Fluctuating sweat and friction may create leaky lipid defects in the maturing skin barrier
In recovering epidermal models and isolated stratum corneum, fluctuating moisture and friction may trigger lipid defects. The hypothesis would lose support if extra vulnerability occurs only in dividing tissue and preventing division errors removes it without changing lipid organization.
Stage of verification
- Hypothesis published2026-09-26
- Indirect evidenceAssessed at 4 of 10
- Direct testAwaited
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Where in the body
Biological function
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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.
Lipid
Stratum corneum lipids
Extracellular lipids between the cells of the skin's outermost layer that contribute to its permeability barrier
Where this hypothesis actsDuring skin barrier recovery, when sweating and friction coincide with an immature stratum corneum
Hypotheses on this target 1
Lower level
Neutralisation
Supplementation
Composition restoration
What is proposed
Stabilize lipid organization against transitions into more permeable states
With whatChange of environment or regimen
HowShift hydration and friction loads to a more mature barrier phase while keeping total hydration, friction work and temperature unchanged
Possible result
Possible reduction in permeability defects and sensitivity to load variability
From the recordПеренос нагрузки на более зрелую фазу повышает устойчивость к таким переходам и стабилизирует SPV_1.
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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
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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.
Recovering skin may respond differently to the same total sweat and friction depending on when they arrive and how unevenly they are delivered. The unexpected move is to propose that brief local fluctuations can switch the skin’s protective fats into a leakier arrangement that persists after the triggering fluctuation. This is a hypothesis generated by the pipeline, not a measured result; its distinctive prediction is that the effect should occur even in an isolated outer skin layer without ongoing cell division.
- Skin maturation is proposed to bring the fats between outer skin cells close to a switch from a sealing arrangement to a leakier one.
- Stronger coordination of maturation is proposed to concentrate that vulnerable state into a shorter, more pronounced interval.
- Local fluctuations in moisture and sideways frictional force are proposed to trigger the switch during that interval.
- Greater fluctuations are predicted to produce disproportionately more leaky defects despite equal total wetting and frictional work.
- The altered fat arrangement is proposed to retain the vulnerability until the defects disappear.
- Moving the same exposure to a more mature phase is predicted to make the switch less likely.
A loosely latched gate can stay shut under a steady push yet spring open under a series of jolts, even when the total effort is the same. Once open, it can remain open after a jolt ends.
Where the picture breaks: The skin’s fats have no literal latch or hinge. The picture does not establish that ordinary sweat and friction can trigger the proposed rearrangement, or that any resulting defect remains after exposure.
- Master questionstep 01 of 04
The intended therapy would bring the functional condition of middle-aged human skin closer to that of young people.
Rests on: The goal takes youthful skin function as the desired treatment outcome.
AssumptionThe goal assumes that youthful function is a usable treatment target, but the supplied material does not define which functions, measurements or degree of improvement would count as reaching it.
- Goal pillarstep 02 of 04
Completion of skin repair should be coordinated with the next exposure to strain.
Rests on: The broader aim of improving skin function is narrowed to the relationship between repair and repeated strain.
AssumptionThe chain takes this timing relationship as a relevant route to better skin function. The master question does not establish that it accounts for differences between middle-aged and young skin.
- Gap questionstep 03 of 04
More tightly coordinated daily healing could increase damage under shift schedules if sweating coincides with an incompletely restored protective layer. Moving the exposure to another time is proposed as a way to remove that effect while keeping its total amount and heat loss unchanged.
Rests on: The preceding stage makes the timing of repeated strain relative to completed repair the issue. This question specifies a possible collision between daily repair timing and sweating.
Stated in the chain - Hypothesisstep 04 of 04
During maturation of the stratum corneum, the outermost protective skin layer, intercellular lipids, the fats between its cells, are proposed to sit close to a switch into a leakier arrangement. More synchronized maturation would concentrate this vulnerable interval, allowing local fluctuations in moisture and sideways force from friction to create persistent leaky defects even when total exposure stays the same. Moving exposure to a more mature phase is predicted to reduce this vulnerability; the stated outcome identifier, SPV_1, is not defined in the supplied material.S9
Rests on: The preceding question supplies the proposed vulnerable interval and the comparison between exposure times. A review in Progress in lipid research (2023), S9, describes changes in lipid arrangement during maturation and effects of hydration in model systems; it supplies a physical basis for the proposal, but does not establish sweat-triggered or friction-triggered defects, their persistence, or protection from changing exposure time. The hypothesis also explicitly borrows a mathematical model of random disturbances driving a system out of a temporarily stable state; applying that model to recovering skin remains a proposed approximation.
Supported by literature
What is carried, and what is not. Individual ingredients have support: a review in Critical reviews in therapeutic drug carrier systems (1991), S3, places the water-loss barrier in the fats between outer skin cells, but does not establish the proposed temporary defects; a human study in Skin research and technology (2021), S5, found increased water loss after forearm friction, but did not test maturation timing or fluctuating exposure. Together with S9’s limited support for changes in fat arrangement during maturation, these findings support background ingredients, while none of the supplied screened sources establishes the proposed sequence from synchronized repair through fluctuating exposure to persistent defects and protection from rescheduling.S3S5S9
Where the reasoning is carried by something unstated · 2
- Master question. The goal assumes that youthful function is a usable treatment target, but the supplied material does not define which functions, measurements or degree of improvement would count as reaching it.
- Goal pillar. The chain takes this timing relationship as a relevant route to better skin function. The master question does not establish that it accounts for differences between middle-aged and young skin.
How a result here could mislead · 3
- More uneven wetting can change measured water flow without proving that a persistent defect has formed. A flow increase could be credited to a changed protective structure when the immediate conditions driving water movement have changed. What closes it: The proposed continuous permeability measurement, meaning measurement of how readily water crosses the layer, needs a corresponding measure of fat arrangement and comparisons under matched conditions for water movement. Persistence must be assessed after the triggering fluctuation has ended; water flow alone cannot identify a lasting structural defect.
- An effect in an isolated outer skin layer could be attributed to the proposed maturation-dependent mechanism even if isolation itself damaged the layer. Conversely, absence of an effect could be read as a refutation even if preparation removed the vulnerable state. What closes it: The isolated preparations need independently established maturation stages and starting integrity, with preparation conditions matched across comparisons. A negative result separates the explanations only if the proposed susceptible state was retained and the imposed local moisture and frictional forces were verified.
- Changing the variability of exposure could also change its total amount, temperature or heat loss, making an apparent timing effect attributable to a different physical exposure. Equal temperature alone does not establish the equal heat loss required by the gap question. What closes it: The comparison must verify total wetting, total frictional work and local exposure patterns, while measuring temperature and heat loss separately. The maturation categories and rule for identifying an abrupt permeability increase must be fixed before results are examined.
What would make this wrong. The proposed distinguishing chain would be contradicted if, with maturation state, starting integrity and local exposure verified, increased exposure variability produced no preferential increase in abrupt permeability changes in immature isolated outer skin layers, while extra vulnerability occurred only in living tissue with dividing cells and disappeared when errors in cell division were prevented without changing fat organization. The supplied hypothesis explicitly identifies that pattern as favoring the rival explanation, in which damage incurred during cell division carries the lasting vulnerability.
What it would change. If the hypothesis held, matching skin repair to daily activity would require attention to brief local fluctuations as well as the total amount of sweat and friction. Stronger coordination of repair could then be harmful when it concentrates vulnerability into a period of repeated exposure, so a therapy pursuing that coordination would also need to account for exposure timing. Even a successful test in laboratory skin models and isolated outer layers would not establish that this mechanism explains middle-aged skin function, occurs under ordinary shift-work conditions, or can restore the broader functions of young human skin.
Sources read · 10
Topical treatments with acylceramide dispersions restored stratum corneum lipid lamellar structures in a reconstructed human epidermis model. · Chemistry and physics of lipids · 2018
“LPP patterns of intercellular lipid matrixes in the SC were disrupted' by surfactant treatments and were recovered by topical acylceramide treatments.”
Does not settle: Источник не устанавливает влияние потоотделения, трения, колебаний увлажнения или сдвигового напряжения на липидные дефекты. Он также не изучает созревание рогового слоя, нелинейную зависимость повреждения от нагрузки, устойчивость более зрелой фазы или SPV_1.
Cutaneous barrier function after cold exposure in hairless mice: a model to demonstrate how cold interferes with barrier homeostasis among workers in the fish-processing industry. · The British journal of dermatology · 1995
“Moreover, histochemical studies showed a delayed reappearance of stratum corneum intercellular lipids following cold exposure.”
Does not settle: Источник не изучает потоотделение, трение, сдвиговое напряжение, колебания нагрузки, нелинейность повреждения или SPV_1. Опыты проведены на безволосых мышах после нарушения барьера ацетоном и воздействия холодом, поэтому они не устанавливают описанный переход липидов при созревании рогового слоя.
The regulation of epidermal lipid synthesis by permeability barrier requirements. · Critical reviews in therapeutic drug carrier systems · 1991
“The barrier to fluid loss resides in the intercellular lipids (primarily sterols, fatty acids, and sphingolipids) of the stratum corneum.”
Does not settle: Источник не проверяет созревание рогового слоя, потоотделение, трение или сдвиговое напряжение. Он не устанавливает временные проницаемые липидные дефекты, нелинейную зависимость повреждения от колебаний нагрузки, сохранение состояния в организации липидов или роль SPV_1.
Poroelastic behavior and water permeability of human skin at the nanoscale. · PNAS nexus · 2023
“Due to its water sensitive nature, a plasticization effect is easily observed for the SC, with the disruption of the intercellular lipid ordering being the target for many dermatological and cosmetic treatments ( ).”
Does not settle: Источник не устанавливает, что потоотделение или сдвиговое трение вызывают проницаемые липидные дефекты во время созревания рогового слоя, не оценивает нелинейность эффекта, сохранение дефектов или SPV_1.
Effect of scratching and friction on human skin in vivo. · Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2021
“Compared to BL, transepidermal water loss (TEWL) value increased significantly at both scratched and friction sites (P<.001) with a significant higher value for friction (P<.001).”
Does not settle: Источник показывает повышение потери воды через кожу после моделируемого трения на предплечье здоровых добровольцев. Он не устанавливает роль потоотделения, колебаний увлажнения или сдвигового напряжения, временное состояние липидов при созревании рогового слоя, нелинейность эффекта нагрузки, сохранение дефектов или влияние переноса нагрузки на SPV_1.
Biophysical and ultrasonographic changes in pityriasis rosea compared with uninvolved skin. · International journal of women's dermatology · 2021
“Stratum corneum hydration ( p < .001), R0 ( p = .003), R2 ( p = .001), R5 ( p = .003), and echodensity of the dermis ( p = .006) were significantly lower, whereas transepidermal water loss ( p = .001), pH ( p < .001), and erythema ( p < .001) were significantly higher in PR lesions.”
Does not settle: Источник сравнивает очаги розового лишая с внешне непоражённой кожей у 21 взрослого пациента. Он не исследует созревание рогового слоя в нормальной коже, потоотделение, сдвиговое напряжение, колебания увлажнения или нагрузки, липидные дефекты, нелинейную зависимость повреждения от нагрузки, их сохранение либо SPV_1.
Comparison of biophysical, biomechanical and ultrasonographic properties of skin in chronic dermatitis, psoriasis and lichen planus. · Medical journal of the Islamic Republic of Iran · 2018
“Elevated TEWL values are observed in a number of diseases with skin barrier abnormalities such as atopic dermatitis and psoriasis ( , ).”
Does not settle: Источник не устанавливает влияние колебаний потоотделения, трения или сдвигового напряжения на межклеточные липиды при созревании рогового слоя, образование проницаемых дефектов, нелинейную зависимость от нагрузки, их сохранение или устойчивость SPV_1.
Glycerol and the skin: holistic approach to its origin and functions. · The British journal of dermatology · 2008
“The diverse actions of the polyol glycerol on the epidermis include improvement of stratum corneum hydration, skin barrier function and skin mechanical properties, inhibition of the stratum corneum lipid phase transition, protection against irritating stimuli, enhancement of desmosomal degradation, and acceleration of wound-healing processes.”
Does not settle: Источник не устанавливает, что колебания потоотделения, увлажнения или сдвигового напряжения при трении вызывают проницаемые липидные дефекты, не оценивает их нелинейную зависимость от нагрузки и не рассматривает созревание рогового слоя, длительность уязвимого интервала или SPV_1.
The skin barrier: An extraordinary interface with an exceptional lipid organization. · Progress in lipid research · 2023
“Within this temperature range the lipid membranes turn gradually from a liquid phase to a crystalline phase [ ]. This phase change occurs due to a drastic change in lipid composition (glucosylceramides, sphingomyelin and phosphoglycerides turn into CERs and FFAs).”
Does not settle: Источник описывает фазовый переход липидов при созревании и влияние гидратации на фазовые переходы в модельных системах. Он не устанавливает роль потоотделения, трения или сдвигового напряжения в образовании проницаемых дефектов, нелинейную зависимость от колебаний нагрузки, длительность сохранения дефектов, влияние переноса нагрузки на зрелую фазу или стабилизацию SPV_1.
Presence and persistence of a highly ordered lipid phase state in the avian stratum corneum. · The Journal of experimental biology · 2018
“However, as temperature increases, lipids of the SC become more disordered, and may pack in more permeable hexagonal or liquid crystalline phase states.”
Does not settle: Не устанавливает влияние потоотделения, трения, колебаний увлажнения или сдвигового напряжения на липидные дефекты. Исследование выполнено на роговом слое домовых воробьёв при изменении температуры кожи, а не во время созревания рогового слоя.
The gap this hypothesis explains
Something is claimed here, but it rests on evidence too thin to carry weight.
Can aligning skin healing worsen shift-work damage, and can rescheduling equal exertion prevent it while preserving cooling?
Original wording · exactly as the pipeline generated it
Может ли усиление суточной синхронизации заживления увеличить повреждение при сменном графике, если потоотделение совпадает с незрелостью барьера, и устраняет ли перенос нагрузки этот эффект при сохранении её дозы и теплоотдачи?
What this question is asking
The question concerns whether making skin repair follow a stronger daily rhythm protects skin or creates recurring periods when it is more easily damaged. It asks whether changing work schedules could place sweating and rubbing against skin at a time when its protective outer layer has not finished recovering, increasing damage. It then asks whether moving the same amount of physical exertion to another time removes that damage while preserving heat loss from the body. The question assumes that repair has distinct daily phases and that sweating during an incompletely recovered phase interferes with protection; the supplied sources establish only parts of that assumption.
- Daily coordination of healing
- The proposed alignment of skin-repair processes with a roughly daily timing pattern, also called circadian synchronization. The input does not specify an intervention or a measure of how strong that alignment is.
- Circadian rhythm
- An internally generated pattern that repeats approximately daily. Alignment means adjusting that pattern to outside timing signals, such as light, as described in S7.
- Shift work
- Work scheduled at changing times or outside usual daytime hours. Here, its role is to change when exertion and sweating occur relative to skin repair.
- Skin barrier
- The protective outer layer of skin. Barrier recovery means restoration of that protection after damage; it is not automatically the same outcome as a wound healing faster.
- Immature barrier
- The question's name for skin protection that has not fully recovered. It describes a degree of recovery, rather than a separate state with a threshold established by the supplied material.
- Wound healing
- The process by which damaged tissue repairs. The cited timing result concerns healing after burns, which does not itself establish resistance to sweat and rubbing.
- Glucose
- A sugar discussed here as a component of sweat. S8 concerns its possible effect on early barrier recovery; that result does not establish the effect of all components of sweat together.
- Exertion dose
- The actual amount of physical activity or effort. The question requires this to remain equal when activity is moved, but supplies no method for defining that equality.
- Heat loss
- Heat leaving the body, providing cooling. The question requires this function to be preserved, so a reduction in sweating alone would not establish the requested outcome.
- Vulnerable window
- A proposed recurring period when incompletely recovered skin would be more easily damaged by sweat and rubbing. Its existence is part of the question, rather than an established finding.
Healing has separate daily recovery phases, and sweating that coincides with an immature skin barrier conflicts with recovery.
The skin barrier is the protective outer layer of skin, and an immature barrier here means that this protection has not fully recovered after damage. The assumption is that daily timing creates a predictable period of incomplete protection and that sweat exposure during that period worsens recovery. If established, this would explain how changing activity times could change damage without changing the amount of activity.
S2 supports an association between injury timing and healing in humans, and S8 supports a narrower possibility that glucose in sweat can delay early barrier recovery, based on the supplied description of mouse experiments. Neither establishes distinct daily periods of barrier immaturity or damage caused by sweat coinciding with those periods. The supplied searches returned related work but no source establishing the combined premise; that does not show that the premise is false.S2S8
The same question asked without the part nothing read establishes:
- Does strengthening daily coordination of skin healing change sweat- and rubbing-related damage during changing work schedules?
- Does moving physical exertion to another time change skin damage during changing work schedules when exertion and heat loss remain equal?
- Damage increases, and rescheduling removes the increase Under the proposed mechanism, stronger daily coordination would leave a vulnerable period that overlaps with sweating and rubbing. Moving equal exertion outside that period would remove the additional damage while preserving cooling, making activity timing consequential.
- Damage increases, but rescheduling does not remove it Stronger coordination would be associated with harm under changing schedules, but moving exertion would leave that harm in place. The proposed overlap would therefore be insufficient to explain a timing-based remedy under the stated conditions.
- Damage does not increase Stronger daily coordination would not create the proposed additional damage under the conditions assessed. There would then be no synchronization-related increase for rescheduling to eliminate, although maintaining cooling would remain a separate requirement.
The proposed chain starts with more tightly timed repair, which could concentrate incomplete recovery into particular hours. If a changed work schedule brings sweating and rubbing into those hours, the question proposes that damage could increase despite better coordination of healing. If timing causes the extra damage, moving exertion could remove it without reducing activity or cooling. Mistaking faster wound healing for protection throughout the day could therefore overlook a vulnerable period, while attributing improvement to timing when exertion or cooling changed would leave the proposed explanation unestablished.
Раздельные фазы восстановления, RL-1, и конфликт потоотделения с барьером, RL-2, не проверены совместно при равной фактической нагрузке.
При смене расписания восстановление и переносимость пота с трением должны сохраняться в молодых границах без снижения теплоотдачи.
Неизвестно, обеспечивает ли синхронизация устойчивость к смене графика или формирует повторяющееся окно уязвимости.
The mechanism it proposes
The engine's own statement of the hypothesis, in full.
Проверяемая гипотеза: во время созревания рогового слоя межклеточные липиды временно находятся близко к переходу в более проницаемое состояние. Усиленная синхронизация созревания делает этот интервал коротким и выраженным. Случайные локальные колебания увлажнения и сдвигового напряжения при потоотделении запускают образование проницаемых липидных дефектов. Их вероятность нелинейно зависит от колебаний нагрузки, поэтому одинаковые суммарные количество пота и работа трения могут давать разное повреждение. Состояние сохраняется в организации внеклеточных липидов до исчезновения дефектов. Перенос нагрузки на более зрелую фазу повышает устойчивость к таким переходам и стабилизирует SPV_1.
Where the idea comes from
The hypothesis borrows a result from another field. This is what it borrows, and from where.
Стохастические процессы, модель Крамерса для выхода из метастабильного состояния при периодической модуляции. Проверяемое приближение: k(t) = k0 × exp(−B(t)/D), B(t) = B0 + B1 × cos(2πt/P + φ) − αh(t) − βs(t); S(t) = exp(−∫₀ᵗ k(u)du). Здесь t и u обозначают время; k(t) обозначает частоту первого возникновения проницаемого липидного дефекта; k0 обозначает частоту попыток локальной перестройки липидов; B(t) обозначает эффективный барьер такой перестройки; B0 обозначает его средний уровень; B1 обозначает амплитуду изменения барьера при синхронном созревании; P обозначает измеренный период этого изменения; φ обозначает фазу созревания относительно начала нагрузки; h(t) обозначает избыток локальной гидратации; s(t) обозначает модуль местного сдвигового напряжения; α и β переводят соответствующие воздействия в изменение эффективного барьера; D обозначает интенсивность быстрых случайных возмущений в тех же единицах, что B; S(t) обозначает вероятность отсутствия первого дефекта к моменту t. Основание переноса: [Activated escape of periodically modulated systems](https://arxiv.org/abs/cond-mat/0504450). Формула применима как проверяемое квазистационарное приближение при B(t) > 0 и подходящем разделении временных масштабов. D нельзя произвольно приравнивать температуре или дисперсии потоотделения; его связь с заданными колебаниями оценивается независимо.
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.
При одинаковых суммарном увлажнении, работе трения и температуре увеличение вариабельности слабых импульсов нагрузки резко повысит частоту скачков проницаемости именно в незрелой фазе. Время первого скачка будет распределено между повторениями даже при одинаковых начальных условиях. Эффект воспроизведётся в изолированных листках рогового слоя соответствующей стадии восстановления и возникнет до любых клеточных повреждений. Перенос нагрузки в зрелую фазу уменьшит эффект вариабельности. Если дополнительная уязвимость обнаруживается только в живой ткани с делящимися клетками и исчезает при предотвращении митотических ошибок без изменения липидной организации, преимущество получает IH_Q_L3_M_G2_4_01.
Would tell it apart from at least one rival. The prediction specifies observable changes in permeability-jump frequency, timing across repetitions, reproduction in isolated tissue, and dependence on recovery phase under stated conditions. 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.
Можно сопоставить восстановленные эпидермальные модели и изолированный роговой слой, используя программируемое увлажнение, трибометр и непрерывную регистрацию проницаемости. Одновременное измерение структуры и потока воды уже продемонстрировано: [Simultaneous Measurements of Structure and Water Permeability in an Isolated Human Skin Stratum Corneum Sheet](https://pmc.ncbi.nlm.nih.gov/articles/PMC6571694/). Главная неопределённость состоит в том, существуют ли предполагаемые метастабильные дефекты в диапазоне обычных бытовых температур и нагрузок.
Other explanations
Every other hypothesis the engine wrote for the same gap, and the observation that would separate the two.
При одинаковых суммарном увлажнении, работе трения и температуре увеличение вариабельности слабых импульсов нагрузки резко повысит частоту скачков проницаемости именно в незрелой фазе. Время первого скачка будет распределено между повторениями даже при одинаковых начальных условиях. Эффект воспроизведётся в изолированных листках рогового слоя соответствующей стадии восстановления и возникнет до любых клеточных повреждений. Перенос нагрузки в зрелую фазу уменьшит эффект вариабельности. Если дополнительная уязвимость обнаруживается только в живой ткани с делящимися клетками и исчезает при предотвращении митотических ошибок без изменения липидной организации, преимущество получает Synchronized skin cell division may let wet friction cause lasting damage through chromosome errors.
- Rival 01 of 01What would separate them
Synchronized skin cell division may let wet friction cause lasting damage through chromosome errors predicts: В восстанавливающихся органотипических моделях кожи доноров 40–60 лет одинаковая влажная механическая нагрузка в пик митозов увеличит число отстающих хромосом, микроядер и дочерних клеток с повреждениями ДНК, а затем вызовет отсроченное ухудшение барьера. Эффект сохранится после выравнивания исходной проницаемости, гидратации и липидной упаковки. Краткая обратимая задержка входа в митоз, полностью прекращённая до последующего восстановления, уменьшит позднее повреждение при той же нагрузке, хотя раннее закрытие замедлится. Если повреждение возникает также в изолированном роговом слое, предшествует митотическим нарушениям и не уменьшается при проверенном предотвращении этих нарушений, преимущество получает this hypothesis.
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.