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Moldakozhayev, A.

Publications and source records attributed to Moldakozhayev, A..

3 recordsLinked to original sources

Causal Language Detection using Text-Document Features: Methodology and Insights from 10 Years of Gut Microbiome Research

Detecting causal language in scientific literature is critical for understanding how research fields frame evidence and inform interventions and policies, yet existing approaches commonly rely on manual annotation. The objective of this study was to evaluate four classifiers for detecting causal language and to apply the best-performing model to assess trends in microbiome research. Microbiome research, with its rapidly expanding observational literature, provides a relevant case study. We extracted Term Frequency-Inverse Document Frequency (TF-IDF) features from the last three sentences of available publication abstracts and trained four classifiers (L1- and L2-regularized logistic regression, Random Forest, and eXtreme Gradient Boosting) to detect causal language. A total of 475 sentences, as determined pragmatically based on annotation feasibility and observed stabilization of model performance, were manually labeled as causal or non-causal following established guidelines for systematic evaluation of causal language in observational health research. Of these, 75% of sentences were used for training and 25% for testing. L1-regularized logistic regression achieved the highest performance (accuracy 76%, F1 72%, prevalence detection accuracy 95%, sensitivity 72%, and specificity 80%) and was applied to 20,022 human gut microbiome abstracts published between 2015 and 2025 grouped into 20 thematic topics using structural topic modeling. Predicted causal language prevalence declined from 52% to 44% between 2015 and 2018, then rose to 51% by 2025, with notable variation across topics (range: 43.1-53.3%). Temporal trends differed across subfields, with increases in Metabolic disorders, Fecal microbiota transplantation, and decreases in Biomarkers and prediction, Antibiotic resistance, and In vitro fermentation. Analysis of influential words confirmed that causal meaning is primarily driven by verbs and modifiers lexically signaling change or intervention. The proposed approach for identifying causal claims in scientific abstracts enables systematic and automated, scalable assessment of how evidence is framed. Its application to the microbiome field highlighted heterogeneity in the reporting of causal relationships and informing the interpretation of microbiome findings for clinical and public health decision-making.

scientific communication and education↗

Rejuvenation of white adipose tissue in a longitudinal heterochronic transplantation model

Exposure to a younger system can induce organismal rejuvenation, yet whether all tissues can be rejuvenated and by what mechanisms remains understudied. We performed heterochronic and isochronic transplantation of subcutaneous white adipose tissue (WAT) between young and old mice and longitudinally tracked changes in biological age. Transplantation accelerated tissue aging, and the molecular age of grafts shifted toward that of the host. Most importantly, old WAT was rejuvenated in a young body. Epigenetic and transcriptomic clocks revealed a reduction of predicted age, accompanied by coordinated activation of canonical and previously unrecognized thermogenic pathways. Molecular rejuvenation was further supported by architectural changes toward a youthful state, including reduced lipid droplet size and decreased cellular heterogeneity. Mitochondrial abundance and morphology remained unchanged, while collagen deposition increased. These results demonstrate that WAT biological age is partially reversible and identify molecular and cellular features underlying its rejuvenation

systems biology↗

Transcriptomic Hallmarks of Mortality Reveal Universal and Specific Mechanisms of Aging, Chronic Disease, and Rejuvenation

Health is strongly affected by aging and lifespan-modulating interventions, but the molecular mechanisms of mortality regulation remain unclear. Here, we conducted an RNA-seq analysis of mice subjected to 20 compound treatments in the Interventions Testing Program (ITP). By integrating it with the data from over 4,000 rodent tissues representing aging and responses to genetic, pharmacological, and dietary interventions with established survival data, we developed robust multi-tissue transcriptomic biomarkers of mortality, capable of quantifying aging and change in lifespan in both short-lived and long-lived models. These tools were further extended to single-cell and human data, demonstrating common mechanisms of molecular aging across cell types and species. Via a network analysis, we identified and annotated 26 co-regulated modules of aging and longevity across tissues, and developed interpretable module-specific clocks that capture aging- and mortality-associated phenotypes of functional components, including, among others, inflammatory response, mitochondrial function, lipid metabolism, and extracellular matrix organization. These tools captured and characterized acceleration of biological age induced by progeria models and chronic diseases in rodents and humans. They also revealed rejuvenation induced by heterochronic parabiosis, early embryogenesis, and cellular reprogramming, highlighting universal signatures of mortality, shared across models of rejuvenation and age-related disease. They included Cdkn1a and Lgals3, whose human plasma levels further demonstrated a strong association with all-cause mortality, disease incidence and risk factors, such as obesity and hypertension. Overall, this study uncovers molecular hallmarks of mammalian mortality shared across organs, cell types, species and models of disease and rejuvenation, exposing fundamental mechanisms of aging and longevity.

systems biology↗