RESUMEN
Human space exploration poses inherent risks to astronauts' health, leading to molecular changes that can significantly impact their well-being. These alterations encompass genomic instability, mitochondrial dysfunction, increased inflammation, homeostatic dysregulation, and various epigenomic changes. Remarkably, these changes bear similarities to those observed during the aging process on Earth. However, our understanding of the connection between these molecular shifts and disease development in space remains limited. Frailty syndrome, a clinical syndrome associated with biological aging, has not been comprehensively investigated during spaceflight. To bridge this knowledge gap, we leveraged murine data obtained from NASA's GeneLab, along with astronaut data gathered from the JAXA and Inspiration4 missions. Our objective was to assess the presence of biological markers and pathways related to frailty, aging, and sarcopenia within the spaceflight context. Through our analysis, we identified notable changes in gene expression patterns that may be indicative of the development of a frailty-like condition during space missions. These findings suggest that the parallels between spaceflight and the aging process may extend to encompass frailty as well. Consequently, further investigations exploring the utility of a frailty index in monitoring astronaut health appear to be warranted.
Asunto(s)
Envejecimiento , Biomarcadores , Fragilidad , Vuelo Espacial , Envejecimiento/genética , Animales , Ratones , Humanos , Astronautas , Masculino , Ingravidez/efectos adversos , Sarcopenia/metabolismoRESUMEN
Background: This study aims to identify the preferred sources for acquiring knowledge about COVID-19 and to evaluate basic knowledge on critical scientific literature appraisal in students from medical schools located in Spanish speaking countries in Latin America. Methods: We designed an online survey of 15 closed-ended questions related to demographics, preferred resources for COVID-19 training, and items to assess critical appraisal skills. A snowball method was used for sampling. We conducted a descriptive analysis and Chi-squared tests to compare the proportion of correct identification of the concept of a preprint and a predatory journal when considering a) self-perceived level of knowledge, b) public vs private school, c) inclusion of a scientific literature appraisal subject in the curriculum, and d) progress in medical school. Results: Our sample included 770 valid responses, out of which most of the participants included were from Mexico (n=283, 36.8%) and Ecuador (n=229, 29.7%). Participants preferred using evidence-based clinical resources (EBCRs) to learn more about COVID-19 (n=182, 23.6%). The preferred study design was case report/series (n=218, 28.1%). We found that only 265 participants correctly identified the concept of a preprint (34.4%), while 243 students (31.6%) correctly identified the characteristics of a predatory journal. We found no significant differences in the proportion of correct answers regardless of the self-perceived level of knowledge, progress in medical school, or scientific literature critical appraisal classes. Conclusion: This study is novel in its approach of identifying sources of knowledge used by Latin American medical students and provides insights into the need to reinforce training in critical appraisal of scientific literature during medical school.
Asunto(s)
COVID-19 , Estudiantes de Medicina , COVID-19/epidemiología , Humanos , América Latina , Alfabetización , PandemiasRESUMEN
Mitochondrial dysfunction is a major hallmark of aging. Mitochondrial DNA (mtDNA) mutations (inherited or acquired) may cause a malfunction of the respiratory chain (RC), and thus negatively affect cell metabolism and function. In contrast, certain mtDNA single nucleotide polymorphisms (SNPs) may be beneficial to mitochondrial electron transport chain function and the extension of cellular health as well as lifespan. The goal of the MitoAging project is to detect key physiological characteristics and mechanisms that improve mitochondrial function and use them to develop therapies to increase longevity and a healthy lifespan. We chose to perform a systematic literature review (SLR) as a tool to collect key mtDNA SNPs associated with an increase in lifespan. Then validated our results by comparing them to the MitoMap database. Next, we assessed the effect of relevant SNPs on protein stability. A total of 28 SNPs were found in protein coding regions. These SNPs were reported in Japan, China, Turkey, and India. Among the studied SNPs, the C5178A mutation in the ND2 gene of Complex I of the RC was detected in all the reviewed reports except in Uygur Chinese centenarians. Then, we found that G9055A (ATP6 gene) and A10398G (ND3 gene) polymorphisms have been associated with a protective effect against Parkinson's disease (PD). Additionally, C8414T in ATP8 was significantly associated with longevity in three Japanese reports. Interestingly, using MitoMap we found that G9055A (ATP6 gene) was the only SNP promoting longevity not associated with any pathology. The identification of SNPs associated with an increase in lifespan opens the possibility to better understand individual differences regarding a decrease in illness susceptibility and find strategies that contribute to healthy aging.