Prolonged histamine action after electrical muscle stimulation may shorten remaining life
In old mice, prolonged histamine action after electrical muscle stimulation could shorten remaining life through low blood pressure and reduced organ blood flow despite strength gains. No histamine-dependent pressure drop, or no protection when it is prevented, would reject this chain.
Omega Point 1.4
Stage of verification
- Hypothesis published2026-10-05
- Indirect evidenceAssessed at 4 of 10
- Direct testAwaited
Map of the hypothesis
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Target map
Every target of every published hypothesis, each with the actions a hypothesis can propose on it. The targets and the actions of this hypothesis are drawn solid.

Signalling molecule
Histamine
A signalling molecule that acts through histamine receptors
Where this hypothesis actsAfter electrical muscle stimulation in old mice, with prolonged local production and systemic effects
Hypotheses on this target 1
Lower level
Synthesis suppression
Neutralisation
Supplementation
Accelerated excretion
What is proposed
Limit pathologically prolonged histamine activity after muscle contraction
With whatSmall molecule
HowUse H1/H2 antagonists during a window selected from the measured response, preserving contractions and the early recovery response
Possible result
Possible longer remaining lifespan and higher SPV_2 through prevention of repeated organ hypoperfusion
From the recordПредлагаемый вариант миметика сохраняет сокращения и ранний восстановительный ответ, но ограничивает патологически затянувшееся действие гистамина.
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Every target read from the published hypotheses, each kind around its pictogram. A larger mark means more hypotheses act on that target. Point at a mark and the actions proposed on it branch out of it.
Solid and named: the targets of this hypothesis
Explore in depth
The logic
The train of thought that ends in this hypothesis. Each stage is the reason the next exists. The master question narrows to a goal, the goal to an unknown nobody has closed, the unknown to the hypothesis proposed here. Every step below says what it rests on and what carries it.
Making muscles stronger might not make an old animal live longer. The unexpected move is to reproduce muscle contractions while deliberately limiting a later part of the recovery response, rather than reproducing the entire response to exercise. This is a proposal generated by the pipeline, not a measured finding: it suggests that prolonged histamine action could lower blood pressure enough to repeatedly deprive organs of adequate blood flow.
- Repeated electrical pulses activate the same muscle regions and are proposed to sustain local histamine production.
- The proposed histamine response shifts from an early recovery signal to excessively prolonged action that affects the wider circulation.
- That prolonged action is proposed to produce a delayed fall in blood pressure.
- Repeated pressure falls are proposed to leave organs with inadequate blood flow and cause injury.
- Repeated organ injury is proposed to shorten remaining life even while the stimulated muscles become stronger.
- Limiting only late histamine action is predicted to prevent these episodes and improve survival while retaining contractions and early recovery.
A tap opened briefly can supply needed water; left open too long, it can lower pressure elsewhere in a shared water system. The proposal is to close it after the useful interval.
Where the picture breaks: Histamine is not a tap, and blood circulation actively adjusts pressure and flow. The picture does not establish that a signal produced in muscle becomes strong or persistent enough to reduce blood delivery to distant organs, or that its early and late effects can be separated.
- Master questionstep 01 of 04
Reproducing selected natural bodily processes might yield new ways to extend life, using substances, combinations or other interventions.
Rests on: The goal treats natural bodily processes as possible starting points for interventions that extend life.
AssumptionIt assumes that at least some benefits of natural bodily processes can be reproduced by an intervention and can translate into longer life; the question itself does not establish either outcome.
- Goal pillarstep 02 of 04
The intended output is a defined set of new interventions that imitate natural bodily processes to extend life.
Rests on: The master question explicitly requests new hypotheses about which processes to reproduce and how their useful effects might extend life.
Stated in the chain - Gap questionstep 03 of 04
Electrical pulses that make muscles contract might increase strength while shortening remaining life if repeatedly activating the same muscle fibres shifts damage to tendons, the tissues connecting muscles to bones, and drains other tissues’ reserves.
Rests on: The preceding goal calls for interventions that imitate useful bodily processes, but does not identify repeated electrical muscle activation as a source of tendon damage or depleted reserves elsewhere.
LeapNeither the preceding stages nor the supplied sources establish the proposed transfer of damage to tendons or depletion of other tissues’ reserves. These are the specific missing connections, rather than evidence that gaining strength and losing lifespan cannot coexist.
- Hypothesisstep 04 of 04
Repeated electrical muscle activation is proposed to sustain histamine production, eventually lower blood pressure and repeatedly reduce blood delivery to organs in old mice, even while strength increases. Selectively limiting the late histamine response is predicted to improve survival while preserving contractions and early recovery.S4S5
Rests on: The preceding question supplies the possibility that strength gains and survival diverge; the endpoint proposes a different route from tendon damage. Experimental Physiology in 2011 found that blocking histamine’s action reduced blood-vessel widening after exercise in recreationally active humans, but did not establish delayed blood-pressure falls or lifespan effects in electrically stimulated old mice. A 1978 report in the Journal of Applied Physiology: Respiratory, Environmental and Exercise Physiology associated drug-induced histamine release in dogs’ lungs with reduced arterial pressure, but did not study muscle stimulation, prolonged recovery or survival.
Supported by literature
What is carried, and what is not. The supplied sources speak to two components of the proposed mechanism: histamine-related effects on blood flow after exercise and an association between histamine release and lower blood pressure; the human recovery study and dog lung study described above establish neither component in electrically stimulated old mice. Nothing supplied establishes the sequence from repeated stimulation through prolonged histamine action and organ injury to shortened life, or the predicted survival benefit of selectively limiting its late action.
Where the reasoning is carried by something unstated · 2
- Master question. It assumes that at least some benefits of natural bodily processes can be reproduced by an intervention and can translate into longer life; the question itself does not establish either outcome.
- Gap question. Neither the preceding stages nor the supplied sources establish the proposed transfer of damage to tendons or depletion of other tissues’ reserves. These are the specific missing connections, rather than evidence that gaining strength and losing lifespan cannot coexist. Establish the missing link before relying on this step.
How a result here could mislead · 3
- Longer survival after a histamine-blocking drug could be credited to preventing late blood-pressure falls even if the benefit came from another drug effect. Conversely, reduced blood flow in the recovering muscle could be mistaken for evidence about inadequate blood delivery to other organs. What closes it: The proposed groups receiving drugs without stimulation are necessary. Pressure, blood delivery to organs, organ injury and survival must be followed together, and the proposed independent prevention of the pressure fall must reproduce the protection before that route can explain the survival effect.
- A failed intervention could be read as disproving the hypothesis when it missed the late histamine response; an apparent success could come from suppressing early recovery or changing the amount of muscle work. What closes it: The intervention window must follow measurements in old mice and be fixed before the survival comparison. The study must verify suppression of late histamine action, preservation of early recovery and comparable muscle work, alongside strength measurements. Physiological Reports in 2013 found that histamine-receptor blockade, meaning prevention of histamine activating its cellular receiving sites, reduced the body’s responsiveness to insulin, a hormone controlling blood sugar, after exercise in healthy humans; this does not establish what selective late blockade would do in old mice.
- A late pressure fall could be treated as excluding the rival explanations even if earlier pressure surges, potassium changes affecting heart rhythm, or renewed virus multiplication also contributed to death. What closes it: Measurements must cover stimulation and recovery, including pressure, heart rhythm and potassium, a mineral whose movement helps control electrical activity in muscle and heart cells. Where the infection rival is applicable, virus multiplication also needs assessment. The proposed corrections of these rival routes require verification that each correction worked; their failure to remove the late response alone would not exclude their contribution to survival.
What would make this wrong. The proposed causal sequence would be broken if electrical stimulation did not produce the predicted late histamine-dependent blood-pressure fall, or if verified elimination of that fall did not protect remaining lifespan during adequate long-term observation. A failure to improve survival would be interpretable only if the intervention demonstrably removed the targeted late response without introducing an offsetting harm. These observations would reject this proposed route, not the broader possibility of developing interventions that imitate natural processes to extend life.
What it would change. If the proposed sequence held, designing an exercise substitute for longer life would require separating useful contraction and early recovery from a late response that harms survival; strength gains alone would not establish benefit. It would support investigating selective timing of an intervention rather than assuming that a more complete reproduction of exercise is always preferable. Even a positive result would leave human lifespan effects and benefits outside the tested old mice and stimulation conditions unestablished. The supplied material also does not define SPV_2, the named outcome measure, so its relationship to remaining lifespan cannot be specified.
Sources read · 5
Distribution oand pharmacological release of histamine in canine lung in vivo. · Journal of applied physiology: respiratory, environmental and exercise physiology · 1978
“This was associated with increased plasma histamine (31.8 +/- 18.4 ng/ml), increased airflow resistance (Rrs: + 452 +/- 257%), decreased lung compliance (-28 +/- 10%), and decreased arterial blood pressure (-41 +/- 6.5%) at 2 min.”
Does not settle: Источник не исследует электрическую стимуляцию или сокращение мышц, старых мышей, длительный гистаминовый ответ, позднюю повторную гипоперфузию органов, рост силы, оставшуюся продолжительность жизни, SPV_2 или избирательное ограничение действия гистамина.
Histamine-receptor blockade reduces blood flow but not muscle glucose uptake during postexercise recovery in humans. · Experimental physiology · 2011
“In conclusion, while oral ingestion of H(1)- and H(2)-receptor antagonists alters postexercise recovery by attenuating vasodilatation, leg glucose uptake is not universally affected in recreationally active individuals.”
Does not settle: Остаются открытыми последствия электрической стимуляции у старых мышей, длительность местного гистаминового ответа, системная гипотензия, повторная гипоперфузия органов, рост силы, продолжительность жизни и показатель SPV_2.
Effect of H1- and H2-histamine receptor blockade on postexercise insulin sensitivity. · Physiological reports · 2013
“In conclusion, H 1 - and H 2 -receptor blockade reduced postexercise whole-body insulin sensitivity by 25%, as estimated by the Matsuda insulin sensitivity index. These findings suggest a histaminergic effect on postexercise glucose regulation in healthy humans.”
Does not settle: Открытыми остаются эффекты у старых мышей, электрической стимуляции мышц, длительность гистаминового ответа, поздняя гипотензия, повторная гипоперфузия органов, рост силы, продолжительность оставшейся жизни и влияние избирательного ограничения позднего действия гистамина на SPV_2.
A single dose of histamine-receptor antagonists before downhill running alters markers of muscle damage and delayed-onset muscle soreness. · Journal of applied physiology (Bethesda, Md. : 1985) · 2017
“In conclusion, histamine-receptor blockade reduced postexercise blood flow, had no effect on the pattern of inflammatory markers, increased serum creatine kinase concentrations, attenuated muscle strength loss, and reduced pain perception following muscle-damaging exercise.”
Does not settle: Источник описывает острый опыт с бегом под уклон у людей и наблюдение в течение 72 часов. Он не устанавливает, что электрическая стимуляция вызывает патологически длительный гистаминовый ответ, системную гипотонию, повторную гипоперфузию органов или сокращение оставшейся жизни старых мышей. Также он не оценивает SPV_2 и не показывает, что ограничение позднего действия гистамина сохраняет раннее восстановление и тренировочную адаптацию.
Efficacy of Neuro-muscular Electrical Stimulation for Orthostatic Hypotension Associated with Long-term Disuse and Diabetic Autonomic Neuropathy: A Case Report. · Physical therapy research · 2024
“Conclusion: The combination of exercise therapy and NMES for OH caused by DAN can alleviate hypotension.”
Does not settle: This single case in a 75-year-old man does not establish effects in old mice, prolonged histamine signaling, delayed systemic hypotension after contraction, organ hypoperfusion, remaining lifespan, SPV_2, or whether selectively limiting histamine preserves strength and improves survival.
The gap this hypothesis explains
Two live hypotheses pull in opposite directions here, and the field has not chosen between them.
Does repeated electrical muscle stimulation shorten remaining life even when it keeps muscles stronger?
Original wording · exactly as the pipeline generated it
Сокращает ли электрический миметик мышечной нагрузки оставшуюся жизнь при устойчивом приросте силы, если повторное включение одних волокон переносит повреждение на сухожилия и истощает резервы других тканей?
What this question is asking
The question concerns whether making muscles contract with electricity can preserve strength while harming the rest of the body enough to shorten life. It asks whether repeated treatment produces lasting strength gains but leaves less remaining life than a comparison without the added stimulation. It assumes that repeatedly activating the same muscle fibers, the cells that contract, can damage tendons and use up other tissues’ capacity to maintain and repair themselves. The stated standard for benefit is stronger muscles together with less accumulated damage across the body and longer remaining life; strength alone would not meet that standard.
- Electrical muscle stimulation
- Use of electrical signals to make muscles contract, called neuromuscular electrical stimulation in the supplied sources. The question treats it as a possible substitute for aspects of muscular activity; the sources describe several treatment settings rather than one uniform regimen.
- Mimetic
- An intervention intended to reproduce part of another process. Here it means electrical stimulation intended to reproduce useful effects of muscle activity; reproducing strength benefits would not establish that it reproduces every effect of exercise.
- Muscle fiber
- A muscle cell that contracts to produce force. The question assumes that stimulation repeatedly activates the same fibers, but the supplied material does not establish that pattern.
- Voluntary contraction and recruitment
- A voluntary contraction is muscle tightening initiated through intentional movement. Recruitment means activating muscle fibers to contribute to a contraction; repeated recruitment of the same fibers is part of the proposed harm mechanism.
- Tendon and tendon loading
- A tendon connects muscle to bone and carries force from a contraction. Loading describes the mechanical demand placed on it, which is not equivalent to injury.
- Force, strain and stress
- Force is the pull applied to a tendon; strain describes how much its length changes relative to its starting length; stress describes force relative to the area carrying it. S8 reports increases in these measures during stimulation, without establishing subsequent damage.
- Tissue reserves
- The question’s shorthand for the capacity of tissues to maintain function and repair damage. The supplied material provides no defined measurement of these reserves or evidence that stimulation exhausts them.
- Residual or accumulated damage
- Damage that remains after the effects of activity and recovery. The pipeline requires a reduction across the body, but supplies no common measurement showing how damage in different tissues would be combined.
- Remaining lifespan
- The time from a specified starting point until death. A remaining-lifespan ratio above one would mean longer remaining life in the treated group than in its comparison group, but no such result is supplied.
- Knee ligament reconstruction and knee replacement
- Ligament reconstruction repairs or replaces a stabilizing band inside the knee; knee replacement substitutes artificial components for damaged joint surfaces. These are the surgical recovery settings for S1 and S3, respectively.
- Quadriceps
- The muscle group at the front of the thigh that straightens the knee. Its strength is a local outcome in the surgical recovery studies, distinct from whole-body damage or lifespan.
- Perfusion and microscopic tissue examination
- Perfusion means passing fluid through tissue; S9 concerns donor limbs maintained outside the body for 24 hours. Microscopic examination checks tissue for visible cellular changes and, in that source, found no muscle-cell injury.
- RL-3 and S-nodes
- Labels used in the supplied pipeline description for a stimulation level and related claims. Their definitions and relationship to the screened studies are not supplied, so they cannot establish a particular protocol or mechanism.
Electrical stimulation preserves strength, while repeated activation of the same muscle fibers transfers damage to tendons and exhausts reserves in other tissues.
Muscle fibers are contracting cells, tendons connect muscles to bones, and other tissues’ reserves here mean their capacity to keep functioning and repair damage. The assumption is that repeatedly stimulating the same cells can strengthen muscles while injuring those connections and consuming maintenance capacity elsewhere. If established, this would explain how a successful muscle treatment could nevertheless shorten life.
S1, S2 and S3 support strength benefits in their respective treatment settings. S8 supports increased tendon loading during a stimulation session, which is narrower than tendon damage. None of the supplied excerpts establishes repeated activation of the same fibers, transfer of damage, exhaustion of other tissues’ reserves, or shortened remaining life. The input’s RL-3 and S-node labels are not defined or connected to an identified treatment protocol in the supplied source material.S1S2S3S8
The same question asked without the part nothing read establishes:
- Does repeated electrical muscle stimulation shorten remaining life when it produces lasting strength gains, compared with treatment without added stimulation?
- When repeated electrical muscle stimulation improves strength, does it also change tendon damage or other tissues’ capacity to maintain and repair themselves?
- How does repeated electrical muscle stimulation affect muscle strength, accumulated bodily damage and remaining life?
- Strength improves, but remaining life shortens This outcome would establish that the local strength benefit can coexist with a worse lifespan outcome. If the proposed tendon damage and loss of repair capacity were also established, they could connect the contractions to that harm; shorter life alone would not identify its cause.
- Strength improves, but remaining life is unchanged The treatment would provide a muscle benefit without extending remaining life. This would fail the stated requirement for life extension, but would not by itself show whether damage elsewhere was absent or offset by other benefits.
- Strength improves and remaining life lengthens This outcome would support a lifespan benefit alongside the strength benefit. The separate requirement for less accumulated bodily damage would still need evidence, because longer life would not by itself establish the proposed damage mechanism.
Electrical stimulation causes muscle contractions, and those contractions place loads on the tendons that connect muscles to bones. The supplied sources report strength benefits in some settings and increased tendon loading during stimulation, but increased loading does not itself establish injury. Under the question’s proposed mechanism, repeated contractions would cause damage or consume repair capacity elsewhere, and those consequences would outweigh the local strength benefit. If that mechanism shortened life, treating stronger muscles as evidence of longer life would give the wrong conclusion. Conversely, treating increased tendon loading as proof of damage and shorter life would also go beyond the evidence supplied.
Электростимуляция уровня RL-3 сохраняет силу; связанные S-узлы допускают перегрузку сухожилий и перенос ресурсных затрат между органами.
Прирост функции после повторных циклов сопровождается снижением совокупного остаточного повреждения и отношением оставшейся продолжительности жизни выше единицы.
Предположение о продлении жизни может оказаться ложным даже при устойчивом достижении главного локального эффекта миметика.
The mechanism it proposes
The engine's own statement of the hypothesis, in full.
Электрический миметик нагрузки может сокращать оставшуюся жизнь старых мышей через чрезмерно длительный гистаминовый ответ после сокращения. Повторное возбуждение одних мышечных участков поддерживает местное образование гистамина; при достаточном системном действии это вызывает позднее падение артериального давления и повторную гипоперфузию органов. Сила при этом продолжает расти. Радикальная часть гипотезы состоит в том, что физиологическую программу, необходимую для полноценной тренировочной адаптации, приходится избирательно ограничивать ради продления жизни: полнота воспроизведения нагрузки и польза для выживания могут причинно расходиться. Предлагаемый вариант миметика сохраняет сокращения и ранний восстановительный ответ, но ограничивает патологически затянувшееся действие гистамина. Он должен повышать SPV_2 за счёт предотвращения повторных эпизодов гипоперфузии.
Testing and possible results
The prediction that would tell it apart
A hypothesis that predicts what its rivals predict is not worth running an experiment over. This is the observation on which this one differs.
После короткой стимуляции обнаруживается отсроченное повышение образования гистамина, за которым следуют падение давления и признаки повреждения органов. Ограничение позднего действия рецепторов H1/H2 улучшает оставшуюся продолжительность жизни при сохранённом приросте силы, даже если часть сосудистой и метаболической адаптации мышцы ослабевает. Независимое предотвращение падения давления воспроизводит защиту. Исправление сенсорного кода, нормализация калиевых колебаний и подавление вирусной репликации не устраняют этот поздний ответ. Отсутствие гистаминзависимой гипотензии либо отсутствие защиты при её устранении опровергает предложенную причинную цепочку.
Would tell it apart from at least one rival. The text predicts observable intervention effects and specifies an explicit rejection condition. No rival prediction is supplied. Only a bench experiment would settle it.
What testing it would take
The engine's own read on whether this is testable with methods that already exist.
Доступны телеметрия давления, определение гистамина и активности гистидиндекарбоксилазы, функциональные исследования мышцы и фармакологические пробы с антагонистами H1/H2. Необходимы отдельные группы с препаратами без стимуляции и независимое подтверждение источника гистамина. Временное окно вмешательства выбирают по измеренному ответу старых мышей. Длительное наблюдение необходимо для вывода о жизни.
Other explanations
Every other hypothesis the engine wrote for the same gap, and the observation that would separate the two.
После короткой стимуляции обнаруживается отсроченное повышение образования гистамина, за которым следуют падение давления и признаки повреждения органов. Ограничение позднего действия рецепторов H1/H2 улучшает оставшуюся продолжительность жизни при сохранённом приросте силы, даже если часть сосудистой и метаболической адаптации мышцы ослабевает. Независимое предотвращение падения давления воспроизводит защиту. Исправление сенсорного кода, нормализация калиевых колебаний и подавление вирусной репликации не устраняют этот поздний ответ. Отсутствие гистаминзависимой гипотензии либо отсутствие защиты при её устранении опровергает предложенную причинную цепочку.
- What would separate them
Shared errors in muscle sensory feedback may drive pressure surges and shorten life predicts: При одинаковых внутримышечных pH, механической работе и калиевой траектории обычная электростимуляция создаёт большую компоненту согласованных сенсорных ошибок и более сильное повышение давления, чем стимуляция с восстановленной сенсорной информативностью. Избирательное изменение сенсорного рисунка при сохранении моторного ответа уменьшает прессорные эпизоды, последующее повреждение сердца и потерю продолжительности жизни. Устранение поздней гистаминовой гипотензии либо подавление вирусной репликации этого эффекта не воспроизводит. Если информативность восстановлена, а избыточный прессорный ответ сохраняется, предложенная связь опровергнута.
- Rival 02 of 03What would separate them
Muscle stimulation may shorten life through potassium-driven heart rhythm disturbances predicts: Избыточные аритмии привязаны к измеренным калиевым пикам или последующим минимумам и возникают до накопления хронического повреждения. Воспроизведение реально зарегистрированной калиевой траектории в изолированном старом сердце вызывает сходные нарушения при постоянных гистамине и вегетативных влияниях. Нормализация калиевой траектории во время миметика устраняет аритмии при сохранении сокращений и сенсорного возбуждения. Если соответствующих системных колебаний нет либо измеренная траектория не нарушает сердечную электрическую активность, эта гипотеза уступает остальным.
- Rival 03 of 03What would separate them
Electrical muscle stimulation may shorten life by reactivating latent herpes in neurons predicts: Избыточное повреждение после повторной стимуляции возникает преимущественно при подтверждённой латентной инфекции и сопровождается вирусной литической транскрипцией и репликацией в соответствующей нейронной территории. Подавление репликации устраняет это повреждение и дефицит выживания, сохраняя мышечную силу, калиевую траекторию и гемодинамические ответы. У животных без соответствующей латентной инфекции такого механизма быть не должно. Отсутствие длительной гипервозбудимости, реактивации или зависимости повреждения от репликации опровергает цепочку.
Why this is not the mainstream account
The engine is asked to say what its hypothesis would overturn and what would surprise a specialist. This is its answer.
У мышей короткая электрическая стимуляция мышцы вызывала отсроченную индукцию гистидиндекарбоксилазы, достигавшую максимума спустя часы; эффект наблюдался также при недостатке тучных клеток. Это показывает возможность длительного химического ответа после краткого сокращения. [Первичное исследование индукции гистидиндекарбоксилазы](https://pubmed.ncbi.nlm.nih.gov/9575306/). У людей блокада H1/H2 ослабляла тренировочную адаптацию. [Исследование роли гистаминовых рецепторов в адаптации](https://pubmed.ncbi.nlm.nih.gov/33853781/). Ни одна из этих работ не устанавливает предложенный эффект на продолжительность жизни.
Интегративная физиология тренировочной адаптации, учебный раздел «Посленагрузочная гиперемия и долговременная адаптация к физической нагрузке». Пересмотра потребует перенос модели, в которой сохранение обязательных звеньев тренировочной адаптации означает повышение общей пользы, на электрические миметики для позднего возраста.
Миметик с ослабленным физиологическим гистаминовым ответом обеспечивает более долгую жизнь, хотя воспроизводит меньше известных тренировочных адаптаций и даёт такой же прирост силы.
Первичное исследование у людей рассматривает рецепторы H1/H2 как необходимые участники интегративного тренировочного ответа. В выполненном целевом поиске не найдено работы, утверждающей, что избирательное ослабление этого ответа продлевает жизнь при электрическом миметике с сохранением прироста силы. Это ограниченная проверка новизны; отсутствие такого утверждения во всех обзорах доказать нельзя. Поэтому статус HERETICAL остаётся предварительным.
What stands behind it
Which of the figures above have a study behind them, which are the engine's own, and what it would take to refute the hypothesis. This audit never judges the idea.
This hypothesis states no figure and cites no study, so there is nothing here to trace.
What it would take to refute it. Nothing already retrieved carries the prediction’s terms and it names no measurement this layer can route to a public dataset, so the bench is the residual — not a finding against it.
0 citation handles extracted; 1 Europe PMC search run; 0 records examined; 0 sources stored for enrichment, 0 with full text. A citation that did not resolve is a bibliographic failure, not proof that no such paper exists, and no hypothesis is blocked by this audit.