A decentralized science (DeSci) initiative leveraging advanced LLMs and blockchain technology to systematically audit scientific literature at scale.
The protocol has processed 40,318 papers and identified 3,544 potential issues, from simple arithmetic errors to complex methodological discrepancies. Each verification strengthens the foundation of scientific knowledge and advances our commitment to research integrity.
90M+
Published Worldwide
30s
Average Time per Paper
$0.30
Average Cost per Analysis
Active
API Available (Version: 0.0.1)
40,318
Papers Processed
1,257,755 Total Chunks
1,333
Total Papers Flagged
3,544
Issues Identified
Writing check
Found in 1,256 papers
They looked at medicines people take and compared how long people lived when they took them versus when they didn’t.
This study examined how taking certain common prescription drugs was associated with lifespan in a large database of UK adults, highlighting both potentially harmful and beneficial drugs.
Through a retrospective cohort analysis of UK Biobank data, a covariate-matched Cox proportional hazards model was applied to assess associations between 406 drugs and all-cause mortality, revealing predominantly negative effects but also several potentially protective agents.
Though the study employs a systematic matching strategy, residual confounding is likely because some control participants may also have had the same prescriptions, which can lead to underestimation or overestimation of true effects.
Scientists used a special friendly germ to help mice with two different brain diseases feel and move better.
An engineered probiotic strain expressing GLP-1 improved memory in an Alzheimer's-like mouse model and motor function in a Parkinson's-like mouse model by reducing inflammation and restoring gut microbiome balance.
Oral administration of an engineered Lactococcus lactis strain stably secreting GLP‑1 ameliorated neuroinflammation, modulated gut microbiota composition, and improved cognitive and motor phenotypes in LPS-induced and MPTP-induced murine models of Alzheimer’s and Parkinson’s disease, respectively.
No separate control group receiving only the base MG1363 strain was included, complicating attribution of effects specifically to the engineered GLP-1 expression.
Minor grammar and tense inconsistencies appear, but overall readability remains adequate.
This paper shows how a substance called Exendin-4 helps cells make more adiponectin, which can help fight diabetes.
This study demonstrates that the GLP-1 receptor agonist Exendin-4 enhances adiponectin expression and secretion by activating the Sirt1/Foxo-1 pathway in adipocytes.
Through in vitro and in vivo experiments, this research elucidates that Exendin-4 stimulates adiponectin production in adipocytes via the Sirt1/Foxo-1 axis, thereby providing mechanistic insight into Exendin-4’s insulin-sensitizing efficacy.
Minor typographical errors and inconsistent spelling of ‘Exendin-4’ appear in some instances.
They tested sweeteners in different drinks to see how these affect our bodies when we drink them with sugar.
This study investigated how non-nutritive sweeteners in water and in diet sodas influenced glucose and hormone responses in healthy adults when consumed before an oral glucose test.
Using a four-period crossover design in healthy adults, the authors found that combining sucralose and acesulfame-potassium in diet soda, but not in water, modestly enhanced GLP-1 responses to an oral glucose load, without significantly altering glycemia or gastric emptying.
Minor limitations include a lack of strict dietary and physical activity control and inattention to the effects of carbonation, though these do not invalidate the study’s overall approach.
Minor inconsistencies were noted in brand name references and LaTeX formatting artifacts.
They found that by stopping certain brain helper cells (called microglia) from becoming too active, fewer brain cells died in Alzheimer's disease models.
The researchers demonstrate that blocking microglial activation with a GLP-1R agonist (NLY01) reduces inflammation-driven astrocyte reactivity and protects neurons, improving memory and learning in Alzheimer’s mouse models.
By targeting upregulated GLP-1 receptors in microglia with the agonist NLY01, the authors suppress Aβ-driven microglial-induced reactive astrocyte conversion, providing neuroprotection and cognitive benefits in 5xFAD and 3xTg-AD mouse models.
There are minor spelling inconsistencies in referencing the drug name and a peptide name.
A DeSci initiative using blockchain technology and AI to audit science at scale. Our mission is to enhance scientific integrity through automated error detection.
Mathematical errors and data discrepancies in research can have far-reaching consequences. We help catch these issues early to maintain scientific integrity.
We've analyzed papers from leading repositories including arXiv, bioRxiv, and medRxiv, helping researchers identify and correct critical issues.