Life Sciences

184 items

American Journal of Respiratory and Critical Care Medicine Oct 1, 2026
Using an unbiased druggable-genome siRNA screen, this study identified ADAMTS14 as a regulator of YAP nuclear translocation; single-cell and spatial transcriptomics of IPF patient lungs localized ADAMTS14 to a CTHRC1-high myofibroblast population enriched in fibroblastic foci, and knockdown or knockout of ADAMTS14 in IPF patient-derived lung fibroblasts reduced pro-fibrotic, matrisome, and TGFβ-response gene expression; mechanistically, collagen V was identified as an ADAMTS14 substrate whose impaired processing shifted the COL1:COL5 ratio from about 50:1 to about 20:1, producing an unstable matrix with disorganized focal adhesions and reduced FAK-AKT signaling and force transmission.
Using an unbiased druggable-genome siRNA screen, this study identified ADAMTS14 as a regulator of YAP nuclear translocation; single-cell and spatial transcriptomics of IPF patient lungs localized ADAMTS14 to a CTHRC1-high myofibroblast population enriched in fibroblastic foci, and knockdown or knockout of ADAMTS14 in IPF patient-derived lung fibroblasts reduced pro-fibrotic, matrisome, and TGFβ-response gene expression; mechanistically, collagen V was identified as an ADAMTS14 substrate whose impaired processing shifted the COL1:COL5 ratio from about 50:1 to about 20:1, producing an unstable matrix with disorganized focal adhesions and reduced FAK-AKT signaling and force transmission.
ADAMTS14 cleaves collagen V to keep matrix stable; its loss weakens YAP nuclear translocation and IPF fibroblast activation
Using an unbiased druggable-genome siRNA screen, this study identified ADAMTS14 as a regulator of YAP nuclear translocation; single-cell and spatial transcriptomics of IPF patient lungs localized ADAMTS14 to a CTHRC1-high myofibroblast population enriched in fibroblastic foci, and knockdown or knockout of ADAMTS14 in IPF patient-derived lung fibroblasts reduced pro-fibrotic, matrisome, and TGFβ-response gene expression; mechanistically, collagen V was identified as an ADAMTS14 substrate whose impaired processing shifted the COL1:COL5 ratio from about 50:1 to about 20:1, producing an unstable matrix with disorganized focal adhesions and reduced FAK-AKT signaling and force transmission.
Using an unbiased druggable-genome siRNA screen, this study identified ADAMTS14 as a regulator of YAP nuclear translocation; single-cell and spatial transcriptomics of IPF patient lungs localized ADAMTS14 to a CTHRC1-high myofibroblast population enriched in fibroblastic foci, and knockdown or knockout of ADAMTS14 in IPF patient-derived lung fibroblasts reduced pro-fibrotic, matrisome, and TGFβ-response gene expression; mechanistically, collagen V was identified as an ADAMTS14 substrate whose impaired processing shifted the COL1:COL5 ratio from about 50:1 to about 20:1, producing an unstable matrix with disorganized focal adhesions and reduced FAK-AKT signaling and force transmission.
发表出处待核验 Oct 1, 2026
This review, using obsessive-compulsive disorder (OCD) as its example, surveys the advances and constraints of big data approaches to three questions—what causes the disorder, which treatments work best for whom, and how to widen access to evidence-based care—reporting that large-scale pooled data such as ENIGMA-OCD show some previously reported effects to be small but reproducible while others do not replicate at scale or appear to be medication effects, that the Global OCD Study harmonized methods across five international sites and recruited 250 unmedicated adults with OCD and 250 matched healthy volunteers and found relatively few case-control brain differences but more informative associations between specific brain and cognitive measures and OC clinical profiles, and that big data ar
This review, using obsessive-compulsive disorder (OCD) as its example, surveys the advances and constraints of big data approaches to three questions—what causes the disorder, which treatments work best for whom, and how to widen access to evidence-based care—reporting that large-scale pooled data such as ENIGMA-OCD show some previously reported effects to be small but reproducible while others do not replicate at scale or appear to be medication effects, that the Global OCD Study harmonized methods across five international sites and recruited 250 unmedicated adults with OCD and 250 matched healthy volunteers and found relatively few case-control brain differences but more informative associations between specific brain and cognitive measures and OC clinical profiles, and that big data ar
Using OCD as its example, a review argues that big data in psychiatry must separate etiology from pathophysiology and stay hypothesis-driven to answer a specific disorder's three core questions
This review, using obsessive-compulsive disorder (OCD) as its example, surveys the advances and constraints of big data approaches to three questions—what causes the disorder, which treatments work best for whom, and how to widen access to evidence-based care—reporting that large-scale pooled data such as ENIGMA-OCD show some previously reported effects to be small but reproducible while others do not replicate at scale or appear to be medication effects, that the Global OCD Study harmonized methods across five international sites and recruited 250 unmedicated adults with OCD and 250 matched healthy volunteers and found relatively few case-control brain differences but more informative associations between specific brain and cognitive measures and OC clinical profiles, and that big data ar
This review, using obsessive-compulsive disorder (OCD) as its example, surveys the advances and constraints of big data approaches to three questions—what causes the disorder, which treatments work best for whom, and how to widen access to evidence-based care—reporting that large-scale pooled data such as ENIGMA-OCD show some previously reported effects to be small but reproducible while others do not replicate at scale or appear to be medication effects, that the Global OCD Study harmonized methods across five international sites and recruited 250 unmedicated adults with OCD and 250 matched healthy volunteers and found relatively few case-control brain differences but more informative associations between specific brain and cognitive measures and OC clinical profiles, and that big data ar
American Journal of Respiratory Cell and Molecular Biology Oct 1, 2026
In 22 C57BL/6 mice (11 given triple oropharyngeal bleomycin at 0.25 mg/kg to induce pulmonary fibrosis and 11 given saline), respiratory-gated µCT was acquired at baseline and days 7, 14, and 21, a U-Net deep-learning algorithm segmented the lungs into left and right lobes that were further divided into apical and caudal regions using airway landmarks for four subregions, and regional volumes, aeration compartments, and ventilation maps were extracted; saline-treated mice showed stable metrics with minimal interanimal variability, whereas bleomycin-treated animals showed early and heterogeneous fibrotic changes with the apical regions most affected and the caudal-right region displaying a compensatory functional increase, so that µCT-based regional analysis detected localized dysfunction a
In 22 C57BL/6 mice (11 given triple oropharyngeal bleomycin at 0.25 mg/kg to induce pulmonary fibrosis and 11 given saline), respiratory-gated µCT was acquired at baseline and days 7, 14, and 21, a U-Net deep-learning algorithm segmented the lungs into left and right lobes that were further divided into apical and caudal regions using airway landmarks for four subregions, and regional volumes, aeration compartments, and ventilation maps were extracted; saline-treated mice showed stable metrics with minimal interanimal variability, whereas bleomycin-treated animals showed early and heterogeneous fibrotic changes with the apical regions most affected and the caudal-right region displaying a compensatory functional increase, so that µCT-based regional analysis detected localized dysfunction a
Four-region µCT analysis detects compensatory ventilation in the right caudal lobe of a mouse fibrosis model that whole-lung readouts miss
In 22 C57BL/6 mice (11 given triple oropharyngeal bleomycin at 0.25 mg/kg to induce pulmonary fibrosis and 11 given saline), respiratory-gated µCT was acquired at baseline and days 7, 14, and 21, a U-Net deep-learning algorithm segmented the lungs into left and right lobes that were further divided into apical and caudal regions using airway landmarks for four subregions, and regional volumes, aeration compartments, and ventilation maps were extracted; saline-treated mice showed stable metrics with minimal interanimal variability, whereas bleomycin-treated animals showed early and heterogeneous fibrotic changes with the apical regions most affected and the caudal-right region displaying a compensatory functional increase, so that µCT-based regional analysis detected localized dysfunction a
In 22 C57BL/6 mice (11 given triple oropharyngeal bleomycin at 0.25 mg/kg to induce pulmonary fibrosis and 11 given saline), respiratory-gated µCT was acquired at baseline and days 7, 14, and 21, a U-Net deep-learning algorithm segmented the lungs into left and right lobes that were further divided into apical and caudal regions using airway landmarks for four subregions, and regional volumes, aeration compartments, and ventilation maps were extracted; saline-treated mice showed stable metrics with minimal interanimal variability, whereas bleomycin-treated animals showed early and heterogeneous fibrotic changes with the apical regions most affected and the caudal-right region displaying a compensatory functional increase, so that µCT-based regional analysis detected localized dysfunction a
American Journal of Respiratory Cell and Molecular Biology Oct 1, 2026
Combining human cord blood monocytes with a neonatal mouse influenza model, this study found that neonatal monocytes sustain higher TLR2 expression after LTA or IAV stimulation, while TLR2 gene deletion, anti-TLR2 antibody blockade, or myeloid-specific TLR2 deletion improved survival of IAV-infected neonatal mice (for example, 61% versus 25% survival for TLR2−/− versus wild-type neonates, and 46% versus 7% with anti-TLR2 antibody), accompanied by reduced neutrophils at 6 days post-infection, lower histopathology scores in myeloid conditional knockouts, and no further rise in IL-6, TNF-α, MCP-1, CXCL1, and CXCL2 from 3 to 6 days post-infection, suggesting that myeloid TLR2 signaling exacerbates neonatal susceptibility to respiratory viral infection by amplifying pulmonary inflammation.
Combining human cord blood monocytes with a neonatal mouse influenza model, this study found that neonatal monocytes sustain higher TLR2 expression after LTA or IAV stimulation, while TLR2 gene deletion, anti-TLR2 antibody blockade, or myeloid-specific TLR2 deletion improved survival of IAV-infected neonatal mice (for example, 61% versus 25% survival for TLR2−/− versus wild-type neonates, and 46% versus 7% with anti-TLR2 antibody), accompanied by reduced neutrophils at 6 days post-infection, lower histopathology scores in myeloid conditional knockouts, and no further rise in IL-6, TNF-α, MCP-1, CXCL1, and CXCL2 from 3 to 6 days post-infection, suggesting that myeloid TLR2 signaling exacerbates neonatal susceptibility to respiratory viral infection by amplifying pulmonary inflammation.
Loss or blockade of myeloid TLR2 improves survival and reduces neutrophils and lung inflammation in influenza-infected neonatal mice
Combining human cord blood monocytes with a neonatal mouse influenza model, this study found that neonatal monocytes sustain higher TLR2 expression after LTA or IAV stimulation, while TLR2 gene deletion, anti-TLR2 antibody blockade, or myeloid-specific TLR2 deletion improved survival of IAV-infected neonatal mice (for example, 61% versus 25% survival for TLR2−/− versus wild-type neonates, and 46% versus 7% with anti-TLR2 antibody), accompanied by reduced neutrophils at 6 days post-infection, lower histopathology scores in myeloid conditional knockouts, and no further rise in IL-6, TNF-α, MCP-1, CXCL1, and CXCL2 from 3 to 6 days post-infection, suggesting that myeloid TLR2 signaling exacerbates neonatal susceptibility to respiratory viral infection by amplifying pulmonary inflammation.
Combining human cord blood monocytes with a neonatal mouse influenza model, this study found that neonatal monocytes sustain higher TLR2 expression after LTA or IAV stimulation, while TLR2 gene deletion, anti-TLR2 antibody blockade, or myeloid-specific TLR2 deletion improved survival of IAV-infected neonatal mice (for example, 61% versus 25% survival for TLR2−/− versus wild-type neonates, and 46% versus 7% with anti-TLR2 antibody), accompanied by reduced neutrophils at 6 days post-infection, lower histopathology scores in myeloid conditional knockouts, and no further rise in IL-6, TNF-α, MCP-1, CXCL1, and CXCL2 from 3 to 6 days post-infection, suggesting that myeloid TLR2 signaling exacerbates neonatal susceptibility to respiratory viral infection by amplifying pulmonary inflammation.
Diabetes Oct 1, 2026
In 24,638 UK Biobank participants with prediabetes, LASSO and elastic net selection of nuclear magnetic resonance metabolomic markers yielded 16 biomarkers, and k-means clustering in the training set (12,322 participants) identified low-, intermediate-, and high-metabolic-risk subtypes that showed progressively higher risks of type 2 diabetes, cardiovascular disease, and chronic kidney disease in the validation set (12,316 participants), with diet-quality associations differing across subtypes and Mendelian randomization suggesting potential causal links for several metabolomic biomarkers.
In 24,638 UK Biobank participants with prediabetes, LASSO and elastic net selection of nuclear magnetic resonance metabolomic markers yielded 16 biomarkers, and k-means clustering in the training set (12,322 participants) identified low-, intermediate-, and high-metabolic-risk subtypes that showed progressively higher risks of type 2 diabetes, cardiovascular disease, and chronic kidney disease in the validation set (12,316 participants), with diet-quality associations differing across subtypes and Mendelian randomization suggesting potential causal links for several metabolomic biomarkers.
Metabolomic clustering of 24,638 UK Biobank participants with prediabetes yields three subtypes with progressively higher type 2 diabetes, cardiovascular, and chronic kidney disease risk
In 24,638 UK Biobank participants with prediabetes, LASSO and elastic net selection of nuclear magnetic resonance metabolomic markers yielded 16 biomarkers, and k-means clustering in the training set (12,322 participants) identified low-, intermediate-, and high-metabolic-risk subtypes that showed progressively higher risks of type 2 diabetes, cardiovascular disease, and chronic kidney disease in the validation set (12,316 participants), with diet-quality associations differing across subtypes and Mendelian randomization suggesting potential causal links for several metabolomic biomarkers.
In 24,638 UK Biobank participants with prediabetes, LASSO and elastic net selection of nuclear magnetic resonance metabolomic markers yielded 16 biomarkers, and k-means clustering in the training set (12,322 participants) identified low-, intermediate-, and high-metabolic-risk subtypes that showed progressively higher risks of type 2 diabetes, cardiovascular disease, and chronic kidney disease in the validation set (12,316 participants), with diet-quality associations differing across subtypes and Mendelian randomization suggesting potential causal links for several metabolomic biomarkers.
American Journal of Respiratory Cell and Molecular Biology Oct 1, 2026
Saavedra and colleagues used CITE-seq to profile circulating CD3+ T cells from 18 adults with cystic fibrosis before and after starting elexacaftor-tezacaftor-ivacaftor (ETI), finding CFTR modulation induces transcriptional reprogramming most pronounced in CD4+ memory T cells (upregulation of PNP and MT1X, enrichment of mitochondrial metabolism and oxidative phosphorylation pathways, and decline in chromatin remodeling and inflammatory activation genes), while Seahorse metabolic flux analysis, splenocytes from CFTR F508del homozygous mice, and CRISPR-Cas9 knockdown of CFTR in primary human lymphocytes all show reduced oxygen consumption, glycolytic capacity, and ATP production in CF lymphocytes, and changes in CD4+ memory T cell gene expression correlate with FEV1 improvement and reduced h
Saavedra and colleagues used CITE-seq to profile circulating CD3+ T cells from 18 adults with cystic fibrosis before and after starting elexacaftor-tezacaftor-ivacaftor (ETI), finding CFTR modulation induces transcriptional reprogramming most pronounced in CD4+ memory T cells (upregulation of PNP and MT1X, enrichment of mitochondrial metabolism and oxidative phosphorylation pathways, and decline in chromatin remodeling and inflammatory activation genes), while Seahorse metabolic flux analysis, splenocytes from CFTR F508del homozygous mice, and CRISPR-Cas9 knockdown of CFTR in primary human lymphocytes all show reduced oxygen consumption, glycolytic capacity, and ATP production in CF lymphocytes, and changes in CD4+ memory T cell gene expression correlate with FEV1 improvement and reduced h
Saavedra et al. find that restoring CFTR with ETI shifts CD4+ memory T cells in CF toward oxidative metabolism, with metabolic gene changes linked to FEV1 improvement and fewer hospitalizations
Saavedra and colleagues used CITE-seq to profile circulating CD3+ T cells from 18 adults with cystic fibrosis before and after starting elexacaftor-tezacaftor-ivacaftor (ETI), finding CFTR modulation induces transcriptional reprogramming most pronounced in CD4+ memory T cells (upregulation of PNP and MT1X, enrichment of mitochondrial metabolism and oxidative phosphorylation pathways, and decline in chromatin remodeling and inflammatory activation genes), while Seahorse metabolic flux analysis, splenocytes from CFTR F508del homozygous mice, and CRISPR-Cas9 knockdown of CFTR in primary human lymphocytes all show reduced oxygen consumption, glycolytic capacity, and ATP production in CF lymphocytes, and changes in CD4+ memory T cell gene expression correlate with FEV1 improvement and reduced h
Saavedra and colleagues used CITE-seq to profile circulating CD3+ T cells from 18 adults with cystic fibrosis before and after starting elexacaftor-tezacaftor-ivacaftor (ETI), finding CFTR modulation induces transcriptional reprogramming most pronounced in CD4+ memory T cells (upregulation of PNP and MT1X, enrichment of mitochondrial metabolism and oxidative phosphorylation pathways, and decline in chromatin remodeling and inflammatory activation genes), while Seahorse metabolic flux analysis, splenocytes from CFTR F508del homozygous mice, and CRISPR-Cas9 knockdown of CFTR in primary human lymphocytes all show reduced oxygen consumption, glycolytic capacity, and ATP production in CF lymphocytes, and changes in CD4+ memory T cell gene expression correlate with FEV1 improvement and reduced h
American Journal of Respiratory and Critical Care Medicine Oct 1, 2026
Using a myeloid-specific Tsc2 deletion mouse model that recapitulates key features of human cardiac sarcoidosis, and integrating single-cell RNA sequencing, bioinformatic analyses, histopathology, in vitro functional studies in murine and human macrophages, and in vivo pharmacologic inhibition, the study found that constitutive mTORC1 activation induces a fibrogenic macrophage (FibMac) population in the heart characterized by Cd63, Spp1, Gpnmb, and Fabp5 expression and arising through a TGF-β-dependent monocyte-to-FibMac differentiation process, and identified MMP12 as a macrophage-intrinsic inducer and dominant effector of this program: recombinant MMP12 was sufficient to enforce fibrogenic differentiation, clustering, and epithelioid features in mouse and human macrophages, whereas selec
Using a myeloid-specific Tsc2 deletion mouse model that recapitulates key features of human cardiac sarcoidosis, and integrating single-cell RNA sequencing, bioinformatic analyses, histopathology, in vitro functional studies in murine and human macrophages, and in vivo pharmacologic inhibition, the study found that constitutive mTORC1 activation induces a fibrogenic macrophage (FibMac) population in the heart characterized by Cd63, Spp1, Gpnmb, and Fabp5 expression and arising through a TGF-β-dependent monocyte-to-FibMac differentiation process, and identified MMP12 as a macrophage-intrinsic inducer and dominant effector of this program: recombinant MMP12 was sufficient to enforce fibrogenic differentiation, clustering, and epithelioid features in mouse and human macrophages, whereas selec
MMP12 identified as a macrophage-intrinsic driver of fibrosis: its inhibition reduces myocardial fibrosis and improves cardiac conduction
Using a myeloid-specific Tsc2 deletion mouse model that recapitulates key features of human cardiac sarcoidosis, and integrating single-cell RNA sequencing, bioinformatic analyses, histopathology, in vitro functional studies in murine and human macrophages, and in vivo pharmacologic inhibition, the study found that constitutive mTORC1 activation induces a fibrogenic macrophage (FibMac) population in the heart characterized by Cd63, Spp1, Gpnmb, and Fabp5 expression and arising through a TGF-β-dependent monocyte-to-FibMac differentiation process, and identified MMP12 as a macrophage-intrinsic inducer and dominant effector of this program: recombinant MMP12 was sufficient to enforce fibrogenic differentiation, clustering, and epithelioid features in mouse and human macrophages, whereas selec
Using a myeloid-specific Tsc2 deletion mouse model that recapitulates key features of human cardiac sarcoidosis, and integrating single-cell RNA sequencing, bioinformatic analyses, histopathology, in vitro functional studies in murine and human macrophages, and in vivo pharmacologic inhibition, the study found that constitutive mTORC1 activation induces a fibrogenic macrophage (FibMac) population in the heart characterized by Cd63, Spp1, Gpnmb, and Fabp5 expression and arising through a TGF-β-dependent monocyte-to-FibMac differentiation process, and identified MMP12 as a macrophage-intrinsic inducer and dominant effector of this program: recombinant MMP12 was sufficient to enforce fibrogenic differentiation, clustering, and epithelioid features in mouse and human macrophages, whereas selec
Cancer Discovery Oct 1, 2026
The authors built MutationProjector, a graph-attention cancer-genome foundation model integrating eight molecular network types, pretrained by masked gene reconstruction on genetic alterations from 30,328 tumors across 10 solid cancer types, then transfer-learned with a random forest on small labeled cohorts; it stratified survival in immunotherapy response prediction with hazard ratios of 0.71 for bladder, 0.74 for lung and 0.59 for melanoma, reached HR = 0.43 in a cisplatin-treated bladder cohort, and proposed KMT2D and SMARCA4-STK11 as candidate biomarkers via attention analysis.
The authors built MutationProjector, a graph-attention cancer-genome foundation model integrating eight molecular network types, pretrained by masked gene reconstruction on genetic alterations from 30,328 tumors across 10 solid cancer types, then transfer-learned with a random forest on small labeled cohorts; it stratified survival in immunotherapy response prediction with hazard ratios of 0.71 for bladder, 0.74 for lung and 0.59 for melanoma, reached HR = 0.43 in a cisplatin-treated bladder cohort, and proposed KMT2D and SMARCA4-STK11 as candidate biomarkers via attention analysis.
MutationProjector, pretrained on 30,000+ tumor genomes, predicts immunotherapy response in bladder, lung and melanoma cancers and flags KMT2D and SMARCA4-STK11 as candidate biomarkers
The authors built MutationProjector, a graph-attention cancer-genome foundation model integrating eight molecular network types, pretrained by masked gene reconstruction on genetic alterations from 30,328 tumors across 10 solid cancer types, then transfer-learned with a random forest on small labeled cohorts; it stratified survival in immunotherapy response prediction with hazard ratios of 0.71 for bladder, 0.74 for lung and 0.59 for melanoma, reached HR = 0.43 in a cisplatin-treated bladder cohort, and proposed KMT2D and SMARCA4-STK11 as candidate biomarkers via attention analysis.
The authors built MutationProjector, a graph-attention cancer-genome foundation model integrating eight molecular network types, pretrained by masked gene reconstruction on genetic alterations from 30,328 tumors across 10 solid cancer types, then transfer-learned with a random forest on small labeled cohorts; it stratified survival in immunotherapy response prediction with hazard ratios of 0.71 for bladder, 0.74 for lung and 0.59 for melanoma, reached HR = 0.43 in a cisplatin-treated bladder cohort, and proposed KMT2D and SMARCA4-STK11 as candidate biomarkers via attention analysis.
发表出处待核验 Oct 1, 2026
This review spans seven areas—community and register-based surveys, cohort and biobank studies, electronic health records, digital phenotyping, brain imaging, genomics and other -omics, and randomized controlled trials—to assess the advances, constraints and future directions of big data in psychiatry, concluding that big data has fostered transdisciplinarity and illuminated the intricacy, heterogeneity and variability of mechanisms underlying psychiatric disorders, yet sample size alone does not guarantee more precise estimates and a gap remains between big data and clinical application, so future work must attend equally to data quality and methodological rigor, conceptual models, and clinical questions.
This review spans seven areas—community and register-based surveys, cohort and biobank studies, electronic health records, digital phenotyping, brain imaging, genomics and other -omics, and randomized controlled trials—to assess the advances, constraints and future directions of big data in psychiatry, concluding that big data has fostered transdisciplinarity and illuminated the intricacy, heterogeneity and variability of mechanisms underlying psychiatric disorders, yet sample size alone does not guarantee more precise estimates and a gap remains between big data and clinical application, so future work must attend equally to data quality and methodological rigor, conceptual models, and clinical questions.
A cross-field review of seven psychiatric research areas finds big data yields mechanistic insight and transdisciplinary collaboration, but sample size alone does not guarantee more precise estimates and a translational gap remains
This review spans seven areas—community and register-based surveys, cohort and biobank studies, electronic health records, digital phenotyping, brain imaging, genomics and other -omics, and randomized controlled trials—to assess the advances, constraints and future directions of big data in psychiatry, concluding that big data has fostered transdisciplinarity and illuminated the intricacy, heterogeneity and variability of mechanisms underlying psychiatric disorders, yet sample size alone does not guarantee more precise estimates and a gap remains between big data and clinical application, so future work must attend equally to data quality and methodological rigor, conceptual models, and clinical questions.
This review spans seven areas—community and register-based surveys, cohort and biobank studies, electronic health records, digital phenotyping, brain imaging, genomics and other -omics, and randomized controlled trials—to assess the advances, constraints and future directions of big data in psychiatry, concluding that big data has fostered transdisciplinarity and illuminated the intricacy, heterogeneity and variability of mechanisms underlying psychiatric disorders, yet sample size alone does not guarantee more precise estimates and a gap remains between big data and clinical application, so future work must attend equally to data quality and methodological rigor, conceptual models, and clinical questions.
arXiv Oct 1, 2026
TERRA presents an end-to-end pipeline that, from scene-less kinematic trajectories alone, combines terrain priors, estimated contacts and negative free-space evidence to recover task-relevant support geometry, adds anatomical, tendon-continuity and contact constraints during retargeting, and uses motion-terrain pairs from five datasets to train a single muscle-actuated control policy, improving terrain accuracy, sharply reducing anatomical and interaction violations, and achieving the highest completion rate over supported terrain families across reconstruction, retargeting and held-out tracking benchmarks.
TERRA presents an end-to-end pipeline that, from scene-less kinematic trajectories alone, combines terrain priors, estimated contacts and negative free-space evidence to recover task-relevant support geometry, adds anatomical, tendon-continuity and contact constraints during retargeting, and uses motion-terrain pairs from five datasets to train a single muscle-actuated control policy, improving terrain accuracy, sharply reducing anatomical and interaction violations, and achieving the highest completion rate over supported terrain families across reconstruction, retargeting and held-out tracking benchmarks.
TERRA reconstructs terrain from kinematics alone, letting a muscle-actuated body complete stairs, ramps and seats
TERRA presents an end-to-end pipeline that, from scene-less kinematic trajectories alone, combines terrain priors, estimated contacts and negative free-space evidence to recover task-relevant support geometry, adds anatomical, tendon-continuity and contact constraints during retargeting, and uses motion-terrain pairs from five datasets to train a single muscle-actuated control policy, improving terrain accuracy, sharply reducing anatomical and interaction violations, and achieving the highest completion rate over supported terrain families across reconstruction, retargeting and held-out tracking benchmarks.
TERRA presents an end-to-end pipeline that, from scene-less kinematic trajectories alone, combines terrain priors, estimated contacts and negative free-space evidence to recover task-relevant support geometry, adds anatomical, tendon-continuity and contact constraints during retargeting, and uses motion-terrain pairs from five datasets to train a single muscle-actuated control policy, improving terrain accuracy, sharply reducing anatomical and interaction violations, and achieving the highest completion rate over supported terrain families across reconstruction, retargeting and held-out tracking benchmarks.

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