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Additive Manufacturing (AM) has revolutionized the production industry by offering design freedom with shorter lead times and reduced material wastage. However, the damage tolerance (DT) of AM parts is a significant concern due to their microstructural and geometric complexities, which affect their mechanical performance. This article aims to provide a comprehensive overview of the manufacturing parameters affecting the components produced by AM specifically selective laser melting (SLM). Detailed discussions are presented on the effects of manufacturing attributes on the microstructure, defects, and mechanical characteristics of AM parts. Depending on these aspects, basic concepts are studied and critically explained specifically for AM materials. The basic criterion for damage‐tolerant component design, the criterion for fatigue and fracture properties, and the effect of the defects on fatigue life are critically presented. In addition, the effect of different types of gradation on the crack growth behavior of samples processed by SLM is also investigated in depth. There is currently a lack of a specific review study in the literature that establishes a connection between process attributes and metallographic properties, and their impact on the damage behavior of additively manufactured parts. This gap in research highlights the need for a comprehensive review to bridge this knowledge deficit and provide valuable insights for understanding the relationships between manufacturing processes, material characteristics, and the structural integrity of additively manufactured components. This review concludes by addressing the challenges and opportunities in designing and qualifying AM parts for damage tolerance. [ABSTRACT FROM AUTHOR]

Systemic environmental disadvantage relates to a host of health and functional outcomes. Specific structural factors have seldom been linked to neural structure, however, clouding understanding of putative mechanisms. Examining relations during childhood/preadolescence, a dynamic period of neurodevelopment, could aid bridge this gap. A total of 10,213 youth were recruited from the Adolescent Brain and Cognitive Development study. Self‐report and objective measures (Census and Federal bureau of investigation metrics extracted using geocoding) of environmental exposures were used, including stimulation indexing lack of safety and high attentional demands, discrepancy indexing social exclusion/lack of belonging, and deprivation indexing lack of environmental enrichment. Environmental measures were related to cortical thickness, surface area, and subcortical volume regions, controlling for other environmental exposures and accounting for other brain regions. Self‐report (|β| =.04–.09) and objective (|β| =.02–.06) environmental domains related to area/thickness in overlapping (e.g., insula, caudal anterior cingulate), and unique regions (e.g., for discrepancy, rostral anterior and isthmus cingulate, implicated in socioemotional functions; for stimulation, precuneus, critical for cue reactivity and integration of environmental cues; and for deprivation, superior frontal, integral to executive functioning). For stimulation and discrepancy exposures, self‐report and objective measures showed similarities in correlate regions, while deprivation exposures evidenced distinct correlates for self‐report and objective measures. Results represent a necessary step toward broader work aimed at establishing mechanisms and correlates of structural disadvantage, highlighting the relevance of going beyond aggregate models by considering types of environmental factors, and the need to incorporate both subjective and objective measurements in these efforts. [ABSTRACT FROM AUTHOR]

Most nations of the world are undergoing rapid and dramatic population ageing, which presents great socio-economic challenges, as well as opportunities, for individuals, families, governments and societies. The prevailing biomedical strategy for reducing the healthcare impact of population ageing has been 'compression of morbidity' and, more recently, to increase healthspan, both of which seek to extend the healthy period of life and delay the development of chronic diseases and disability until a brief period at the end of life. Indeed, a recently established field within biological ageing research, 'geroscience', is focused on healthspan extension. Superimposed on this background are new attitudes and demand for 'optimal longevity' - living long, but with good health and quality of life. A key obstacle to achieving optimal longevity is the progressive decline in physiological function that occurs with ageing, which causes functional limitations (e.g. reduced mobility) and increases the risk of chronic diseases, disability and mortality. Current efforts to increase healthspan centre on slowing the fundamental biological processes of ageing such as inflammation/oxidative stress, increased senescence, mitochondrial dysfunction, impaired proteostasis and reduced stress resistance. We propose that optimization of physiological function throughout the lifespan should be a major emphasis of any contemporary biomedical policy addressing global ageing. Effective strategies should delay, reduce in magnitude or abolish reductions in function with ageing (primary prevention) and/or improve function or slow further declines in older adults with already impaired function (secondary prevention). Healthy lifestyle practices featuring regular physical activity and ideal energy intake/diet composition represent first-line function-preserving strategies, with pharmacological agents, including existing and new pharmaceuticals and novel 'nutraceutical' compounds, serving as potential complementary approaches. Future research efforts should focus on defining the temporal patterns of functional declines with ageing, identifying the underlying mechanisms and modulatory factors involved, and establishing the most effective lifestyle practices and pharmacological options for maintaining function. Continuing development of effective behavioural approaches for enhancing adherence to healthy ageing practices in diverse populations, and ongoing analysis of the socio-economic costs and benefits of healthspan extension will be important supporting goals. To meet the demands created by rapid population ageing, a new emphasis in physiological geroscience is needed, which will require the collaborative, interdisciplinary efforts of investigators working throughout the translational research continuum from basic science to public health. [ABSTRACT FROM AUTHOR]

1. This study investigates the mechanistic and ecological basis of phenotypic sorting in the sociable weaver Philetairus socius (Latham). In this colonially and communally breeding African bird, morphology, condition, age-specific survival rates and reproductive investment vary with colony size. 2. This variation might arise from non-adaptive constraints imposed by density dependence, or from adaptive life-history responses to colony size-dependent selection pressures. To attempt to distinguish these, the environments in which adults made reproductive decisions and in which offspring developed were manipulated. 3. When food supplementation improved the pre-breeding environment of adults, they bred earlier but did not change investment in eggs or incubation. 4. Nestling and subsequent adult phenotypes were unaffected by supplementary feeding, although post-fledging survival improved. Nestling origin and not rearing environment predicted phenotype in a cross-fostering experiment between colonies. 5. Phenotypic differences among colonies hence seemed not to be plastic responses to resource availability. Life-history differentiation, mediated either genetically or maternally, might have taken place over relatively narrow temporal and spatial scales. 6. Adaptive variation in reproductive investment could thus mitigate costs of large colony size, by reducing costs of reproduction and hence improving adult survival. If so, then fine-scale life-history adjustment could help to maintain stable variation in colony size. [ABSTRACT FROM AUTHOR]

The mechanistic target of rapamycin (mTOR) is an evolutionarily conserved protein kinase that regulates growth and metabolism. mTOR is found in two protein complexes, mTORC1 and mTORC2, that have distinct components and substrates and are both inhibited by rapamycin, a macrolide drug that robustly extends lifespan in multiple species including worms and mice. Although the beneficial effect of rapamycin on longevity is generally attributed to reduced mTORC1 signaling, disruption of mTORC2 signaling can also influence the longevity of worms, either positively or negatively depending on the temperature and food source. Here, we show that loss of hypothalamic mTORC2 signaling in mice decreases activity level, increases the set point for adiposity, and renders the animals susceptible to diet‐induced obesity. Hypothalamic mTORC2 signaling normally increases with age, and mice lacking this pathway display higher fat mass and impaired glucose homeostasis throughout life, become more frail with age, and have decreased overall survival. We conclude that hypothalamic mTORC2 is essential for the normal metabolic health, fitness, and lifespan of mice. Our results have implications for the use of mTORC2‐inhibiting pharmaceuticals in the treatment of brain cancer and diseases of aging. [ABSTRACT FROM AUTHOR]