Evolution, Medicine, and Public Health最新文献

Cancer cells are highly cooperative in a nepotistic way and evolutionarily dynamic. Present cancer treatments often overlook these aspects, inducing the selection of resistant cancer cells and the corresponding relapse. As an alternative method of cancer elimination, autologous cell defection (ACD) was suggested by which modified cancer cells parasitically reliant on other cancer cells are implemented to the cancer cluster. Specifically, modified cancer cells should not produce costly growth factors that promote the growth of other cancer cells while receiving the benefit of exposure to such growth factors. Analytical models and rudimentary experiments up to date provide the medical feasibility of this method. In this study, I built comprehensive spatial simulation models by embracing the effects of the multiple growth factors, the Warburg effect, mutations and immunity. The simulation results based on planar spatial structures indicate that implementation of the defective modified tumours may replace the existing cancer cluster and defective cells would later collapse by themselves. Furthermore, I built a mathematical model that compares the fitness of the cells adjacent to the hypertumour-cancer interface. I also calculated whether anticancer drugs that reduce the effects of the growth factors promote or demote the utility of ACD under diverse fitness functions. The computational examination implies that anticancer drugs may impede the therapeutic effect of ACD when there is a strong concavity in the fitness function. The analysis results could work as a general guidance for effective ACD that may expand the paradigm of cancer treatment.

Background and objectives: Good sleep quality, associated with few arousals, no daytime sleepiness and self-satisfaction with one's sleep, is pivotal for adolescent growth, maturation, cognition and overall health. This article aims to identify what ecological factors impact adolescent sleep quality across three distinct sleep ecologies representing a gradient of dense urbanity to small, rural environments with scarce artificial lighting and no Internet.

Methodology: We analyze variation of sleep efficiency, a quantitative measure of sleep quality-defined as the ratio of total time spent asleep to total time dedicated to sleep-in two agricultural indigenous populations and one post-industrial group in Mexico (Campeche = 44, Puebla = 51, Mexico City = 50, respectively). Data collection included actigraphy, sleep diaries, questionnaires, interviews and ethnographic observations. We fit linear models to examine sleep efficiency variation within and between groups.

Results: We found that sleep efficiency varied significantly across sites, being highest in Mexico City (88%) and lowest in Campeche (75%). We found that variation in sleep efficiency was significantly associated with nightly exposure to light and social sleep practices.

Conclusions and implications: Our findings point toward contextual cost-benefits of sleep disruption in adolescence. We highlight the need to prioritize research on adolescent sleep quality across distinct developmental ecologies and its impact on health to improve adolescent wellbeing through evidence-based health practices.

Background: In industrialized populations, low male testosterone is associated with higher rates of cardiovascular mortality. However, coronary risk factors like obesity impact both testosterone and cardiovascular outcomes. Here, we assess the role of endogenous testosterone on coronary artery calcium in an active subsistence population with relatively low testosterone levels, low cardiovascular risk and low coronary artery calcium scores.

Methodology: In this cross-sectional community-based study, 719 Tsimane forager-horticulturalists in the Bolivian Amazon aged 40+ years underwent computed tomography (49.8% male, mean age 57.6 years).

Results: Coronary artery calcium levels were low; 84.5% had no coronary artery calcium. Zero-inflated negative binomial models found testosterone was positively associated with coronary artery calcium for the full sample (Incidence Rate Ratio [IRR] = 1.477, 95% Confidence Interval [CI] 1.001-2.170, P = 0.031), and in a male-only subset (IRR = 1.532, 95% CI 0.993-2.360, P = 0.053). Testosterone was also positively associated with clinically relevant coronary atherosclerosis (calcium >100 Agatston units) in the full sample (Odds Ratio [OR] = 1.984, 95% CI 1.202-3.275, P = 0.007) and when limited to male-only sample (OR = 2.032, 95% CI 1.118-4.816, P = 0.024). Individuals with coronary artery calcium >100 had 20% higher levels of testosterone than those with calcium <100 (t = -3.201, P = 0.007).

Conclusions and implications: Among Tsimane, testosterone is positively associated with coronary artery calcium despite generally low normal testosterone levels, minimal atherosclerosis and rare cardiovascular disease (CVD) events. Associations between low testosterone and CVD events in industrialized populations are likely confounded by obesity and other lifestyle factors.