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PubMed2005

Phosphoproteomics for oncology discovery and treatment.

Reversible protein phosphorylation is one of the most important forms of cellular regulation. For this reason, phosphoproteomic analysis of protein phosphorylation in cells is a powerful tool for evaluating the functional status of cells. The importance of protein kinase-regulated signal transduction pathways in human cancer has led to the development of drugs that inhibit protein kinases at the apex or intermediary levels of these pathways. Phosphoproteomic analysis of these signalling pathways will provide important insights into the operation and connectivity of these pathways that will facilitate the identification of the best targets for cancer therapies. Moreover, phosphoproteomic analysis of individual tumours will help match targeted cancer drugs to the appropriate patients.

Antineoplastic Agents↗

PubMed1992

Secretory pathway function in Saccharomyces cerevisiae.

A genetic analysis of secretory pathway function in yeast was initiated some 12 years ago in the laboratory of Randy Schekman. These mutants held great promise in terms of providing an experimental system with which molecular participants of secretory pathway function could be investigated. This early promise has not failed. For the last five years, analysis of yeast secretory pathway function has been at the cutting edge of our understanding of the mechanisms by which proteins travel between intracellular compartments. In some cases, Sacch. cerevisiae has provided a valuable in vivo corroboration of the concepts derived from biochemical studies of mammalian intercompartmental protein transport in vitro. In other cases, studies conducted in the yeast system have defined previously unanticipated involvements for known catalytic activities in the secretory process. It is clear that yeast will continue to play a major role in setting the pace of research directed towards a detailed molecular understanding of protein secretion. Since it is now apparent that the basic strategies that underlie secretory pathway function have been conserved among eukaryotes, further exploitation of the powerful and complementary yeast and mammalian experimental systems guarantees that the next decade will see even greater progress towards our understanding of protein secretion in eukaryotic cells than did the first.

Biological Transport↗

PubMed1995

Comet assay analysis of repair of DNA strand breaks in normal and deficient human cells exposed to radiations and chemicals. Evidence for a repair pathway specificity of DNA ligation.

The induction and resealing of DNA strand breaks in a cell line with a proven defect in DNA ligase I, 46BR, and in two Bloom's syndrome cell lines, YBL6 and GM 1492, were compared to those observed in normal human 1BR/3 fibroblasts after treatment with a variety of genotoxic agents whose lesions are processed by different repair pathways. This analysis was performed using the single-cell gel electrophoresis assay. The three types of cells were found to have similar capabilities to recognize and incise ultraviolet photoproducts and also demonstrated similar amounts of DNA breaks immediately after gamma irradiation. During post-treatment incubation, 46BR cells showed a marked DNA re-ligation defect after ultraviolet radiation damage, GM 1492 cells demonstrated a highly reduced DNA joining ability after relatively high doses of ultraviolet radiation, and YBL6 cells were particularly affected in DNA re-ligation after damage by 4-nitroquinoline-1-oxide. The two Bloom's syndrome cell lines and 46BR cells had a nearly normal ability to reseal breaks resulting from gamma irradiation or treatment with xanthine plus xanthine oxidase. These findings suggest that different DNA ligases may be involved in different DNA repair pathways in human cells.

4-Nitroquinoline-1-oxide↗

PubMed2006

Analysis of bridge-mediated pathways for long-range charge transfer systems.

With the density matrix decomposition scheme of the path integral method, an accurate quantitative analysis on bridge-mediated pathways in long-range charge transfer processes is presented. Unlike a donor-bridge-acceptor triad, a long-range charge transfer process with a number of bridges has additional pathways in which charges always migrate through bridges but not necessarily by incoherent nearest-neighbor hopping. By employing the density matrix decomposition and sorting the incoherent nearest-neighbor and the coherent next-nearest-neighbor hopping pathways, respective contributions to the charge transfer are evaluated quantitatively. Numerical results of two series of configurations with varying degrees of coherence within the system have found that, depending on the configuration, the contribution of the coherent pathways other than superexchange pathways is significant. In the presence of the coherence, long-range charge transfer dynamics may be dominated by the through-bridge mechanism that consists of the coherent through-bridge pathways as well as the incoherent nearest-neighbor hopping pathways.

Letter↗

PubMed2026

Epigenetic alterations of AKT1 orchestrate a metabolic reprogramming in advanced lipedema: translational insights from an integrated multi-omics study.

BACKGROUND: lipedema is a chronic, progressive adipose disorder predominantly affecting women, characterized by painful, symmetrical subcutaneous fat accumulation, and typically resistant to lifestyle interventions. The pathophysiology of advanced-stage lipedema remains poorly defined, and no validated biomarkers or targeted therapies are currently available. METHODS: in this observational study, we applied a comprehensive multi-omics approach to dissect the molecular and metabolic alterations underlying late-stage lipedema. RESULTS: Genome-wide DNA methylation profiling identified over 5,000 differentially methylated CpG sites affecting genes involved in receptor tyrosine kinase signaling, phospho-metabolism, and immune pathways. Transcriptomic analysis revealed profound downregulation of mitochondrial functions, including oxidative phosphorylation, the TCA cycle, and fatty acid β-oxidation, alongside disruption of the sirtuin pathway and extracellular matrix remodeling. Integrative analysis pinpointed AKT1 as a central regulatory node: its promoter region was hypomethylated, correlating with increased gene expression and protein phosphorylation. Metabolomic profiling confirmed AKT1-linked metabolic dysregulation, including altered levels of L-arginine, NADP+, ATP, guanosine, glycerol, and glutamate, indicating impaired redox balance and energy metabolism. Trans-omic network analysis positioned AKT1 at the intersection of multiple dysregulated pathways, suggesting its key role in advanced-stage lipedema. CONCLUSIONS: the consistent enhancing of AKT pathway signaling across omic layers highlights its potential not only as a biomarker for disease stratification but also as a putative druggable target for therapeutic intervention. These findings offer new mechanistic insights into lipedema pathophysiology and provide a rationale for future personalized treatment strategies guided by AKT1-centric molecular profiling.

Proto-Oncogene Proteins c-akt↗

PubMed2006

Reconstruction and in silico analysis of the MAPK signaling pathways in the human blood fluke, Schistosoma japonicum.

At present, little is known about signal transduction mechanisms in schistosomes, which cause the disease of schistosomiasis. The mitogen-activated protein kinase (MAPK) signaling pathways, which are evolutionarily conserved from yeast to Homo sapiens, play key roles in multiple cellular processes. Here, we reconstructed the hypothetical MAPK signaling pathways in Schistosoma japonicum and compared the schistosome pathways with those of model eukaryote species. We identified 60 homologous components in the S. japonciumMAPK signaling pathways. Among these, 27 were predicted to be full-length sequences. Phylogenetic analysis of these proteins confirmed the evolutionary conservation of the MAPK signaling pathways. Remarkably, we identified S. japonicum homologues of GTP-binding protein beta and alpha-I subunits in the yeast mating pathway, which might be involved in the regulation of different life stages and female sexual maturation processes as well in schistosomes. In addition, several pathway member genes, including ERK, JNK, Sja-DSP, MRAS and RAS, were determined through quantitative PCR analysis to be expressed in a stage-specific manner, with ERK, JNK and their inhibitor Sja-DSP markedly upregulated in adult female schistosomes.

Amino Acid Sequence↗

PubMed2026

Multi-omics profiling of cerebrospinal fluid in autoimmune encephalitis: insights into pathogenesis and therapeutic targets.

BACKGROUND: Autoimmune encephalitis (AIE) is a rare, severe inflammatory brain disease, with its pathogenesis not yet fully elucidated. This study aimed to characterize proteomic and metabolomic alterations in the cerebrospinal fluid (CSF) of AIE patients and identify potential therapeutic targets. METHODS: 65 consecutive AIE patients and age-matched concurrent controls were enrolled, respectively. Clinical characteristics, including blood and CSF laboratory findings, were compared between the two groups, and CSF samples were collected for multi-omics analysis. Differentially expressed proteins (DEPs) and metabolites (DEMs) between AIE patients and controls were identified using data-independent acquisition-based proteomics and targeted liquid chromatography-mass spectrometry-based metabolomics, followed by integrated multi-omics analysis. RESULTS: Compared with controls, AIE patients had lower levels of triglyceride and C1q, but higher HDL-CH levels, neutrophil counts, and eosinophil counts in blood. CSF leukocyte, erythrocyte, lymphocyte, and mononuclear cell counts were also elevated in AIE patients. Proteomic analysis identified 163 DEPs, with enrichment of 87 canonical pathways primarily associated with immune-inflammatory responses, neuronal-synaptic dysfunction, and cell signaling and metabolic pathways. Metabolomic analysis recognized 21 DEMs, predominantly amino acids, lipids, and carbohydrates, which were involved in lipid-carbohydrate metabolism and immune regulation. Integrated multi-omics analysis validated these findings and identified several potential therapeutic targets for AIE, including the IL6-STAT3 axis. CONCLUSIONS: Integrated multi-omics analysis systematically delineates cellular and molecular alterations underlying AIE. Immune-inflammatory response and lipid metabolism are pivotal in AIE progression and the IL6-STAT3 axis holds promise as a potential therapeutic target.

Humans↗

PubMed1995

sli-1, a negative regulator of let-23-mediated signaling in C. elegans.

By screening for suppressors of hypomorphic mutations of let-23, a receptor tyrosine kinase necessary for vulval induction in Caenorhabditis elegans, we recovered > or = 12 mutations defining the sli-1 (suppressor of lineage defect) locus. sli-1 mutations suppress four of five phenotypes associated with hypomorphic alleles of let-23 but do not suppress let-23 null alleles. Thus, a sli-1 mutation does not bypass the requirement for functional let-23 but rather allows more potent LET-23-dependent signaling. Mutations at the sli-1 locus are otherwise silent with respect to vulval differentiation and cause only a low-penetrance abnormal head phenotype. Mutations at sli-1 also suppress the vulval defects but not other defects associated with mutations of sem-5, whose product likely interacts with LET-23 protein during vulval induction. Mutations at sli-1 suppress lin-2, lin-7 and lin-10 mutations but only partially suppress lin-3 and let-60 mutations and do not suppress a lin-45 mutation. The sli-1 locus displays dosage sensitivity: severe reduction of function alleles of sli-1 are semidominant suppressors; a duplication of the sli-1(+) region enhances the vulvaless phenotype of hypomorphic mutations of let-23. We propose that sli-1 is a negative regulator that acts at or near the LET-23-mediated step of the vulval induction pathway. Our analysis suggests that let-23 can activate distinct signaling pathways in different tissues: one pathway is required for vulval induction; another pathway is involved in hermaphrodite fertility and is not regulated by sli-1.

Alleles↗

PubMed2026

Study on the mechanism of SW inhibiting testosterone synthesis in mouse Leydig cells.

BACKGROUND: Swainsonine (SW), the main toxic component of locoweed, can cause livestock poisoning and reproductive damage in male animals; however, the mechanism by which it affects testosterone secretion remains unclear. METHODS: Ten-week-old male C57BL/6 mice were orally administered SW at doses of 0, 0.05, and 0.25 mg/(kg·d) for 28 days. TM3 mouse Leydig cells were treated with SW at concentrations of 0, 1, and 10 nM for 24 h. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was performed on RNA-seq data from mouse testicular tissues to identify differentially enriched pathways between the control and SW-treated groups. Testosterone secretion levels were measured using an enzyme-linked immunosorbent assay (ELISA). The mRNA expression levels of steroidogenesis-related genes (StAR, Cyp11a1, Hsd3b2, and Hsd17b3) were detected by qPCR, while the expression of the steroidogenic acute regulatory (STAR) protein was detected by western blotting. AutoDock Vina molecular docking was used to predict the binding affinity between SW and the STAR protein. RESULTS: KEGG analysis revealed a significant enrichment of pathways related to steroid synthesis. In both the mouse model and TM3 cells, SW significantly inhibited testosterone secretion, downregulated the mRNA expression of StAR, Cyp11a1, Hsd3b2, and Hsd17b3, and reduced the protein expression of STAR. Molecular docking analysis revealed multiple potential hydrogen-bond interaction sites between SW and STAR. CONCLUSION: SW downregulates the expression of steroidogenesis-related genes and STAR protein, thereby suppressing testosterone secretion in male mice and TM3 cells.

Swainsonine↗

PubMed2002

Integrated care pathways for vascular surgery: an analysis of the first 18 months.

OBJECTIVES: A review of the use of previously described integrated care pathways (ICPs) established for three elective vascular surgical procedures. DESIGN: A retrospective analysis of information gathered prospectively over an initial 18 month period of use of vascular surgical ICPs. SUBJECT: Patients admitted to a single vascular unit for "open" repair of abdominal aortic aneurysm (AAA), carotid endarterectomy, or femoropopliteal bypass grafting. METHODS: An analysis of variance data, length of stay, and costings after the use of ICPs, compared with previous clinical practice. RESULTS: Variance data were gathered for each of the three procedures. Variances of medication prescribing and delays in discharge were common to all procedures. In particular: (i) gastrointestinal complications were more specific to AAA repair and (ii) wound drains were removed a day later than originally proposed after femoropopliteal bypass. Overall, improved efficiency due to use of ICPs reduced the length of stay for all procedures, which was reflected in a potential cost saving of some 25%. CONCLUSION: There are clear benefits to the use of ICPs, resulting in more structured, efficient, and cost effective patient care. Recommended changes to current practice based on variance analysis will require continued audit to sustain this "evidence based" approach.

Aortic Aneurysm, Abdominal↗

PubMed2025

Bioinformatics analysis of miR-2861 and miR-5011-5p that function as potential tumor suppressors in colorectal carcinogenesis.

BACKGROUND: The study aimed to was to investigate the relationship between miR-2861, miR-5011-5p, and colorectal carcinogenesis. METHOD: In the present study, it was isolated RNA from both the tumor and non-tumor tissue of a total of 80 CRC patients and after synthesizing the cDNA, it was performed qRT-PCR to determine the expression levels of miR‑2861 and miR‑5011-5p. In addition, it was predicted that dysregulated miRNAs targets, pathways and functional gene annotations that may be important in colorectal carcinogenesis using KEGG pathway and GO analysis. RESULTS: The resulting data revealed that both expression levels of miR-2861 and miR-5011-5p were significantly decreased in tumor tissues compared with non-tumor tissues of CRC patients. The GO and KEGG pathway analysis showed that miR-2861 and miR-5011-5p may participate in multiple the biological process, cellular components, and molecular function subcategories such as mitotic cell cycle, regulation of small GTPase mediated signal transduction, cell death, and acid binding transcription factor activity. It was also revealed that target genes of miRNAs can be found in signaling pathways such as TGF-beta, Rap1, Ras, cAMP, Wnt, mTOR and, PI3K-Akt signaling pathways. CONCLUSION: These findings imply that miR-2861 and miR-5011-5p might function as tumor suppressors in the development of CRC.

MicroRNAs↗

PubMed2007

Rheumatoid arthritis subtypes identified by genomic profiling of peripheral blood cells: assignment of a type I interferon signature in a subpopulation of patients.

BACKGROUND: Rheumatoid arthritis (RA) is a heterogeneous disease with unknown cause. AIM: To identify peripheral blood (PB) gene expression profiles that may distinguish RA subtypes. METHODS: Large-scale expression profiling by cDNA microarrays was performed on PB from 35 patients and 15 healthy individuals. Differential gene expression was analysed by significance analysis of microarrays (SAM), followed by gene ontology analysis of the significant genes. Gene set enrichment analysis was applied to identify pathways relevant to disease. RESULTS: A substantially raised expression of a spectrum of genes involved in immune defence was found in the PB of patients with RA compared with healthy individuals. SAM analysis revealed a highly significant elevated expression of interferon (IFN) type I regulated genes in patients with RA compared with healthy individuals, which was confirmed by gene ontology and pathway analysis, suggesting that this pathway was activated systemically in RA. A quantitative analysis revealed that increased expression of IFN-response genes was characteristic of approximately half of the patients (IFN(high) patients). Application of pathway analysis revealed that the IFN(high) group was largely different from the controls, with evidence for upregulated pathways involved in coagulation and complement cascades, and fatty acid metabolism, while the IFN(low) group was similar to the controls. CONCLUSION: The IFN type I signature defines a subgroup of patients with RA, with a distinct biomolecular phenotype, characterised by increased activity of the innate defence system, coagulation and complement cascades, and fatty acid metabolism.

Adult↗

PubMed2007

Unified structural equation modeling approach for the analysis of multisubject, multivariate functional MRI data.

The ultimate goal of brain connectivity studies is to propose, test, modify, and compare certain directional brain pathways. Path analysis or structural equation modeling (SEM) is an ideal statistical method for such studies. In this work, we propose a two-stage unified SEM plus GLM (General Linear Model) approach for the analysis of multisubject, multivariate functional magnetic resonance imaging (fMRI) time series data with subject-level covariates. In Stage 1, we analyze the fMRI multivariate time series for each subject individually via a unified SEM model by combining longitudinal pathways represented by a multivariate autoregressive (MAR) model, and contemporaneous pathways represented by a conventional SEM. In Stage 2, the resulting subject-level path coefficients are merged with subject-level covariates such as gender, age, IQ, etc., to examine the impact of these covariates on effective connectivity via a GLM. Our approach is exemplified via the analysis of an fMRI visual attention experiment. Furthermore, the significant path network from the unified SEM analysis is compared to that from a conventional SEM analysis without incorporating the longitudinal information as well as that from a Dynamic Causal Modeling (DCM) approach.

Attention↗

PubMed2004

Model reduction and analysis of robustness for the Wnt/beta-catenin signal transduction pathway.

We present a framework for model reduction of signal transduction networks. The methods are explained by considering a recent model for Wnt/beta-catenin signalling which plays an important regulatory role in cell development and oncogenesis. The procedure results in a reduction of system variables and parameters while maintaining the ability of the model to describe experimental data and to predict the in-vivo behaviour of the pathway. Using metabolic control analysis we quantified the response of the pathway towards random fluctuations of model parameters. This allows to characterise the robustness of the pathway against perturbations in stimulated and unstimulated states. We show that robustness depends on structural as well as kinetic properties of the pathway.

Animals↗

PubMed1993

Biochemical analysis of germination mutants to characterize germinant receptors of Bacillus subtilis 1604 spores.

Spores of Bacillus subtilis 1604 can be induced to germinate by incubation in L-Ala (the ALA pathway) or in a combination of beta-D-glucose (Glc), beta-fructose (Fru), L-Asn and K+ (the GFAK pathway). Biochemical analysis of the germination response of a gerA mutant deficient in the ALA pathway revealed that L-Ala can replace L-Asn in the GFAK pathway (the GFAlaK pathway). In contrast to the ALA pathway of both the wild-type and of a gerB mutant, the GFAlaK pathway was insensitive to D-Ala and showed the same overall inhibitor profile as the GFAK pathway of wild-type and gerA spores. It is deduced that a second L-Ala receptor with different characteristics to that functioning in the ALA pathway is present in wild-type spores. Analysis of the germination response of a gerB mutant showed that whilst the rate of ALA germination could be stimulated by Glc as well as by Fru in the presence of Glc, the spores could not germinate in GFAK. In addition, Glc and Fru were unable to reverse D-Ala inhibition of L-Ala germination which they do in the wild-type. Thus, in the gerB mutant, the L-Ala/L-Asn receptor in the GFAK pathway is defective. It is concluded that the germination receptors in the ALA and GFAK pathways can functionally interact with each other to initiate B. subtilis spore germination. This conclusion is discussed in relation to proposed models of triggering of spore germination.

Amino Acids↗

PubMed2025

Construction of cDNA library of Dalbergia odorifera induced by low temperature stress and screening of low temperature tolerant genes.

To systematically analyze the gene function of Dalbergia odorifera, the seedlings of D. odorifera were treated with low-temperature stress for 6 h. Total RNA was extracted from a mixture of seedling roots, stems, and leaves, and a low-temperature-induced D. odorifera yeast cDNA expression library was constructed. The library volume was 1.032 × 108 CFU, and the PCR (Polymerase Chain Reaction) identification of the library bacterial fluid showed that the amplification was around 1000 bp, with a single randomly distributed band, indicating that the library had been recombinantly inserted into the pYES2 vector. The GO (Gene Ontology) analysis showed that the library genes were mainly involved in metabolic and stress signaling pathways. The KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis showed that the genes were primarily related to energy and metabolic pathways. Twenty-one genes were screened or obtained at -20°C for low-temperature tolerance. In addition, the organ expression profiles of the candidate genes were analyzed based on RNA-seq data, and the expression profiles of the candidate genes under low-temperature stress were also examined. The construction of the yeast library provides genetic resources for the analysis of the mechanism of low-temperature tolerance of D. odorifera, which is important for comprehending and utilizing the genetic resources of D. odorifera.

Gene Library↗

PubMed2000

Clinical pathways--an evaluation of its impact on the quality of care in an acute care general hospital in Singapore.

A critical or clinical pathway defines the optimal care process, sequencing and timing of interventions by healthcare professionals for a particular diagnosis or procedure. It is a relatively new clinical process improvement tool that has been gaining popularity across hospitals and various healthcare organisations in many parts of the world. It is now slowly gaining momentum and popularity in Asia and Singapore. Clinical pathways are developed through collaborative efforts of clinicians, case managers, nurses, and other allied healthcare professionals with the aim of improving the quality of patient care, while minimising cost to the patient. Clinical pathways have been shown to reduce unnecessary variation in patient care, reduce delays in discharge through more efficient discharge planning, and improve the cost-effectiveness of clinical services. The approach and objectives of clinical pathways are consistent with those of total quality management (TQM) and continuous clinical quality improvement (CQI), and is essentially the application of these principles at the patient's bedside. However, despite the growing popularity of pathways, their impact on clinical outcomes and their clinical effectiveness remains largely untested and unproven through rigorous clinical trials. This paper begins with an overview of the nature of clinical pathways and the analysis of variances from the pathway, their benefits to the healthcare organisation, their application as a tool for CQI activities in direct relation to patient care, and their effectiveness in a variety of healthcare settings. The paper describes an evaluation of the impact of a clinical pathway on the quality of care for patients admitted for uncomplicated acute myocardial infarction (AMI) through an analysis of variances. The author carried out a one year evaluation of a clinical pathway on uncomplicated AMI in Changi General Hospital (CGH) to determine its effectiveness and impact on a defined set of outcomes. A before and after nonrandomized study of two groups of patients admitted to the Hospital for uncomplicated AMI was done. A total of 169 patients were managed on the clinical pathway compared to 100 patients in the control (historical comparison) group. Outcomes were compared between the two groups of patients. Restriction and matching of study subjects in both groups ensured that the patients selected were comparable in terms of severity of illness. The results showed that the patients on the clinical pathway and the comparison group were similar with respect to demographic variables, prevalence of risk factors and comorbidities. There was a statistically significant reduction in the average length of stay after implementation of the clinical pathway. This was achieved without any adverse effect on short term clinical outcomes such as in-hospital mortality, complication rate and morbidity. There were no significant difference in readmission rates at 6 months after discharge. The paper concludes that clinical pathways, implemented in the context of an acute care general hospital, is able to significantly improve care processes through better collaboration among healthcare professionals and improvements in work systems.

Analysis of Variance↗

PubMed2026

Is impulsivity simply a failure of self-control? Evidence based on multi-omics analyses of genomics, metabolomics and brain imaging.

High impulsivity-a hallmark of various adverse life outcomes such as substance abuse, impulsive buying, violence, and crime-has typically been considered as a failure of self-control. However, is impulsivity simply a failure of self-control? To address this issue, we employed multi-omics combined with brain imaging approach in a large-scale sample (Nbrain imaging=1524, Ngenomics=835, Nmetabolomics=946) to elucidate the relationship between impulsivity and self-control. Mendelian randomization showed a bidirectional association between impulsivity and self-control, suggesting that they influenced each other. Partial least squares analysis highlighted that self-control primarily implicates the frontal lobe regions (e.g., superior frontal gyrus), whereas impulsivity involves the amygdala, insula, and basal ganglia. The cerebellum, superior frontal gyrus, and middle frontal gyrus were identified as shared areas in impulsivity and self-control. Furthermore, gene-based association analysis identified heterochromatin protein 1 binding protein 3 as specifically related to impulsivity, while pathway enrichment analysis demonstrated that arginine and proline metabolism was a common metabolic pathway associated with both impulsivity and self-control. Overall findings demonstrate that impulsivity and self-control involve both shared and distinct brain regions, genetic and metabolic foundations. The brain imaging results suggest that impulsivity is related not only to self-control-related processes but also to the motivation to pursue rewards. Together, this large-scale integrative study firstly provides a side-by-side map of genomic, metabolic, and limbic-network signatures of impulsivity distinct from self-control, offering a foundation for mechanism-driven biomarker and intervention research in maladaptive impulsivity.

Impulsive Behavior↗