Evidence for the stress-linked immunocompetence handicap hypothesis in humans.
Ontology highlight
ABSTRACT:
SUBMITTER: Rantala MJ
PROVIDER: S-EPMC4355638 | biostudies-other | 2012
REPOSITORIES: biostudies-other
Similar Datasets
Project description:The observations that testosterone might be immunosuppressive, form the basis for the immunocompetence handicap hypothesis (ICHH). According to ICHH only high-quality individuals can maintain high levels of testosterone and afford the physiological cost of hormone-derived immunosuppression. The animal and human studies that attempted to support the ICHH by precisely defined impairment of immunity associated with high testosterone levels are inconclusive. Furthermore, human studies have used only selected immune functions and varying testosterone fractions. This is the first study examining the relationship between multiple innate and adaptive immunity and serum levels of free testosterone, total testosterone, DHT and DHEA in ninety-seven healthy men. Free testosterone and marginally DHT levels were positively correlated with the strength of the influenza post-vaccination response. Total testosterone and DHEA showed no immunomodulatory properties. Our findings did not support ICHH assumptions about immunosuppressive function of androgens. In the affluent society studied here, men with higher levels of free testosterone could afford to invest more in adaptive immunity. Since the hormone-immune relationship is complex and may depend on multiple factors, including access to food resources, androgens should be treated as immunomodulators rather than implicit immunosuppressants.
| S-EPMC5943526 | biostudies-literature
Project description:The dual-hit hypothesis of neurodegeneration states that severe stress sensitizes vulnerable cells to subsequent challenges so that the two hits are synergistic in their toxic effects. Although the hippocampus is vulnerable to a number of neurodegenerative disorders, there are no models of synergistic cell death in hippocampal neurons in response to combined proteotoxic and oxidative stressors, the two major characteristics of these diseases. Therefore, a relatively high-throughput dual-hit model of stress synergy was developed in primary hippocampal neurons. In order to increase the rigor of the study and strengthen the interpretations, three independent, unbiased viability assays were employed at multiple timepoints. Stress synergy was elicited when hippocampal neurons were treated with the proteasome inhibitor MG132 followed by exposure to the oxidative toxicant paraquat, but only after 48 h. MG132 and paraquat only elicited additive effects 24 h after the final hit and even loss of heat shock protein 70 activity and glutathione did not promote stress synergy at this early timepoint. Dual hits of MG132 elicited modest glutathione loss and slightly synergistic toxic effects 48 h after the second hit, but only at some concentrations and only according to two viability assays (metabolic fitness and cytoskeletal integrity). The thiol N-acetyl cysteine protected hippocampal neurons against dual MG132/MG132 hits but not dual MG132/paraquat hits. These findings support the view that proteotoxic and oxidative stress propel and propagate each other in hippocampal neurons, leading to synergistically toxic effects, but not as the default response and only after a delay. The neuronal stress synergy observed here lies in contrast to astrocytic responses to dual hits, because astrocytes that survive severe proteotoxic stress resist additional cell loss following second hits. In conclusion, a new model of hippocampal vulnerability was developed for the testing of therapies, because neuroprotective treatments that are effective against severe, synergistic stress are more likely to succeed in the clinic. © 2016 Wiley Periodicals, Inc.
| S-EPMC4949116 | biostudies-literature
Project description:Fixed differences of chromosomal rearrangements between isolated populations may promote speciation by preventing between-population gene flow upon secondary contact, either because hybrids suffer from lowered fitness or, more likely, because recombination is reduced in rearranged chromosomal regions. This chromosomal speciation hypothesis thus predicts more rapid genetic divergence on rearranged than on colinear chromosomes because the former are less porous to gene flow. A number of studies of fungi, plants, and animals, including limited genetic data of humans and chimpanzees, support the hypothesis. Here we reexamine the hypothesis for humans and chimpanzees with substantially more genomic data than were used previously. No difference is observed between rearranged and colinear chromosomes in the level of genomic DNA sequence divergence between species. The same is also true for protein sequences. When the gorilla is used as an outgroup, no acceleration in protein sequence evolution associated with chromosomal rearrangements is found. Furthermore, divergence in expression pattern between orthologous genes is not significantly different for rearranged and colinear chromosomes. These results, showing that chromosomal rearrangements did not affect the rate of genetic divergence between humans and chimpanzees, are expected if incipient species on the evolutionary lineages separating humans and chimpanzees did not hybridize.
| S-EPMC479111 | biostudies-literature
Project description: Not available
| S-EPMC7423596 | biostudies-literature
Project description:We report on a study of whether people believe that the rich are richer than the poor because they have been more selfish in life, using data from more than 26,000 individuals in 60 countries. The findings show a strong belief in the selfish rich inequality hypothesis at the global level; in the majority of countries, the mode is to strongly agree with it. However, we also identify important between- and within-country variation. We find that the belief in selfish rich inequality is much stronger in countries with extensive corruption and weak institutions and less strong among people who are higher in the income distribution in their society. Finally, we show that the belief in selfish rich inequality is predictive of people's policy views on inequality and redistribution: It is significantly positively associated with agreeing that inequality in their country is unfair, and it is significantly positively associated with agreeing that the government should aim to reduce inequality. These relationships are highly significant both across and within countries and robust to including country-level or individual-level controls and using Lasso-selected regressors. Thus, the data provide compelling evidence of people believing that the rich are richer because they have been more selfish in life and perceiving selfish behavior as creating unfair inequality and justifying equalizing policies.
| S-EPMC8784141 | biostudies-literature
Project description:The formation of the Ontong Java Nui super oceanic plateau (OJN), which is based on the model that the submarine Ontong Java Plateau (OJP), Manihiki Plateau (MP), and Hikurangi Plateau (HP) were once its contiguous fragments, could have been the largest globally consequential volcanic event in Earth's history. This OJN hypothesis has been debated given the paucity of evidence, for example, the differences in crustal thickness, the compositional gap between MP and OJP basalts and the apparent older age of both plateaus relative to HP remain unresolved. Here we investigate the geochemical and 40Ar-39Ar ages of dredged rocks recovered from the OJP's eastern margin. Volcanic rocks having compositions that match the low-Ti MP basalts are reported for the first time on the OJP and new ~ 96-116 Ma and 67-68 Ma 40Ar-39Ar age data bridge the temporal gap between OJP and HP. These results provide new evidence for the Ontong Java Nui hypothesis and a framework for an integrated tectonomagmatic evolution of the OJP, MP, and HP. The isotopic data imply four mantle components in the source of OJN that are also expressed in present-day Pacific hotspots sources, indicating origin from (and longevity of) the Pacific Large Low Shear-wave Velocity Province.
| S-EPMC10213030 | biostudies-literature
Project description:Integrative explanations of why obesity is more prevalent in some sectors of the human population than others are lacking. Here, we outline and evaluate one candidate explanation, the insurance hypothesis (IH). The IH is rooted in adaptive evolutionary thinking: The function of storing fat is to provide a buffer against shortfall in the food supply. Thus, individuals should store more fat when they receive cues that access to food is uncertain. Applied to humans, this implies that an important proximate driver of obesity should be food insecurity rather than food abundance per se. We integrate several distinct lines of theory and evidence that bear on this hypothesis. We present a theoretical model that shows it is optimal to store more fat when food access is uncertain, and we review the experimental literature from non-human animals showing that fat reserves increase when access to food is restricted. We provide a meta-analysis of 125 epidemiological studies of the association between perceived food insecurity and high body weight in humans. There is a robust positive association, but it is restricted to adult women in high-income countries. We explore why this could be in light of the IH and our theoretical model. We conclude that although the IH alone cannot explain the distribution of obesity in the human population, it may represent a very important component of a pluralistic explanation. We also discuss insights it may offer into the developmental origins of obesity, dieting-induced weight gain, and anorexia nervosa.
| S-EPMC5266557 | biostudies-literature
Project description:A well-recognized theory of Alzheimer's disease (AD) pathogenesis suggests ectopic cell cycle events to mediate neurodegeneration. Vulnerable neurons of the AD brain exhibit biomarkers of cell cycle progression and DNA replication suggesting a reentry into the cell cycle. Chromosome reduplication without proper cell cycle completion and mitotic division probably causes neuronal cell dysfunction and death. However, this theory seems to require some inputs in accordance with the generally recognized amyloid cascade theory as well as to explain causes and consequences of genomic instability (aneuploidy) in the AD brain. We propose that unscheduled and incomplete DNA replication (replication stress) destabilizes (epi)genomic landscape in the brain and leads to DNA replication "catastrophe" causing cell death during the S phase (replicative cell death). DNA replication stress can be a key element of the pathogenetic cascade explaining the interplay between ectopic cell cycle events and genetic instabilities in the AD brain. Abnormal cell cycle reentry and somatic genome variations can be used for updating the cell cycle theory introducing replication stress as a missing link between cell genetics and neurobiology of AD.
| S-EPMC3254013 | biostudies-other
Project description:Pointing gestures play a foundational role in human language, but up to now, we have not known where these gestures come from. Here, we investigated the hypothesis that pointing originates in touch. We found, first, that when pointing at a target, children and adults oriented their fingers not as though trying to create an "arrow" that picks out the target but instead as though they were aiming to touch it; second, that when pointing at a target at an angle, participants rotated their wrists to match that angle as they would if they were trying to touch the target; and last, that young children interpret pointing gestures as if they were attempts to touch things, not as arrows. These results provide the first substantial evidence that pointing originates in touch.
| S-EPMC6620103 | biostudies-literature
Project description:Restoration efforts have been escalating worldwide in response to widespread habitat degradation. However, coastal restoration attempts notoriously vary in their ability to establish resilient, high-functioning ecosystems. Conventional restoration attempts disperse transplants in competition-minimizing arrays, yet recent studies suggest that clumping transplants to maximize facilitative interactions may improve restoration success. Here, we modify the stress gradient hypothesis to generate predictions about where each restoration design will perform best across environmental stress gradients. We then test this conceptual model with field experiments manipulating transplant density and configuration across dune elevations and latitudes. In hurricane-damaged Georgia (USA) dunes, grass transplanted in competition-minimizing (low-density, dispersed) arrays exhibited the highest growth, resilience to disturbance and dune formation in low-stress conditions. In contrast, transplants survived best in facilitation-maximizing (high-density, clumped) arrays in high-stress conditions, but these benefits did not translate to higher transplant growth or resilience. In a parallel experiment in Massachusetts where dune grasses experience frequent saltwater inundation, fewer transplants survived, suggesting that there are thresholds above which intraspecific facilitation cannot overcome local stressors. These results suggest that ecological theory can be used to guide restoration strategies based on local stress regimes, maximizing potential restoration success and return-on-investment of future efforts.
| S-EPMC6939925 | biostudies-literature