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Whatever factor or factors enabled extreme human longevity in the pre- and immediate post-Flood worlds likely also affected the animal kingdom. Thus, direct or indirect evidence for greater past animal longevity is also de facto evidence for greater past human longevity. The field of skeletochronology is making it possible to deduce information about the ontogenetic growth trajectories of giant fossil crocodilians such as Deinosuchus riograndensis (alternately, D. hatcheri) and Sarcosuchus imperator. Their growth curves indicate that these crocodilians grew for at least 50-60 years, a duration significantly greater than even the total typical 30-year lifespan of extant crocodilians. Moreover, a smoothed Deinosuchus growth curve published in the mainstream evolutionary literature suggests this age of 50 years likely significantly underestimates the true age at maturity. Given the evidence from longevity studies linking both larger adult body sizes and greater ages at maturation to greater longevity, the large adult body sizes of Deinosuchus and Sarcosuchus and their prolonged maturation intervals are indirect evidence of lifespans greater than extant crocodilians. Other giant fossil crocodilians, some of which may be direct ancestors of extant crocodilians, were also likely experiencing greater longevity. Moreover, the similarity of giant crocodilian body sizes in Cretaceous, Miocene, and Pliocene strata suggest that these crocodilians obtained their giant sizes under similar environmental conditions. This could suggest they all lived in the pre-Flood world and would be another argument for a 'high' Cenozoic Flood/post-Flood boundary. [ABSTRACT FROM AUTHOR]

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tRNAs are evolutionarily ancient molecular decoders essential for protein translation. In eukaryotes, tRNAs and other short, noncoding RNAs are transcribed by RNA polymerase (Pol) III, an enzyme that promotes ageing in yeast, worms, and flies. Here, we show that a partial reduction in Pol III activity specifically disrupts tRNA levels. This effect is conserved across worms, flies, and mice, where computational models indicate that it impacts mRNA decoding. In all 3 species, reduced Pol III activity increases proteostatic resilience. In worms, it activates the unfolded protein response (UPR) and direct disruption of tRNA metabolism is sufficient to recapitulate this. In flies, decreasing Pol III's transcriptional initiation on tRNA genes by a loss-of-function in the TFIIIC transcription factor robustly extends lifespan, improves proteostatic resilience and recapitulates the broad-spectrum benefits to late-life health seen following partial Pol III inhibition. We provide evidence that a partial reduction in Pol III activity impacts translation, quantitatively or qualitatively, in both worms and flies, indicating a potential mode of action. Our work demonstrates a conserved and previously unappreciated role of tRNAs in animal ageing. tRNAs are important for protein translation, but whether they influence aging is unknown. In this paper, by manipulating RNA polymerase III-mediated transcription of tRNAs across three animal species, the authors demonstrate previously unappreciated roles of tRNA in proteostasis, old-age health and animal longevity. [ABSTRACT FROM AUTHOR]

Methylation profiles of animals are known to differ by age and disease status. Bovine respiratory disease (BRD), a complex infectious disease, primarily affects calves and has significant impact on animal welfare and the cattle industry, due to production losses, increased veterinary costs as well as animal losses. BRD susceptibility is multifactorial, influenced by both environmental and genetic factors. We have performed a pilot study to investigate the epigenetic profile of BRD susceptibility in six calves (three healthy versus three diagnosed with BRD) and age-related methylation differences between healthy calves and adult dairy cows (three calves versus four adult cows) using Reduced Representation Bisulfite Sequencing (RRBS). We identified 2537 genes within differentially methylated regions between calves and adults. Functional analysis revealed enrichment of developmental pathways including cell fate commitment and tissue morphogenesis. Between healthy and BRD affected calves, 964 genes were identified within differentially methylated regions. Immune and vasculature regulatory pathways were enriched and key candidates in BRD susceptibility involved in complement cascade regulation, vasoconstriction and respiratory cilia structure and function were identified. Further studies with a greater sample size are needed to validate these findings and formulate integration into breeding programmes aiming to increase animal longevity and disease resistance. Epigenetic profiling using reduced representation bisulfite sequencing provides preliminary insights into the role of DNA methylation in ageing and bovine respiratory disease in UK dairy cattle. [ABSTRACT FROM AUTHOR]

Huntington's disease (HD) is a devastating neurodegenerative disease that is manifested by a gradual loss of physical, cognitive, and mental abilities. As the disease advances, age has a major impact on the pathogenic signature of mutant huntingtin (mHTT) protein aggregation. This review aims to explore the intricate relationship between aging, mHTT toxicity, and cellular senescence in HD. Scientific data on the interplay between aging, mHTT, and cellular senescence in HD were collected from several academic databases, including PubMed, Google Scholar, Google, and ScienceDirect. The search terms employed were "AGING," "HUNTINGTON'S DISEASE," "MUTANT HUNTINGTIN," and "CELLULAR SENESCENCE." Additionally, to gather information on the molecular mechanisms and potential therapeutic targets, the search was extended to include relevant terms such as "DNA DAMAGE," "OXIDATIVE STRESS," and "AUTOPHAGY." According to research, aging leads to worsening HD pathophysiology through some processes. As a result of the mHTT accumulation, cellular senescence is promoted, which causes DNA damage, oxidative stress, decreased autophagy, and increased inflammatory responses. Pro‐inflammatory cytokines and other substances are released by senescent cells, which may worsen the neuronal damage and the course of the disease. It has been shown that treatments directed at these pathways reduce some of the HD symptoms and enhance longevity in experimental animals, pointing to a new possibility of treating the condition. Through their amplification of the harmful effects of mHTT, aging and cellular senescence play crucial roles in the development of HD. Comprehending these interplays creates novel opportunities for therapeutic measures targeted at alleviating cellular aging and enhancing HD patients' quality of life. [ABSTRACT FROM AUTHOR]

Mechanical stress is a measure of internal resistance exhibited by a body or material when external forces, such as compression, tension, bending, etc. are applied. The study of mechanical stress on health and aging is a continuously growing field, as major changes to the extracellular matrix and cell-to-cell adhesions can result in dramatic changes to tissue stiffness during aging and diseased conditions. For example, during normal aging, many tissues including the ovaries, skin, blood vessels, and heart exhibit increased stiffness, which can result in a significant reduction in function of that organ. As such, numerous model systems have recently emerged to study the impact of mechanical and physical stress on cell and tissue health, including cell-culture conditions with matrigels and other surfaces that alter substrate stiffness and ex vivo tissue models that can apply stress directly to organs like muscle or tendons. Here, we sought to develop a novel method in an in vivo model organism setting to study the impact of altering substrate stiffness on aging by changing the stiffness of solid agar medium used for growth of C. elegans. We found that greater substrate stiffness had limited effects on cellular health, gene expression, organismal health, stress resilience, and longevity. Overall, our study reveals that altering substrate stiffness of growth medium for C. elegans has only mild impact on animal health and longevity; however, these impacts were not nominal and open up important considerations for C. elegans biologists in standardizing agar medium choice for experimental assays. [ABSTRACT FROM AUTHOR]

In this study, we show the improvement in life longevity in an experimental mouse model after step-by-step autologous ovarian transplantation and compare its effects with exogenic transdermal estradiol usage. This has proven to be more efficient than "traditional" hormonal replacement therapy. Despite the high speed and effectiveness of estradiol replacement deficiency in blood by its oral or transdermal use, no significant increase in the life longevity of animals and possibly in women was noted. The function of the transplanted fragment is usually limited to 6-12 months. This is enough for oncofertility purposes, sometimes, but not for longevity improvement. We performed periodical tissue return (autologous transplantation), containing both the cortex and medulla in the experimental mouse model, which resulted in a statistically reliable improvement in longevity. Our experience indicates the important role of medullary ovarian factors in slowing the aging process in the body and increasing the life expectancy in the experiment. As shown, the transdermal estrogen supportive therapy for ovarian deficiency improves estrogen levels but causes much slower decreases in the follicle stimulating hormone (FSH) and luteinizing hormone (LH). Moreover, we attained the best longevity with step-bystep periodic ovarian autotransplantation, thus making "prosthetics" of ovarian function longer than it is preplanned physiologically [direct correlation between the levels of FSH and lifespan (r = 0.98)]. The experimental model we suggested could be projected to other mammals or humans as cortical transplantation provides the same results for reproduction restoration in mice and humans and even for hormone level normalization, but there is still a lack of information about anti-aging factors in the ovarian medulla and cortex. Hence, we consider that the most important factor for the anti-aging ovarian transplantation technology is to preserve and transfer both the medulla and cortex as parts of the whole ovary. [ABSTRACT FROM AUTHOR]

Background: Longevity and resilience are two fundamental traits for more sustainable livestock production. These traits are closely related, as resilient animals tend to have longer lifespans. An interesting criterion for increasing longevity in rabbit could be based on the information provided by its gut microbiome. The gut microbiome is essential for regulating health and plays crucial roles in the development of the immune system. The aim of this research was to investigate if animals with different longevities have different microbial profiles. We sequenced the 16S rRNA gene from soft faeces from 95 does. First, we compared two maternal rabbit lines with different longevities; a standard longevity maternal line (A) and a maternal line (LP) that was founded based on longevity criteria: females with a minimum of 25 parities with an average prolificacy per parity of 9 or more. Second, we compared the gut microbiota of two groups of animals from line LP with different longevities: females that died/were culled with two parities or less (LLP) and females with more than 15 parities (HLP). Results: Differences in alpha and beta diversity were observed between lines A and LP, and a partial least square discriminant analysis (PLS-DA) showed a high prediction accuracy (> 91%) of classification of animals to line A versus LP (146 amplicon sequence variants (ASV)). The PLS-DA also showed a high prediction accuracy (> 94%) to classify animals to the LLP and HLP groups (53 ASV). Interestingly, some of the most important taxa identified in the PLS-DA were common to both comparisons (Akkermansia, Christensenellaceae R-7, UnculturedEubacteriaceae, among others) and have been reported to be related to resilience and longevity. Conclusions: Our results indicate that the first parity gut microbiome profile differs between the two rabbit maternal lines (A and LP) and, to a lesser extent, between animals of line LP with different longevities (LLP and HLP). Several genera were able to discriminate animals from the two lines and animals with different longevities, which shows that the gut microbiome could be used as a predictive factor for longevity, or as a selection criterion for these traits. [ABSTRACT FROM AUTHOR]

The Bengal tiger (Panthera tigris tigris) is a species belonging to the Felidae family. In Argentina, tigers are currently only found in captivity. The longevity of individual animals in human‐controlled environments depends on proper management and practices that prioritize animal welfare. Regular veterinary care is essential to maintain optimal health conditions. Professionals must have a comprehensive understanding of the anatomy and physiology of tigers to effectively perform medical procedures and administer treatments. The study described in the text focuses on the trajectory and distribution of nerves in the pelvic limb of a Bengal tiger specimen, providing detailed dissection findings. The results revealed that the lumbosacral plexus is formed from the ventral rami of the LIV, LV, LVI, LVII, SI, SII and SIII nerves. Among the observations to highlight is the great development of the nerves N. cutaneus femoris lateralis and N. cutaneus femoris caudalis some differences were observed in the distribution of the N. femoralis and N. obturatorius; the N. ischiadicus, together with its division into the fibularis communis and tibialis nerves, showed the same configuration observed in other cats. Finally, it was observed that the nerves N. gluteus cranialis and N. gluteus caudalis also originated from the truncus lumbosacralis. The similarities and differences with studies carried out on other cats are relevant and provide anatomical data for medical procedures in the Bengal tiger. [ABSTRACT FROM AUTHOR]

Simple Summary: Technological and social progress are often closely linked. There is a consensus that future medicine will benefit from the use of available health data. The form in which these health data will be available is crucial. For a comprehensive analysis, it is necessary to harmonize and link these data and enable seamless use across system boundaries. In this paper, we consider the field of equine veterinary health data. We propose a vision that data from the entire global horse population are utilized for the benefit of animal health and longevity. With this in mind, we examine social aspects influencing technical progress. Here, we use a socio-technical matrix as a tool. We reduce the overall complexity by limiting ourselves to the following: Technically, we consider the treasure trove of data from veterinary diagnostics and the Internet of Medical Things (IoMT). Regarding social interactions, we focus on veterinarians and horse owners. Utilizing this socio-technical matrix, we branch out to identify barriers and enablers on the way to the vision. Additional elements, such as the slowly maturing awareness of horse owners regarding the value of these data as well as training of all parties in the handling of data, are identified to be crucial. There is a consensus that future medicine will benefit from a comprehensive analysis of harmonized, interconnected, and interoperable health data. These data can originate from a variety of sources. In particular, data from veterinary diagnostics and the monitoring of health-related life parameters using the Internet of Medical Things are considered here. To foster the usage of collected data in this way, not only do technical aspects need to be addressed but so do organizational ones, and to this end, a socio-technical matrix is first presented that complements the literature. It is used in an exemplary analysis of the system. Such a socio-technical matrix is an interesting tool for analyzing the process of data sharing between actors in the system dependent on their social relations. With the help of such a socio-technical tool and using equine veterinary medicine as an example, the social system of veterinarians and owners as actors is explored in terms of barriers and enablers of an effective digital representation of the global equine population. [ABSTRACT FROM AUTHOR]

One of the challenges facing science/biology today is uncovering the molecular bases that support and determine animal and human longevity. Nature, in offering a diversity of animal species that differ in longevity by more than 5 orders of magnitude, is the best 'experimental laboratory' to achieve this aim. Mammals, in particular, can differ by more than 200-fold in longevity. For this reason, most of the available evidence on this topic derives from comparative physiology studies. But why can human beings, for instance, reach 120 years whereas rats only last at best 4 years? How does nature change the longevity of species? Longevity is a species-specific feature resulting from an evolutionary process. Long-lived animal species, including humans, show adaptations at all levels of biological organization, from metabolites to genome, supported by signaling and regulatory networks. The structural and functional features that define a long-lived species may suggest that longevity is a programmed biological property. Compendium of phenotypic features present in long-lived animal species. [Display omitted] • Animal longevity is a species-specific biological trait. • Oxidative metabolism is an endogenous process present throughout life at a characteristic rate in each animal species. • Oxidative metabolism is the basic biologic mechanism whose adaptations define animal longevity. • The molecular features of long-lived animal species may suggest that longevity is a programmed species-specific trait. [ABSTRACT FROM AUTHOR]

Huntington's Disease (HD) is a rare genetic disease causing progressive nerve cell breakdown due to an overabundance of CAG repeats in the Htt gene. Although no cure exists, symptoms like chorea, an abrupt dance-like movements due to high dopamine levels, can be treated. Caenorhabditis elegans, which shares genetic similarities with humans and is easy to maintain in the lab, is an ideal model for studying HD. We examined the effects of Lithium Chloride (LiCl), which potentially reduces dopamine in presynaptic cells, on HD symptoms in C. elegans. Paraquat, known to negatively affect longevity and mitochondrial function in C. elegans, served as a negative control. Three strains of C. elegans were utilized: the N2 wild-type strain, the EAK102 strain (mild HD), and the EAK103 strain (severe HD). EAK 102 and 103 are transgenic animals containing a yellow fluorescent protein (YFP) linked to HD repeats. We performed longevity, imaging, and thrashing assays to assess phenotypical change upon LiCl or Paraquat exposure. Longevity assay showed that the EAK103 strain treated with paraquat had significantly reduced median survival than lithium chloride or untreated. LiCl had no negative impact on the longevity of the animals. The EAK strains were utilized to determine if there was a change in YFP levels indicative of HD protein levels. Imaging results showed a significant increase in fluorescence after both paraquat and lithium chloride exposure, suggesting an increase in HD protein levels. Thrashing assays demonstrated significant results: paraquat significantly decreased thrashes, while LiCl increased thrashing in the EAK103 strain. Overall, lithium chloride did not significantly affect lifespan but improved motility in the thrashing assay. Future research will include changing the drugs' concentrations and testing mithramycin in conjunction with LiCl, which has previously been beneficial for HD worms. These findings suggest potential therapeutic avenues for managing HD symptoms using Lithium Chloride. [ABSTRACT FROM AUTHOR]

Glia have an emergent role in brain aging and disease. In the Drosophila melanogaster brain, ensheathing glia function as phagocytic cells and respond to acute neuronal damage, analogous to mammalian microglia. We previously reported changes in glia composition over the life of ants and fruit flies, including a decline in the relative proportion of ensheathing glia with time. How these changes influence brain health and life expectancy is unknown. Here, we show that ensheathing glia but not astrocytes decrease in number during Drosophila melanogaster brain aging. The remaining ensheathing glia display dysregulated expression of genes involved in lipid metabolism and apoptosis, which may lead to lipid droplet accumulation, cellular dysfunction, and death. Inhibition of apoptosis rescued the decline of ensheathing glia with age, improved the neuromotor performance of aged flies, and extended lifespan. Furthermore, an expanded ensheathing glia population prevented amyloid‐beta accumulation in a fly model of Alzheimer's disease and delayed the premature death of the diseased animals. These findings suggest that ensheathing glia play a vital role in regulating brain health and animal longevity. [ABSTRACT FROM AUTHOR]

A dairy farmer's decision to cull or keep dairy cows is likely a complex decision based on animal health and farm management practices. The present paper investigated the relationship between cow longevity and animal health, and between longevity and farm investments, while controlling for farm-specific characteristics and animal management practices, by using Swedish dairy farm and production data for the period 2009 to 2018. We used the ordinary least square and unconditional quantile regression model to perform mean-based and heterogeneous-based analysis, respectively. Findings from the study indicate that, on average, animal health has a negative but insignificant effect on dairy herd longevity. This implies that culling is predominantly done for other reasons than poor health status. Investment in farm infrastructure has a positive and significant effect on dairy herd longevity. The investment in farm infrastructure creates room for new or superior recruitment heifers without the need to cull existing dairy cows. Production variables that prolong dairy cow longevity include higher milk yield and an extended calving interval. Findings from this study imply that the relatively short longevity of dairy cows in Sweden compared with some dairy producing countries is not a result of problems with health and welfare. Rather, dairy cow longevity in Sweden hinges on the farmers' investment decisions, farm-specific characteristics and animal management practices. [ABSTRACT FROM AUTHOR]

The evolutionary meaning and basic molecular mechanisms involved in the determination of longevity remain an unresolved problem. Currently, different theories are on offer in response to these biological traits and to explain the enormous range of longevities observed in the animal kingdom. These theories may be grouped into those that defend non-programmed aging (non-PA) and those that propose the existence of programmed aging (PA). In the present article we examine many observational and experimental data from both the field and from the laboratory and sound reasoning accumulated in recent decades both compatible and not with PA and non-PA evolutionary theories of aging. These analyses are briefly summarized and discussed. Our conclusion is that most of the data favour programmed aging with a possible contribution of non-PA antagonist pleiotropy in various cases.

Mitochondria play a wide diversity of roles in cell physiology and have a key functional implication in cell bioenergetics and biology of free radicals. As the main cellular source of oxygen radicals, mitochondria have been postulated as the mediators of the cellular decline associated with the biological aging. Recent evidences have shown that mitochondrial free radical production is a highly regulated mechanism contributing to the biological determination of longevity which is species-specific. This mitochondrial free radical generation rate induces a diversity of adaptive responses and derived molecular damage to cell components, highlighting mitochondrial DNA damage, with biological consequences that influence the rate of aging of a given animal species. In this review, we explore the idea that mitochondria play a fundamental role in the determination of animal longevity. Once the basic mechanisms are discerned, molecular approaches to counter aging may be designed and developed to prevent or reverse functional decline, and to modify longevity.

(1) Background: Desalination is a developing industry that keeps expanding, nowadays counting >15,000 infrastructures worldwide. A byproduct of the desalination process is concentrated brine, further containing operational chemicals, including antiscalants and coagulants. Yet, the potential genotoxic impacts of the inclusive brine are inadequately studied. (2) Methods: In vitro and in vivo assays were used to test the impacts of a representative antiscalant and a coagulant. The model cnidarian Nematostella vectensis was employed to assess the impacts of the tested pollutants on animal longevity. Additionally, the genotoxicity of seawater sampled near four desalination plants was tested using the comet assay. (3) Results: In vitro analyses of the antiscalant and coagulant revealed neither genotoxic nor cytotoxic effects at environmentally relevant concentrations, but they were destructive to whole organisms (N. vectensis) at various developmental stages. Part of the seawater samples from sites near desalination plants were genotoxic, revealing ephemeral and mosaic genotoxicity. Since desalination plants are situated in highly anthropogenic-impacted areas, it is impossible at this stage to evaluate the possible contribution of the brine to overall marine genotoxicity. (4) Conclusions: Exact desalination-associated chemicals and the brine itself should be evaluated directly for potential genotoxicity. [ABSTRACT FROM AUTHOR]

The nucleolus is the site of ribosome biogenesis, one of the most resource-intensive processes in eukaryotic cells. Accordingly, nucleolar morphology and activity are highly responsive to growth signaling and nucleolar insults which are collectively included in the actively evolving concept of nucleolar stress. Importantly, nucleolar alterations are a prominent feature of multiple human pathologies, including cancer and neurodegeneration, as well as being associated with aging. The past decades have seen numerous attempts to isolate compounds targeting different facets of nucleolar activity. We provide an overview of therapeutic opportunities for targeting nucleoli in different pathologies and currently available therapies. Changes in nucleolar activity and/or morphology are often associated with human disease, opening new opportunities to develop novel biomarkers and therapies. Although cancer cells often present enlarged nucleoli and increased ribosome biogenesis, mutations impairing translation can also lead to tumor development. An extended lifespan has been associated with smaller nucleoli, and partial reduction in nucleolar activity increases longevity in multiple animal models. Nucleolar stress-generating agents targeting different steps of ribosome biogenesis are been developed for their use in cancer therapy, although the specificity of currently available drugs is limited. [ABSTRACT FROM AUTHOR]

Niemann-Pick C disease (NPC) is an autosomal recessive genetic disorder resulting from mutation in one of two cholesterol transport genes: NPC1 or NPC2, causing accumulation of unesterified cholesterol, together with glycosphingolipids, within the endosomal/lysosomal compartment of cells. The result is a severe disease in both multiple peripheral organs and the central nervous system, causing neurodegeneration and early death. However, the pathophysiological mechanisms of NPC1 remain poorly understood. Recent studies have shown that the primary lysosomal defect found in fibroblasts from NPC1 patients is accompanied by a deregulation of mitochondrial organization and function. There is currently no cure for NPC1, but recently the potential of β-cyclodextrin (β-CD) for the treatment of the disease was discovered, which resulted in the redistribution of cholesterol from subcellular compartments to the circulation and increased longevity in an animal model of NPC1. Considering the above, the present work evaluated the in vitro therapeutic potential of β-CD to reduce cholesterol in fibroblasts from NPC1 patients. β-CD was used in its free and nanoparticulate form. We also evaluated the β-CD potential to restore mitochondrial functions, as well as the beneficial combined effects of treatment with antioxidants N-Acetylcysteine (NAC) and Coenzyme Q10 (CoQ10). Besides, we evaluated oxidative and nitrative stress parameters in NPC1 patients. We showed that oxidative and nitrative stress could contribute to the pathophysiology of NPC1, as the levels of lipoperoxidation and the nitrite and nitrate levels were increased in these patients when compared to healthy individuals, as well as DNA damage. The nanoparticles containing β-CD reduced the cholesterol accumulated in the NPC1 fibroblasts. This result was potentiated by the concomitant use of the nanoparticles with the antioxidants NAC and CoQ10 compared to those presented by healthy individuals cells ́. In addition, treatments combining β-CD nanoparticles and antioxidants could reduce mitochondrial oxidative stress, demonstrating advantages compared to free β-CD. The results obtained are promising regarding the combined use of β-CD loaded nanoparticles and antioxidants in the treatment of NPC1 disease. [ABSTRACT FROM AUTHOR]

In pig breeding, the integration of phenotypes into genetic improvement has been employed for decades. With today’s advancements in modern sensors, digital phenotyping provides a promising avenue for further enhancing accuracy through genomic selection. This integration also creates opportunities to study areas that used to be challenging due to limitations in data collection. We present four examples of digital phenotypes to illustrate how a company may leverage digital phenotyping for genetic implementation: individual feed intake, computer vision leg scoring, behavior, and metabolomics. Phenotypes recorded using automated electronic devices such as feed intake devices enable continuous tracking and recording of individual feed intake events when animals enter the feeder station during performance testing. The full series of events is often condensed into a single average per individual prior to genetic evaluation. By implementing computer vision, the precision of leg scoring phenotypes has increased from subjective, human-measured categorical scores of 1 to 9 to objective, camera-based continuous assessments. We have implemented convolutional neural networks (CNNs) to predict leg scores in our selection process. Using automation, the camera-based leg scoring system enables us to extend the scale of data used in genetic evaluations to improve animal welfare and longevity. Digital phenotyping holds promise for behavioral studies. Traditional methods of phenotype collection for individual behavior have been hindered by challenges such as the difficulty of capturing individual identification and the time-consuming nature of data collection. We have developed a proprietary, custom ear tag reading method and tracking algorithm that enables the automated identification of unique pigs even in visually challenging conditions. The method estimates behavior traits including time spent eating, drinking, lying, sitting, standing, and meters of distance traveled. These are used for genetic parameter estimation with investigations on association with production traits. Understanding metabolic profiles of pigs offers the potential to uncover new traits that were previously difficult to measure, and to identify biomarkers associated with traits. In conclusion, the integration of digital phenotyping into pig breeding programs offers a path toward more precise and efficient genetic improvement. Digital data capture yields a large amount of data which still provides novel opportunities for research and application. [ABSTRACT FROM AUTHOR]

Metabolic diseases often share common traits, including accumulation of unfolded proteins in the endoplasmic reticulum (ER). Upon ER stress, the unfolded protein response (UPR) is activated to limit cellular damage which weakens with age. Here, we show that Caenorhabditis elegans fed a bacterial diet supplemented high glucose at day 5 of adulthood (HGD-5) extends their lifespan, whereas exposed at day 1 (HGD-1) experience shortened longevity. We observed a metabolic shift only in HGD-1, while glucose and infertility synergistically prolonged the lifespan of HGD-5, independently of DAF-16. Notably, we identified that UPR stress sensors ATF-6 and PEK-1 contributed to the longevity of HGD-5 worms, while ire-1 ablation drastically increased HGD-1 lifespan. Together, we postulate that HGD activates the otherwise quiescent UPR in aged worms to overcome ageing-related stress and restore ER homeostasis. In contrast, young animals subjected to HGD provokes unresolved ER stress, conversely leading to a detrimental stress response. Endoplasmic reticulum stress activates the unfolded protein response (UPR). The authors show that glucose extends the lifespan of aged animals by activating the otherwise quiescent UPR while causing a UPR-dependent reduced longevity in young animals [ABSTRACT FROM AUTHOR]

Simple Summary: In the dairy farming system that uses compost barns, animals remain in a large area covered with organic material and are free to move and express their behaviors in a more natural way. The compost barn system has become popular in recent years because it provides greater well-being and quality of life, favoring animal productivity and longevity. The aim of this paper is to develop a bibliometric analysis to evaluate scientific studies about compost barn systems. A total of 108 databases, considering articles and literature reviews obtained from the Scopus and Web of Science databases were considered for this analysis. After standardizing the data, the resulting spreadsheet was analyzed with VOSviewer software. The keywords most used by the authors were "compost-bedded pack barn", "dairy cow", and "dairy cattle". The most relevant countries, journals, institutions, researchers, and co-citation networks to compost barn research were highlighted. The analysis confirmed a significant interest in the spatial variation in the sheds and their relationship with milk quality, heat stress, and animal welfare. This paper provides a great contribution related to the scientific evolution and the research and publishing tendencies of studies on the compost barn animal housing system. The objective of this study was to evaluate the main scientific studies addressing the topic of compost barns in recent years, highlighting the main journals, authors, countries, organizations, and keywords associated with the publications and trends in this type of research through a bibliometric analysis. For this analysis, publications (articles and literature reviews) addressing compost barns were obtained from the Scopus and Web of Science databases. A total of 108 studies published between 2007 and April 2022 were included. A greater number of publications was observed starting in 2017, with 2021 having the largest number of publications. The Journal of Dairy Science was the most highly cited journal. Marcia I. Endres was the author with the greatest academic impact. The most influential country was the United States, followed by Brazil. Among the organizations that have published studies on compost barns, the Federal University of Lavras, and the University of Florence had the largest numbers of publications. In conclusion, this bibliometric analysis allowed us to evaluate the scientific evolution, research, and publishing tendencies of studies on the compost barn animal housing system, and the results make it possible to deduce current trends in scientific research and publications. [ABSTRACT FROM AUTHOR]

Antioxidants are often associated with a variety of anti-aging compounds that can ensure human and animal health longevity. Foods and diet supplements from animals and plants are the common exogenous sources of antioxidants. However, microbial-based products, including probiotics and their derivatives, have been recognized for their antioxidant properties through numerous studies and clinical trials. While the number of publications on probiotic antioxidant capacities and action mechanisms is expanding, that of synbiotics combining probiotics with prebiotics is still emerging. Here, the antioxidant metabolites and properties of synbiotics, their modes of action, and their different effects on human and animal health are reviewed and discussed. Synbiotics can generate almost unlimited possibilities of antioxidant compounds, which may have superior performance compared to those of their components through additive or complementary effects, and especially by synergistic actions. Either combined with antioxidant prebiotics or not, probiotics can convert these substrates to generate antioxidant compounds with superior activities. Such synbiotic-based new routes for supplying natural antioxidants appear relevant and promising in human and animal health prevention and treatment. A better understanding of various component interactions within synbiotics is key to generating a higher quality, quantity, and bioavailability of antioxidants from these biotic sources. [ABSTRACT FROM AUTHOR]

[Display omitted] • Children are exposed to the highest levels of food additive carrageenan. • High carrageenan intake affects anxiety, immune function and oxidative stress. • Carrageenan increases oxidative-inflammatory stress that accelerate the aging process. The rate of aging can be determined, among other factors, by the diet during childhood and adolescence. Many additives are currently added to food, including carrageenan (E-407), a thickener derived from red algae. Although the acceptable daily intake for carrageenan is periodically re-evaluated, children show the highest levels of exposure with unknown potential effects on the aging process and longevity. Therefore, the aim of the present study is to know the effects in young mice of carrageenan intake, at the maximum level exposure scenario surveyed in children, on the homeostatic (nervous and immune) systems, the redox-inflammatory state and the repercussion that this may have on the aging and longevity of the animals. Swiss mice of 2 months of age (equivalent to 8 years old children) were used and 4 experimental groups were created (N = 10 animals/group): females and males that ingested carrageenan (540 mg/kg of κ-carrageenan in 200 μL of drinking water by pipette tip administration) and control females and males that took 200 μL of water, daily for 15 days. After that time, a battery of behavioral tests was performed, and peritoneal leukocytes were extracted to assess different immune functions and their redox and inflammatory state. These tests were repeated when the mice reached adulthood (7 months) and old age (18 months). Fecal microbiota was analyzed at the same sampling times. The results showed that animals that ingested carrageenan presented elevated levels of anxiety, impaired immune function and increased oxidative-inflammatory stress, with these effects extending into adulthood and old age and leading to reduced longevity in these mice. Overall, observed microbiota changes were related more to the aging process than the carrageenan intake. In conclusion, the exposure to high doses of the food additive carrageenan in childhood may contribute to an impairment of homeostasis, and consequently of health, with an increased oxidative-inflammatory stress, which implies an accelerated aging process, leading to a lower longevity. [ABSTRACT FROM AUTHOR]

Sirtuins are a family of proteins that protect against cellular injury and aging; understanding their evolution should reveal fundamental mechanisms governing longevity. "Early-branching" animals such as sea sponges and jellyfish have been understudied in previous analyses of sirtuin diversity. These organisms not only hold important positions at the base of the evolutionary tree, but also have unique aging dynamics that defy convention, such as quasi-immortality and high regenerative capacity. In this study, we survey the evolution of sirtuin proteins in animals, with a focus on the oldest living lineages. We describe previously unrecognized expansions of "Class IV" and "Class I" sirtuins around the origin of animals, raising the number of sirtuin families in the last common ancestor to at least nine. Most of these undescribed sirtuins have been lost in vertebrates and other bilaterian animals. Our work also clarifies the evolution of PNC1 and NAMPT enzymes that carry out the rate-limiting step in sirtuin-related NAD+ biosynthesis. The genes for PNC1 and NAMPT enzymes were both present in the first animals, with the genes being lost a minimum of 11 and 13 times, respectively, over the course of animal evolution. We propose that species with these ancestral gene repertoires are ideal model organisms for studying the genetic regulation of animal longevity and will provide clues to increasing longevity in humans. [ABSTRACT FROM AUTHOR]

Decreased content and activity of the mechanistic target of rapamycin (mTOR) signalling pathway, as well as the mTOR complex 1 (mTORC1) itself, are key traits for animal species and human longevity. Since mTORC1 acts as a master regulator of intracellular metabolism, it is responsible, at least in part, for the longevous phenotype. Conversely, increased content and activity of mTOR signalling and mTORC1 are hallmarks of ageing. Additionally, constitutive and aberrant activity of mTORC1 is also found in age-related diseases such as Alzheimer's disease (AD) and cancer. The downstream processes regulated through this network are diverse, and depend upon nutrient availability. Hence, multiple nutritional strategies capable of regulating mTORC1 activity and, consequently, delaying the ageing process and the development of age-related diseases, are under continuous study. Among these, the restriction of calories is still the most studied and robust intervention capable of downregulating mTOR signalling and feasible for application in the human population. [ABSTRACT FROM AUTHOR]

Thiyl radicals are exceptionally interesting reactive sulfur species (RSS), but rather rarely considered in a biological or medical context. We here review the reactivity of protein thiyl radicals in aqueous and lipid phases and provide an overview of their most relevant reaction partners in biological systems. We deduce that polyunsaturated fatty acids (PUFAs) are their preferred reaction substrates in lipid phases, whereas protein side chains arguably prevail in aqueous phases. In both cellular compartments, a single, dominating thiyl radical-specific antioxidant does not seem to exist. This conclusion is rationalized by the high reaction rate constants of thiyl radicals with several highly concentrated substrates in the cell, precluding effective interception by antioxidants, especially in lipid bilayers. The intractable reactivity of thiyl radicals may account for a series of long-standing, but still startling biochemical observations surrounding the amino acid cysteine: (i) its global underrepresentation on protein surfaces, (ii) its selective avoidance in aerobic lipid bilayers, especially the inner mitochondrial membrane, (iii) the inverse correlation between cysteine usage and longevity in animals, (iv) the mitochondrial synthesis and translational incorporation of cysteine persulfide, and potentially (v) the ex post introduction of selenocysteine into the genetic code. [ABSTRACT FROM AUTHOR]

Geroprotectors slow down aging and promote healthy longevity in model animals. Although hundreds of compounds have been shown to extend the life of laboratory model organisms, clinical studies on potential geroprotectors are exceedingly rare, especially in healthy elders. This review aims to classify potential geroprotectors based on the mechanisms by which they influence aging. These pharmacological interventions can be classified into the following groups: those that prevent oxidation; proteostasis regulators; suppressors of genomic instability; epigenetic drugs; those that preserve mitochondrial function; inhibitors of aging-associated signaling pathways; hormetins; senolytics/senostatics; anti-inflammatory drugs; antifibrotic agents; neurotrophic factors; factors preventing the impairment of barrier function; immunomodulators; and prebiotics, metabiotics, and enterosorbents. Geroprotectors or anti-aging drugs can slow down aging and promote a healthy lifespan. Pharmacological interventions in aging can be classified based on the mechanism of aging. Many geroprotectors may act in multiple pathways. Clinical studies are needed for approval of potential candidates as human geroprotectors. [ABSTRACT FROM AUTHOR]

A species-specific lipidome profile is an inherent feature linked to longevity in the animal kingdom. However, there is a lack of lipidomic studies on human longevity. Here, we use mass spectrometry-based lipidomics to detect and quantify 151 sphingolipid molecular species and use these to define a phenotype of healthy humans with exceptional life span. Our results demonstrate that this profile specifically comprises a higher content of complex glycosphingolipids (hexosylceramides and gangliosides), and lower levels of ceramide species from the de novo pathway, sphingomyelin and sulfatide; while for ceramide-derived signaling compounds, their content remains unchanged. Our findings suggest that structural glycosphingolipids may be more relevant to achieve the centenarian condition than signaling sphingolipids. [ABSTRACT FROM AUTHOR]

Sulfonylureas are widely used oral anti-diabetic drugs. However, its long-term usage effects on patients' lifespan remain controversial, with no reports of influence on animal longevity. Hence, the anti-aging effects of chlorpropamide along with glimepiride, glibenclamide, and tolbutamide were studied with special emphasis on the interaction of chlorpropamide with mitochondrial ATP-sensitive K+ (mitoK-ATP) channels and mitochondrial complex II. Chlorpropamide delayed aging in Caenorhabditis elegans , human lung fibroblast MRC-5 cells and reduced doxorubicin-induced senescence in both MRC-5 cells and mice. In addition, the mitochondrial membrane potential and ATP levels were significantly increased in chlorpropamide-treated worms, which is consistent with the function of its reported targets, mitoK-ATP channels. Increased levels of mitochondrial reactive oxygen species (mtROS) were observed in chlorpropamide-treated worms. Moreover, the lifespan extension by chlorpropamide required complex II and increased mtROS levels, indicating that chlorpropamide acts on complex II directly or indirectly via mitoK-ATP to increase the production of mtROS as a pro-longevity signal. This study provides mechanistic insight into the anti-aging effects of sulfonylureas in C. elegans. Chlorpropamide delayed aging in Caenorhabditis elegans , MRC-5 cells and doxorubicin-induced aging mice. It acts on complex II directly or indirectly via mitoK-ATP to produce mtROS as a pro-longevity signal. [Display omitted] [ABSTRACT FROM AUTHOR]

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There are many costs associated with increased body size and longevity in animals, including the accumulation of genotoxic and cytotoxic damage that comes with having more cells and living longer. Yet, some species have overcome these barriers and have evolved remarkably large body sizes and long lifespans, sometimes within a narrow window of evolutionary time. Here, we demonstrate through phylogenetic comparative analysis that multiple turtle lineages, including Galapagos giant tortoises, concurrently evolved large bodies, long lifespans, and reduced cancer risk. We also show through comparative genomic analysis that Galapagos giant tortoises have gene duplications related to longevity and tumor suppression. To examine the molecular basis underlying increased body size and lifespan in turtles, we treated cell lines from multiple species, including Galapagos giant tortoises, with drugs that induce different types of cytotoxic stress. Our results indicate that turtle cells, in general, are resistant to oxidative stress related to aging, whereas Galapagos giant tortoise cells, specifically, are sensitive to endoplasmic reticulum stress, which may give this species an ability to mitigate the effects of cellular stress associated with increased body size and longevity. [ABSTRACT FROM AUTHOR]

Complex I, a component of the electron transport chain, plays a central functional role in cell bioenergetics and the biology of free radicals. The structural and functional N module of complex I is one of the main sites of the generation of free radicals. The NDUFV2 subunit/N1a cluster is a component of this module. Furthermore, the rate of free radical production is linked to animal longevity. In this review, we explore the hypothesis that NDUFV2 is the only conserved core subunit designed with a regulatory function to ensure correct electron transfer and free radical production, that low gene expression and protein abundance of the NDUFV2 subunit is an evolutionary adaptation needed to achieve a longevity phenotype, and that these features are determinants of the lower free radical generation at the mitochondrial level and a slower rate of aging of long‐lived animals. [ABSTRACT FROM AUTHOR]

Insulin/IGF-1 signaling (IIS) regulates various physiological aspects in numerous species. In Caenorhabditis elegans, mutations in the daf-2/insulin/IGF-1 receptor dramatically increase lifespan and immunity, but generally impair motility, growth, and reproduction. Whether these pleiotropic effects can be dissociated at a specific step in insulin/IGF-1 signaling pathway remains unknown. Through performing a mutagenesis screen, we identified a missense mutation daf-18(yh1) that alters a cysteine to tyrosine in DAF-18/PTEN phosphatase, which maintained the long lifespan and enhanced immunity, while improving the reduced motility in adult daf-2 mutants. We showed that the daf-18(yh1) mutation decreased the lipid phosphatase activity of DAF-18/PTEN, while retaining a partial protein tyrosine phosphatase activity. We found that daf-18(yh1) maintained the partial activity of DAF-16/FOXO but restricted the detrimental upregulation of SKN-1/NRF2, contributing to beneficial physiological traits in daf-2 mutants. Our work provides important insights into how one evolutionarily conserved component, PTEN, can coordinate animal health and longevity. Mutations in daf-2/insulin/IGF-1 receptor impair the growth and reproduction of C. elegans but conversely enhance immunity and lifespan. Here, the authors show that a missense mutation in the gene retains the effects on lifespan and immunity and improves motility. [ABSTRACT FROM AUTHOR]

Circular RNA (circRNA) is a closed, single-stranded transcript widely detected in eukaryotes. Recent studies indicate that the levels of circRNAs change with age in various tissues in multiple species, ranging from nematodes to mammals. Here we discuss the functional roles of circRNAs in animal aging and longevity. We review studies regarding the differential expression of circRNAs that contributes to cellular senescence and the pathogenesis of aging-associated diseases. We explore the features of aging-associated circRNAs by discussing their potential as biomarkers of aging, tissue specificity, physiological roles, action mechanisms, and evolutionarily conserved characteristics. Our review provides insights into current progress in circRNA research and their significant functions in the aging process. Circular RNAs (circRNAs) are closed and cyclic RNAs that are widely expressed in eukaryotes and have multiple functions, including interacting with proteins, sponging miRNAs, encoding proteins, and regulating gene expression via binding promoters. The expression patterns and stability of circRNAs have emerged as promising candidate biomarkers of aging and age-associated diseases. The levels of circRNAs generally increase with age in various species and may play roles in aging and cellular senescence. Specifically, ciRS-7/circCDR1as and circSfl are associated with Alzheimer's disease and fruit fly longevity, respectively. It will be important to identify functional circRNAs to elucidate the underlying mechanisms regarding their roles in aging and/or age-related diseases. [ABSTRACT FROM AUTHOR]

• Aging can be pharmacologically retarded in animals. • The challenge now is to translate longevity drugs to the clinic. • A growing number of companies and clinical trials promise to shed light on which drugs extend healthy life. • Longevity pharmacology promises to revolutionize medicine. With a globally aging population, longevity is becoming the most promising market for the biotech industry. In animals, aging can be retarded and longevity extended, which, if translated to humans, would result in huge health benefits with remarkable commercial value. The potential to slow down human aging has led to a race to discover the most promising longevity drugs in animals and ultimately translate them to humans. Indeed, in recent years, there has been exponential growth in longevity drugs discovered in animal models. Investment in longevity biotech is also booming, and several clinical trials will soon shed light on which drugs extend healthy lives. Thus, the longevity pharmacology field promises to revolutionize the healthcare of a growing aging population. [ABSTRACT FROM AUTHOR]

We recently described two outbred mouse lines that were selected for large litter size at first delivery. However, lifetime fecundity appears to be economically more important for the husbandry of many polytocous species for which mouse lines might serve as bona fide animal models (e.g. for pigs). In the present study, we compared the lifetime fecundities of two highly fertile mouse lines (FL1 and FL2: >20 offspring/litter at first delivery) with those of an unselected control line (ctrl) and two lines that were selected for high body weight (DU6) and high protein mass (DU6P) without selection pressure on fertility. We tested the hypothesis that selection for large litter size at first parturition would also increase lifetime fecundity in mice, and we observed very large differences between lines. Whereas FL1 and ctrl delivered up to nine and ten litters, none of the DU6 and DU6P females gave birth to more than five litters. In line with this observation, FL1 delivered the most pups per lifetime (85.7/female). FL2 females produced the largest average litter sizes (20.4 pups/litter) in the first four litters; however, they displayed a reduced number of litters. With the exception of ctrl, litter sizes declined from litter to litter. Repeated delivery of litters with high offspring numbers did not affect the general health of FL females. The presented data demonstrate that two biodiverse, highly fertile mouse lines selected for large litter size at first delivery show different lifetime reproductive fitness levels. Thus, these mouse lines might serve as valuable mouse models for investigating lifetime productivity and longevity in farm animals. [ABSTRACT FROM AUTHOR]

Coordinated regulation of stress response pathways is crucial for cellular homeostasis. However, crosstalk between the different stress pathways and the physiological significance of this crosstalk remain poorly understood. In this study, using the model organism C. elegans, we discovered that suppression of the transcription factor LET-607/CREBH, a regulator of cellular defense and proteostatic responses, triggers adaptive induction of DAF-16-dependent stress responses. Suppression of LET-607 improves stress resistance and extends C. elegans lifespan in a DAF-16-dependent manner. We identified the sphingomyelin synthase SMS-5 to be a central mediator in the communication between LET-607 and DAF-16. SMS-5 reduces the contents of unsaturated phosphatidylcholine (PC), which activates DAF-16 through ITR-1-dependent calcium signaling and calcium-sensitive kinase PKC-2. Our data reveal the significance of crosstalk between different stress pathways in animal fitness and identify LET-607/CREBH and specific PC as regulators of DAF-16 and longevity. Author summary: In order to cope with stresses, cells have evolved complex and elegant adaptive mechanisms, which are also referred to as stress responses. Central to these responses are core transcription factors. It is widely hypothesized that interruption of one key stress response pathway could compromise overall cellular function and survival. In order to avoid such an issue, stress response pathways communicate with each other. A defect in one pathway may adaptively activate other pathways, thus restoring homeostasis and increasing fitness. However, how these pathways communicate is largely unexplored. In this study, we unraveled crosstalk between the LET-607 and DAF-16 pathways in C. elegans. Suppression of LET-607, a regulator of defense and proteostatic responses, was shown to adaptively activate DAF-16, which is a crucial regulator of general stress responses. This crosstalk was shown to be vital for animal fitness, as suppression of LET-607 extends lifespan in a DAF-16-dependent manner. Intriguingly, loss of LET-607 results in increased levels of the sphingomyelin synthase SMS-5, which metabolizes membrane lipid PC. Consequently, the reduction in PC causes activation of DAF-16 via membrane-located calcium channel ITR-1 and calcium-sensitive kinase PKC-2. This study identifies a novel crosstalk between stress response pathways, which is potentially significant in animal longevity. [ABSTRACT FROM AUTHOR]

Mitochondrial ATP production is a well-known regulator of neuronal excitability. The reciprocal influence of plasma-membrane potential on ATP production, however, remains poorly understood. Here, we describe a mechanism by which depolarized neurons elevate the somatic ATP/ADP ratio in Drosophila glutamatergic neurons. We show that depolarization increased phospholipase-Cß (PLC-ß) activity by promoting the association of the enzyme with its phosphoinositide substrate. Augmented PLC-ß activity led to greater release of endoplasmic reticulum Ca2+ via the inositol trisphosphate receptor (IP3R), increased mitochondrial Ca2+ uptake, and promoted ATP synthesis. Perturbations that decoupled membrane potential from this mode of ATP synthesis led to untrammeled PLC-ß-IP3R activation and a dramatic shortening of Drosophila lifespan. Upon investigating the underlying mechanisms, we found that increased sequestration of Ca2+ into endolysosomes was an intermediary in the regulation of lifespan by IP3Rs. Manipulations that either lowered PLC-ß/IP3R abundance or attenuated endolysosomal Ca2+ overload restored animal longevity. Collectively, our findings demonstrate that depolarization-dependent regulation of PLC-ß-IP3R signaling is required for modulation of the ATP/ADP ratio in healthy glutamatergic neurons, whereas hyperactivation of this axis in chronically depolarized glutamatergic neurons shortens animal lifespan by promoting endolysosomal Ca2+ overload. [ABSTRACT FROM AUTHOR]

Cells use a variety of mechanisms to maintain optimal mitochondrial function including the mitochondrial unfolded protein response (UPRmt). The UPRmt mitigates mitochondrial dysfunction by differentially regulating mitoprotective gene expression through the transcription factor ATFS-1. Since UPRmt activation is commensurate with organismal benefits such as extended lifespan and host protection during infection, we sought to identify pathways that promote its stimulation. Using unbiased forward genetics screening, we isolated novel mutant alleles that could activate the UPRmt. Interestingly, we identified one reduction of function mutant allele (osa3) in the mitochondrial ribosomal gene mrpl-2 that activated the UPRmt in a diet-dependent manner. We find that mrpl-2(osa3) mutants lived longer and survived better during pathogen infection depending on the diet they were fed. A diet containing low levels of vitamin B12 could activate the UPRmt in mrpl-2(osa3) animals. Also, we find that the vitamin B12-dependent enzyme methionine synthase intersects with mrpl-2(osa3) to activate the UPRmt and confer animal lifespan extension at the level of ATFS-1. Thus, we present a novel gene-diet pairing that promotes animal longevity that is mediated by the UPRmt. Author summary: The mitochondrial unfolded protein response (UPRmt) is a cellular pathway that mediates recovery of damaged mitochondria. Mitigation of mitochondrial dysfunction is critical due to the essential nature of the organelle. The UPRmt controls the expression of genes that help restore mitochondrial homeostasis via the bZIP transcription factor ATFS-1. The activation of the UPRmt is associated not only with extended animal lifespan but also with increased host protection during infection with bacterial pathogens. Using a genetic screen to identify pathways that activate the UPRmt, we recovered a novel reduction of function mutation in the mitochondrial ribosomal gene mrpl-2 that mediates protein translation in mitochondria. Interestingly, our isolated mrpl-2 mutant activates the UPRmt and promotes longevity when fed a specific diet which is low in the metabolite vitamin B12. We find that impaired function of methionine synthase, an enzyme that uses vitamin B12 as a cofactor to convert homocysteine to methionine, genetically interacts with the isolated mrpl-2 mutant to activate the UPRmt and extend lifespan. Our findings suggest that the lifespan-extending benefits of impaired mitochondrial translation and that of methionine restriction occur through a common mechanism that includes the activation of the UPRmt. [ABSTRACT FROM AUTHOR]

The American lobster (Homarus americanus) is a commercially important crustacean with an unusual long life span up to 100 years and a comparative animal model of longevity. Therefore, research into its immune system and physiology is of considerable importance both for industry and comparative immunology studies. Peptidylarginine deiminases (PADs) are a phylogenetically conserved enzyme family that catalyses post-translational protein deimination via the conversion of arginine to citrulline. This can lead to structural and functional protein changes, sometimes contributing to protein moonlighting, in health and disease. PADs also regulate the cellular release of extracellular vesicles (EVs), which is an important part of cellular communication, both in normal physiology and in immune responses. Hitherto, studies on EVs in Crustacea are limited and neither PADs nor associated protein deimination have been studied in a Crustacean species. The current study assessed EV and deimination signatures in haemolymph of the American lobster. Lobster EVs were found to be a poly-dispersed population in the 10–500 nm size range, with the majority of smaller EVs, which fell within 22–115 nm. In lobster haemolymph, 9 key immune and metabolic proteins were identified to be post-translationally deiminated, while further 41 deiminated protein hits were identified when searching against a Crustacean database. KEGG (Kyoto encyclopedia of genes and genomes) and GO (gene ontology) enrichment analysis of these deiminated proteins revealed KEGG and GO pathways relating to a number of immune, including anti-pathogenic (viral, bacterial, fungal) and host-pathogen interactions, as well as metabolic pathways, regulation of vesicle and exosome release, mitochondrial function, ATP generation, gene regulation, telomerase homeostasis and developmental processes. The characterisation of EVs, and post-translational deimination signatures, reported in lobster in the current study, and the first time in Crustacea, provides insights into protein moonlighting functions of both species-specific and phylogenetically conserved proteins and EV-mediated communication in this long-lived crustacean. The current study furthermore lays foundation for novel biomarker discovery for lobster aquaculture. Image 1 • PAD and protein deimination signatures are novel biomarkers in haemolymph of American lobster (Homarus americanus). • Extracellular vesicles (EVs) were profiled in lobster. • Deiminated proteins in lobster are involved in key immune, gene regulatory, metabolic and developmental functions. • Deimination may cause protein moonlighting in Crustacean physiology, immunology and in phylogenetically conserved proteins. [ABSTRACT FROM AUTHOR]

Summary: Thyroid function is central in the control of physiological and pathophysiological processes. Studies in animal models and human research have determined that thyroid hormones modulate cellular processes relevant for aging and for the majority of age‐related diseases. While several studies have associated mild reductions on thyroid hormone function with exceptional longevity in animals and humans, alterations in thyroid hormones are serious medical conditions associated with unhealthy aging and premature death. Moreover, both hyperthyroidism and hypothyroidism have been associated with the development of certain types of diabetes and cancers, indicating a great complexity of the molecular mechanisms controlled by thyroid hormones. In this review, we describe the latest findings in thyroid hormone research in the field of aging, diabetes, and cancer, with a special focus on hepatocellular carcinomas. While aging studies indicate that the direct modulation of thyroid hormones is not a viable strategy to promote healthy aging or longevity and the development of thyromimetics is challenging due to inefficacy and potential toxicity, we argue that interventions based on the use of modulators of thyroid hormone function might provide therapeutic benefit in certain types of diabetes and cancers. [ABSTRACT FROM AUTHOR]

In livestock activity, profitability can be evaluated by calculating zootechnical indices, because of their relation with production and, consequently, to the main income source for the farmer. The aim of this study was to evaluate the importance of a group of productive-reproductive indicators, not always valued, in the economic results of milk production in system based on grazing. Retrospective data was used, corresponding to lactations of 1,785 primiparous Holstein cows, American-Canadian biotype, collected between 1999-2016 in two establishments located in Entre Ríos province, Argentina. Fifty members from each of the following three age groups at first calving were randomly chosen: Group 1: 750 days (24 months), Group 2: 840 days (27 months) and Group 3: 1,098 days (32 months). Group characterization was based on values of the following indicators: total productive life, total milk production, milk index, productive days, number of calvings, production per lactation and mean calving interval. Significant differences between groups (p<0.05) were only observed for total productive life. Although all three groups produced similar amounts of milk, cows in the late calving age group resulted in higher incomes. It is concluded that indicators calving interval, efficiency in rearing, age at first calving and longevity, all of which are easy to register, acquire relevance when evaluating their impact while modeling the final economic result of the establishment, thus enabling the technical and managerial decision making, aimed to improve system profitability. [ABSTRACT FROM AUTHOR]

The gut microbiome (GM) represents a large and very complex ecosystem of different microorganisms. There is an extensive interest in the potential role of the GM in different diseases including cancer, diabetes, cardiovascular diseases, and aging. The GM changes over the lifespan and is strongly associated with various age-related diseases. Ames dwarf (df/df) mice are characterized by an extended life- and healthspan, and although these mice are protected from many age-related diseases, their microbiome has not been studied. To determine the role of microbiota on longevity animal models, we investigated the changes in the GM of df/df and normal control (N) mice, by comparing parents before mating and littermate mice at three distinct time points during early life. Furthermore, we studied the effects of a 6-month calorie restriction (CR), the most powerful intervention extending the lifespan. Our data revealed significant changes of the GM composition during early life development, and we detected differences in the abundance of some bacteria between df/df and N mice, already in early life. Overall, the variability of the microbiota by genotype, time-point, and breeding pair showed significant differences. In addition, CR caused significant changes in microbiome according to gastrointestinal (GI) location (distal colon, ileum, and cecum), genotype, and diet. However, the overall impact of the genotype was more prominent than that of the CR. In conclusion, our findings suggest that the gut microbiota plays an important role during postnatal development in long-living df/df mice and CR dietary regimen can significantly modulate the GM. [ABSTRACT FROM AUTHOR]

Copyright of Revista Biociências is the property of Revista Biociencias and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The senescence of the immune system contributes considerably to the age-related diseases that are the main causes of death after the age of 65. In this study, we present an appealing option for the prevention of immune senescence and slowing or reversing the aging process, which can be achieved by heterochronous autologous hematopoietic stem cell transplantation (haHSCT), where healthy autologous bone marrow stem cells are collected from donors while young, cryopreserved and stored for a long period, and reinfused at a later time when indicated. After reinfusion and homing, these young HSCs could participate in normal hemato- and immunopoiesis and improve several immune functions by expanding the immune- as well as hematopoietic cell repertoire. Several animal studies have already confirmed the feasibility of this procedure, which extended the longevity of the treated animals. If translated to human medicine, haHSCT could prevent or mitigate age-related immune defects and extend the healthy life span. In this review, we describe the concept of haHSCT, recent studies that confirm its feasibility, and discuss the further research needed to translate this heterochronous methodology. [ABSTRACT FROM AUTHOR]

Survival and longevity are very important traits in pig breeding. From an economic standpoint, it is favorable to keep the sows for another parity instead of replacing them and, from the animal's perspective, better welfare is achieved if they do not experience health problems. It is challenging to record longevity in purebred (PB) nucleus herds because animals are more likely to be replaced based on breeding value and high replacement rates rather than inability to produce. Crossbred (CB) sows are, however, submitted to lower replacement rates and are more likely to be kept in the farm longer if they can produce large and robust litters. Therefore, the objective of this study was to investigate whether the use of CB phenotypes could improve prediction accuracy of longevity for PBs. In addition, a new definition of survival was investigated. The analyzed data included phenotypes from two PB dam lines and their F1 cross. Three traits were evaluated: 1) whether or not the sow got inseminated for a second litter within 85 d of first farrowing (Longevity 1–2), 2) how many litters the sow can produce within 570 d of first farrowing [Longevity 1–5 (LGY15)], and 3) a repeatability trait that indicates whether or not the sow survived until the next parity (Survival). Traits were evaluated both as the same across breeds and as different between breeds. Results indicated that longevity is not the same trait in PB and CB animals (low genetic correlation). In addition, there were differences between the two PB lines in terms of which trait definition gave the greatest prediction accuracy. The repeatability trait (Survival) gave the greatest prediction accuracy for breed B, but LGY15 gave the greatest prediction accuracy for breed A. Prediction accuracy for CBs was generally poor. The Survival trait is recorded earlier in life than LGY15 and seemed to give a greater prediction accuracy for young animals than LGY15 (until own phenotype was available). Thus, for selection of young animals for breeding, Survival would be the preferred trait definition. In addition, results indicated that lots of data were needed to get accurate estimates of breeding values and that, if CB performance is the breeding goal, CB phenotypes should be used in the genetic evaluation. [ABSTRACT FROM AUTHOR]