Restoring blood flow and sweating may destabilize heat loss if response delays persist
In some people aged 40–60, weaker blood flow and sweating responses may protect against heat-loss oscillations caused by delays. Reject this explanation if dysfunction persists after confirmed delay reduction and depends exclusively on prior stimulus count or the spatial arrangement of active sites.
Stage of verification
- Hypothesis published2026-09-26
- Indirect evidenceAssessed at 4 of 10
- Direct testAwaited
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Rhythm or programme
Thermoregulatory feedback
The feedback process that adjusts vascular and sweating responses to regulate body heat
Where this hypothesis actsPeople aged 40–60 with delayed vascular and sweating responses during repeated climatic transitions
Hypotheses on this target 1
Inhibition
Activation
Function preservation
Feedback restoration1
Rhythm restoration
Direct measurement

What is proposed
Feedback restoration
Shorten response delays to allow stronger vascular and sweating responses
With whatNot stated in the record
HowTest controlled ventilation to reduce cooling delay while preserving peak responses; a method for shortening biological response delays is not stated
Possible result
Possible restoration of heat-loss capacity with damped thermal oscillations and stable SPV_8
From the recordСокращение полной задержки позволяет восстановить мощность без потери устойчивости и тем самым стабилизирует SPV_8.
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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.
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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.
Restoring younger skin function may require cooling the body at the right time as well as cooling it strongly enough. The unexpected move is to propose that weaker responses in some people aged 40–60 are a protective adjustment: strengthening them while leaving their delays intact could make cooling repeatedly overshoot the body's needs. That protective role is a hypothesis generated by the pipeline, not a measured result.
- Persistent reductions in responsiveness to nerve signals are proposed to limit blood-flow and sweating responses in some people aged 40–60.
- Those weaker responses are proposed to keep delayed cooling corrections small enough for temperature swings to settle.
- Restoring response strength while retaining the delay would make cooling peak after the need for it has passed.
- Excess late cooling would trigger an opposite correction, changing shrinking swings in heat loss into growing swings.
- Shortening the total delay would let strong cooling arrive in time, changing growing swings back into shrinking ones.
A shower with a slow temperature response can swing between too hot and too cold when each turn of the tap is large and its effect arrives late. Smaller turns can keep the swings manageable even while the delay remains.
Where the picture breaks: The picture illustrates how correction size and delay could interact. It does not establish that human skin deliberately or biologically acquires weaker responses for this protective purpose, or account for differences between sweating, blood flow and evaporation.
- Master questionstep 01 of 04
The goal is a treatment that brings the functional condition of middle-aged people's skin closer to that of young people's skin.
Rests on: The supplied goal explicitly names this treatment objective; it does not establish that it is achievable.
Stated in the chain - Goal pillarstep 02 of 04
Skin's protective responses must work compatibly when several demands occur together.
Rests on: The broad goal of restoring skin function is narrowed to how protective responses work together.
AssumptionThe chain takes compatibility under simultaneous demands as a component of youthful skin function, without explaining that choice in the master question.
- Gap questionstep 03 of 04
Stronger skin blood-flow and sweating responses might destabilize heat loss if they still arrive late. Repeated transitions between humid warmth and dry coolness would provide the setting for asking whether changing activation timing removes that instability.
Rests on: The preceding stage calls for compatible protective responses but supplies no account of why delayed blood flow and sweating are the particular coordination problem to investigate.
LeapThe missing connection is a stated basis for selecting delayed heat-loss responses during these climate transitions from the broader problem of simultaneous demands. The screened sources provide related background but do not establish this specific connection.
- Hypothesisstep 04 of 04
In some people aged 40–60, persistently reduced responsiveness to sympathetic nerve signals, signals from the body's involuntary control system, is proposed to keep delayed cooling stable. Strengthening blood-flow and sweating responses without shortening their delay would remove that protection, producing progressively larger swings in heat loss; shortening the delay would permit strong, stable responses. The proposal calls the intended outcome stabilization of SPV_8, an outcome identifier whose definition is not supplied.
Rests on: The preceding question explicitly supplies the proposed interaction between response strength and delay, and asks whether changing timing prevents instability. The endpoint develops that possibility into a mechanism in which reduced responsiveness is protective and late cooling triggers repeated opposite corrections.
Stated in the chain
What is carried, and what is not. Two background ingredients have relevant screened material: a 2020 European Journal of Applied Physiology study found later onset of the skin blood-flow response during exercise in young men than in boys, without testing middle-aged people or unstable cooling; a 2016 Temperature review described reduced sweating sensitivity in type 1 diabetes, a condition affecting blood-sugar regulation, and reported possible explanations involving sweat glands and their nerve signals, without establishing protective weakening in people aged 40–60. These sources speak to response delays and reduced responsiveness separately; neither establishes the proposed protective role or the sequence from stronger delayed responses to growing heat-loss swings and rescue by shortening the delay.
Where the reasoning is carried by something unstated · 2
- Goal pillar. The chain takes compatibility under simultaneous demands as a component of youthful skin function, without explaining that choice in the master question.
- Gap question. The missing connection is a stated basis for selecting delayed heat-loss responses during these climate transitions from the broader problem of simultaneous demands. The screened sources provide related background but do not establish this specific connection. Establish the missing link before relying on this step.
How a result here could mislead · 3
- Improvement under controlled ventilation could be credited to faster biological responses even if moving air merely makes cooling take effect sooner. Equal peak responses could also conceal changes in how strongly responses increase with the driving signal. What closes it: Measure the intervals from nerve signals to blood-flow and sweating responses independently of the interval until cooling occurs. Assess starting levels, maximum responses and response gain, the amount a response changes for a given change in its driving signal, separately; a timing rescue must establish which delay changed and whether response gain also changed.
- Repeated temperature swings could reflect the imposed climate transitions rather than an instability that continues within the body's cooling control. Smaller temperature peaks after weakening responses could also be mistaken for better heat control while a sustained heat imbalance remains. What closes it: Measure actual heat loss and temperature after periodic transitions stop, with criteria fixed beforehand for distinguishing shrinking from growing swings. Alongside peak temperatures, assess the proposed integral of absolute heat-content deviation, the accumulated size of departures from the reference amount of heat stored in the body; the reference and observation period are not specified in the supplied design and must be fixed.
- Changing activation timing could stabilize cooling by separating neighboring active skin areas or allowing recovery between repeated signals, rather than by correcting the proposed interaction between response gain and delay. What closes it: The comparison must distinguish total response delay from the timing and arrangement of active skin areas, the number of preceding signals and the intervals between them. The supplied testing outline does not specify controls that separate these alternatives; a timing intervention alone cannot identify which explanation produced the improvement.
What would make this wrong. The proposal's stated rejection condition is that instability persists after a confirmed reduction in the relevant delay and is determined exclusively by the number of preceding signals or the spatial arrangement of active skin areas. That observation would break the claim that excessive response gain interacting with persistent delay explains the instability, provided the intervention demonstrably changed the intended delay.
What it would change. If the mechanism held, restoring youthful skin function would require preserving stable coordination while strengthening responses: a weaker response could sometimes be part of a protective adjustment. Work on restoring skin cooling would therefore have to assess response timing and actual heat balance alongside response strength. Even a successful test in the proposed subgroup would not establish a treatment that restores overall youthful skin function, lasting benefit, or applicability to all middle-aged people; the meaning of improvement in SPV_8 would also remain unresolved until that outcome is defined.
Sources read · 9
The skin blood flow response to exercise in boys and men and the role of nitric oxide. · European journal of applied physiology · 2020
“Boys had a shorter delay from the onset of exercise to onset of SkBF response compared with men (205 ± 48 and 309 ± 71 s, respectively; p < 0.01, d = 1.7 [0.9-2.8]).”
Does not settle: Источник сравнивает мальчиков и мужчин 22 ± 2 лет при нагрузке. Он не изучает людей 40–60 лет, потоотделение, устойчивость терморегуляции, колебания теплоотдачи, восстановление амплитуды при сохранённой задержке или компенсаторные изменения чувствительности периферических симпатических путей.
Restoration of thermoregulation after exercise. · Journal of applied physiology (Bethesda, Md. : 1985) · 2017
“This delay in the restoration of postexercise thermoregulation has been associated with disturbances in cardiovascular function which manifest most commonly as postexercise hypotension.”
Does not settle: Источник описывает задержку восстановления терморегуляции после нагрузки, но не устанавливает компенсаторное снижение чувствительности у людей 40-60 лет, усиление амплитуды при сохранённой задержке, нарастающие колебания теплоотдачи, сокращение полной задержки или стабилизацию SPV_8.
Body temperature regulation in diabetes. · Temperature (Austin, Tex.) · 2016
“Given the reduced thermosensitivity of the sweating response in those with type 1 diabetes, Carter et al. surmised that the diabetes-related changes in sweating were due to peripherally-mediated changes such as reduced acetylcholine sensitivity, altered physical properties of the actual sweat glands and/or interruptions in the thermoeffector neural pathways.”
Does not settle: Источник описывает нарушения теплоотдачи при диабете 1 типа. Он не устанавливает наличие компенсаторного ограничения у людей 40–60 лет, сохранённые задержки реакций, восстановление амплитуды, колебания теплоотдачи, устойчивость терморегуляции или показатель SPV_8.
Effect of sinusoidal leg cycling exercise period on brachial artery blood flow dynamics in humans. · The journal of physiological sciences : JPS · 2020
“Contrarily, the BF-BA response showed anti-phase (approximately 180°) regardless of the period, whereas the θ of forearm SBF and SR were similar to gas exchange and central circulation.”
Does not settle: Источник изучал семь здоровых молодых мужчин при синусоидальной нагрузке на велоэргометре. Он не устанавливает возрастные изменения у людей 40-60 лет, компенсаторное снижение чувствительности симпатических путей, устойчивость терморегуляции, нарастающие колебания теплоотдачи, влияние восстановления амплитуды при сохранённой задержке или сокращения полной задержки на SPV_8.
Thermoregulation in the Aging Population and Practical Strategies to Overcome a Warmer Tomorrow. · Proteomics · 2020
“Mechanisms underlying a compromised cutaneous vasodilation are suggested to include reduced sympathetic neural drive, diminished cholinergic co-transmitter contribution, and altered second messenger signaling events.”
Does not settle: Абстракт не устанавливает, что снижение чувствительности у людей 40–60 лет является компенсаторным ограничением усиления. Он не оценивает задержки терморегуляторных реакций, устойчивость системы, колебания теплоотдачи, восстановление амплитуды либо SPV_8.
Autonomic control of body temperature and blood pressure: influences of female sex hormones. · Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2017
“Changes in thermoregulation over the course of the menstrual cycle and with hot flashes at menopause are mediated by hormonal influences on neural control of skin blood flow and sweating.”
Does not settle: It does not establish compensatory reductions in peripheral response sensitivity in people aged 40–60, persistent response delays, restoration of response amplitude, oscillations in heat loss, or stabilization of SPV_8.
Heat tolerance and aging. · Medicine and science in sports · 1979
“Whether the decrease in responsiveness of sweating noted for some older individuals is an age related change or a reflection of their lower fitness levels is not known.”
Does not settle: Источник не устанавливает возраст 40-60 лет, изменения чувствительности сосудистых путей, задержки реакций, усиление амплитуды, колебания теплоотдачи или стабилизацию SPV_8.
Circulatory and thermal responses of men with different training status to prolonged physical work in dry and humid heat. · Scandinavian journal of work, environment & health · 1987
“The impaired work performance in the heat seemed mainly to be related to the circulatory instability accompanying the increased cutaneous circulation.”
Does not settle: Возраст участников, связь нестабильности с задержкой реакции, роль потоотделения, компенсаторное снижение чувствительности периферических путей, нарастающие колебания теплоотдачи и показатель SPV_8 остаются открытыми.
Mechanisms of Heat-Induced Sleep Disruption in Aging: A Narrative Review. · 2026
“Thermoregulatory efficiency declines with aging due to reduced sensitivity of hypo-thalamic POA neurons and impairments in peripheral heat-dissipation mechanisms, including sweating and vasodilation, as demonstrated primarily in systematic reviews and human studies [ , ].”
Does not settle: Источник не устанавливает возрастную группу 40–60 лет, компенсаторную роль сниженной чувствительности периферических путей, сохранение задержки реакции, восстановление амплитуды, нарастающие колебания теплоотдачи, сокращение полной задержки или стабилизацию SPV_8.
The gap this hypothesis explains
Can restoring skin blood flow and sweating disrupt heat loss, and can retiming them prevent it?
Original wording · exactly as the pipeline generated it
Может ли восстановление мощности сосудистой и потовой реакций дестабилизировать теплоотдачу, если их задержки сохраняются, и устраняет ли изменение времени активации этот сбой при повторных переходах между влажным теплом и сухой прохладой?
What this question is asking
The question concerns whether restoring the strength of skin responses also restores their ability to regulate heat loss. It asks what happens when blood-vessel responses and sweating become stronger but still respond late during repeated switches between warm, humid air and cool, dry air. The comparison is between restoring response strength alone and also changing when those responses begin, with the stability of heat loss as the outcome. It assumes that response strength can be restored while delays remain; the supplied sources do not establish that combination. The stated context concerns middle-aged skin, but the supplied evidence does not establish the answer for that population.
- Skin blood-vessel response
- A change in blood flow through the skin associated with changes in its blood vessels. Here, the question distinguishes the strength of that response from how late it occurs.
- Sweating response
- The production of sweat by the skin. The question treats the amount produced and its pattern over time as separate aspects of the response.
- Response strength
- How large a blood-flow or sweating response becomes. The supplied question calls this its power, but gives no measurement or target that defines restoration.
- Response delay and activation timing
- Response delay is the interval between a change in conditions and the body's response; activation timing concerns when that response starts. Changing the start time does not, by definition alone, establish that every part of the response becomes faster.
- Heat loss and its stability
- Heat loss is the transfer of heat from the body to its surroundings. Stability here refers to the question's proposed ability to keep that loss appropriately controlled during repeated environmental changes; the input supplies no formal criterion.
- Thermoregulation
- The body's regulation of temperature through control of heat production and heat loss. It involves multiple responses, so a change in sweating alone does not describe the entire process.
- Autonomic responses
- Bodily responses regulated automatically rather than through deliberate action. S9 describes their coordination as necessary for heat production and heat loss.
- Epidermal transient receptor potential vanilloid 3 channels
- Temperature-sensitive channels in the epidermis, the skin's outer layer, referred to as TRPV3 in S6. That source links age-related changes in these channels to a possible delay in detecting skin-temperature changes and limited local blood-vessel responses.
- Heat acclimation
- Adaptation associated with exposure to heat. S4 reports increased sweating and other changes after this adaptation, without establishing that it restored skin function to a younger state.
- Core temperature
- Temperature within the body's interior, distinguished from skin temperature. S4 reports a slower rise in this measure after heat acclimation.
- Sleep deprivation
- A condition of insufficient sleep. It is the condition examined in S3, whose cooling result does not directly answer the question about restoring skin responses.
The strength of vascular and sweating responses can be restored while their delays remain.
The blood-vessel response concerns changes in blood flow through the skin, and the sweating response concerns sweat production. The assumption is that both responses can regain strength without becoming quicker to respond to changing conditions. If this combination occurs, it allows the effects of response strength and response timing on heat loss to be distinguished.
The supplied search results do not establish restoration of both responses with persistent delays. S6 reports age-related changes in temperature-sensitive channels in the outer skin layer and suggests that these might delay detection of skin-temperature changes; it does not demonstrate persistent delays after restoration or address sweating delays. S4 reports increased sweating after adaptation to heat, but does not establish the proposed separation between restored strength and unchanged timing. These limitations leave the assumption unestablished, rather than showing it to be false.S6S4
The same question asked without the part nothing read establishes:
- During repeated switches between warm, humid air and cool, dry air, does restoring skin blood-vessel responses and sweating alter their timing and the stability of heat loss?
- During repeated switches between warm, humid air and cool, dry air, does changing when skin blood-vessel responses and sweating begin improve the stability of heat loss?
- Stronger delayed responses disrupt heat loss; changing timing prevents it Under the proposed mechanism, restored responses would act too late for the current surroundings and disturb heat loss across repeated switches. If changing activation timing removed that disturbance, response strength alone would be an insufficient measure of restored function.
- Stronger delayed responses disrupt heat loss; changing timing does not prevent it Restoring strength would produce the proposed disturbance, but changing when responses begin would leave it unresolved. That outcome would show that the timing change examined does not suffice to restore stable heat loss; it would not identify the remaining cause.
- Stronger responses do not disrupt heat loss despite persistent delays The remaining delays would not produce the proposed disturbance under the conditions examined. There would consequently be no demonstrated disturbance of this kind for changing activation timing to remove.
Heat production and heat loss depend on coordinated automatic bodily responses, according to S9. The question therefore distinguishes how strongly a response acts from whether it acts at the appropriate time. Under its proposed mechanism, a stronger response that arrives late could continue affecting heat loss after the surroundings have changed; this is a conditional interpretation, not a reported finding. If that mechanism operates, restoring strength alone could fail to restore temperature control, whereas correcting timing could matter. If it does not operate, treating persistent delays as a demonstrated cause of unstable heat loss would misrepresent the evidence.
The mechanism it proposes
The engine's own statement of the hypothesis, in full.
У части людей 40–60 лет снижение чувствительности сосудистой и секреторной реакций представляет собой компенсаторное ограничение усиления, которое удерживает запаздывающую терморегуляцию в устойчивом режиме. Субстрат компенсации составляют устойчивые изменения чувствительности периферических исполнительных путей к симпатическому сигналу. Восстановление амплитуды при сохранённой задержке снимает это ограничение: охлаждение достигает максимума после исчезновения потребности в нём, затем вызывает противоположную коррекцию. Возникают нарастающие колебания фактической теплоотдачи. Сокращение полной задержки позволяет восстановить мощность без потери устойчивости и тем самым стабилизирует SPV_8.
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 повторных климатических переходах повышение измеренного усиления должно менять затухание тепловых колебаний на нарастание только при достаточно большой задержке. Сокращение задержки должно возвращать затухание при прежних пиковых сосудистой и секреторной реакциях. После прекращения периодических переходов колебания некоторое время сохраняются, что отделяет собственную неустойчивость от обычного следования внешней нагрузке. Решающий результат: временное возвращение пониженного усиления уменьшает одновременно температурные выбросы и интеграл абсолютного отклонения теплосодержания, хотя отдельные реакции становятся слабее. Гипотезу отвергают, если сбой сохраняется после подтверждённого сокращения задержки и определяется исключительно предшествующим числом стимулов либо пространственным расположением активных участков.
Would tell it apart from at least one rival. The prediction specifies observable changes in oscillation damping, temperature excursions and integrated absolute heat-content deviation, plus an explicit rejection condition. No rival prediction is supplied. A paper already fetched for this hypothesis bears on it.
What testing it would take
The engine's own read on whether this is testable with methods that already exist.
Климатическая камера, лазерная оценка перфузии, измерение потоотделения, калориметрия и микронейрография позволяют оценить усиление и задержки раздельно. Управляемая вентиляция проверяет вклад исполнительной задержки охлаждения. Её эффект сам по себе ещё не доказывает исправление биологической задержки: для этого требуется независимое измерение интервалов от нервного сигнала до сосудистой и секреторной реакций. Максимальную мощность, наклон ответа и исходный уровень следует оценивать отдельно.
Other explanations
Every other hypothesis the engine wrote for the same gap, and the observation that would separate the two.
При повторных климатических переходах повышение измеренного усиления должно менять затухание тепловых колебаний на нарастание только при достаточно большой задержке. Сокращение задержки должно возвращать затухание при прежних пиковых сосудистой и секреторной реакциях. После прекращения периодических переходов колебания некоторое время сохраняются, что отделяет собственную неустойчивость от обычного следования внешней нагрузке. Решающий результат: временное возвращение пониженного усиления уменьшает одновременно температурные выбросы и интеграл абсолютного отклонения теплосодержания, хотя отдельные реакции становятся слабее. Гипотезу отвергают, если сбой сохраняется после подтверждённого сокращения задержки и определяется исключительно предшествующим числом стимулов либо пространственным расположением активных участков.
- What would separate them
Loss of alternating activation across skin regions may destabilize heat loss predicts: При одинаковых суммарной секреции, среднем кровотоке, средней задержке и распределении индивидуальных порогов компактное размещение одновременно активных участков должно давать большие температурные выбросы, чем их чередующееся размещение. Перестановка пространственного порядка импульсов должна улучшать теплоотдачу без сокращения средней задержки. Дополнительный признак отрицательной частотной зависимости: при усилении активности соседних участков вероятность включения ещё не активированного участка падает сильнее, чем предсказывает модель общего центрального теплового сигнала. Отсутствие влияния пространственного порядка при достаточной точности измерений опровергает эту гипотезу в пользу общего временного или рецепторного механизма.
- Rival 02 of 02What would separate them
Repeated climate transitions may destabilize heat loss by reducing vascular receptor sensitivity predicts: После одинакового исходного отдыха первая реакция должна быть сохранной. Отношение сосудистой амплитуды второго ответа к первому должно падать при сокращении межстимульного интервала и восстанавливаться после паузы даже при фиксированной температуре и одинаковом внешнем нервном или фармакологическом входе. Ответ на стимул, обходящий исследуемый рецептор, должен сохраняться. Простое опережение второго импульса при прежнем коротком интервале не исправит сбой и может его усилить. Гипотеза теряет поддержку, если одинаковые повторные входы дают неизменный сосудистый ответ, а теплоотдача нормализуется только после коррекции общей задержки или перестановки активных участков.
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.
В исследовании местного введения тетрагидробиоптерина поздняя сосудистая реакция возрастной кожи приблизилась к молодой, тогда как различия на более ранних этапах нагревания сохранялись. Это показывает возможность разделения восстановленной величины ответа и его динамики. Исследование не проверяло колебательную неустойчивость. [Первичное исследование восстановления вазодилатации](https://pmc.ncbi.nlm.nih.gov/articles/PMC3311663/).
Геронтологическая физиология терморегуляции; учебная глава «Температура тела, регуляция температуры и лихорадка» в Guyton and Hall Textbook of Medical Physiology. Пересмотра потребует трактовка ослабленной возрастной реакции как однозначно утраченной функции: для выделенного фенотипа она окажется необходимой компенсацией задержки, которую опасно устранять изолированно.
Участок с восстановленной молодой амплитудой объективно хуже переносит повторную смену климата, чем тот же участок после частичного обратимого ослабления ответа; после сокращения задержки преимущество переходит к восстановленной амплитуде. Такой обратимый переход должен воспроизводиться без изменения гидратации, артериального давления и условий испарения.
При целевом поиске сочетаний aging, cutaneous vasodilation, adaptive attenuation, delayed feedback и oscillations не найдено обзора, утверждающего именно такую компенсаторную причинность. Это ограниченная проверка новизны; доказать отсутствие соответствующего утверждения во всей литературе невозможно. Общая идея неустойчивости запаздывающей обратной связи давно известна. Радикальная часть гипотезы состоит в функционально защитной роли конкретного возрастного ослабления.
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. 6 paper(s) already retrieved for this hypothesis carry its prediction’s terms. Reading them comes before running anything. Already retrieved: [The unbearable versatility of endocrine aging].; [Features of water-electrolyte balance in persons of the older age group].; [Adaptation of the 12-item medication adherence scale ( the Questionnaire for assessment of adherence to Medication) on a Russian-speaking sample of patients with type 1 and type 2 diabetes mellitus]..
6 papers retrieved around this hypothesis
- [The unbearable versatility of endocrine aging].PMID 42733379 · full_text · 50,301 characters stored
- [Association of vitiligo with endocrine autoimmune diseases: literature review].PMID 42733372 · full_text · 37,212 characters stored
- [Features of water-electrolyte balance in persons of the older age group].PMID 38311992 · full_text · 51,603 characters stored
- [Determination of prolactin reference intervals in different age groups].PMID 37448243 · full_text · 16,490 characters stored
- [The causes of obesity relapse after weight loss].PMID 39069774 · full_text · 33,542 characters stored
- [Adaptation of the 12-item medication adherence scale ( the Questionnaire for assessment of adherence to Medication) on a Russian-speaking sample of patients with type 1 and type 2 diabetes mellitus].PMID 39302863 · full_text · 46,786 characters stored
0 citation handles extracted; 1 Europe PMC search run; 8 records examined; 6 sources stored for enrichment, 6 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.