Innate Ability (innate + ability)

Distribution by Scientific Domains


Selected Abstracts


Cell proliferation and apoptosis: dual-signal hypothesis tested in tuberculous pleuritis using mycobacterial antigens

FEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2004
Sulochana D. Das
Abstract Antigens and mitogens have the innate ability to trigger cell proliferation and apoptosis thus exhibiting a dual-signal phenomenon. This dual-signal hypothesis was tested with mycobacterial antigens (PPD and heat killed Mycobacterium tuberculosis, MTB) in tuberculous pleuritis patients where the immune response is protective and compartmentalized. We compared and correlated the cell-cycle analysis and antigen-induced apoptosis in normal and patients' peripheral blood mononuclear cells (PBMCs) and patients' pleural fluid mononuclear cells (PFMCs). In cell-cycle analysis, PFMCs showed good mitotic response with PPD and MTB antigens where 10% and 7% of resting cells entered the S and G2/M phases of cell cycle, respectively. This antigen-induced proliferation of PFMCs correlated well with the lymphocyte transformation test (LTT) results. On the other hand, PFMCs also showed 21% of spontaneous apoptosis, which further increased to 43%, by induction with known apoptotic agent like Dexamethasone (DEX) and the mycobacterial antigens PPD and MTB. Further we demonstrated by anti-CD3 induction experiments that prior activation of cells is prerequisite for them to undergo apoptosis. Our results showed that PPD and MTB antigens induced both cell proliferation and apoptosis in PFMCs, which were pre-sensitized to mycobacterial antigens in vivo. Thus the dual-signal phenomenon was operative against these antigens in tuberculous pleuritis. We also demonstrated that the activated cells are more predisposed to apoptosis. [source]


Variation in the degree and costs of adaptive phenotypic plasticity among Rana temporaria populations

JOURNAL OF EVOLUTIONARY BIOLOGY, Issue 5 2004
J. Merilä
Abstract Adaptive phenotypic plasticity in the form of capacity to accelerate development as a response to pond drying risk is known from many amphibian species. However, very little is known about factors that might constrain the evolution of this type of plasticity, and few studies have explored to what degree plasticity might be constrained by trade-offs dictated by adaptation to different environmental conditions. We compared the ability of southern and northern Scandinavian common frog (Rana temporaria) larvae originating from 10 different populations to accelerate their development in response to simulated pond drying risk and the resulting costs in metamorphic size in a factorial laboratory experiment. We found that (i) northern larvae developed faster than the southern larvae in all treatments, (ii) a capacity to accelerate the response was present in all five southern and all five northern populations tested, but that the magnitude of the response was much larger (and less variable) in the southern than in the northern populations, and that (iii) significant plasticity costs in metamorphic size were present in the southern populations, the plastic genotypes having smaller metamorphic size in the absence of desiccation risk, but no evidence for plasticity costs was found in the northern populations. We suggest that the weaker response to pond drying risk in the northern populations is due to stronger selection on large metamorphic size as compared with southern populations. In other words, seasonal time constraints that have selected the northern larvae to be fast growing and developing, may also constrain their innate ability for adaptive phenotypic plasticity. [source]


Fast foods, energy density and obesity: a possible mechanistic link

OBESITY REVIEWS, Issue 4 2003
A. M. Prentice
Summary Fast foods are frequently linked to the epidemic of obesity, but there has been very little scientific appraisal of a possible causal role. Here we review a series of studies demonstrating that the energy density of foods is a key determinant of energy intake. These studies show that humans have a weak innate ability to recognise foods with a high energy density and to appropriately down-regulate the bulk of food eaten in order to maintain energy balance. This induces so called ,passive over-consumption'. Composition data from leading fast food company websites are then used to illustrate that most fast foods have an extremely high energy density. At some typical outlets the average energy density of the entire menus is ,1100 kJ 100 g,1. This is 65% higher than the average British diet (,670 kJ 100 g,1) and more than twice the energy density of recommended healthy diets (,525 kJ 100 g,1). It is 145% higher than traditional African diets (,450 kJ 100 g,1) that probably represent the levels against which human weight regulatory mechanisms have evolved. We conclude that the high energy densities of many fast foods challenge human appetite control systems with conditions for which they were never designed. Among regular consumers they are likely to result in the accidental consumption of excess energy and hence to promote weight gain and obesity. [source]


On the Specification and Estimation of the Production Function for Cognitive Achievement*

THE ECONOMIC JOURNAL, Issue 485 2003
Petra E. Todd
This paper considers methods for modelling the production function for cognitive achievement in a way that captures theoretical notions that child development is a cumulative process depending on the history of family and school inputs and on innate ability. It develops a general modelling framework that accommodates many of the estimating equations used in the literatures. It considers different ways of addressing data limitations, and it makes precise the identifying assumptions needed to justify alternative approaches. Commonly used specifications are shown to place restrictive assumptions on the production technology. Ways of testing modelling assumptions and of relaxing them are discussed. [source]


The geography of tyranny and despair: development indicators and the hypothesis of genetic inevitability of national inequality

THE GEOGRAPHICAL JOURNAL, Issue 3 2008
STEPHEN MORSE
Development geography has long sought to understand why inequalities exist and the best ways to address them. Dependency theory sets out an historical rationale for under development based on colonialism and a legacy of developed core and under-developed periphery. Race is relevant in this theory only insofar that Europeans are white and the places they colonised were occupied by people with darker skin colour. There are no innate biological reasons why it happened in that order. However, a new theory for national inequalities proposed by Lynn and Vanhanen in a series of publications makes the case that poorer countries have that status because of a poorer genetic stock rather than an accident of history. They argue that IQ has a genetic basis and IQ is linked to ability. Thus races with a poorer IQ have less ability, and thus national IQ can be positively correlated with performance as measured by an indicator like GDP/capita. Their thesis is one of despair, as little can be done to improve genetic stock significantly other than a programme of eugenics. This paper summarises and critiques the Lynn and Vanhanen hypothesis and the assumptions upon which it is based, and uses this analysis to show how a human desire to simplify in order to manage can be dangerous in development geography. While the attention may naturally be focused on the ,national IQ' variables as a proxy measure of ,innate ability', the assumption of GDP per capita as an indicator of ,success' and ,achievement' is far more readily accepted without criticism. The paper makes the case that the current vogue for indicators, indices and cause,effect can be tyrannical. [source]