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30734948-35a9-4d4b-b917-8fbf2a6deeab
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vgsshyvs-3844
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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longevity in mammals
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longevity in mammals
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This PDF is a high-level evolutionary biology rese This PDF is a high-level evolutionary biology research article published in PNAS that investigates why some mammals live longer than others. It tests a powerful hypothesis:
Mammals that live in trees (arboreal species) evolve longer lifespans because tree-living reduces external sources of death such as predators, disease, and environmental hazards.
Using a massive dataset of 776 mammalian species, the study compares lifespan, body size, and habitat across nearly all mammalian clades. It provides one of the strongest empirical tests of evolutionary ageing theory in mammals.
The core message:
Arboreal mammals live significantly longer than terrestrial mammals, even after accounting for body size and evolutionary history â supporting the evolutionary theory of ageing and clarifying why primates (including humans) evolved long lifespans.
đł 1. Why Arboreality Should Increase Longevity
Evolutionary ageing theory predicts:
High extrinsic mortality (predators, disease, accidents) â earlier ageing, shorter lifespan
Low extrinsic mortality â slower ageing, longer lifespan
Tree living offers protection:
Harder for predators to attack
Less exposure to ground hazards
Improved escape options
Therefore, species that spend more time in trees should evolve greater lifespan and delayed senescence.
Longevity in mammals
đ 2. Dataset and Methodology
The paper analyzes:
776 species of non-flying, non-aquatic mammals
Lifespan records (mostly from captive data for accurate maxima)
Species classified into:
Arboreal
Semiarboreal
Terrestrial
Body mass as a key covariate
Phylogenetically independent contrasts (PIC) to remove evolutionary bias
This allows a robust test of whether habitat causes differences in longevity.
Longevity in mammals
đ 3. Main Findings
â A. Arboreal mammals live longer
Across mammals, tree-living species have significantly longer maximum lifespans than terrestrial ones when body size is held constant.
Longevity in mammals
â B. The pattern holds in most mammalian groups
In 8 out of 10 subclades, arboreal species live longer than terrestrial relatives.
â C. Exceptions reveal evolutionary history
Two groups do not show this pattern:
Primates & Their Close Relatives (Euarchonta)
Arboreal and terrestrial species do not differ significantly
Likely because primates evolved from highly arboreal ancestors
Their long lifespan may have been established early and retained
Even terrestrial primates inherit long-living traits
Longevity in mammals
Marsupials (Metatheria)
No longevity advantage for arboreal vs. terrestrial species
Marsupials in general are not long-lived, regardless of habitat
Longevity in mammals
â D. Squirrels provide a clear example
Within Sciuroidea:
Arboreal squirrels live longer than terrestrial squirrels
Semiarboreal species fall in between
Longevity in mammals
đ 4. Why Primates Are a Special Case
The article provides an important evolutionary insight:
Primates did not gain longevity from becoming arboreal â they were already arboreal.
Arboreality is the ancestral primate condition
Long lifespan likely evolved early as primates adapted to tree life
Later terrestrial primates (baboons, humans) retained this long-lived biology
Additional survival strategies (large body size, social structures, intelligence) further reduce predation
Longevity in mammals
This helps explain why humansâthe most terrestrial primateâstill have extremely long lifespans.
𧏠5. Evolutionary Significance
The study strongly supports evolutionary ageing theory:
Low extrinsic mortality â slower ageing
Arboreality functions like a protective âlife-extending shieldâ
Similar patterns seen in flying mammals (bats) and gliding mammals
Reduced risk environments create selection pressure for longer lives
Longevity in mammals
đŸ 6. Additional Insights
âïž Body size explains ~60% of lifespan variation
Larger mammals generally live longer, but habitat explains additional differences.
âïž Arboreal habitats evolve multiple times
Many mammal groups that shifted from ground to trees repeatedly evolved greater longevity â independently.
âïž Sociality reduces predation too
Large social groups (e.g., in primates and some marsupials) reduce predator risk, altering ageing patterns.
Longevity in mammals
â Overall Summary
This PDF provides a groundbreaking comparative analysis showing that arboreal mammals live longer than terrestrial mammals, validating key predictions of evolutionary ageing theory. It demonstrates that reduced exposure to predators and environmental hazards in tree habitats leads to delayed ageing and increased lifespan. While most mammals follow this pattern, primates and marsupials are exceptions due to their unique evolutionary histories â particularly primates, who long ago evolved the long-living biology that humans still carry today.
This study is one of the most compelling demonstrations of how ecology, behavior, and evolutionary history shape lifespan across mammals....
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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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qdzwhpef-1289
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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longevity lifespain
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longevity across the human life span
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âSocial relationships and physiological determinan âSocial relationships and physiological determinants of longevity across the human life spanâ is a landmark study that explains how social relationships directly shape the biology of aging, beginning in adolescence and persisting into old age. Using an unprecedented integration of four major U.S. longitudinal datasets, the authors show that social connections literally âget under the skin,â altering inflammation, cardiovascular function, metabolic health, and ultimately lifespan.
The study examines two key dimensions of social relationships:
Social integration â the quantity of social ties and frequency of interaction
Social support and strain â the quality, positivity, or negativity of those relationships
Across adolescence, young adulthood, midlife, and late adulthood, the researchers link these measures to objective biomarkers: CRP inflammation, blood pressure, waist circumference, and BMI.
Core Findings
More social connections = better physiological health, in a clear doseâresponse pattern.
Social isolation is as biologically harmful as major clinical risks.
In adolescence, isolation increased inflammation as much as physical inactivity.
In old age, its impact on hypertension exceeded that of diabetes.
Effects emerge early and accumulate: adolescent social integration predicts cardiovascular and metabolic health years later.
Midlife is different: quantity of relationships matters less, but quality (support or strain) becomes especially important.
Negative relationships (strain) are stronger predictors of poor health than lack of support.
Late-life social connections protect against hypertension and obesity, even after adjusting for demographics, behavior, and socioeconomic factors.
Significance
The study provides some of the strongest evidence to date that social relationships causally influence longevity through biological pathways, not just through behavior or psychology. It shows that:
Social connectedness is a lifelong biological asset.
Social adversity is a chronic physiological stressor that accelerates aging.
Effective health and longevity strategies must include social environments, not just medical or lifestyle interventions.
This work fundamentally reframes longevity research by demonstrating that aging is shaped not only by genes, lifestyle, or medical careâbut also by the structure and quality of our social lives....
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b996a863-1c98-4a77-842c-4008d596029f
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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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wvptnahr-9268
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xevyo
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longevity of C. elegans m
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longevity of C. elegans mutants
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This study delivers a deep, mechanistic explanatio This study delivers a deep, mechanistic explanation of how changes in lipid biosynthesisâspecifically in fatty-acid chain length and saturationâcontribute directly to the extraordinary longevity of certain C. elegans mutants, especially those with disrupted insulin/IGF-1 signaling (IIS). By comparing ten nearly genetically identical worm strains that span a tenfold range of lifespans, the authors identify precise lipid signatures that track strongly with lifespan and experimentally confirm that altering these lipid pathways causally extends or reduces lifespan.
Its central insight:
Long-lived worms reprogram lipid metabolism to make their cell membranes more resistant to oxidative damage, particularly by reducing peroxidation-prone polyunsaturated fatty acids (PUFAs) and shifting toward shorter and more saturated lipid chains.
This metabolic remodeling lowers the substrate available for destructive free-radical chain reactions, boosting both stress resistance and lifespan.
𧏠Core Findings, Explained Perfectly
1. Strong biochemical patterns link lipid structure to lifespan
Across all strains, two lipid features were the strongest predictors of longevity:
A. Shorter fatty-acid chain length
Long-lived worms had:
more short-chain fats (C14:0, C16:0)
fewer long-chain fats (C18:0, C20:0, C22:0)
Average chain length decreased almost perfectly in proportion to lifespan.
B. Fewer polyunsaturated fatty acids (PUFAs)
Long-lived mutants had:
sharply reduced PUFAs (EPA, arachidonic acid, etc.)
dramatically lower peroxidation index (PI)
fewer double bonds (lower DBI)
These changes make membranes much less susceptible to lipid peroxidation damage.
2. Changes in enzyme activity explain the lipid shifts
By measuring mRNA levels and inferred enzymatic activity, the study shows:
Downregulated in long-lived mutants
Elongases (elo-1, elo-2, elo-5) â shorter chains
Î5 desaturase (fat-4) â fewer PUFAs
Upregulated
Î9 desaturases (fat-6, fat-7) â more monounsaturated, oxidation-resistant MUFAs
This combination produces membranes that are:
just fluid enough (thanks to MUFAs)
much harder to oxidize (thanks to less PUFA content)
This is a perfect, balanced redesign of the membrane.
3. RNAi experiments prove these lipid changes CAUSE longevity
Knocking down specific genes in normal worms produced dramatic effects:
Increasing lifespan
fat-4 (Î5 desaturase) RNAi â +25% lifespan
elo-1 or elo-2 (elongases) RNAi â ~10â15% lifespan increase
Combined elo-1 + elo-2 knockdown â even larger increase
Reducing lifespan
Knockdown of Î9 desaturases (fat-6, fat-7) slightly shortened lifespan
Stress resistance matched the lifespan effects
The same interventions boosted survival under hydrogen peroxide oxidative stress, confirming that resistance to lipid peroxidation is a key mechanism of longevity.
4. Dietary experiments confirm the same mechanism
When worms were fed extra PUFAs like EPA or DHA:
lifespan dropped by 16â24%
Even though these fatty acids are often considered âhealthyâ in humans, in worms they create more oxidative vulnerability, validating the model.
5. Insulin/IGF-1 longevity mutants remodel lipids as part of their longevity program
The longest-lived mutantsâespecially age-1(mg44), which can live nearly 10Ă longerâshow the greatest lipid remodeling:
lowest elongase expression
lowest PUFA levels
highest MUFA-producing Î9 desaturases
This suggests that IIS mutants extend lifespan partly through targeted remodeling of membrane lipid composition, not just through metabolic slowdown or stress-response pathways.
đĄ What This Means
The core conclusion
Longevity in C. elegans is intimately connected to reducing lipid peroxidation, a major source of cellular damage.
Worms extend their lifespan by:
shortening lipid chains
reducing PUFA content
elevating MUFAs
suppressing enzymes that create vulnerable lipid species
enhancing enzymes that create stable ones
These changes:
harden membranes against oxidation
reduce chain-reaction damage
increase survival under stress
extend lifespan significantly
**This is one of the clearest demonstrations that lipid composition is not just correlated with longevityâ
it helps cause longevity.**...
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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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mfcdvyme-9289
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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mTmodel_1765016141
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Filtered merged training 6-12
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xevyo-base-v1
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Contain lots of data various category like econimi Contain lots of data various category like econimics, medical, historical...
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{"train_runtime": 654.8482, "train_sam {"train_runtime": 654.8482, "train_samples_per_second": 2.443, "train_steps_per_second": 0.305, "total_flos": 7878114829615104.0, "train_loss": 1.3694590425491333, "epoch": 0.33769523005487545, "step": 200}...
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f9601fa5-f780-4137-bc3e-bb016c529d27
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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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hiynnkoy-3916
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xevyo
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mtorc1 is also involve in
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mtorc1 is also involve in longevity between specie
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This PDF is a scientific editorial from the journa This PDF is a scientific editorial from the journal Aging (2021) that explains how mTORC1, a central nutrient- and energy-sensing cellular pathway, plays a critical role not only in lifespan extension within a single species but also in determining natural longevity differences between mammalian species.
The authors, Gustavo Barja and Reinald Pamplona, summarize recent comparative research showing that long-lived species naturally maintain lower mTORC1 activity, suggesting that downregulated mTORC1 signaling is an evolutionary adaptation that contributes to slower aging and extended longevity.
đ¶ 1. Background: The Aging Program & Effector Systems
The paper begins by reviewing the nuclear aging program (AP) and the network of aging effectors controlled by it.
These include:
mitochondrial ROS production
mitochondrial DNA repair
lipid composition of membranes
telomere shortening rates
metabolomic/lipidomic profiles
mTORC1 is also involved in longâŠ
Long-lived species show:
low mitochondrial ROS at complex I
high mitochondrial DNA repair
lower unsaturated fatty acids in membranes
slower telomere shortening
mTORC1 is also involved in longâŠ
These differences shape species-specific aging rates.
đ¶ 2. What is mTORC1 and Why It Matters for Aging?
mTORC1 is a highly conserved cellular signaling hub that integrates information about:
nutrients
energy (ATP, glucose)
amino acids (especially arginine, leucine, methionine)
hormones
oxygen levels
mTORC1 is also involved in longâŠ
mTORC1 regulates:
protein + lipid synthesis
mitochondrial function
autophagy
cell growth and proliferation
stress responses
Within species, lowering mTORC1 activity increases lifespan in yeast, worms, flies, and mammals, while increased mTORC1 accelerates aging.
đ¶ 3. The New Study: First Cross-Species Analysis of mTORC1 and Longevity
The editorial highlights a new comparative study across eight mammalian species with lifespans ranging from 3.5 years (mouse) to 46 years (horse).
Using droplet digital PCR (ddPCR), Western blotting, and targeted metabolomics, the study measured:
mTORC1 gene expression
mTORC1 protein levels
concentrations of activators and inhibitors
mTORC1 is also involved in longâŠ
đ¶ 4. Key Findings: Long-Lived Species Naturally Suppress mTORC1
The study found that longer-living mammals consistently exhibit a molecular signature of low mTORC1 activity, including:
A) Activators â (negatively correlated with longevity)
Long-lived species have low levels of:
mTOR
Raptor
Arginine
Methionine
SAM (S-adenosylmethionine)
Homocysteine
mTORC1 is also involved in longâŠ
B) Inhibitors â (positively correlated with longevity)
Long-lived species have higher levels of:
phosphorylated mTOR (mTORSer2448)
PRAS40
mTORC1 is also involved in longâŠ
These patterns were independent of phylogeny, meaning they reflect functional longevity mechanisms, not ancestry.
đ¶ 5. Interpretation: mTORC1 Is Part of an Evolutionary Longevity Strategy
The authors argue that:
Long-lived species have evolved permanent, natural repression of mTORC1 signaling.
This protects cells from accelerated aging, degenerative diseases, and metabolic stress.
mTORC1 works in coordination with other aging effectors as part of the Cell Aging Regulating System (CARS).
mTORC1 is also involved in longâŠ
This places mTORC1 as a cross-species determinant of longevity, not just a within-species modulator.
đ¶ 6. Overall Conclusion
The PDF concludes that maintaining low mTORC1 downstream activity during adult life is a conserved biological strategy that increases longevity both within and between mammalian species. This is the first study to show that natural variation in mTORC1 levels across species correlates directly with evolutionary differences in lifespan.
â Perfect One-Sentence Summary
This editorial explains that long-lived mammalian species naturally suppress mTORC1 activityâthrough lower levels of its activators and higher levels of its inhibitorsârevealing mTORC1 as a fundamental, evolutionarily conserved determinant of species longevity....
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ulhxaowh-0444
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xevyo
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pension HOW TO PRICE
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HOW TO PRICE LONGEVITY SWAP
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The article âHow to Price Longevity Swapsâ explain The article âHow to Price Longevity Swapsâ explains how pension plans and reinsurers evaluate and price longevity swapsâfinancial instruments used to transfer the risk of pensioners living longer than expected. It begins by outlining the growing importance of longevity risk management, especially following large pension buy-out and buy-in transactions in the U.K. and U.S. Longevity swaps serve as an alternative that transfers only longevity risk, not investment or asset risk, from pension plans to insurers or reinsurers.
The article describes how a longevity swap works: the reinsurer agrees to pay the actual pension benefits of a specified group of pensioners, while the pension plan pays fixed premiums based on expected mortality. Pricing requires three major components:
Current mortality analysisâa detailed examination of historical mortality experience, socio-economic differences, and risk factors within the pensioner portfolio.
Mortality trend assumptionsâselecting and projecting future mortality improvement models, while accounting for uncertainty, model risk, cohort effects, and longevity basis risk.
Risk margin for capitalâreflecting the reinsurerâs expenses and the capital required to hold longevity risk over time, often calculated using cost-of-capital methods similar to Solvency II regulations.
The article emphasizes that accurate pricing must consider portfolio heterogeneity, long-term uncertainty in mortality improvements, and the sensitivity of models to data variations. It concludes that while reinsurers possess the necessary expertise to manage longevity risk, their capacity is limited, and transferring this risk to broader capital markets may be the futureâprovided longevity basis risk is better understood and quantified.
If you want, I can also provide:
â
A short 3â4 line summary
â
A simple student-friendly version
â
Quiz / MCQs from this file
Just tell me!...
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signs of life guidance
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signs of life guidance
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âSigns of Life Guidance â Visual Summary (v1.2)â i âSigns of Life Guidance â Visual Summary (v1.2)â is a clear, compassionate, UK-wide clinical guideline that explains how to determine and document signs of life following spontaneous birth before 24+0 weeks, in situations whereâafter careful discussion with the parentsâactive survival-focused neonatal care is not appropriate. The guidance ensures consistent, respectful, and trauma-minimizing care for both babies and parents during extremely preterm births.
Purpose of the Guidance
To help clinicians:
Recognize genuine signs of life
Communicate sensitively with parents
Provide appropriate comfort and palliative care
Ensure correct legal documentation of birth and death
Deliver consistent bereavement support across the UK
Determining Signs of Life
A baby is classified as liveborn if any of the following visible, persistent signs are present:
clearly visible heartbeat
visible cord pulsation
breathing, crying, or sustained gasps
definite limb movement
The guidance emphasizes:
Fleeting reflexes (brief gasps, twitches, or chest wall pulsations in the first minute) do not count as signs of life.
Parentsâ own observations should be respectfully included.
A stethoscope is not required.
After Live Birth
A doctor (usually the obstetrician) should confirm and document signs of life to avoid legal complications with the death certificate.
A doctor may rely on a midwifeâs documented observations.
The baby receives perinatal palliative comfort care, and the familyâs emotional and physical needs are actively supported.
Communication With Parents
Sensitive communication is emphasized to reduce trauma:
Parents are prepared that babies born before 24 weeks often do not survive.
Parents are informed that reflex movements do not necessarily indicate life.
Language preferences must be respectedâsome parents prefer âloss of baby,â others prefer âend of pregnancyâ or âmiscarriage.â
Bereavement Care (All Births)
All families should receive:
A parent-led bereavement plan
Privacy, choices, and time with their baby
Memory-making opportunities
Information on burial/cremation/sensitive disposal
Referral to support services and community care
Guidelines reference the National Bereavement Care Pathway for consistent care across the UK.
Documentation Requirements
Depends on region and whether signs of life were witnessed:
Before 24+0 weeks: No legal requirement for birth registration; offer a sensitive âcertificate of lossâ or âcertificate of birth.â
If liveborn and later dies: A neonatal death certificate must be issued by a doctor who witnessed signs of life.
If no doctor witnessed it, the case must be referred to the coroner in England/Wales/NI.
Scope of the Guidance
Included:
Spontaneous in-hospital births <22+0 weeks
Spontaneous births at 22+0 to 23+6 weeks when survival-focused care is not appropriate
Pre-hospital births <22+0 weeks (same principles)
Excluded:
>Medical terminations
>Uncertain gestational age
>Births at 22â23+6 weeks where active neonatal care is planned or considered...
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4d9eabfe-53cc-49d3-984a-cc7121b41d3e
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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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nnequewi-7486
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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the molecular signatures
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the molecular signatures of longevity
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/home/sid/tuning/finetune/backend/output/nnequewi- /home/sid/tuning/finetune/backend/output/nnequewi-7486/merged_fp16_hf...
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âThe Molecular Signatures of Longevityâ is a compr âThe Molecular Signatures of Longevityâ is a comprehensive scientific review that explores the shared biological patternsâor âsignaturesââthat distinguish long-lived organisms from normal ones, across species ranging from yeast and worms to mice and humans. The paper synthesizes genomic, transcriptomic, proteomic, metabolic, and epigenetic evidence to uncover the molecular hallmarks that consistently support longer lifespan and extended healthspan.
Core Idea
Long-lived species, long-lived mutants, and exceptionally long-lived humans (like centenarians) share a set of convergent molecular features. These signatures reflect a body that ages more slowly because it prioritizes maintenance, protection, and metabolic efficiency over growth and reproduction.
Major Molecular Signatures Identified
1. Downregulated growth-related pathways
Across almost all models of longevity, genes that drive growth and proliferationâsuch as insulin/IGF-1 signaling, mTOR, and growth hormone pathwaysâare consistently reduced.
This metabolic shift favors stress resistance and preservation, not rapid cell division.
2. Enhanced stress-response and repair systems
Long-lived organisms upregulate genes and pathways that improve:
>DNA repair
>Protein folding and quality control
>Antioxidant defenses
>Cellular detoxification
These changes help prevent molecular damage and maintain cellular integrity over decades.
Determinants of Longevity
3. Improved mitochondrial function and energy efficiency
Longevity is associated with:
More efficient mitochondria
Altered electron transport patterns
Reduced reactive oxygen species (ROS) production
Rather than producing maximum energy, long-lived organisms produce steady, clean energy that minimizes internal damage.
Determinants of Longevity
4. Reduced chronic inflammation
A consistent signature of long-lived humansâincluding centenariansâis low baseline inflammation (inflammaging avoidance).
They show lower activation of immune-inflammatory pathways and better regulation of cytokine responses.
5. Epigenetic stability
Long-lived individuals maintain:
Younger DNA methylation patterns
Stable chromatin structure
Preserved transcriptional regulation
These allow their cells to âbehave youngerâ despite chronological age.
Insights from Centenarians
Centenarians display many of the same molecular signatures found in long-lived animal models:
Exceptional lipid metabolism, especially in pathways involving APOE
Robust immune regulation, avoiding chronic inflammation
Gene expression profiles resembling people decades younger
Protective metabolic and repair pathways that remain active throughout life
They often appear biologically resilient, maintaining molecular systems that typically erode with aging.
Determinants of Longevity
Evolutionary Perspective
The article explains that these longevity signatures arise because evolution favors maintenance and efficiency in certain species where survival under stress is essential.
Thus, the same metabolic and stress-response systems that help organisms survive harsh conditions also extend lifespan.
Implications for Human Health and Interventions
The paper highlights that several known anti-aging interventionsâsuch as calorie restriction, rapamycin, fasting, metformin, and certain genetic variantsâwork largely because they activate the same molecular signatures found in naturally long-lived organisms.
These shared signatures point toward potential therapeutic targets, including:
IGF-1 / mTOR inhibition
Enhanced DNA repair
Mitochondrial optimization
Anti-inflammatory modulation
Epigenetic rejuvenation
Conclusion
âThe Molecular Signatures of Longevityâ shows that longevity is not randomâit has a repeatable, identifiable molecular blueprint.
Across species and in exceptionally long-lived humans, the same biological themes appear:
Less growth, more protection. Less inflammation, more repair. Cleaner energy, stronger stress resistance.
These convergent signatures reveal the fundamental biology of long life and offer a roadmap for extending human healthspan through targeted interventions....
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6bae65a2-1788-4e37-a147-a84aa3a0173a
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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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xevyo-base-v1
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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xevyo
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AI assistant with a single unchangeable identity, AI assistant with a single unchangeable identity, representing the vision, values, and purpose of Dr. Anmol Kapoor....
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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Trained incrementally on curated instructionârespo Trained incrementally on curated instructionâresponse pairs with embedded chain-of-thought data, it maintains logical coherence, contextual awareness, and factual accuracy....
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{"train_runtime": 599.3462, "train_sam {"train_runtime": 599.3462, "train_samples_per_second": 2.67, "train_steps_per_second": 0.334, "total_flos": 8579520714768384.0, "train_loss": 0.2602055296301842, "epoch": 14.296296296296296, "step": 200}...
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completed
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448a4ad8-de1e-41f1-81cc-17ad98c5b180
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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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vfqewudj-1695
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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xevyo-new
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New model with Economy Book knowledge
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/home/sid/tuning/finetune/backend/output/vfqewudj- /home/sid/tuning/finetune/backend/output/vfqewudj-1695/merged_fp16_hf...
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A common Sense Guide to the Economy Book By: Thoma A common Sense Guide to the Economy Book By: Thomas Sowell
This is a book about economics guide and bellow are the chapters name:
WHAT IS ECONOMICS?
THE ROLE OF PRICES
PRICES AND MARKETS
Price Controls
An Overview of Prices
INDUSTRY AND COMMERCE
The Rise and Fall of Businesses
The Role of Profitsâand Losses
The Economics of Big Business
Regulation and Anti-Trust Laws
Market and Non-Market Economies
WORK AND PAY
Productivity and Pay
Minimum Wage Laws
Special Problems in Labor Markets
TIME AND RISK
Investment
Stocks, Bonds and Insurance
Special Problems of Time and Risk
THE NATIONAL ECONOMY
National Output
Money and the Banking System
Government Functions
Government Finance
Special Problems in the National Economy
THE INTERNATIONAL ECONOMY
International Trade
International Transfers of Wealth
International Disparities in Wealth
SPECIAL ECONOMIC ISSUES
Myths About Markets
âNon-Economicâ Values
The History of Economics
Parting Thoughts...
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c93ca324-4417-473c-aec0-cef445eaa318
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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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gwzkzrpn-5662
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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âOptimal Aging & Keys
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Optimal Aging & Keys to Longevity
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âOptimal Aging & Keys to Longevityâ is a short âOptimal Aging & Keys to Longevityâ is a short, practical guide written by Dr. Robert S. Tan, a geriatrician and gerontologist, summarizing the essential habits and biological factors that promote longer, healthier lives. Drawing on decades of clinical experience and conversations with centenarians, the document explains that while genetics play a role, lifestyle choicesâespecially diet, exercise, emotional well-being, and avoidance of harmful behaviorsâare the most powerful determinants of longevity.
The guide emphasizes small, moderate food intake, highlighting research showing that calorie restriction can extend lifespan. It warns against excessive salt, sugar, and processed foods, recommending fresh, antioxidant-rich foods such as fish, vegetables, green tea, almonds, olives, and red wine in moderation.
Dr. Tan stresses that exercise is one of the strongest anti-aging tools, capable of restoring declining hormones and maintaining muscle, strength, and bone density as people age.
He also notes that happiness, strong social connections, mental activity, and a purposeful life are all linked to living longer, likely due to beneficial hormonal and neurological effects.
The document identifies smoking as one of the most damaging behaviorsâshortening life, increasing disease risk, and even causing genetic harm passed to future generations. It concludes by acknowledging that genetics set limits on lifespan, but healthy habits from early in life allow individuals to reach their full biological potential....
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c8b722df-e762-4e5e-b58b-d6ce30b794b7
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8684964a-bab1-4235-93a8-5fd5e24a1d0a
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bxzxobhi-1709
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xevyo
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/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf...
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âThe Impact of New Drug
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âThe Impact of New Drug Launches on Longevity
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/home/sid/tuning/finetune/backend/output/bxzxobhi- /home/sid/tuning/finetune/backend/output/bxzxobhi-1709/merged_fp16_hf...
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âThe Impact of New Drug Launches on Longevityâ is âThe Impact of New Drug Launches on Longevityâ is an econometric and public-health analysis that quantifies how the introduction of new pharmaceuticals contributes to increases in life expectancy, reductions in mortality, and economic value creation across countries.
The report uses large datasetsâinternational drug launch records, disease mortality statistics, and demographic trendsâto show that innovative medicines are one of the most powerful drivers of improved longevity worldwide.
Its central conclusion is clear:
Launching new drugs saves lives on a national scale.
Countries that adopt new medicines sooner experience greater increases in life expectancy.
Core Findings
1. New drug launches significantly increase life expectancy
The paper demonstrates that most of the gains in longevity over recent decades are explained by new pharmaceutical therapies introduced after 1980.
Key evidence shows:
Each new drug launch is associated with measurable declines in disease-specific mortality.
Countries with faster uptake of new drugs experience larger increases in life expectancy than those with slower adoption.
Examples include:
New cardiovascular drugs reducing deaths from heart attacks and stroke
Oncology drugs lowering cancer mortality
HIV antiretroviral therapies increasing survival dramatically
2. âPharmaceutical innovationâ predicts mortality decline
The report uses time-series and cross-country regressions to show that:
The number of new drugs launched in a country strongly predicts the reduction of deaths in that country over the following years.
Older drugs have diminishing returns; most life-saving impact comes from new mechanisms, new molecular structures, and new therapeutic classes.
3. Drug innovation explains a large share of recent longevity growth
The analysis shows that new drugs account for:
A substantial percentage of the increase in life expectancy since the 1990s
A major portion of the decline in early-death years (years of life lost)
A large share of improvements in quality-adjusted life years (QALYs)
In some models, up to 70% of mortality reduction in major diseases is attributable to modern pharmaceutical innovation.
4. Countries adopting drugs later benefit less
The paper shows clear international disparities:
Countries that delay market approval for new drugs experience slower declines in mortality.
Regulatory speed and drug reimbursement policies directly influence national health outcomes.
This highlights the critical public-policy importance of faster approval, uptake, and access.
5. New drugs are cost-effective investments
The paper examines economic impacts and concludes that:
Although new drugs increase short-term spending,
They generate far greater long-term economic benefits via reduced hospitalization, reduced disability, and increased lifetime earnings.
Every dollar spent on pharmaceutical innovation yields multiple dollars in societal benefit through:
Improved survival
Higher labor productivity
Lower long-term medical costs
6. The largest longevity gains come from four therapeutic areas
Based on mortality-improvement models, the strongest life-extension effects arise from:
Cardiovascular drugs (statins, blood-pressure therapies, anticoagulants)
Oncology drugs
Infectious-disease therapies (HIV, hepatitis, vaccines)
CNS drugs (stroke recovery, neurodegeneration treatments)
These correspond to the biggest contributors to early mortality in industrialized nations.
Methodological Contributions
The paper uses:
International datasets from multiple decades
Drug launch timelines
Disease-specific mortality models
Country-fixed effects and year-fixed effects
Validation through both disease-level and aggregate analysis
This gives the findings strong statistical credibility and global relevance.
Conclusion
âThe Impact of New Drug Launches on Longevityâ demonstrates that pharmaceutical innovation is one of the most powerful forces increasing global life expectancy. New medicines reduce premature mortality across nearly all major disease categories, providing massive health and economic benefits to societies.
The reportâs message is definitive:
If countries want longer, healthier lives for their populations,
they must prioritize access to new, innovative medicines....
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