazo o tras una sesión de entrenamiento. Conclusiones: El AE, RT, Combo e INT muestran eficacia en el control glucémico tanto en el entrenamiento prolongado como en las 24-48h post-entrenamiento. Es necesaria la prescripción de un entrenamiento estructurado con una frecuencia, volumen e intensidad determinados para lograr beneficios en el control glucémico. El combo es la modalidad que obtiene mejores resultados a través del entrenamiento a largo plazo.
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Background: Celiac disease (CD) has a negative impact on the health-related quality of life (HRQL) of affected patients. Although HRQL and its determinants have been examined in Spanish CD patients specifically recruited in hospital settings, these aspects of CD have not been assessed among the general Spanish population. Methods: An observational, transversal study of a non-randomized, representative sample of adult celiac patients throughout all of Spain's Autonomous Regions. Subjects were recruited through celiac patient associations. A Spanish version of the self-administered Celiac Disease-Quality of Life (CD-QOL) questionnaire was used. Determinant factors of HRQL were assessed with the aid of multivariate analysis to control for confounding factors. Results: We analyzed the responses provided by 1,230 patients, 1,092 (89.2%) of whom were women. The overall mean value for the CD-QOL index was 56.3 ± 18.27 points. The dimension that obtained the most points was dysphoria, with 81.3 ± 19.56 points, followed by limitations with 52.3 ± 23.43 points; health problems, with 51.6 ± 26.08 points, and inadequate treatment, with 36.1 ± 21.18 points. Patient age and sex, along with time to diagnosis, and length of time on a gluten-free diet were all independent determinant factors of certain dimensions of HRQL: women aged 31 to 40 expressed poorer HRQL while time to diagnosis and length of time on a gluten-free diet were determinant factors for better HRQL scores. Conclusions: The HRQL of adult Spanish celiac subjects is moderate, improving with the length of time patients remain on a gluten-free diet.
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" ... Through the financial assistance of the AID" (U.S. Agency for International Development) ISP (International Statistical Programs) of the Bureau of the Census.
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Bibliography: p. 53-54.
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"May, 1982".
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Mode of access: Internet.
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Mode of access: Internet.
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"June 1975."
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"Funding for this project was provided through a Cooperative Agreement (U32/CCU515667-04) with the Centers for Disease Control and Prevention/Division of Diabetes Translation"--P. i.
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Mode of access: Internet.
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Mode of access: Internet.