tbuckley/cabot-search huggingface dataset:
Timing of Renal-Replacement Therapy in Patients with Acute Kidney Injury and Sepsis
Authors: Saber D Barbar, Raphaël Clere-Jehl, Abderrahmane Bourredjem, Romain Hernu, Florent Montini, Rémi Bruyère, Christine Lebert, Julien Bohé, Julio Badie, Jean-Pierre Eraldi, Jean-Philippe Rigaud, Bruno Levy, Shidasp Siami, Guillaume Louis, Lila Bouadma, Jean-Michel Constantin, Emmanuelle Mercier, Kada Klouche, Damien du Cheyron, Gaël Piton, Djillali Annane, Samir Jaber, Thierry van der Linden, Gilles Blasco, Jean-Paul Mira, Carole Schwebel, Loïc Chimot, Philippe Guiot, Mai-Anh Nay, Ferhat Meziani, Julie Helms, Claire Roger, Benjamin Louart, Remi Trusson, Auguste Dargent, Christine Binquet, Jean-Pierre Quenot
Journal: New England Journal of Medicine (2018)

Acute kidney injury is the most frequent complication in patients with septic shock and is an independent risk factor for death. Although renal-replacement therapy is the standard of care for severe acute kidney injury, the ideal time for initiation remains controversial. In a multicenter, randomized, controlled trial, we assigned patients with early-stage septic shock who had severe acute kidney injury at the failure stage of the risk, injury, failure, loss, and end-stage kidney disease (RIFLE) classification system but without life-threatening complications related to acute kidney injury to receive renal-replacement therapy either within 12 hours after documentation of failure-stage acute kidney injury (early strategy) or after a delay of 48 hours if renal recovery had not occurred (delayed strategy). The failure stage of the RIFLE classification system is characterized by a serum creatinine level 3 times the baseline level (or ≥4 mg per deciliter with a rapid increase of ≥0.5 mg per deciliter), urine output less than 0.3 ml per kilogram of body weight per hour for 24 hours or longer, or anuria for at least 12 hours. The primary outcome was death at 90 days. The trial was stopped early for futility after the second planned interim analysis. A total of 488 patients underwent randomization; there were no significant between-group differences in the characteristics at baseline. Among the 477 patients for whom follow-up data at 90 days were available, 58% of the patients in the early-strategy group (138 of 239 patients) and 54% in the delayed-strategy group (128 of 238 patients) had died (P=0.38). In the delayed-strategy group, 38% (93 patients) did not receive renal-replacement therapy. Criteria for emergency renal-replacement therapy were met in 17% of the patients in the delayed-strategy group (41 patients). Among patients with septic shock who had severe acute kidney injury, there was no significant difference in overall mortality at 90 days between patients who were assigned to an early strategy for the initiation of renal-replacement therapy and those who were assigned to a delayed strategy. (Funded by the French Ministry of Health; IDEAL-ICU ClinicalTrials.gov number, NCT01682590 .).
GW29-e0401 Late detection of left ventricular mechanical dyssynchrony and impaired morphology after high dose of anthracycline chemotherapy using real-time three-dimensional echocardiography: a 5-year retrospective follow-up study
Authors: Chujie Zhang, Jinyi Lin, Yuchen Xu, Rui zhao, Yiyao He, Leilei Cheng
Journal: Journal of the American College of Cardiology (2018)
P3.15-13 Surgical Management of Huge Pulmonary Arteriovenous Malformations: Our Experience
Authors: F. Gradica, L. Lisha, D. Argjiri, A. Cani, F. Kokici, V. Rexha, F. Gradica, S. Beqiri, S. Demaci, S. Maliqi
Journal: Journal of Thoracic Oncology (2018)
Chronic hydroxychloroquine/chloroquine exposure for connective tissue diseases and risk of Alzheimer’s disease
Authors: Young Ho Lee
Journal: Annals of the Rheumatic Diseases (2018)

I have read with interest the article by Fardet et al 1 regarding chronic hydroxychloroquine/chloroquine exposure for connective tissue diseases and risk of Alzheimer’s disease. This population-based cohort study reported that people who had been chronically exposed to hydroxychloroquine/chloroquine were not at a higher risk of Alzheimer’s disease than the control individuals. However, the manuscript has some issues. The …
The case for calling alcohol a drug
Authors: Helen Macdonald
Journal: BMJ (2018)

The words that clinicians use matter. Professors Kypros Kypri and Jim McCambridge argue that the way we categorise these words is also important, particularly in relation to drug and addiction policy (doi:10.1136/bmj.k3944). Policy could deal with smoking, drugs, and alcohol separately. Or it could bring all addictive drugs together, including alcohol, among others.

“The clear identification of alcohol as a drug matters …
Longitudinal analysis of circulating biomarkers to monitor advanced EGFR mutated (EGFR+) non-small cell lung cancer (NSCLC)
Authors: P.N. Ding, T. Becker, V.J. Bray, W. Chua, Y.F. Ma, A. Luk, J. Po, D. Lynch, N. Caixeiro, P. de Souza, T.L. Roberts
Journal: Annals of Oncology (2018)
BMJ Awards: nominations open with six new categories for 2019
Authors: Susan Mayor
Journal: BMJ (2018)

Nominations opened on 22 October for The BMJ Awards 2019, celebrating outstanding achievement in medicine.

Doctors have until Friday 18 January 2019 to put themselves—or colleagues—forward in 15 categories across a range of specialties in the UK’s leading medical awards. They aim to recognise the inspirational work of healthcare teams across the country and promote excellence in healthcare.

The award winners will be announced at a ceremony on Wednesday 24 April 2019 after a rigorous judging process in which shortlisted teams present their work and answer questions from …
Targeting VEGFR2 with Ramucirumab strongly impacts effector/ activated regulatory T cells and CD8+ T cells in the tumor microenvironment
Authors: Yasuko Tada, Yosuke Togashi, Daisuke Kotani, Takeshi Kuwata, Eichi Sato, Akihito Kawazoe, Toshihiko Doi, Hisashi Wada, Hiroyoshi Nishikawa, Kohei Shitara
Journal: Journal for ImmunoTherapy of Cancer (2018)

Several studies have established a correlation between the VEGF-VEGFR2 axis and an immunosuppressive microenvironment; this immunosuppression can be overcome by anti-angiogenic reagents, such as ramucirumab (RAM). However, little is known about the immunological impact of anti-angiogenic reagents within the tumor microenvironment in human clinical samples. This study aimed at investigating the effects of RAM on the tumor microenvironmental immune status in human cancers.
GW29-e0031 Perturbations of the anti-ageing hormone Klotho in patients with diagonal earlobe crease
Authors: Fuqiang Liu, Shuang Shi, Ling Zhu, Yujie Xing, Jiang Lei, Weifeng Tian, Gongchang Guan, Junkuai Wang
Journal: Journal of the American College of Cardiology (2018)
ITGBL1 modulates integrin activity to promote cartilage formation and protect against arthritis
Authors: Eun Kyung Song, Jimin Jeon, Dong Gil Jang, Ha Eun Kim, Hyo Jung Sim, Keun Yeong Kwon, Sofia Medina-Ruiz, Hyun-Jun Jang, Ah Reum Lee, Jun Gi Rho, Hyun-Shik Lee, Seok Jung Kim, Chan Young Park, Kyungjae Myung, Wook Kim, Taejoon Kwon, Siyoung Yang, Tae Joo Park
Journal: Science Translational Medicine (2018)

ITGBL1 promotes chondrogenesis and protects joint cartilage from osteoarthritis by inhibiting integrin-extracellular matrix interaction.
Abstract B32: A novel role for the EWS portion of EWS/FLI in binding GGAA-microsatellites required for oncogenic transformation in Ewing sarcoma
Authors: K. M. Johnson, S. L. Lessnick
Journal: Cancer Research (2018)

Abstract Objective: Ewing sarcoma is a pediatric bone malignancy initiated by a t(11;22) chromosomal translocation that produces the EWS/FLI oncoprotein. EWS/FLI transcriptionally activates and represses its target genes to mediate oncogenic reprogramming. Expression of its upregulated targets correlates with EWS/FLI binding to associated GGAA-microsatellites, which show length polymorphisms. These microsatellite polymorphisms may critically affect EWS/FLI-responsiveness of key gene targets. For example, NR0B1 is necessary for EWS/FLI mediated oncogenic transformation, and we found a “sweet spot” of 18-26 repeat length as optimal for EWS/FLI mediated transcriptional activity at NR0B1 through clinical observations and in vitro studies. The mechanism underlying this optimal length is unknown. Methods: We explored the stoichiometry and binding affinity of EWS/FLI for different GGAA-repeat lengths through biochemical studies, including fluorescence polarization, ChIP-seq, and RNA-seq, combined with bioinformatics analysis. Additionally, use of mutant constructs of EWS/FLI has been critical for elucidating particular binding behavior of EWS/FLI at different microsatellite repeat lengths. Results: Our biochemical studies, using recombinant Δ22 (a version of EWS/FLI containing only the FLI portion) demonstrate a stoichiometry of one Δ22-monomer binding to every two consecutive GGAA-repeats on shorter microsatellite sequences. Surprisingly, the affinity for Δ22 binding to GGAA-microsatellites significantly decreased, and ultimately became unmeasurable, when the size of the microsatellite was increased to the “sweet spot” length. In contrast, a fully functional EWS/FLI mutant (Mut9, which retains approximately half of the EWS portion of the fusion) showed low affinity for smaller GGAA-microsatellites, but instead significantly increased its affinity at “sweet spot” microsatellite lengths. Single-gene ChIP and genome-wide ChIP-seq and RNA-seq studies extended these findings to the in vivo setting. Conclusion: Together, these data reveal an unexpected novel role for the EWS portion of the EWS/FLI fusion in DNA binding. Additionally, our data suggest a length-dependent biochemical mechanism for EWS/FLI binding and transcriptional regulation at GGAA-microsatellites. Citation Format: K. M. Johnson, S. L. Lessnick. A novel role for the EWS portion of EWS/FLI in binding GGAA-microsatellites required for oncogenic transformation in Ewing sarcoma [abstract]. In: Proceedings of the AACR Special Conference: Pediatric Cancer Research: From Basic Science to the Clinic; 2017 Dec 3-6; Atlanta, Georgia. Philadelphia (PA): AACR; Cancer Res 2018;78(19 Suppl):Abstract nr B32.
Reassessment of 4-Cycle Etoposide and Cisplatin as the Standard of Care for Good-Risk Metastatic Germ Cell Tumors
Authors: Daniel E. Fein, Jessica K. Paulus, Paul Mathew
Journal: JAMA Oncology (2018)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Oncology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Oncology journal
Intertumoral Heterogeneity of CD3+ and CD8+ T-Cell Densities in the Microenvironment of DNA Mismatch-Repair–Deficient Colon Cancers: Implications for Prognosis
Authors: Harry H. Yoon, Qian Shi, Erica N. Heying, Andrea Muranyi, Joerg Bredno, Faith Ough, Azita Djalilvand, June Clements, Rebecca Bowermaster, Wen-Wei Liu, Michael Barnes, Steven R. Alberts, Kandavel Shanmugam, Frank A. Sinicrope
Journal: Clinical Cancer Research (2018)

Abstract Purpose: Colorectal cancers with deficient DNA mismatch repair (dMMR) are presumed to uniformly have dense lymphocytic infiltration that underlies their favorable prognosis and is critical to their responsiveness to immunotherapy, as compared with MMR-proficient (pMMR) tumors. We examined T-cell densities and their potential heterogeneity in a large cohort of dMMR tumors. Experimental Design: CD3+ and CD8+ T-cell densities were quantified at the invasive margin (IM) and tumor core (CT) in 561 stage III colon cancers (dMMR, n = 278; pMMR, n = 283) from a phase III adjuvant trial (N0147). Their association with overall survival (OS) was determined using multivariable Cox analysis. Results: Although CD3+ and CD8+ T-cell densities in the tumor microenvironment were higher in dMMR versus pMMR tumors overall, intertumoral heterogeneity in densities between tumors was significantly higher by 30% to 88% among dMMR versus pMMR cancers (P &amp;lt; 0.0001 for all four T-cell subtypes [CD3+IM, CD3+CT, CD8+IM, CD8+CT]). A substantial proportion of dMMR tumors (26% to 35% depending on the T-cell subtype) exhibited T-cell densities as low as that in the bottom half of pMMR tumors. All four T-cell subtypes were prognostic in dMMR with CD3+IM being the most strongly prognostic. Low (vs. high) CD3+IM was independently associated with poorer OS among dMMR (HR, 4.76; 95% confidence interval, 1.43–15.87; P = 0.0019) and pMMR tumors (P = 0.0103). Conclusions: Tumor-infiltrating T-cell densities exhibited greater intertumoral heterogeneity among dMMR than pMMR colon cancers, with CD3+IM providing robust stratification of both dMMR and pMMR tumors for prognosis. Potentially, lower T-cell densities among dMMR tumors may contribute to immunotherapy resistance.
Abstract 19422: Origin of Ventricular Fibrillation in Bileaflet Mitral Valve Prolapse Syndrome
Authors: Faisal F Syed, Michael Ackerman, Christopher J McLeod, Suraj Kapa, Siva K Mulpuru, Chenni S Sriram, Bryan C Cannon, Samuel J Asirvatham, Peter A Noseworthy
Journal: Circulation (2015)

Introduction: Although most patients with mitral valve prolapse (MVP) have a benign prognosis, there is a subgroup with bileaflet MVP syndrome (biMVPS) at increased risk of idiopathic ventricular fibrillation (VF). The phenotypic features of this syndrome include myxomatous bileaflet prolapse, complex ventricular ectopy (VE), T-wave inversion in inferolateral ECG leads, and female predominance. The mechanism of ventricular arrhythmia in these patients is unknown. Methods: We reviewed our center’s ablation experience of 14 consecutive patients with biMVPS patients between February 2007 and October 2013 (n=13 female, median [range] age at index ablation 33.8 [21.0 - 58.7] years, left ventricular ejection fraction [EF] 60 [45-67] %, all ≤ moderate mitral regurgitation [MR]). We compared findings from 6 with prior sudden cardiac arrest (SCA) and recurrent ICD shocks for drug refractory VF with 8 who had symptomatic drug-refractory complex VE but without prior SCA. Results: All patients with prior SCA had a predominant VE trigger for the VF. There was no difference between the two groups in EF, MR severity, VE burden, and number of different VE morphologies or foci ablated. Sites of successful VE ablation at index procedure were the LV papillary muscles (PM, n=6 anterior, 6 posterior), fascicular system (n=5 anterior, 4 posterior), mitral annulus (n=2), outflow tracts (3 RVOT, 1 LVOT), and coronary sinus (n=1). All patients had at least one LV papillary or fascicular VE focus. Purkinje origin VE was identified as the VF trigger in 6/6 SCA patients (3 from PM, 3 from LV fascicles) and only 4/8 (none from PM) non-SCA patients (p=0.04). Acute success was seen in 17/19 procedures with no complications. VF storm occurred within 24 hours of ablation in a single patient. At 310 (39 - 2099) days follow-up, 1 SCA patient received a single shock (p=0.031 compared to pre-ablation), and symptoms from VE were reduced in 12/14. Conclusions: BiMVPS is characterized by VE from the LV fascicles and papillary muscles that trigger VF. The VE is invariably multifocal and may also involve the outflow tracts and mitral annulus. Ablation of clinically dominant VE foci alleviates symptoms and reduces the number of VF-terminating ICD shocks.
Association of sarcopenia with dose-limiting toxicties and survival in oesophageal adenocarcinoma treated with neoadjuvant chemotherapy
Authors: J.M.J. Weaver, C. Cipriano, A. McWilliam, Z. Kordatou, M. Abraham, T. Germetaki, G. Papaxoinis, W. Mansoor
Journal: Annals of Oncology (2018)
Unique pattern of neutrophil migration and function during tumor progression
Authors: Sima Patel, Shuyu Fu, Jerome Mastio, George A. Dominguez, Abhilasha Purohit, Andrew Kossenkov, Cindy Lin, Kevin Alicea-Torres, Mohit Sehgal, Yulia Nefedova, Jie Zhou, Lucia R. Languino, Cynthia Clendenin, Robert H. Vonderheide, Charles Mulligan, Brian Nam, Neil Hockstein, Gregory Masters, Michael Guarino, Zachary T. Schug, Dario C Altieri, Dmitry I. Gabrilovich
Journal: Nature Immunology (2018)
Abstract B22: Antitumor effects of selective PRMT1 inhibitors on neuroblastoma in vitro and in vivo
Authors: Jeanne N. Hansen, Louis T. Lotta, Allison Eberhardt, Yujun George Zheng, Sen Ji, Shengyong Yang, Nina F. Schor, Xingguo Li
Journal: Cancer Research (2018)

Abstract The MYC family of transcription factors is one of the most frequently overexpressed oncogenes in human malignancies, including tumors that are derived from the nervous system. MYCN plays a causative role in neuroblastoma, a common and fatal childhood cancer of the developing sympathetic nervous system. Thus, the MYC family has been considered as a promising cancer target; however, so far, no small molecules can directly target MYC or MYCN in vivo. We have recently reported that PRMT1 functions as a key regulator of the stability and oncogenicity of MYCN. In this study, we have performed the structure-activity relationship analysis of diamidine-related PRMT1-seletive inhibitors. In correlation with their inhibition against PRMT1 in biochemical assays, these compounds showed remarkable anticancer properties both in neuroblastoma cell lines in vitro and in a preclinical mouse model of neuroblastoma in vivo. Mechanistically, these potent PRMT1 inhibitors destabilized MYCN, caused cell cycle arrest, and restored normal developmental signals of the developing sympathetic neuroblast precursors. Together, our results demonstrate that PRMT1-seletive inhibitors are promising anti-neuroblastoma agents and may represent a general strategy to target certain MYC/MYCN-driven cancers. Citation Format: Jeanne N. Hansen, Louis T. Lotta, Allison Eberhardt, Yujun George Zheng, Sen Ji, Shengyong Yang, Nina F. Schor, Xingguo Li. Antitumor effects of selective PRMT1 inhibitors on neuroblastoma in vitro and in vivo [abstract]. In: Proceedings of the AACR Special Conference: Pediatric Cancer Research: From Basic Science to the Clinic; 2017 Dec 3-6; Atlanta, Georgia. Philadelphia (PA): AACR; Cancer Res 2018;78(19 Suppl):Abstract nr B22.
Comprehensive biomarker analyses and updated results of PURE-01 study: Neoadjuvant pembrolizumab (pembro) in muscle-invasive urothelial bladder carcinoma (MIBC)
Authors: A. Necchi, A. Briganti, D. Raggi, R. Luciano, M. Colecchia, S. Massa, P. Giannatempo, R. Colombo, A. Gallina, R. Salvioni, R. Mortarini, F. Montorsi, R. Madison, S.M. Ali, J.S. Ross, J. Chung, A. Anichini
Journal: Annals of Oncology (2018)
Pan-cancer analysis of tumor metabolic landscape associated with genomic alterations
Authors: Hongyoon Choi, Kwon Joong Na
Journal: Molecular Cancer (2018)

Although metabolic alterations are one of the hallmarks of cancer, there is a lack of understanding of how metabolic landscape is reconstituted according to cancer progression and which genetic alterations underlie its heterogeneity within cancer cells. Here, the configuration of the metabolic landscape according to genetic alteration is examined across 7648 subjects representing 29 cancers. The metabolic landscape and its reconfiguration according to the accumulated mutation maintained characteristics of their tissue of origin. However, there were some common patterns across cancers in terms of the association with cancer progression. Carbohydrate and pyrimidine metabolism showed the highest positive correlation with tumor metabolic burden and they were also common poor prognostic pathways in several cancer types. We additionally examined whether genetic alterations associated with the heterogeneity of metabolic landscape. Genetic alterations associated with each metabolic pathway differed between cancers, however, they were a part of cancer drivers in most cancer types.
Prediabetes Is Associated With Structural Brain Abnormalities: The Maastricht Study
Authors: Marnix J.M. van Agtmaal, Alfons J.H.M. Houben, Vera de Wit, Ronald M.A. Henry, Nicolaas C. Schaper, Pieter C. Dagnelie, Carla J. van der Kallen, Annemarie Koster, Simone J. Sep, Abraham A. Kroon, Jacobus F.A. Jansen, Paul A. Hofman, Walter H. Backes, Miranda T. Schram, Coen D.A. Stehouwer
Journal: Diabetes Care (2018)

Structural brain abnormalities are key risk factors for brain diseases, such as dementia, stroke, and depression, in type 2 diabetes. It is unknown whether structural brain abnormalities already occur in prediabetes. Therefore, we investigated whether both prediabetes and type 2 diabetes are associated with lacunar infarcts (LIs), white matter hyperintensities (WMHs), cerebral microbleeds (CMBs), and brain atrophy.We used data from 2,228 participants (1,373 with normal glucose metabolism [NGM], 347 with prediabetes, and 508 with type 2 diabetes (oversampled); mean age 59.2 ± 8.2 years; 48.3% women) of the Maastricht Study, a population-based cohort study. Diabetes status was determined with an oral glucose tolerance test. Brain imaging was performed with 3 Tesla MRI. Results were analyzed with multivariable logistic and linear regression analyses.Prediabetes and type 2 diabetes were associated with the presence of LIs (odds ratio 1.61 [95% CI 0.98-2.63] and 1.67 [1.04-2.68], respectively; Ptrend = 0.027), larger WMH (β 0.07 log10-transformed mL [log-mL] [95% CI 0.00-0.15] and 0.21 log-mL [0.14-0.28], respectively; Ptrend <0.001), and smaller white matter volumes (β -4.0 mL [-7.3 to -0.6] and -7.2 mL [-10.4 to -4.0], respectively; Ptrend <0.001) compared with NGM. Prediabetes was not associated with gray matter volumes or the presence of CMBs.Prediabetes is associated with structural brain abnormalities, with further deterioration in type 2 diabetes. These results indicate that, in middle-aged populations, structural brain abnormalities already occur in prediabetes, which may suggest that the treatment of early dysglycemia may contribute to the prevention of brain diseases.
A phase II study of low-dose erlotinib in frail patients with EGFR-mutant non-small cell lung cancer: TORG1425
Authors: Akihiro Bessho, Shingo Miyamoto, Koichi Azuma, Hidenobu Ishii, Shinobu Hosokawa, Hideo Kunitoh, Tsuneo Shimokawa, Hiroshi Tanaka, Hiromi Aono, Yoshiro Nakahara, Yukio Hosomi, Kei Kusaka, Kazuhiko Yamada, Hiroaki Okamoto
Journal: Annals of Oncology (2018)
Use of red clover in premenopausal breast cancer patients receiving hormonal adjuvant treatment: Biological and clinical implications from a randomized clinical trial
Authors: C. Ferraris, B. Ballestra, V. Cappelletti, C. Listorti, P. Miodini, I. Pulice, L. Mariani, E. Ferrari, A. Gambaro, I. Maugeri, G. Martelli, S. Folli
Journal: Annals of Oncology (2018)
GW29-e1174 The H19 long noncoding RNA is a novel negative regulator of cardiomyocyte hypertrophy
Authors: Lantao Liu, Yao Song, Linling Li, Song Zuo, Nian Liu, Guan Yang, Haijing Wang, Xuan Cheng, Youyi Zhang, Xiao Yang, Xiangbo An, Zhenhua Li, Jian Wang
Journal: Journal of the American College of Cardiology (2018)
The Thalamostriatal Projections Contribute to the Initiation and Execution of a Sequence of Movements
Authors: Edgar Díaz-Hernández, Rubén Contreras-López, Asai Sánchez-Fuentes, Luis Rodríguez-Sibrían, Josué O. Ramírez-Jarquín, Fatuel Tecuapetla
Journal: Neuron (2018)