tbuckley/cabot-search huggingface dataset:
Distinct epigenetic and transcriptional profiles of Epstein-Barr virus (EBV) positive and negative primary CNS lymphomas
Authors: Ling Hai, Dennis Friedel, Felix Hinz, Dirk C Hoffmann, Sofia Doubrovinskaia, Hannah Rohdjess, Katharina Weidenauer, Evgeniya Denisova, Georg T Scheffler, Tobias Kessler, Alexandros Kourtesakis, Christel Herold-Mende, Octavian Henegariu, Joachim M Baehring, Jorg Dietrich, Benedikt Brors, Wolfgang Wick, Felix Sahm, Leon D Kaulen
Journal: Neuro-Oncology (2024)

Abstract Background Epstein-Barr virus (EBV)+ and EBV- primary CNS lymphomas (PCNSL) carry distinct mutational landscapes, but their transcriptional and epigenetic profiles have not been integrated and compared. This precludes further insights into pathobiology and molecular differences, relevant for classification and targeted therapy. Methods Twenty-three EBV- and 15 EBV+ PCNSL, histologically classified as diffuse large B-cell lymphomas, were subjected to RNA-sequencing and EPIC methylation arrays. Unsupervised clustering analyses were performed. Differentially expressed and differentially methylated genes were identified and integrated. Results Two distinct transcriptional clusters were found, which separated EBV- and EBV+ PCNSL (P &amp;lt; .0001). The EBV+ transcriptional signature contained genes (GPR15, FCER2/CD23, SLAMF1/CD150) closely regulated by EBV oncogenes in B cells. Pathway enrichment analysis uncovered enhanced B-cell receptor (BCR) and WNT/beta-catenin signaling in EBV- lymphomas, whereas Interleukin-10, NOTCH, and viral life cycle pathways were upregulated in EBV+ PCNSL. Correspondingly, BCR-associated SYK kinase activity was enriched in EBV- tumors while JAK2 was overrepresented in EBV+ PCNSL. Epigenetic profiling revealed reduced global promoter methylation in EBV+ PCNSL. Two methylation clusters were recognized, which separated EBV- and EBV+ PCNSL (P &amp;lt; .0001). Epigenetic profiles were distinct from 2,788 other brain tumor and nonmalignant reference samples. Promoter region hypermethylation of CD79B, a BCR subunit critical for sustained proliferation in EBV- disease, highly correlated (R = −0.7) with its transcriptional downregulation in EBV+ PCNSL. Conclusions EBV+ and EBV- PCNSL harbor distinct transcriptional and epigenetic profiles, corroborating them as distinctive biological subtypes. Uncovered differences provide novel insights into their pathobiology, may guide molecular diagnostics and targeted therapies.
Hyperthermic Intraperitoneal Chemotherapy in Platinum-Sensitive Recurrent Ovarian Cancer: A Randomized Trial on Survival Evaluation (HORSE; MITO-18)
Authors: Anna Fagotti, Barbara Costantini, Francesco Fanfani, Diana Giannarelli, Pierandrea De Iaco, Vito Chiantera, Vincenzo Mandato, Giorgio Giorda, Giovanni Aletti, Stefano Greggi, A. Myriam Perrone, Vanda Salutari, Rita Trozzi, Giovanni Scambia
Journal: Journal of Clinical Oncology (2024)

PURPOSE To investigate whether the addition of hyperthermic intraperitoneal chemotherapy (HIPEC) to secondary cytoreductive surgery (SCS) without neoadjuvant chemotherapy has a benefit on progression-free survival (PFS), as opposed to SCS alone in patients with platinum-sensitive recurrent epithelial ovarian cancer (platinum-free interval, &gt;6 months). METHODS This was a multicenter randomized phase III study. Random assignment was performed at the time of surgery in cases with residual tumor ≤0.25 cm. HIPEC with cisplatin (CDDP) 75 mg/m 2 for 60 minutes at 41.5°C was administered at the end of surgery in the experimental arm. Both groups received postoperative platinum-based chemotherapy. The primary end point was PFS. The safety profile and postrecurrence survival (PRS) were the secondary end points. RESULTS A total of 167 patients underwent random assignment, 82 patients to SCS plus HIPEC (experimental arm) and 85 to SCS alone (control arm). The median follow-up was 83 months (IQR, 64-102). The median PFS was 23 months (95% CI, 17 to 29) in the group that underwent surgery alone and 25 months (95% CI, 18 to 32) in the group that underwent cytoreductive surgery with HIPEC. The probability of PRS at 5 years was 61.6% (95% CI, 50.8 to 72.4) in the SCS group and 75.9% (95% CI, 66.5 to 85.3) in the SCS plus HIPEC group. The incidence of postoperative adverse events of any grade was similar between the two groups. CONCLUSION The addition of HIPEC to complete or nearly complete primary SCS did not confer a benefit in terms of PFS in patients with platinum-sensitive peritoneal recurrence.
Effectiveness of a Cardiovascular Health Electronic Health Record Application for Cancer Survivors in Community Oncology Practice: Results From WF-1804CD
Authors: Kathryn E. Weaver, Emily V. Dressler, Heidi D. Klepin, Simon C. Lee, Brian J. Wells, Sydney Smith, W. Gregory Hundley, Glenn J. Lesser, Chandylen L. Nightingale, Julie C. Turner, Ian Lackey, Kevin Heard, Randi Foraker, Kathryn E. Weaver, Randi Foraker, Emily V. Dressler, Brian Wells, W. Gregory Hundley, Heidi Klepin, Philip Payne, Albert Lai, Simon Craddock Lee, Glenn J. Lesser, Jay W. Carlson, Marcia L. Hernandez, Jenny Hanna, Heide Alexandra Rodgers, Sonia J. Varghese, Alyssa D. Throckmorton, Rajiv Panikkar, Paula Ronjon, Joshua Lukenbill, Ann Louise Stroh, Adedayo A. Onitilo, Lindsey W. Kulbacki, Khalid Matin, Mary Helen Hackney
Journal: Journal of Clinical Oncology (2024)

PURPOSE Guidelines recommend cardiovascular (CV) risk assessment and counseling for cancer survivors. This study evaluated the automated heart-health assessment (AH-HA) clinical decision support tool to promote provider-patient CV health (CVH) discussions in outpatient oncology. METHODS The AH-HA trial (WF-1804CD), coordinated by the Wake Forest National Cancer Institute Community Oncology Research Program Research Base, randomized practices to the AH-HA tool or usual care (UC) and enrolled survivors receiving routine care ≥6 months after curative cancer treatment. The tool displayed American Heart Association Life's Simple 7 CVH factors (BMI, physical activity, diet, smoking status, blood pressure, cholesterol, and glucose), populated from the electronic health record (EHR), alongside cancer treatments received with cardiotoxic potential. The primary end point was survivor-reported discussion of nonideal or missing CVH factors. A mixed-effects logistic regression model assessed the effect of AH-HA on CVH discussions, adjusting for practice. RESULTS Five UC and four AH-HA practices enrolled 645 survivors (82% breast, 8% endometrial, 5% colorectal, and 5% lymphoma, prostate, or multiple types) from October 1, 2020, to February 28, 2023. Most survivors were female (96%; 84% White/non-Hispanic, 8% Black; 3% Hispanic). Nearly all survivors (98%) in AH-HA practices reported a discussion for ≥1 nonideal or missing CVH factor compared with 55% in UC ( P &lt; .001). The average number of survivor-reported factors discussed was higher in AH-HA compared with UC (mean, 4.06 v 1.27; P &lt; .001), as were EHR-documented discussions (3.83 v 0.77; P = .03). Survivors in AH-HA practices were also significantly more likely to report a recommendation to see a primary care provider (39%) compared with UC practices (25%, P = .02). Reported recommendations to see a cardiologist were low (approximately 6%) and did not differ between groups. CONCLUSION The AH-HA tool was effective at promoting CVH discussions during routine follow-up care for survivors and recommendations to consult primary care.
Artificial daylight – the future for PDT in an uncertain climate?
Authors: Terence H Wong, Colin A Morton
Journal: British Journal of Dermatology (2024)

Journal Article Accepted manuscript Artificial daylight – the future for PDT in an uncertain climate? Get access Terence H Wong, Terence H Wong Department of Dermatology, Stirling Community Hospital, Stirling, UK Correspondence: Terence H. Wong, Email:terence.wong@nhs.scot https://orcid.org/0000-0002-3711-2976 Search for other works by this author on: Oxford Academic Google Scholar Colin A Morton Colin A Morton Department of Dermatology, Stirling Community Hospital, Stirling, UK https://orcid.org/0000-0002-4824-3090 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, ljae466, https://doi.org/10.1093/bjd/ljae466 Published: 22 November 2024 Article history Received: 19 November 2024 Accepted: 21 November 2024 Published: 22 November 2024
Skin microbiome dynamics in patients with polymorphic light eruption in response to UV radiations
Authors: Yacine Amar, Sebastian Niedermeier, Rafaela Silva, Susanne Kublik, Michael Schloter, Tilo Biedermann, Martin Köberle, Bernadette Eberlein
Journal: British Journal of Dermatology (2024)

Abstract Background Polymorphic light eruption (PLE) is the most frequent photodermatosis in Europe with an estimated prevalence of 10 to 20%, particularly in temperate climates. Itching or burning lesions appear only in sun-exposed areas, predominantly on the chest, the arms and forearms within a few hours following exposure. The disease’s cause is still unknown, yet studies have suggested that skin microbial elements may play a role in its pathogenesis. Objectives We investigated in this cohort the skin microbiome of PLE patients upon exposure to ultraviolet radiation (UVR), to assess its role in the onset of PLE lesions. Methods Forty-one skin swabs have been collected from eleven PLE patients at baseline and following a three-day exposure to UVR and from healthy controls. The collected swabs were analyzed for their microbial composition using a 16S amplicon sequencing approach. Results The PLE skin showed a dysbalanced microbiome, already at baseline, with significantly reduced microbial diversity and noticeable colonization by bacterial pathogens as Staphylococcus aureus. Upon UVR exposure, the PLE microbiome exhibited a further loss of diversity and decline of beneficial skin commensals. In line with this, we observed that UVR exerted strong antimicrobial effects in vitro against representative skin residents. Conclusions Taken together, UVR can lead to profound skin microbiome changes, allowing the proliferation of dysbiotic members that can release a variety of elements able to trigger PLE lesions. This is the first study investigating the cutaneous microbiome changes in PLE patients upon UVR, offering new insights into disease pathogenesis, so far unexplored.
The use and implementation of omalizumab as food allergy treatment: Consensus-based guidance and Work Group Report of the Adverse Reactions to Foods Committee of the American Academy of Allergy, Asthma &amp; Immunology
Authors: Aikaterini Anagnostou, J Andrew Bird, Sharon Chinthrajah, Timothy E Dribin, David M Fleischer, Edwin Kim, Anna Nowak-Wegrzyn, Rima Rachid, Marcus S Shaker, Wayne Shreffler, Scott Sicherer, Jonathan Tam, Brian P Vickery, Yamini V Virkud, Julie Wang, Michael Young, Matthew Greenhawt
Journal: Journal of Allergy and Clinical Immunology (2024)
Nuclear pore and nucleocytoplasmic transport impairment in oxidative stress-induced neurodegeneration: relevance to molecular mechanisms in Pathogenesis of Parkinson’s and other related neurodegenerative diseases
Authors: Zainab Riaz, Gabriel S. Richardson, Huajun Jin, Gary Zenitsky, Vellareddy Anantharam, Arthi Kanthasamy, Anumantha G. Kanthasamy
Journal: Molecular Neurodegeneration (2024)
LTBK-02. EVALUATION OF PAXALISIB IN GBM AGILE PHASE 3 REGISTRATION PLATFORM TRIAL FOR NEWLY DIAGNOSED AND RECURRENT GLIOBLASTOMA
Authors: Ingo K Mellinghoff, Timothy Cloughesy, Brian Alexander, Donald A Berry, Meredith Buxton, Webster Cavenee, Howard Colman, John de Groot, Benjamin M Ellingson, Gary B Gordon, Andrew B Lassman, Michael Lim, Mustafa Khasraw, James Perry, Erik P Sulman, Michael Weller, Patrick Wen, W K Alfred Yung, Nicholas Berry, Todd Graves, Michelle Detry, E M Viktoria Hyddmark, Adam Johnsson, Heather Kling, Anna McGlothlin, Ashley Powell, Sarah Untch, Elisa Aquilanti, Nicholas Blondin, Brian Boulmay, Macarena de la Fuente, Jan Drappatz, Justin Jordan, Thomas J Kaley, Mina Lobbous, Tom Mikkelsen, Herbert Newton, Scott Owen, Katherine Peters, David Schiff, Wendy Sherman, Shiao-Pei Weathers, Michael Youssef, John Friend, Eudocia Lee
Journal: Neuro-Oncology (2024)

Abstract GBM AGILE(NCT03970447) is a phase 2/3 Bayesian adaptive registration platform trial testing multiple therapies against a common control. Paxalisib, a PI3K/mTOR inhibitor, is the 3rd arm in the trial to conclude evaluation. METHODS Paxalisib was open to patients with newly diagnosed unmethylated (NDU) and recurrent (RD) glioblastoma, with three possible signatures: NDU, RD, and All(NDU+RD). Arm enrollment occurred Dec2020 through May2022. Control patients were enrolled from study initiation (July2019) and were treated with temozolomide(NDU) or lomustine(RD). GBM AGILE investigational arms have 1 or 2 stages, with adaptive randomization in stage 1 and fixed randomization if arms continue to stage 2. Efficacy is based on OS hazard ratio(HR) of Arm/Control. Efficacy goal is final Bayesian probability ≥ 98% for HR&amp;lt;1.00 in combined Stages. An Arm continues to Stage 2 if Bayesian predictive power (PP) ≥ 0.8. An Arm stops accruing in Stage 1 if it reaches maximal sample size(N) or does not meet a minimum efficacy threshold (PP&amp;lt;0.25 for all signatures when N&amp;gt;50). Clinical cut-off is 12 months after accrual stops. The maximum N for paxalisib was approximately 150(Stage 1) and 50(Stage 2). RESULTS After paxalisib reached &amp;gt;150 patients in Stage 1, accrual stopped [Paxalisib/control N 54/75(NDU), 100/188(RD)]. Neither PP thresholds for moving to Stage 2 nor stopping for minimum efficacy were met. Following an unplanned public disclosure that the arm did not continue to stage 2, clinical cut-off for final analysis (planned May2023) was updated to public disclosure date (August2022). At final analysis mean HRs were 0.89(NDU), 1.25(RD), 1.05(All), probabilities of HR&amp;lt;1.00 of 0.72(NDU), 0.076(RD), 0.398(All). Model estimated median OS paxalisib/control (months) were 14.77/13.84(NDU) and 8.58/10.06(RD). CONCLUSION Paxalisib did not show survival benefit over cumulative control in final primary analysis; additional secondary analyses are being considered. GBM AGILE continues to rapidly and efficiently assess therapies in ND and RD glioblastoma.
LTBK-01. PHASE 3 STELLAR STUDY SHOWS EFLORNITHINE IMPROVES OVERALL SURVIVAL (OS) AND PROGRESSION FREE SURVIVAL (PFS) IN PATIENTS WITH RECURRENT 2021 WHO ASTROCYTOMA, IDH-MUTANT GRADE 3
Authors: Howard Colman, Giuseppe Lombardi, Eric Wong, Tobias Walbert, Marica Eoli, Andrew Lassman, David Peereboom, Sani Kizilbash, Carlos Kamiya-Matsuoka, Marshall Pitz, Roy Strowd, Annick Desjardins, Priya Kumthekar, Warren Mason, Alessia Pellerino, Ricardo Soffietti, Nicholas Butowski, Peter Forsyth, Mohamed Hamza, Peter Hau, Enrico Lallana, Burt Nabors, David Piccioni, Erik Uhlmann, Liam Welsh, Patrick Wen, Jorg Dietrich, Victor Levin
Journal: Neuro-Oncology (2024)

Abstract BACKGROUND Recurrent anaplastic astrocytoma (AA), a grade 3 brain cancer, remains an unmet medical need. STELLAR was a phase III randomized, open-label trial of eflornithine (ornithine decarboxylase inhibitor) with lomustine versus lomustine alone, originally for patients with recurrent AA. However, as the WHO definition of AA evolved during trial conduct (e.g., excluding IDH wild-type disease), we determined results in both the original ITT population and by revised molecularly defined WHO 2021 diagnoses in pre-planned analyses. METHOD Key eligibility: age ≥ 18, AA (2016 WHO criteria), first recurrence ≥ 6 months after radiation and temozolomide, KPS ≥ 70, no imaging findings consistent with grade 4 glioblastoma. Stratification: IDH, age, resection extent, and geography. Patients were randomized to Arm A: eflornithine (2.8 g/m2 TID Q 2/3 weeks) with lomustine (90 mg/m2 Q 6 weeks) or Arm B: lomustine (110 mg/m2 Q 6 weeks). Primary endpoint was OS. The pre-specified hazard ratio (HR) goal was 0.667 based on projected median OS (mOS) increase to 18 months from 12 months. RESULTS 343 pts (172/171 Arms A/B) were randomized (105 sites, 8 countries). ITT analysis found no difference between arms (mOS 23.4 vs. 20.3 months, HR = 0.94). However, a pre-specified subset analysis in IDH mutant, 2021 WHO-defined grade 3 astrocytoma (n=194), showed significant improvement with eflornithine (mOS 34.9 vs. 23.5 months, HR = 0.64, log rank p = 0.016) and PFS (15.8 vs. 7.2 months, HR = 0.58, log rank p = 0.015). No difference was observed in the IDH wild-type subset. AEs were consistent with historic data. CONCLUSION There was no difference in OS between arms in the ITT analysis. However, medically meaningful and statistically significant OS and PFS benefits were observed with eflornithine in the pre-planned analysis of patients with molecularly defined 2021 WHO CNS grade 3 astrocytoma.
Transcriptomic analysis of skeletal muscle regeneration across mouse lifespan identifies altered stem cell states
Authors: Lauren D. Walter, Jessica L. Orton, Ioannis Ntekas, Ern Hwei Hannah Fong, Viviana I. Maymi, Brian D. Rudd, Iwijn De Vlaminck, Jennifer H. Elisseeff, Benjamin D. Cosgrove
Journal: Nature Aging (2024)

In aging, skeletal muscle regeneration declines due to alterations in both myogenic and non-myogenic cells and their interactions. This regenerative dysfunction is not understood comprehensively or with high spatiotemporal resolution. We collected an integrated atlas of 273,923 single-cell transcriptomes and high-resolution spatial transcriptomic maps from muscles of young, old and geriatric mice (~5, 20 and 26 months old) at multiple time points following myotoxin injury. We identified eight immune cell types that displayed accelerated or delayed dynamics by age. We observed muscle stem cell states and trajectories specific to old and geriatric muscles and evaluated their association with senescence by scoring experimentally derived and curated gene signatures in both single-cell and spatial transcriptomic data. This revealed an elevation of senescent-like muscle stem cell subsets within injury zones uniquely in aged muscles. This Resource provides a holistic portrait of the altered cellular states underlying muscle regenerative decline across mouse lifespan. Skeletal muscle regeneration declines during aging but the underlying processes are incompletely understood. Here the authors generated single-cell and spatial transcriptomics data from uninjured and injured muscles across mouse lifespan and observed age-specific immune cell dynamics and an elevation of senescent-like muscle stem cells in aged muscles.
Molecular and genetic insights into human ovarian aging from single-nuclei multi-omics analyses
Authors: Chen Jin, Xizhe Wang, Jiping Yang, Seungsoo Kim, Adam D. Hudgins, Amir Gamliel, Mingzhuo Pei, Daniela Contreras, Melody Devos, Qinghua Guo, Jan Vijg, Marco Conti, Jan Hoeijmakers, Judith Campisi, Rogerio Lobo, Zev Williams, Michael G. Rosenfeld, Yousin Suh
Journal: Nature Aging (2024)

The ovary is the first organ to age in the human body, affecting both fertility and overall health. However, the biological mechanisms underlying human ovarian aging remain poorly understood. Here we present a comprehensive single-nuclei multi-omics atlas of four young (ages 23–29 years) and four reproductively aged (ages 49–54 years) human ovaries. Our analyses reveal coordinated changes in transcriptomes and chromatin accessibilities across cell types in the ovary during aging, notably mTOR signaling being a prominent ovary-specific aging pathway. Cell-type-specific regulatory networks reveal enhanced activity of the transcription factor CEBPD across cell types in the aged ovary. Integration of our multi-omics data with genetic variants associated with age at natural menopause demonstrates a global impact of functional variants on gene regulatory networks across ovarian cell types. We nominate functional non-coding regulatory variants, their target genes and ovarian cell types and regulatory mechanisms. This atlas provides a valuable resource for understanding the cellular, molecular and genetic basis of human ovarian aging. The molecular and cellular mechanisms underlying ovarian aging are incompletely understood. Here the authors provide single-nuclei RNA and ATAC-seq of human ovarian tissue from four young and four reproductively aged donors, revealing coordinated transcriptomic and epigenomic changes across cell types and highlighting a role for mTOR signaling in reproductive aging.
Pathogenic role of acyl coenzyme A binding protein (ACBP) in Cushing’s syndrome
Authors: Hui Pan, Ai-Ling Tian, Hui Chen, Yifan Xia, Allan Sauvat, Stephanie Moriceau, Flavia Lambertucci, Omar Motiño, Liwei Zhao, Peng Liu, Misha Mao, Sijing Li, Shuai Zhang, Adrien Joseph, Sylvère Durand, Fanny Aprahamian, Zeyu Luo, Yang Ou, Zhe Shen, Enfu Xue, Yuhong Pan, Vincent Carbonnier, Gautier Stoll, Sabrina Forveille, Marion Leduc, Giulia Cerrato, Alexandra Cerone, Maria Chiara Maiuri, Frederic Castinetti, Thierry Brue, Hongsheng Wang, Yuting Ma, Isabelle Martins, Oliver Kepp, Guido Kroemer
Journal: Nature Metabolism (2024)

Abstract Cushing’s syndrome is caused by an elevation of endogenous or pharmacologically administered glucocorticoids. Acyl coenzyme A binding protein (ACBP, encoded by the gene diazepam binding inhibitor, Dbi ) stimulates food intake and lipo-anabolic reactions. Here we found that plasma ACBP/DBI concentrations were elevated in patients and mice with Cushing’s syndrome. We used several methods for ACBP/DBI inhibition in mice, namely, (1) induction of ACBP/DBI autoantibodies, (2) injection of a neutralizing monoclonal antibody, (3) body-wide or hepatocyte-specific knockout of the Dbi gene, (4) mutation of the ACBP/DBI receptor Gabrg2 and (5) injections of triiodothyronine or (6) the thyroid hormone receptor-β agonist resmetirom to block Dbi transcription. These six approaches abolished manifestations of Cushing’s syndrome such as increased food intake, weight gain, excessive adiposity, liver damage, hypertriglyceridaemia and type 2 diabetes. In conclusion, it appears that ACBP/DBI constitutes an actionable target that is causally involved in the development of Cushing’s syndrome.
Predicting modular functions and neural coding of behavior from a synaptic wiring diagram
Authors: Ashwin Vishwanathan, Alex Sood, Jingpeng Wu, Alexandro D. Ramirez, Runzhe Yang, Nico Kemnitz, Dodam Ih, Nicholas Turner, Kisuk Lee, Ignacio Tartavull, William M. Silversmith, Chris S. Jordan, Celia David, Doug Bland, Amy Sterling, H. Sebastian Seung, Mark S. Goldman, Emre R. F. Aksay, Kyle Wille, Ben Silverman, Ryan Willie, Sarah Morejohn, Selden Koolman, Marissa Sorek, Devon Jones, Amy Sterling, Celia David, Sujata Reddy, Anthony Pelegrino, Sarah Williams
Journal: Nature Neuroscience (2024)

A long-standing goal in neuroscience is to understand how a circuit's form influences its function. Here, we reconstruct and analyze a synaptic wiring diagram of the larval zebrafish brainstem to predict key functional properties and validate them through comparison with physiological data. We identify modules of strongly connected neurons that turn out to be specialized for different behavioral functions, the control of eye and body movements. The eye movement module is further organized into two three-block cycles that support the positive feedback long hypothesized to underlie low-dimensional attractor dynamics in oculomotor control. We construct a neural network model based directly on the reconstructed wiring diagram that makes predictions for the cellular-resolution coding of eye position and neural dynamics. These predictions are verified statistically with calcium imaging-based neural activity recordings. This work demonstrates how connectome-based brain modeling can reveal previously unknown anatomical structure in a neural circuit and provide insights linking network form to function. The authors determine the synaptic wiring diagram of a vertebrate circuit and reveal behaviorally associated modules. A model based on this connectome predicts neural coding and dynamics that are verified with calcium imaging data.