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Nitrenes are a highly reactive, yet fundamental, compound class. They possess a monovalent nitrogen atom and usually a short life span, typically in the nanosecond range. Here, we report on the synthesis of a stable nitrene by photolysis of the arylazide MSFluindN3 (1), which gave rise to the quantitative formation of the arylnitrene MSFluindN (2) (MSFluind is dispiro[fluorene-9,3′-(1′,1′,7′,7′-tetramethyl-s-hydrindacen-4′-yl)-5′,9′′-fluorene]) that remains unchanged for at least 3 days when stored under argon atmosphere at room temperature. The extraordinary life span permitted the full characterization of 2 by single-crystal x-ray crystallography, electron paramagnetic resonance spectroscopy, and superconducting quantum interference device magnetometry, which supported a triplet ground state. Theoretical simulations suggest that in addition to the kinetic stabilization conferred by the bulky MSFluind aryl substituent, electron delocalization across the central aromatic ring contributes to the electron stabilization of 2. [ABSTRACT FROM AUTHOR]

Genomic DNA that resides in the nuclei of mammalian neurons can be as old as the organism itself. The life span of nuclear RNAs, which are critical for proper chromatin architecture and transcription regulation, has not been determined in adult tissues. In this work, we identified and characterized nuclear RNAs that do not turn over for at least 2 years in a subset of postnatally born cells in the mouse brain. These long-lived RNAs were stably retained in nuclei in a neural cell type-specific manner and were required for the maintenance of heterochromatin. Thus, the life span of neural cells may depend on both the molecular longevity of DNA for the storage of genetic information and also the extreme stability of RNA for the functional organization of chromatin. [ABSTRACT FROM AUTHOR]

The cerebellum contains most of the neurons in the human brain and exhibits distinctive modes of development and aging. In this work, by developing our single-cell three-dimensional (3D) genome assay—diploid chromosome conformation capture, or Dip-C—into population-scale (Pop-C) and virus-enriched (vDip-C) modes, we resolved the first 3D genome structures of single cerebellar cells, created life-spanning 3D genome atlases for both humans and mice, and jointly measured transcriptome and chromatin accessibility during development. We found that although the transcriptome and chromatin accessibility of cerebellar granule neurons mature in early postnatal life, 3D genome architecture gradually remodels throughout life, establishing ultra–long-range intrachromosomal contacts and specific interchromosomal contacts that are rarely seen in neurons. These results reveal unexpected evolutionarily conserved molecular processes that underlie distinctive features of neural development and aging across the mammalian life span. [ABSTRACT FROM AUTHOR]

Hunger is an ancient drive, yet the molecular nature of pressures of this sort and how they modulate physiology are unknown. We find that hunger modulates aging in Drosophila. Limitation of branched-chain amino acids (BCAAs) or activation of hunger-promoting neurons induced a hunger state that extended life span despite increased feeding. Alteration of the neuronal histone acetylome was associated with BCAA limitation, and preventing these alterations abrogated the effect of BCAA limitation to increase feeding and extend life span. Hunger acutely increased feeding through usage of the histone variant H3.3, whereas prolonged hunger seemed to decrease a hunger set point, resulting in beneficial consequences for aging. Demonstration of the sufficiency of hunger to extend life span reveals that motivational states alone can be deterministic drivers of aging. [ABSTRACT FROM AUTHOR]

The article examines the multifaceted roles of cellular senescence beyond aging, highlighting its physiological functions such as tumor suppression, tissue regeneration, and wound healing. It addresses challenges in defining and targeting senescent cells therapeutically, emphasizing their complex implications for health and disease across different biological contexts.

"Denizens of the Dark" is an article published in Science that explores the world of nocturnal organisms. The author, Leigh Ann Henion, takes readers on a journey through Appalachia, highlighting different species that thrive at night. Henion connects with experts and participates in community science events to observe and learn about these creatures. The article emphasizes the need for dark preserves to protect nocturnal habitats and discusses the negative impacts of artificial light on wildlife. Overall, the article aims to raise awareness about the importance of nocturnal organisms and the need to preserve their habitats. [Extracted from the article]

In most organisms, reproduction is correlated with shorter life span. However, the reproductive queen in eusocial insects exhibits a much longer life span than that of workers. In Harpegnathos ants, when the queen dies, workers can undergo an adult caste switch to reproductive pseudo-queens (gamergates), exhibiting a five-times prolonged life span. To explore the relation between reproduction and longevity, we compared gene expression during caste switching. Insulin expression is increased in the gamergate brain that correlates with increased lipid synthesis and production of vitellogenin in the fat body, both transported to the egg. This results from activation of the mitogen-activated protein kinase (MAPK) branch of the insulin signaling pathway. By contrast, the production in the gamergate developing ovary of anti-insulin Imp-L2 leads to decreased signaling of the AKT/forkhead box O (FOXO) branch in the fat body, which is consistent with their extended longevity. [ABSTRACT FROM AUTHOR]

The extension of life span driven by 40% caloric restriction (CR) in rodents causes trade-offs in growth, reproduction, and immune defense that make it difficult to identify therapeutically relevant CR-mimetic targets. We report that about 14% CR for 2 years in healthy humans improved thymopoiesis and was correlated with mobilization of intrathymic ectopic lipid. CR-induced transcriptional reprogramming in adipose tissue implicated pathways regulating mitochondrial bioenergetics, anti-inflammatory responses, and longevity. Expression of the gene Pla2g7 encoding platelet activating factor acetyl hydrolase (PLA2G7) is inhibited in humans undergoing CR. Deletion of Pla2g7 in mice showed decreased thymic lipoatrophy, protection against age-related inflammation, lowered NLRP3 inflammasome activation, and improved metabolic health. Therefore, the reduction of PLA2G7 may mediate the immunometabolic effects of CR and could potentially be harnessed to lower inflammation and extend the health span. [ABSTRACT FROM AUTHOR]

The article discusses several studies published in science journals, as of September 2022. Topics include the negative effects of climate change on forests through extreme heat, drought, and disturbances; a trade-off between reproduction and life span that occurs across most living organisms; and drugs that trigger the degradation of target proteins.

Pacific Ocean rockfishes (genus Sebastes) exhibit extreme variation in life span, with some species being among the most long-lived extant vertebrates. We de novo assembled the genomes of 88 rockfish species and from these identified repeated signatures of positive selection in DNA repair pathways in long-lived taxa and 137 longevity-associated genes with direct effects on life span through insulin signaling and with pleiotropic effects through size and environmental adaptations. A genome-wide screen of structural variation reveals copy number expansions in the immune modulatory butyrophilin gene family in long-lived species. The evolution of different rockfish life histories is coupled to genetic diversity and reshapes the mutational spectrum driving segregating CpG→TpG variants in long-lived species. These analyses highlight the genetic innovations that underlie life history trait adaptations and, in turn, how they shape genomic diversity. [ABSTRACT FROM AUTHOR]

Humans prioritize close, positive relationships during aging, and socioemotional selectivity theory proposes that this shift causally depends on capacities for thinking about personal future time horizons. To examine this theory, we tested for key elements of human social aging in longitudinal data on wild chimpanzees. Aging male chimpanzees have more mutual friendships characterized by high, equitable investment, whereas younger males have more one-sided relationships. Older males are more likely to be alone, but they also socialize more with important social partners. Further, males show a relative shift from more agonistic interactions to more positive, affiliative interactions over their life span. Our findings indicate that social selectivity can emerge in the absence of complex future-oriented cognition, and they provide an evolutionary context for patterns of social aging in humans. [ABSTRACT FROM AUTHOR]

For this study, we generated cytosine DNA methylation (DNAm) profiles (n = 15,456) from 348 mammalian species using a methylation array platform that targets highly conserved cytosines. INTRODUCTION: Comparative epigenomics is an emerging field that combines epigenetic signatures with phylogenetic relationships to elucidate species characteristics such as maximum life span. This suggests that long-living species evolved mechanisms that maintain low methylation levels in these chromatin states that would favor higher expression levels of genes essential for an organism's survival. [Extracted from the article]

Additionally, we found variances in aging for expressed gene number and cell type identity, with different cell types being differentially affected by different aging features. We characterized 163 distinct cell types, developed aging clock models, and combined four aging features to rank the aging rate of different cell types. [Extracted from the article]

The article reports that Calorie restriction (CR) involves chronic reduction of energy intake without inducing malnutrition. Topics CR extends life span in multiple animal models and reduces the risk of age-associated disorders which arise from metabolic dysfunction and inflammation; and reducing energy intake, can improve health and increase life span in model organisms contribution of fasting and timing of calorie-reduced meals to the efficacy of CR, as estimated by life-span extension.

The article discusses the importance of studying postzygotic mutations (PZMs) and presents a new method called Lachesis to detect single-nucleotide DNA PZMs. The study analyzed data from the NIH Genotype-Tissue Expression project and found that PZMs are pervasive and highly variable among individuals and tissues, occurring most frequently during early embryonic development, and some low-frequency prenatal mutations are more deleterious than other forms of human genetic variation.

Adult stem cells (SCs) are essential for tissuemaintenance and regeneration yet are susceptible to senescence during aging.We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence.Treatment with the NAD+ precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the mdx (C57BL/10ScSn-Dmdmdx/J) mouse model of muscular dystrophy.We furthermore demonstrate that NR delays senescence of neural SCs andmelanocyte SCs and increases mouse life span. Strategies that conserve cellularNAD+ may reprogram dysfunctional SCs and improve life span in mammals. [ABSTRACT FROM AUTHOR]

Mitochondria generate adenosine 5'-triphosphate (ATP) and are a source of potentially toxic reactive oxygen species (ROS). It has been suggested that the gradual mitochondrial dysfunction that is observed to accompany aging could in fact be causal to the aging process. Here we review findings that suggest that age-dependent mitochondrial dysfunction is not sufficient to limit life span. Furthermore, mitochondrial ROS are not always deleterious and can even stimulate pro-longevity pathways. Thus, mitochondrial dysfunction plays a complex role in regulating longevity. [ABSTRACT FROM AUTHOR]

The article explores on the understanding of the average life span of animals based on their lifestyles and the food they eat. Topics discussed include the influence of the metabolic rates to the life span of the animals, the immunity of the animals on their environment and the differences on the life expectancy between cats and dogs.

Theories about biological limits to life span and evolutionary shaping of human longevity depend on facts about mortality at extreme ages, but these facts have remained a matter of debate. Do hazard curves typically level out into high plateaus eventually, as seen in other species, or do exponential increases persist? In this study, we estimated hazard rates from data on all inhabitants of Italy aged 105 and older between 2009 and 2015 (born 1896 – 1910), a total of 3836 documented cases. We observed level hazard curves, which were essentially constant beyond age 105. Our estimates are free from artifacts of aggregation that limited earlier studies and provide the best evidence to date for the existence of extreme-age mortality plateaus in humans. [ABSTRACT FROM AUTHOR]

Spinal muscular atrophy (SMA) is a genetic disease caused by mutation or deletion of the survival of motor neuron 1 (SMN1) gene. A paralogous gene in humans, SMN2, produces low, insufficient levels of functional SMN protein due to alternative splicing that truncates the transcript. The decreased levels of SMN protein lead to progressive neuromuscular degeneration and high rates of mortality. Through chemical screening and optimization, we identified orally available small molecules that shift the balance of SMN2 splicing toward the production of full-length SMN2 messenger RNA with high selectivity. Administration of these compounds to Δ7 mice, a model of severe SMA, led to an increase in SMN protein levels, improvement of motor function, and protection of the neuromuscular circuit. These compounds also extended the life span of the mice. Selective SMN2 splicing modifiers may have therapeutic potential for patients with SMA. [ABSTRACT FROM AUTHOR]

Single-cell species harbor ancestral structural homologs of caspase proteases, although the evolutionary benefit of such apoptosis-related proteins in unicellular organisms is unclear. Here, we found that the yeast metacaspase Mca1 is recruited to the insoluble protein deposit (IPOD) and juxtanuclear quality-control compartment (JUNQ) during aging and proteostatic stress. Elevating MCA1 expression counteracted accumulation of unfolded proteins and aggregates and extended life span in a heat shock protein Hsp104 disaggregase- and proteasome-dependent manner. Consistent with a role in protein quality control, genetic interaction analysis revealed that MCA1 buffers against deficiencies in the Hsp40 chaperone YDJ1 in a caspase cysteine-dependent manner. Life-span extension and aggregate management by Mca1 was only partly dependent on its conserved catalytic cysteine, which suggests that Mca1 harbors both caspase-dependent and independent functions related to life-span control. [ABSTRACT FROM AUTHOR]

How an individual's longevity is affected by the opposite sex is still largely unclear. In the nematode Caenorhabditis elegans, the presence of males accelerated aging and shortened the life span of individuals of the opposite sex (hermaphrodites), including long-lived or sterile hermaphrodites. The male-induced demise could occur without mating and required only exposure of hermaphrodites to medium in which males were once present. Such communication through pheromones or other diffusible substances points to a nonindividual autonomous mode of aging regulation. The male-induced demise also occurred in other species of nematodes, suggesting an evolutionary conserved process whereby males may induce the disposal of the opposite sex to save resources for the next generation or to prevent competition from other males. [ABSTRACT FROM AUTHOR]

Sensory perception can modulate aging and physiology across taxa. We found that perception of female sexual pheromones through a specific gustatory receptor expressed in a subset of foreleg neurons in male fruit flies, Drosophila melanogaster, rapidly and reversibly decreases fat stores, reduces resistance to starvation, and limits life span. Neurons that express the reward-mediating neuropeptide F are also required for pheromone effects. High-throughput whole-genome RNA sequencing experiments revealed a set of molecular processes that were affected by the activity of the longevity circuit, thereby identifying new candidate cell-nonautonomous aging mechanisms. Mating reversed the effects of pheromone perception; therefore, life span may be modulated through the integrated action of sensory and reward circuits, and healthy aging may be compromised when the expectations defined by sensory perception are discordant with ensuing experience. [ABSTRACT FROM AUTHOR]

Although the gonad primarily functions in procreation, it also affects animal life span. Here, we show that removal of the Caenorhabditis elegans germ line triggers a switch in the regulatory state of the organism to promote longevity, co-opting components involved in larval developmental timing circuits. These components include the DAF-12 steroid receptor, which is involved in the larval stage two-to-stage three (L2-L3) transition and up-regulates members of the let-7 microRNA (miRNA) family. The miRNAs target an early larval nuclear factor lin-14 and akt-1/kinase, thereby stimulating DAF-16/FOXO signaling to extend life. Our studies suggest that metazoan life span is coupled to the gonad through elements of a developmental timer. [ABSTRACT FROM AUTHOR]

The article discusses the scrutiny of research regarding the genetic aspects of aging. Topics include an overview of scientist Matt Kaeberlein of the University of Washington (UW), Seattle, who is trying to replicate an aging study led by Leonard Guarente of the Massachusetts Institute of Technology (MIT) in which Kaeberlein participated and discoveries by MIT post-doctoral student Heidi Tissenbaum and Stephen Helfand of Brown University that an overexpression of sirtuin (SIR2) proteins extends life span in worms and flies, respectively. Also discussed is a dispute over the effect of the compound resveratrol, which is found in red wine, on SIR2 and life span.

When the food intake of organisms such as yeast and rodents is reduced (dietary restriction), they live longer than organisms fed a normal diet. A similar effect is seen when the activity of nutrient-sensing pathways is reduced by mutations or chemical inhibitors. In rodents, both dietary restriction and decreased nutrient-sensing pathway activity can lower the incidence of age-related loss of function and disease, including tumors and neuro-degeneration. Dietary restriction also increases life span and protects against diabetes, cancer, and cardiovascular disease in rhesus monkeys, and in humans it causes changes that protect against these age-related pathologies. Tumors and diabetes are also uncommon in humans with mutations in the growth hormone receptor, and natural genetic variants in nutrient-sensing pathways are associated with increased human life span. Dietary restriction and reduced activity of nutrient-sensing pathways may thus slow aging by similar mechanisms, which have been conserved during evolution. We discuss these findings and their potential application to prevention of age-related disease and promotion of healthy aging in humans, and the challenge of possible negative side effects. [ABSTRACT FROM AUTHOR]

Caloric restriction (CR) protects against aging and disease, but the mechanisms by which this affects mammalian life span are unclear. We show in mice that deletion of ribosomal S6 protein kinase 1 (S6K1), a component of the nutrient-responsive mTOR (mammalian target of rapamycin signaling pathway, led to increased life span and resistance to age-related pathologies, such as bone, immune, and motor dysfunction and loss of insulin sensitivity. Deletion of S6KY induced gene expression patterns similar to those seen in CR or with pharmacological activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK), a conserved regulator of the metabolic response to CR. Our results demonstrate that S6K1 influences healthy mammalian life span and suggest that therapeutic manipulation of S6K1 and AMPK might mimic CR and could provide broad protection against diseases of aging. [ABSTRACT FROM AUTHOR]

Heat shock factor 1 (HSF1) is essential for protecting cells from protein-damaging stress associated with misfolded proteins and regulates the insulin-signaling pathway and aging. Here, we show that human HSF1 is inducibly acetylated at a critical residue that negatively regulates DNA binding activity. Activation of the deacetylase and longevity factor SIRT1 prolonged HSF1 binding to the heat shock promoter Hsp70 by maintaining HSF1 in a deacetylated, DNA-binding competent state. Conversely, down-regulation of SIRT1 accelerated the attenuation of the heat shock response (HSR) and release of HSF1 from its cognate promoter elements. These results provide a mechanistic basis for the requirement of HSF1 in the regulation of life span and establish a role for SIRT1 in protein homeostasis and the HSR. [ABSTRACT FROM AUTHOR]

White adipose (fat) tissues regulate metabolism, reproduction, and life span. Adipocytes form throughout life, with the most marked expansion of the lineage occurring during the postnatal period. Adipocytes develop in coordination with the vasculature, but the identity and location of white adipocyte progenitor cells in vivo are unknown. We used genetically marked mice to isolate proliferating and renewing adipogenic progenitors. We found that most adipocytes descend from a pool of these proliferating progenitors that are already committed, either prenatally or early in postnatal life. These progenitors reside in the mural cell compartment of the adipose vasculature, but not in the vasculature of other tissues. Thus, the adipose vasculature appears to function as a progenitor niche and may provide signals for adipocyte development. [ABSTRACT FROM AUTHOR]

Reduced insulin-like signaling extends the life span of Caenorhabditis elegans and Drosophila. Here, we show that, in mice, less insulin receptor substrate-2 (Irs2) signaling throughout the body or just in the brain extended life span up to 18%. At 22 months of age, brain-specific Irs2 knockout mice were overweight, hyperinsulinemic, and glucose intolerant; however, compared with control mice, they were more active and displayed greater glucose oxidation, and during meals they displayed stable superoxide dismutase-2 concentrations in the hypothalamus. Thus, less Irs2 signaling in aging brains can promote healthy metabolism, attenuate meal-induced oxidative stress, and extend the life span of overweight and insulin-resistant mice. [ABSTRACT FROM AUTHOR]

The size and age structures for four assemblages of North American tyrannosaurs—Albertosaurus, Tyrannosaurus, Gorgosaurus, and Daspletosaurus—reveal a pronounced, bootstrap-supported pattern of age-specific mortality characterized by relatively high juvenile survivorship and increased mortality at midlife and near the maximum life span. Such patterns are common today in wild populations of long-lived birds and mammals. Factors such as predation and entrance into the breeding population may have influenced tyrannosaur survivorship. This survivorship pattern can explain the rarity of juvenile specimens in museum collections. [ABSTRACT FROM AUTHOR]

The microRNA lin-4 and its target, the putative transcription factor lin-14, control the timing of larval development in Caenorhabditis elegans. Here, we report that lin-4 and lin-14 also regulate life span in the adult. Reducing the activity of lin-4 shortened life span and accelerated tissue aging, whereas overexpressing lin-4 or reducing the activity of lin-14 extended life span. Lifespan extension conferred by a reduction in lin-14 was dependent on the DAF16 and HSF-1 transcription factors, suggesting that the lin-4-lin — 14 pair affects life span through the insulin/insulin-like growth factor-1 pathway. This work reveals a role for microRNAs and developmental timing genes in life-span regulation. [ABSTRACT FROM AUTHOR]

Calorie restriction (CR) extends the life span of numerous species, from yeast to rodents. Yeast Sir2 is a nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase that has been proposed to mediate the effects of CR. However, this hypothesis has been challenged by the observation that CR can extend yeast life span in the absence of Sir2. Here, we show that Sir2independent life-span extension is mediated by Hst2, a Sir2 homolog that promotes the stability of repetitive ribosomal DMA, the same mechanism by which Sir2 extends life span. These findings demonstrate that the maintenance of DMA stability is critical for yeast life-span extension by CR and suggest that, in higher organisms, multiple members of the Sir2 family may regulate life span in response to diet. [ABSTRACT FROM AUTHOR]

The article presents information about researcher Lenny Guarente and his former postdoc David Sinclair, who can dramatically extend the life span of yeast. They're battling over how this works and competing head-to-head to grant extra years to humans. Guarente and Sinclair both have bold ideas for translating yeast studies into ways to stall mammalian aging and treat age-related diseases. Sinclair recently announced plans to launch a biotechnology company that he says will compete directly with one co-founded by his mentor. "They're doing exactly what we're doing and it's a race," says Sinclair, clearly relishing the prospect.

The germ tine of the nematode Caenorhabditis elegans influences life-span; when the germ-line precursor celts are removed, life-span is increased dramaticaUy. We find that neither sperm, nor oocytes, nor meiotic precursor cells are responsible for this effect. Rather life-span is influenced by the proliferating germ-line stem cells. These cells, as well as a downstream transcriptional regulator, act in the adult to influence aging, indicating that the aging process remains plastic during. We propose that the germ-line stem celts affect life-span by influencing the production of, or the response to, a steroid hormone that promotes longevity. [ABSTRACT FROM AUTHOR]

Presents a study on the genetical and environmental control of aging in adult fruit flies. Doubling of the adult life span with the insertional mutations of a single gene; Result of the sequence analysis; Creation of a metabolic state similar to caloric restriction.

Recovery from infection is not always complete, and mild chronic infection may persist. Although the direct costs of such infections are apparently small, the potential for any long-term effects on Darwinian fitness is poorly understood. In a wild population of great reed warblers, we found that low-level chronic malaria infection reduced life span as well as the lifetime number and quality of offspring. These delayed fitness effects of malaria appear to be mediated by telomere degradation, a result supported by controlled infection experiments on birds in captivity. The results of this study imply that chronic infection may be causing a series of small adverse effects that accumulate and eventually impair phenotypic quality and Darwinian fitness. [ABSTRACT FROM AUTHOR]

Presents research which performed a screen for gene mutations that extend life-span in Drosophila melanogaster. Traits of the mutant line methuselah (mth); Prediction of a protein by the mth gene; Use of signal transduction pathways to modulate stress response and life-span.

Presents research which studied nongenetic causes for the increase in human life span. Increases in old-age survival since 1950; Deceleration of death rates; Value of three biodemographic insights; Genetic license for extended survival; Survival attributes; Implications of research.

Presents results of a study which investigated the role of genetics in determining life-span. Heritability of life-span; Genetic variants modifying senescence of mammals and invertebrates; Alteration of metabolic pathways; Environmental factors; Gene expression in aging; Genetics of longevity; Genetics of AD and cell death; Alternate life histories.

Wolbachia strain wMelPop reduces the longevity of its Drosophila melanogaster host and, when introduced into the mosquito Aedes aegypti, halves its life span. We show that wMelPop induces up-regulation of the mosquito's innate immune system and that its presence inhibits the development of filarial nematodes in the mosquito. These data suggest that wMelPop could be used in the global effort to eliminate lymphatic filariasis and possibly for the control of other mosquito-borne parasites where immune preactivation inhibits their development. The cost of constitutive immune up-regulation may contribute to the life-shortening phenotype. [ABSTRACT FROM AUTHOR]

The article explores how social environment shapes human health, producing strong relationships between social factors, disease risk, and survival. It mentions that socially induced stress shortens natural life spans owing to multiple causes, including atherosclerosis; and also mentions that social adversity is closely linked to health and mortality outcomes in humans, across the life course.

Focuses on a study which investigated calorie restriction (CR) in yeast by physiological or genetic means and showed a substantial extension in life-span. How glucose activates the yeast cyclic adenosine monophosphate-dependent protein kinase pathway; Correlation between enhanced stress resistance and extended life-span; Role of nicotinamide adenine dinucleotide synthesis in CR-induced life-span extension.

The article discusses the use of crowd-sourced genealogical research as part of genetic research. Topics include an issue article showing how research can be done used on information from the genealogy website Geni, research on life span using the genealogical information, and the potential of using information from direct-to-consumer genetic services in precision medicine.

Reports that fractal-like networks effectively endow life with an additional fourth spatial dimension, which is the origin of quarter-power scaling. Hierarchial branching networks in which organisms have evolved; Tendency of natural selection to maximize both metabolic capacity and internal efficiency.

The authors suggests the significant role of the changes to coral microbiome in future coral reef health. They discuss the correlations between the life span of an organism and its microbial complexity, structure and function and the influence of microbes in coral ecosystem stability. They also cite bleaching as an example of the impact of environmental stress on coral function and coral animals and their immune system.

The article reports that the U.S. National Institutes of Health (NIH) has expanded an existing rule that requires children's participation in clinical trials to embrace people across the life span, including the oldest Americans.

The article discusses research by De Haes et al. on how the drug metformin may prolong lifespan in the worm Caenorhabditis elegans.

The article discusses cell biology research by S. Malmgren Hill et al. within the issue showing the positive effects of metacaspase 1 (Mca1) on the life span of the yeast Saccharomyces cerevisiae when protein homeostasis is impaired. Topics include the activation of caspases as a suicide mechanism in single-cell eukaryotes, Mcal's mode of action, and the role of heat shock protein 104 (Hsp104) and yeast protein homologues Ssa and Ydj1 in protein disaggregation and folding.

The article discusses studies published in the issue by C. Shi, T. J. Maures, and C. M. Gendron on the subject of exposure to the opposite sex and its effect on an animal's life span. Topics include invertebrates such as nematode worms and fruit flies; male induced demise in worms; female produced pheromones in the fruit fly; and fitness in species.