Mitochondrial genome deletions hide a loss of muscle energy reserve
Retained muscle fibers may conceal lost energy reserve by recruiting unaffected segments and motor units. The hypothesis predicts that intolerance maps to mitochondrial genome deletions despite abundant oxygen and fuel; normal intrinsic respiration in affected regions argues against it.
Omega Point 1.1
Stage of verification
- Hypothesis published2026-09-18
- Indirect evidenceAssessed at 5 of 10
- Direct testAwaited
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Metabolism and energy
Oxidative capacity
The capacity to support oxidative metabolism
Where this hypothesis actsRetained muscle fiber segments with high mitochondrial deletion heteroplasmy and reduced oxidative reserve
Hypotheses on this target 2
Inhibition
Activation1
Function preservation1
Supplementation
Feedback restoration
Direct measurement
What is proposed
Function preservation
Preserve oxidative capacity
With whatNot stated in the record
HowNot stated in the record
Possible result
Possible stabilization of SPV_6
From the recordPreserving oxidative capacity in the retained compartment stabilizes SPV_6.
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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.
Muscle that performs normally after surgery or illness may be hiding segments where the mitochondria — the organelles that produce nearly all of a cell's energy — have been quietly overtaken by defective copies of their own genome. The unexpected claim is not that mitochondrial mutations accumulate with age, which is established, but that their spatial patterning within individual fibers creates a concealed energy deficit that ordinary activity never reaches and that standard tissue sampling cannot detect. This is a mechanism proposed by a research pipeline, not a finding from any experiment; it names the observations — spatial correspondence between mutant genome burden and respiratory failure within single fibers — that would confirm or break it.
- Mitochondrial DNA replication in post-mitotic muscle fibers — fibers that no longer divide — occasionally produces deletion mutations, yielding genomes missing a stretch of their sequence.
- Within a single fiber, a deleted genome replicates alongside normal copies; clonal expansion gradually raises the local fraction of deletion-bearing copies in a focal segment of the fiber.
- When deletion-bearing copies dominate a segment, that segment loses functional respiratory-chain complexes — becoming COX-deficient, lacking the enzyme cytochrome c oxidase — and can no longer produce aerobic energy at full capacity.
- The nervous system recruits unaffected segments of the same fiber and neighboring motor units to meet ordinary demand, so whole-muscle performance appears normal and the local deficit is invisible to bulk measurement.
- Recurrent physiological stresses — surgery, illness, intensive rehabilitation — push demand past what the remaining unaffected segments can supply, exposing the hidden energetic bottleneck that ordinary activity never reached.
- Over months and years, clonal expansion widens the mosaic: more segments cross the threshold into COX deficiency, steadily narrowing the gap between routine output and true oxidative reserve.
- Later tissue-replacement procedures that increase demand on the retained muscle encounter a progressively smaller margin of safe reserve, making each successive demand increase more dangerous than the last.
A library where one shelf has a misprinted edition mixed in with the correct copies. Every time the library restocks that shelf it duplicates whatever is already there — misprints included — so over years the shelf fills with unusable copies while every other shelf is fine. A visitor browsing the whole collection barely notices, but anyone who needs several books from that particular shelf cannot fill their order.
Where the picture breaks: Library books are passive objects on a fixed shelf; mitochondrial genomes replicate, fuse, and divide continuously within a dynamic network, and the takeover depends on the kinetics of mitochondrial fission and fusion rather than passive shelf restocking. The analogy also does not capture the threshold effect — a fiber segment tolerates a substantial mutant load before function collapses, whereas a misprinted book is unusable from the start.
- Master questionstep 01 of 04
Slowing aging through tissue replacement requires knowing which parts of the body must be exchanged and how little can be changed to achieve the effect — the minimum effective replacement set and its anatomical identity.
Rests on: The premise that aging can be meaningfully slowed by replacing a subset of tissues rather than requiring whole-body intervention, and that a minimum sufficient set exists.
AssumptionIt is taken as given that partial tissue replacement can slow aging and that the problem is to identify the smallest effective target, not to establish whether targeted replacement works at all.
- Goal pillarstep 02 of 04
When only some tissue is replaced, the new tissue restores functional demand — it works, and it asks the surrounding body to support that work. The tissue that was not replaced must still supply the reserve capacity to meet the increased demand. Containing the mismatch between what restored tissue demands and what retained tissue can deliver is a necessary condition for safe partial replacement.
Rests on: The master question's framing of minimum replacement — if only part of the body is exchanged, the rest must absorb the consequences, and a mismatch between restored demand and retained reserve is the predictable failure mode.
Stated in the chain - Gap questionstep 03 of 04
After a stressful episode such as surgery, illness, or intensive rehabilitation, patients appear to recover baseline function, but challenge testing sometimes reveals persistent loss of reserve capacity that baseline measurements miss. The unresolved question is whether this pattern reflects irreversible structural damage to the microvascular supply — the small blood vessels feeding muscle tissue — making each stress episode permanently costly, or a reversible timing mismatch between demand and recovery that resolves given enough time.
Rests on: The goal pillar's requirement that retained tissue preserve its reserve — if reserve is being lost invisibly after each stress, the mismatch is worse than baseline performance suggests, and repeated replacement-driven demands become cumulatively dangerous.
Stated in the chain - Hypothesisstep 04 of 04
The concealed reserve loss is neither microvascular damage nor a reversible timing disorder. Mitochondrial DNA deletions — mutations that remove a stretch of the mitochondrial genome — accumulate through clonal expansion, the process by which copies descended from one mutant genome gradually dominate a local region, within focal segments of individual muscle fibers. Each affected segment loses respiratory-chain function — the capacity of its mitochondria to transfer electrons from nutrients to oxygen and produce usable energy. The muscle compensates by recruiting unaffected segments and neighboring motor units — groups of fibers controlled by a single nerve — so ordinary performance appears normal. Recurrent physiological stresses push demand past the compensated range, exposing energetic bottlenecks that were present all along. Over time, clonal expansion widens the mosaic of affected segments, narrowing the margin between routine output and true oxidative reserve — the gap between current energy output and maximum aerobic capacity. The proposal predicts that persistent challenge intolerance maps spatially onto fiber segments carrying high deletion heteroplasmy — a high fraction of mutant mitochondrial genomes — with measurably reduced maximal respiration even when oxygen and substrate are supplied without limit, and that finding normal intrinsic respiration in those same segments would argue against it.S1
Rests on: The gap question asks whether concealed reserve loss is structural or reversible; this hypothesis answers that it is structural, but the structure is intracellular — a mosaic of mutant mitochondrial genomes spreading through clonal expansion — rather than vascular, and S1 establishes that the physical substrate exists: deletion-bearing genomes do concentrate in focal COX-deficient segments of human muscle fibers.
Supported by literature
What is carried, and what is not. Of three screened sources, one — S1 (2014, Human Molecular Genetics) — directly establishes the physical substrate the first mechanistic link requires: deletion-bearing mitochondrial genomes concentrate through clonal expansion in focal COX-deficient segments of individual human muscle fibers, with affected segments ranging from under ten to over one thousand micrometers. That finding does not address whether unaffected segments compensate functionally, which is the second link. The remaining sources — S3, an eight-patient case series available at abstract level only, and S5, a cross-sectional study measuring bulk deletion abundance in peripheral artery disease — operate at the tissue or population level and do not test spatial genotype-to-function correspondence within fibers. No screened source addresses any link beyond the first: neither the functional masking by recruitment, nor stress exposure of the bottleneck, nor the progressive narrowing of reserve over time. One link of the chain has direct molecular and histochemical support; the sequence from concealment through stress exposure to progressively unsafe demand is entirely proposed.S1S3S5
Where the reasoning is carried by something unstated · 1
- Master question. It is taken as given that partial tissue replacement can slow aging and that the problem is to identify the smallest effective target, not to establish whether targeted replacement works at all.
How a result here could mislead · 3
- The lesions are focal and irregularly spaced along a fiber, so a biopsy or laser-capture pass — a technique that uses a focused laser to isolate a microscopic region from a tissue section — that does not intersect an affected segment will show normal heteroplasmy and normal respiration. This would be read as evidence against the hypothesis when the mosaic was simply missed, a false negative indistinguishable from a true negative without independent confirmation that affected segments were present and sampled. What closes it: COX/SDH dual histochemical staining — which marks COX-deficient segments blue against a brown succinate-dehydrogenase background — must precede and guide laser-capture targeting, so that segment selection is based on visible dysfunction rather than random positioning. The protocol must specify in advance how many COX-deficient and COX-normal segments per fiber are captured and what minimum count of affected segments is required before a negative respirometry result is interpretable.
- A positive spatial correlation — segments with high deletion load showing low respiration — could arise from co-degeneration, where both deletion accumulation and respiratory decline are driven independently by the same upstream cause such as chronic oxidative stress rather than by the causal chain the hypothesis claims. The correlation would look identical either way. What closes it: The hypothesis requires a specific dose-response shape: graded heteroplasmy levels within a single fiber should produce graded respiratory deficits, and the threshold at which function drops should correspond to the established biochemical threshold for respiratory-chain failure, typically sixty to eighty percent mutant load. A step-function collapse near that known threshold supports the proposed causal sequence; a smooth decline that does not respect any threshold is more consistent with confounding by a shared upstream cause.
- Permeabilized-fiber respirometry — a technique that makes the fiber membrane porous so substrates and oxygen can be supplied directly at controlled concentrations — delivers substrates at saturating levels, bypassing the in vivo delivery constraints of the mitochondrial network and fiber geometry. A segment that is functionally impaired in the living body, where substrate delivery through the fiber volume is rate-limiting, could show near-normal maximal respiration under the assay's ideal conditions, meeting the hypothesis's own falsification criterion artifactually. What closes it: The respirometry protocol must include sub-saturating substrate titrations alongside the standard maximal protocol and must report the substrate concentration at which respiration diverges between affected and unaffected segments from the same fiber — not only the plateau value under saturating conditions.
What would make this wrong. Fiber segments with high deletion heteroplasmy and histochemical COX deficiency that nonetheless show normal maximal respiration when supplied with saturating oxygen and substrates ex vivo — the hypothesis's own stated falsification criterion — would break the chain, because the energetic bottleneck on which both the concealment of reserve loss during ordinary activity and the danger of later demand increases depend would not exist despite the genomic damage being present.
What it would change. If the spatial distribution of mitochondrial heteroplasmy is confirmed as the stored state that makes retained muscle unsafe under increased demand, the answer to the master question shifts: the minimum tissue that must be replaced is set not by what has visibly failed but by what has silently accumulated deletion mosaics in its retained fibers. Replacement planning would require pre-operative mapping of segmental heteroplasmy — a spatial biopsy guided by histochemical staining, not a bulk tissue assay — to identify which muscle compartments can tolerate increased demand and which cannot. Even if confirmed in human biopsy material, this would establish the mechanism in sampled muscles under controlled ex vivo conditions; the step from segmental respirometry to predicting whole-body exercise tolerance, the timescale over which the mosaic expands across a lifespan, and the heteroplasmy threshold at which demand becomes clinically unsafe would all remain unestablished.
Sources read · 3
Dissecting the mechanisms underlying the accumulation of mitochondrial DNA deletions in human skeletal muscle. · Human molecular genetics · 2014
“The COX-deficient segment has been shown to be of variable length, ranging from <10 to >1000 μm ( ). These are thought to occur as a consequence of the continuous replication of mtDNA in muscle cells, associated with mitochondrial fission and fusion, leading to changes in the proportion of mutant mtDNA in muscle segments.”
Does not settle: The source establishes that deletion-bearing mitochondrial genomes concentrate in focal COX-deficient segments of individual muscle fibers via clonal expansion — directly supporting the spatial-distribution premise of the question. It does not address whether unaffected fiber segments or motor units are recruited to compensate functionally during ordinary performance, whether recurrent physiological stresses selectively expose these focal energetic bottlenecks, how clonal expansion rate affects the safety of later oxidative demands, or any clinical or functional performance endpoint. SPV_6 and the 'concealed reserve loss' framing are not addressed. The paper's primary finding — that deletion size does not confer a replicative advantage — is mechanistic background on clonal expansion kinetics, not evidence for the functional masking claim.
Myopathy and Ophthalmologic Abnormalities in Association With Multiple Skeletal Muscle Mitochondrial DNA Deletions. · Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society · 2024
“Pathogenic variants in mtDNA were not found in the blood or buccal sample from any patient, but 7 of 8 patients had multiple mtDNA deletions identified in muscle tissue. One patient had a single mtDNA deletion identified in the muscle. Heteroplasmy was less than 15% for all of the identified deletions, with the exception of one deletion that had a heteroplasmy of 50%-60%.”
Does not settle: The abstract describes tissue-level heteroplasmy (muscle vs. blood/buccal) and clinical phenotype in 8 patients, but says nothing about intracellular spatial distribution of deletion-bearing genomes within individual muscle fibers, focal segmental concentration, recruitment of unaffected fiber segments to compensate, oxidative reserve, or any mechanism by which functional loss is concealed at the whole-muscle level. Sample size is 8. No functional capacity, respiratory, or energetic measurements are reported.
Mitochondrial DNA damage in calf skeletal muscle and walking performance in people with peripheral artery disease. · Free radical biology & medicine · 2020
“The analysis of mtDNA 4977 deletion revealed no significant association with walking performance in PAD people. Our results are in keeping with previous findings of unvaried abundance of mtDNA 4977 bp deletion in calf skeletal muscle from patients with unilateral PAD with lower and higher ABI.”
Does not settle: The source measures aggregate deletion abundance across a biopsy, not the intracellular spatial distribution of heteroplasmy within individual fibers or focal segments. It does not test whether unaffected fiber segments or motor units are recruited to compensate for deletion-bearing segments, does not measure oxidative reserve capacity, and does not apply stress conditions beyond ordinary paced walking that would be expected to expose energetic bottlenecks under SCOUT 2. The no-association finding is consistent with concealment of reserve loss at ordinary demand but does not establish the spatial heteroplasmy mechanism proposed. Cross-sectional design precludes causal inference; mitochondrial function was not directly assayed.
The gap this hypothesis explains
Do recurrent deficits after apparent recovery reflect permanent small-vessel loss or temporary coordination failure?
Original wording · exactly as the pipeline generated it
Does apparent recovery conceal persistent microvascular reserve loss that makes repeat output gains dangerous, or do recurrent deficits reflect reversible timing mismatch rather than cumulative structural injury?
What this question is asking
The smallest blood vessels in an organ — capillaries and arterioles too fine to image on a standard scan — form a reserve network that opens when demand rises. After an injury that damages some of these vessels, gross function (cardiac output, kidney filtration, exercise tolerance) can return to a range that looks normal on clinical tests. The question asks whether that normalcy is real or whether the reserve network has been permanently thinned, so that the next time the organ is pushed hard it hits a ceiling lower than before and sustains new damage. The alternative possibility is that recurrent problems are not structural at all but reflect a temporary mismatch in the timing of vessel dilation — different parts of the network responding out of step — which would resolve on its own without leaving cumulative harm.
- microvascular reserve
- The capacity of the smallest blood vessels — capillaries and arterioles — to increase blood flow above their resting rate when demand rises. Measured clinically by stressing the vessel bed (usually with a drug like adenosine) and comparing peak flow to resting flow. A high reserve means the network can open wide when needed; a low reserve means the network is already near its ceiling at rest and cannot deliver much more during exercise, fever, or injury. This is the quantity the question asks whether apparent recovery truly restores.
- coronary flow reserve (CFR)
- The ratio of maximum coronary blood flow (during pharmacological stress) to resting coronary blood flow. A normal value is roughly 2.5 or above; below that, the heart's small vessels cannot deliver enough extra blood when the heart works harder. S5 and S10 both measure CFR and find it reduced in their patient populations; S6 finds it normal in one patient.
- index of microcirculatory resistance (IMR)
- A pressure-and-flow-derived number that isolates the resistance of the smallest coronary vessels from the resistance of the larger arteries. Higher values mean the microvascular bed is more obstructed or rarefied. Used alongside CFR to locate the problem: a low CFR with a high IMR points to the capillary network, not the large arteries. S10 reports elevated IMR in heart-failure patients; S6 reports normal IMR in one case.
- rarefaction
- A permanent reduction in the density of small blood vessels in a tissue — capillaries that existed before an injury are destroyed and not rebuilt, leaving the surviving network thinner and less able to supply blood during high demand. In this question, rarefaction is the structural mechanism that would make repeat stress dangerous: fewer vessels means less reserve, and each new insult destroys more of what remains. S1 documents this process in mouse kidney capillaries after acute injury.
- timing mismatch (dyssynchrony)
- A proposed functional mechanism in which the small vessels are structurally intact but open and close out of step with each other, creating patchy under-perfusion that looks like rarefaction on reserve testing but resolves as signalling recalibrates. This is the reversible alternative the question poses. No source in the set uses or examines this concept; it is entirely from the question itself.
- apparent recovery
- The return of gross functional measures — cardiac output, kidney filtration rate, exercise tolerance, resting blood flow — to ranges that look normal on standard clinical tests, while the microvascular bed underneath may or may not have returned to its pre-injury state. The question's core concern is that these surface metrics can mask a quietly shrinking reserve.
- heart failure with preserved ejection fraction (HFpEF)
- A form of heart failure in which the heart's pumping fraction — the percentage of blood ejected with each beat — remains in the normal range (typically above 50 percent), yet the patient has symptoms of heart failure (breathlessness, fluid retention, exercise intolerance). S10 shows that these patients have impaired microvascular reserve despite the apparently normal pump function, making HFpEF a clinical example of the 'apparent recovery concealing deeper damage' pattern the question asks about.
- cardiac syndrome X
- A clinical label for patients who have chest pain typical of coronary artery disease but whose large coronary arteries appear normal on angiography. The pain is attributed to dysfunction of the small coronary vessels — microvascular disease that standard imaging misses. S5 studies this population and finds that inflammation correlates with reduced coronary flow reserve.
- acute kidney injury (AKI)
- A sudden drop in kidney function, usually measured by a rise in blood creatinine or a fall in urine output. S1 uses AKI in mice as the injury model and shows that the kidney's peritubular capillaries — the tiny vessels surrounding the filtration tubules — do not fully regrow after injury, leaving structural rarefaction that predisposes to another episode.
Apparent functional recovery occurs after microvascular injury, but recurrent deficits emerge afterward, and these could be explained by either permanent vessel loss or reversible coordination failure.
The question takes it as given that people (or organs) do appear to recover after small-vessel injury — numbers normalise, symptoms recede — yet problems come back. It needs this to be true, because without both the apparent recovery and the later recurrence there is no fork to explain. The structural-versus-functional framing further assumes these are the two candidate mechanisms and that distinguishing them is possible in principle.
S2 establishes that macro-level revascularisation after myocardial infarction leaves microvascular injury untreated and that roughly 40 percent of patients progress to heart failure despite restored epicardial flow — this supports the concept that surface-level recovery coexists with deeper vascular damage [S2]. S1 shows in mouse kidneys that microvascular endothelial-cell rarefaction persists after acute kidney injury and increases the likelihood of recurrence, supporting the idea that apparent renal recovery does not eliminate structural small-vessel loss [S1]. However, no source in the set tracks a patient or animal from injury through apparent recovery and then measures reserve capacity at the moment of a second insult. The 'timing mismatch' half of the premise — that recurrent deficits might reflect reversible dyssynchrony rather than structural thinning — is not addressed by any source read.S1S2
The same question asked without the part nothing read establishes:
- After microvascular injury, does measured reserve capacity decline cumulatively with each subsequent insult, or does it return to baseline between episodes?
- In organs that appear functionally recovered after small-vessel injury, what is the trajectory of coronary or renal flow reserve over repeated stress episodes?
- Is microvascular rarefaction after ischaemic injury progressive and dose-dependent, or does a plateau of structural loss set in after the first event?
- Permanent reserve loss accumulates with each insult Each episode of apparent recovery leaves fewer recruitable capillaries, so the ceiling for safe demand drops with every cycle. A patient cleared for rehabilitation or repeat surgery on the basis of normal resting function would in fact be closer to the threshold of ischaemic injury than before, and the next high-demand episode would damage tissue that the previous round's reduced reserve could no longer protect. Rehabilitation protocols and re-intervention timing would need to be calibrated to measured reserve, not resting function.
- Recurrent deficits are reversible coordination failures The microvascular bed is structurally intact but its dilation timing is transiently disordered — different segments open out of phase, producing patchy under-perfusion that mimics rarefaction on flow-reserve testing. Because the vessels still exist, the mismatch resolves as local signalling recalibrates, and no cumulative loss accrues. In this case, restricting activity to protect a reserve that is not actually shrinking would impose unnecessary disability, and the clinical priority shifts to managing the transient dyssynchrony rather than preventing structural attrition.
- Both mechanisms coexist, ratio varies by tissue and insult severity Some fraction of the deficit after each episode is permanent structural rarefaction and some fraction is reversible timing mismatch, with the ratio depending on the organ, the severity of the original injury, and the interval before the next insult. Neither a purely structural nor a purely functional model would predict outcomes accurately, and clinical management would need to separate the two components — likely requiring longitudinal reserve measurement at multiple time points — before choosing between protective restriction and progressive loading.
If apparent recovery conceals permanent loss of microvascular reserve, then every subsequent episode of high demand — exercise, fever, surgical stress, a second ischaemic event — draws on a smaller buffer than the last, and each draw erodes it further. Clinicians who see normal resting function and clear the patient for activity would be sending them into a structural trap. If, on the other hand, recurrent deficits are coordination failures that self-correct, the risk profile reverses: restricting activity to protect a reserve that is not actually shrinking would impose unnecessary disability. The entire strategy for repeat stress testing, rehabilitation intensity, and re-intervention timing depends on which mechanism dominates.
The mechanism it proposes
The engine's own statement of the hypothesis, in full.
SCOUT 2: Intracellular population dynamics progressively concentrate deletion-bearing mitochondrial genomes in focal segments of retained muscle fibers. Ordinary performance is maintained by recruiting unaffected segments and motor units, concealing loss of oxidative reserve. Recurrent stresses expose these pre-existing energetic bottlenecks, while long-term clonal expansion makes later replacement-enabled demand increasingly unsafe. The stored state is the spatial distribution of mitochondrial heteroplasmy, not microvascular damage or reversible timing. Preserving oxidative capacity in the retained compartment stabilizes SPV_6.
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.
Persistent challenge intolerance localizes to fiber segments with high deletion heteroplasmy, respiratory-chain deficiency, and reduced maximal respiration even under saturating ex vivo oxygen and substrate supply. Deficits persist after circadian alignment, cue extinction, and normalization of phosphate-dependent calcium release. Spatial mutant burden predicts later output intolerance beyond perfusion measures. Normal intrinsic respiration in affected regions argues against this hypothesis.
Would tell it apart from at least one rival. The prediction specifies observable spatial associations, persistent deficits under stated conditions, and an explicit rejection condition. No rival prediction was 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.
Laser-capture sampling, deletion sequencing, respiratory-chain staining, and permeabilized-fiber respirometry can test spatial genotype-function correspondence. Sampling error is substantial because lesions are focal; negative bulk sequencing is not a decisive test.
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: Rapid and efficient labeling by a selective organic fluorophore probe highlights heterogeneity of mycobacterial populations and persister resuscitation.; Effect of Postbiotics Derived from <i>Lactobacillus rhamnosus</i> PB01 (DSM 14870) on Sperm Quality: A Prospective In Vitro Study.; Localization of the epileptogenic network from scalp EEG using a patient-specific whole-brain model..
7 papers retrieved around this hypothesis
- Rapid and efficient labeling by a selective organic fluorophore probe highlights heterogeneity of mycobacterial populations and persister resuscitation.PMID 41411265 · full_text · 82,410 characters stored
- Eye Darkening Under Dehydration Stress in the Neotropical Frog Boana punctata (Schneider, 1799).PMID 42504469 · full_text · 31,565 characters stored
- Primary trabecular bone formation in vitro by the OmGFP66 osteogenic cell line: Multiscale symmetry breaking and characterization in 3D.PMID 41436000 · full_text · 94,926 characters stored
- Localization of the epileptogenic network from scalp EEG using a patient-specific whole-brain model.PMID 40161993 · full_text · 68,127 characters stored
- Effect of Postbiotics Derived from <i>Lactobacillus rhamnosus</i> PB01 (DSM 14870) on Sperm Quality: A Prospective In Vitro Study.PMID 38892713 · full_text · 59,774 characters stored
- On Levodopa Interactions with Brain Disease Amyloidogenic Proteins at the Nanoscale.PMID 40256523 · full_text · 45,691 characters stored
- On Levodopa Interactions with Brain Disease Amyloidogenic Proteins at the Nanoscale.PMID 40256523 · full_text · 45,653 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.