tbuckley/cabot-search huggingface dataset:
Association of Abnormal Elevations in <scp>IFIT</scp>3 With Overactive Cyclic <scp>GMP</scp>‐<scp>AMP</scp> Synthase/Stimulator of Interferon Genes Signaling in Human Systemic Lupus Erythematosus Monocytes
Authors: Jiehua Wang, Min Dai, Yange Cui, Guojun Hou, Jun Deng, Xin Gao, Zhuojun Liao, Ya Liu, Yao Meng, Lingling Wu, Chao Yao, Yan Wang, Jie Qian, Qiang Guo, Huihua Ding, Bo Qu, Nan Shen
Journal: Arthritis & Rheumatology (2018)

Objective Increasing evidence indicates that the cyclic GMP ‐ AMP synthase/stimulator of interferon genes ( cGAS / STING ) signaling pathway has a critical pathogenic role in systemic lupus erythematosus ( SLE ). Expression levels of the interferon (IFN)–inducible gene IFIT 3 are elevated in SLE patients. However, it is still not clear how IFIT 3 contributes to the pathogenesis of SLE . This study was undertaken to investigate the activation of the cGAS / STING signaling pathway in human SLE monocytes, and to determine how elevated expression of IFIT 3 could contribute to overactive cGAS / STING signaling in patients with SLE. Methods Monocytes from SLE patients or healthy controls were examined for activity of the cGAS / STING signaling pathway and expression levels of IFIT 3. Correlations between cGAS / STING signaling activity and SLE clinical features were analyzed. Gain‐ or loss‐of‐function experiments were used to determine the role of IFIT 3 in cGAS / STING signaling. Coimmunoprecipitation assays were used to identify the interaction between IFIT 3 and other proteins. Results The cGAS / STING signaling pathway was found to have enhanced activity in monocytes from SLE patients compared to healthy controls, as indicated by the higher expression of IFN β downstream. Levels of IFIT 3 were significantly elevated in human SLE monocytes, and this was positively correlated with the activity of the cGAS / STING signaling pathway. In vitro, the expression of VACV 70‐induced IFN β was reduced by knockdown of IFIT 3, whereas overexpression of IFIT 3 produced an opposite effect. Finally, IFIT 3 was found to interact with both STING and TANK ‐binding kinase 1. Conclusion These findings suggest that IFIT 3 is one of the genes that contributes to the overactive cGAS / STING signaling pathway in human SLE monocytes. IFIT 3 may therefore serve as a novel therapeutic target for blocking the production of type I IFN and other proinflammatory cytokines by the cGAS / STING signaling pathway in patients with SLE.
Platelets play an essential role in murine lung development through Clec-2/podoplanin interaction
Authors: Nagaharu Tsukiji, Osamu Inoue, Mitsuru Morimoto, Norifumi Tatsumi, Hiroaki Nagatomo, Koji Ueta, Toshiaki Shirai, Tomoyuki Sasaki, Shimon Otake, Shogo Tamura, Toshiaki Tachibana, Masataka Okabe, Masanori Hirashima, Yukio Ozaki, Katsue Suzuki-Inoue
Journal: Blood (2018)
Alcohol intake in relation to non-fatal and fatal coronary heart disease and stroke: EPIC-CVD case-cohort study
Authors: Cristian Ricci, Angela Wood, David Muller, Marc J Gunter, Antonio Agudo, Heiner Boeing, Yvonne T van der Schouw, Samantha Warnakula, Calogero Saieva, Annemieke Spijkerman, Ivonne Sluijs, Anne Tjønneland, Cecilie Kyrø, Elisabete Weiderpass, Tilman Kühn, Rudolf Kaaks, Maria-Jose Sánchez, Salvatore Panico, Claudia Agnoli, Domenico Palli, Rosario Tumino, Gunnar Engström, Olle Melander, Fabrice Bonnet, Jolanda M A Boer, Timothy J Key, Ruth C Travis, Kim Overvad, W M Monique Verschuren, J Ramón Quirós, Antonia Trichopoulou, Eleni-Maria Papatesta, Eleni Peppa, Conchi Moreno Iribas, Diana Gavrila, Ann-Sofie Forslund, Jan-Håkan Jansson, Giuseppe Matullo, Larraitz Arriola, Heinz Freisling, Camille Lassale, Ioanna Tzoulaki, Stephen J Sharp, Nita G Forouhi, Claudia Langenberg, Rodolfo Saracci, Michael Sweeting, Paul Brennan, Adam S Butterworth, Elio Riboli, Nick J Wareham, John Danesh, Pietro Ferrari
Journal: BMJ (2018)

<h3>Abstract</h3> <h3>Objective</h3> To investigate the association between alcohol consumption (at baseline and over lifetime) and non-fatal and fatal coronary heart disease (CHD) and stroke. <h3>Design</h3> Multicentre case-cohort study. <h3>Setting</h3> A study of cardiovascular disease (CVD) determinants within the European Prospective Investigation into Cancer and nutrition cohort (EPIC-CVD) from eight European countries. <h3>Participants</h3> 32 549 participants without baseline CVD, comprised of incident CVD cases and a subcohort for comparison. <h3>Main outcome measures</h3> Non-fatal and fatal CHD and stroke (including ischaemic and haemorrhagic stroke). <h3>Results</h3> There were 9307 non-fatal CHD events, 1699 fatal CHD, 5855 non-fatal stroke, and 733 fatal stroke. Baseline alcohol intake was inversely associated with non-fatal CHD, with a hazard ratio of 0.94 (95% confidence interval 0.92 to 0.96) per 12 g/day higher intake. There was a J shaped association between baseline alcohol intake and risk of fatal CHD. The hazard ratios were 0.83 (0.70 to 0.98), 0.65 (0.53 to 0.81), and 0.82 (0.65 to 1.03) for categories 5.0-14.9 g/day, 15.0-29.9 g/day, and 30.0-59.9 g/day of total alcohol intake, respectively, compared with 0.1-4.9 g/day. In contrast, hazard ratios for non-fatal and fatal stroke risk were 1.04 (1.02 to 1.07), and 1.05 (0.98 to 1.13) per 12 g/day increase in baseline alcohol intake, respectively, including broadly similar findings for ischaemic and haemorrhagic stroke. Associations with cardiovascular outcomes were broadly similar with average lifetime alcohol consumption as for baseline alcohol intake, and across the eight countries studied. There was no strong evidence for interactions of alcohol consumption with smoking status on the risk of CVD events. <h3>Conclusions</h3> Alcohol intake was inversely associated with non-fatal CHD risk but positively associated with the risk of different stroke subtypes. This highlights the opposing associations of alcohol intake with different CVD types and strengthens the evidence for policies to reduce alcohol consumption.
In silico evaluation of the 12-gene molecular score (EndoPredict) and the recurrence score (Oncotype DX) as predictors of response to neo-adjuvant chemotherapy in estrogen receptor positive (ER+), HER2 negative (HER2-) breast cancer.
Authors: Hatem Hussein Soliman, Mark E. Robson, Susanne Wagner, Darl D Flake, Lee Steven Schwartzberg, Priyanka Sharma, Anthony Martin Magliocco, Ralf Kronenwett, Johnathan M. Lancaster, Jerry S Lanchbury, Alexander Gutin, William John Gradishar
Journal: Journal of Clinical Oncology (2018)

539 Background: Neo-adjuvant chemotherapy (NaCT) facilitates complete surgical resection in locally advanced, ER+, HER2- breast cancer. Due to its association with improved outcome, pathologic complete response (pCR) to NaCT treatment has been accepted as a surrogate for long-term outcome in clinical trials of patients with HER2+, triple-negative, or luminal B breast cancer. However, only 7-10% of patients with ER+, HER2- disease who receive NaCT achieve pCR. Biomarkers predictive of NaCT response would facilitate patient stratification and enable individualized therapeutic strategies. Here we evaluated the ability of two prognostic biomarker assays to predict NaCT response in ER+, HER2- breast cancer by means of a microarray-based in silico analysis. Methods: Expression and corresponding clinical data associated with pre-treatment biopsies obtained from patients with breast cancer who subsequently received NaCT were obtained from public datasets (GSE entries 16716, 20271, 25066, 32646, 41656, 41998). ER+, HER2- samples were selected based on available immunohistochemistry (IHC) data. The 12-gene molecular score (12-MS) and 21-gene recurrence score (21-RS) were approximated in silico according to published algorithms using expression means of array probes corresponding to the respective genes. Association with pCR was tested by logistic regression with adjustment for cohort. Results: A total of 764 patients with ER+, HER2- disease had available IHC data; 59 experienced pCR (response rate 8%). 12-MS and 21-RS were moderately well correlated (0.71). Both scores were predictive of pCR (12-MS p = 6.9x10-5; 21-RS p = 0.0023). In bivariate analysis the 12-MS remained a significant predictor of response (p = 0.01) while the 21-RS did not (p = 0.73). Conclusions: In this microarray-based in silico analysis, 12-MS was highly predictive of ER+, HER2- response to NaCT. Optimal stratification of patients with ER+, HER2- breast cancer for NaCT offers the opportunity to individualize care, improve response rates, and possibly avoid ineffective treatment.
Characteristics and Outcome of ROS1-Positive Non–Small Cell Lung Cancer Patients in Routine Clinical Practice
Authors: Sehhoon Park, Beung-Chul Ahn, Sung Won Lim, Jong-Mu Sun, Hye Ryun Kim, Min Hee Hong, Se-Hoon Lee, Jin Seok Ahn, Keunchil Park, Yoon La Choi, Byoung Chul Cho, Myung-Ju Ahn
Journal: Journal of Thoracic Oncology (2018)
Expansion of IL-23 receptor bearing TNFR2+ T cells is associated with molecular resistance to anti-TNF therapy in Crohn’s disease
Authors: Heike Schmitt, Ulrike Billmeier, Walburga Dieterich, Timo Rath, Sophia Sonnewald, Stephen Reid, Simon Hirschmann, Kai Hildner, Maximilian J Waldner, Jonas Mudter, Arndt Hartmann, Robert Grützmann, Clemens Neufert, Tino Münster, Markus F Neurath, Raja Atreya
Journal: Gut (2018)

Objective Anti-tumour necrosis factor (TNF) antibodies are successfully used for treatment of Crohn’s disease. Nevertheless, approximately 40% of patients display failure to anti-TNF therapy. Here, we characterised molecular mechanisms that are associated with endoscopic resistance to anti-TNF therapy. Design Mucosal and blood cells were isolated from patients with Crohn’s disease prior and during anti-TNF therapy. Cytokine profiles, cell surface markers, signalling proteins and cell apoptosis were assessed by microarray, immunohistochemistry, qPCR, ELISA, whole organ cultures and FACS. Results Responders to anti-TNF therapy displayed a significantly higher expression of TNF receptor 2 (TNFR2) but not IL23R on T cells than non-responders prior to anti-TNF therapy. During anti-TNF therapy, there was a significant upregulation of mucosal IL-23p19, IL23R and IL-17A in anti-TNF non-responders but not in responders. Apoptosis-resistant TNFR2+IL23R+ T cells were significantly expanded in anti-TNF non-responders compared with responders, expressed the gut tropic integrins α4β7, and exhibited increased expression of IFN-γ, T-bet, IL-17A and RORγt compared with TNFR2+IL23R− cells, indicating a mixed Th1/Th17-like phenotype. Intestinal TNFR2+IL23R+ T cells were activated by IL-23 derived from CD14+ macrophages, which were significantly more present in non-responders prior to anti-TNF treatment. Administration of IL-23 to anti-TNF-treated mucosal organ cultures led to the expansion of CD4+IL23R+TNFR2+ lymphocytes. Functional studies demonstrated that anti-TNF-induced apoptosis in mucosal T cells is abrogated by IL-23. Conclusions Expansion of apoptosis-resistant intestinal TNFR2+IL23R+ T cells is associated with resistance to anti-TNF therapy in Crohn’s disease. These findings identify IL-23 as a suitable molecular target in patients with Crohn’s disease refractory to anti-TNF therapy.
Treatment Facility Volume and Survival in Patients with Metastatic Renal Cell Carcinoma: A Registry-based Analysis
Authors: Shreyas S. Joshi, Elizabeth A. Handorf, Matthew Zibelman, Elizabeth R. Plimack, Robert G. Uzzo, Alexander Kutikov, Marc C. Smaldone, Daniel M. Geynisman
Journal: European Urology (2018)
Ornithine Decarboxylase in Macrophages Exacerbates Colitis and Promotes Colitis-Associated Colon Carcinogenesis by Impairing M1 Immune Responses
Authors: Kshipra Singh, Lori A. Coburn, Mohammad Asim, Daniel P. Barry, Margaret M. Allaman, Chanjuan Shi, M. Kay Washington, Paula B. Luis, Claus Schneider, Alberto G. Delgado, M. Blanca Piazuelo, John L. Cleveland, Alain P. Gobert, Keith T. Wilson
Journal: Cancer Research (2018)

Ornithine decarboxylase (ODC) is the rate-limiting enzyme for polyamine biosynthesis and restricts M1 macrophage activation in gastrointestinal (GI) infections. However, the role of macrophage ODC in colonic epithelial-driven inflammation is unknown. Here, we investigate cell-specific effects of ODC in colitis and colitis-associated carcinogenesis (CAC). Human colonic macrophages expressed increased ODC levels in active ulcerative colitis and Crohn's disease, colitis-associated dysplasia, and CAC. Mice lacking Odc in myeloid cells (OdcΔmye mice) that were treated with dextran sulfate sodium (DSS) exhibited improved survival, body weight, and colon length and reduced histologic injury versus control mice. In contrast, GI epithelial-specific Odc knockout had no effect on clinical parameters. Despite reduced histologic damage, colitis tissues of OdcΔmye mice had increased levels of multiple proinflammatory cytokines and chemokines and enhanced expression of M1, but not M2 markers. In the azoxymethane-DSS model of CAC, OdcΔmye mice had reduced tumor number, burden, and high-grade dysplasia. Tumors from OdcΔmye mice had increased M1, but not M2 macrophages. Increased levels of histone 3, lysine 9 acetylation, a marker of open chromatin, were manifest in tumor macrophages of OdcΔmye mice, consistent with our findings that macrophage ODC affects histone modifications that upregulate M1 gene transcription during GI infections. These findings support the concept that macrophage ODC augments epithelial injury-associated colitis and CAC by impairing the M1 responses that stimulate epithelial repair, antimicrobial defense, and antitumoral immunity. They also suggest that macrophage ODC is an important target for colon cancer chemoprevention.Significance: Ornithine decarboxylase contributes to the pathogenesis of colitis and associated carcinogenesis by impairing M1 macrophage responses needed for antitumoral immunity; targeting ODC in macrophages may represent a new strategy for chemoprevention. Cancer Res; 78(15); 4303-15. ©2018 AACR.
Promising activity of farnesyltransferase inhibitors across seven different sarcoma subtypes
Authors: William D. Tap, Chen Jiang, Fritz C. Eilber, Juran Kato-Stankiewicz, Jed P. Needle, Amrita Desai, John A. Glaspy, Dennis J. Slamon, Fuyuhiko Tamanoi
Journal: Cancer Research (2006)

3805   Sarcomas are a heterogeneous group of mesenchymal malignancies whose benefit from traditional chemotherapy has been maximized. A diagnosis of sarcoma still portends a poor prognosis with a disease specific mortality of up to 50%. Sarcomas are fertile ground for the application of novel, targeted therapies with the hope of identifying a treatment effective across histologic subtypes. We report that farnesyltransferase inhibitors (FTIs) demonstrate in vitro activity against sarcoma cell lines of variable histologies. Seven different sarcoma subtypes, including osteosarcoma, synovial sarcoma, uterine sarcoma and Ewing’s sarcoma were examined for their sensitivity to two FTI compounds, BMS214662 and BMS225975. Both compounds demonstrated exquisite growth inhibition as detected by cell count and MTT assays. IC50’s were in the range of 125-400 nanomolars, concentrations known to inhibit farnesylation. FTIs inhibited cellular growth in every histology tested. This is in contrast to other signal transduction inhibitors, i.e. of the MAPK pathway, whose effects were limited to specific pathologies alone. BMS214662 and BMS225975 differ in their potency and mechanism of action, providing an accurate tool to evaluate reasons for their efficacy. In most cell lines, FACS analysis showed an accumulation in the G1 phase of the cell cycle with little or no increase in apoptosis. Investigations of signaling properties after exposure to FTI revealed inhibition of S6 phosphorylation in some cell lines in a fashion similar to that seen with the use of rapamycin. S6 is a downstream effector of mTOR. The activation of mTOR/S6K relies on the farnesylation of Rheb. These results suggest that FTIs may inhibit the growth of some of our sarcoma cell lines by down regulating the TSC/Rheb/mTOR pathway. Effects of combining FTIs with other reagents such as taxanes are currently being investigated. These results are forthcoming and will be discussed.
Mortality in Puerto Rico after Hurricane Maria
Authors: Nishant Kishore, Domingo Marqués, Ayesha Mahmud, Mathew V. Kiang, Irmary Rodriguez, Arlan Fuller, Peggy Ebner, Cecilia Sorensen, Fabio Racy, Jay Lemery, Leslie Maas, Jennifer Leaning, Rafael A. Irizarry, Satchit Balsari, Caroline O. Buckee
Journal: New England Journal of Medicine (2018)

Quantifying the effect of natural disasters on society is critical for recovery of public health services and infrastructure. The death toll can be difficult to assess in the aftermath of a major disaster. In September 2017, Hurricane Maria caused massive infrastructural damage to Puerto Rico, but its effect on mortality remains contentious. The official death count is 64.
A randomized phase II trial evaluating <i>CYP2D6</i> genotype-guided tamoxifen dosing in hormone receptor-positive metastatic breast cancer: TARGET-1.
Authors: Toshimi Takano, Chiyo K. Imamura, Kenji Tamura, Shigehira Saji, Takeharu Yamanaka, Kan Yonemori, Masato Takahashi, Junji Tsurutani, Reiki Nishimura, Kazuhiko Sato, Akira Kitani, Naoto T. Ueno, Taisei Mushiroda, Michiaki Kubo, Yasuhiro Fujiwara, Yusuke Tanigawara
Journal: Journal of Clinical Oncology (2018)

1046 Background: Tamoxifen (TAM) is a prodrug that requires metabolic activation by CYP2D6. Genetic polymorphism of CYP2D6 has been speculated to cause suboptimal efficacy of TAM. Methods: In a phase II multicenter open-label randomized controlled study, we enrolled candidates for first-line TAM therapy who had hormone receptor–positive (HR+) metastatic breast cancer. CYP2D6 genotyping was performed using DNA extracted from whole blood at baseline. Patients with heterozygous (wt/V) or homozygous (V/V) variant alleles of decreased or no function were randomly assigned to TAM at regular dose (20 mg/day, RD arm) or increased dose (40 mg/day, ID arm), and patients with homozygous wild-type alleles (wt/wt) received TAM at 20 mg/day. The primary endpoint was 6-month (6M) progression-free survival (PFS) rate. Secondary endpoints included PFS and plasma levels of TAM and its metabolites. Results: From December 2012 to July 2016, 186 Japanese patients were enrolled. Of 184 evaluable patients, 136 carried wt/V or V/V (ID arm, 70; RD arm, 66), and 48 carried wt/wt. Patient characteristics (genotype; proportion of HR+ cells; status by recurrent or stage IV disease, bone metastasis, menopause, concurrent LHRH agonist therapy) did not differ significantly between the ID arm and RD arm. PFS rates at 6M were not significantly different between arms (67.6% ID arm vs. 66.7% RD arm; P = .45). Median PFS was longer in the ID arm than in the RD arm (14.2 M vs. 11.7 M; HR, 0.75; P = .15) with a median follow-up of 22.9 M. The trough levels of key active metabolite endoxifen (END) were significantly higher in the ID arm than in the RD arm (median 89.2 nM vs. 51.1 nM; P < .0001). Compared with the levels of END in patients with wt/wt receiving TAM 20 mg/day (72.0 nM), those in patients in the ID arm were not significantly different (P = .0680), and those in patients in the RD arm were significantly lower (P = .0026). Adverse events did not differ significantly between arms. Conclusions: In patients with CYP2D6 variant alleles, increasing TAM dosing resulted in higher plasma END levels. There was no PFS rate difference at 6M, but there was a trend for longer PFS for TAM at 40 mg/day than at 20 mg/day. Long-term follow-up is needed. Clinical trial information: UMIN000009155.
Deadly DAaRTS destroy cancer cells via a tumor microenvironment–mediated trigger
Authors: James V. McCann, Jamie L. Null, Andrew C. Dudley
Journal: Journal of Clinical Investigation (2018)

Stromal cells within the tumor microenvironment play a supportive role in tumor growth, progression, and treatment resistance; therefore, these nonmalignant cells are potential therapeutic targets. In this issue of the JCI, Szot et al. devised a strategy to exploit the cell-surface marker TEM8 (also known as ANTXR1), which is expressed by cancer-associated stromal cells, as a zip code to deliver an antibody-drug conjugate (ADC) linked to the potent cancer-killing drug monomethyl auristatin E (MMAE). In preclinical tumor and experimental metastasis models of multiple cancer types, TEM8-ADC targeted TEM8-expressing cancer-associated stromal cells, which processed and liberated membrane-permeable MMAE and released this drug via the P-glycoprotein (P-gp) drug transporter. Released MMAE killed cancer cells through a bystander mechanism that did minimal damage to the stromal cells themselves. P-gp-expressing tumor cells displayed MMAE resistance, suggesting that P-gp expression status may identify patients who might benefit the most from TEM8-ADC. This strategy, termed DAaRTS (drug activation and release through stroma), represents an elegant example of how selective expression of a cell-surface molecule on cancer-associated stroma can be exploited to facilitate drug delivery and shrink solid tumors.
Neoadjuvant talazoparib (TALA) for operable breast cancer patients with a BRCA mutation (BRCA+).
Authors: Jennifer Keating Litton, Marion Scoggins, Kenneth R. Hess, Beatriz Adrada, Carlos Hernando Barcenas, Rashmi Krishna Murthy, Senthil Damodaran, Sarah Marie DeSnyder, Abenaa M. Brewster, Alastair Mark Thompson, Gary J Whitman, Nuhad K. Ibrahim, Stacy L. Moulder, Jill Schwartz-Gomez, Elizabeth A. Mittendorf, Banu Arun
Journal: Journal of Clinical Oncology (2018)

508 Background: TALA has demonstrated efficacy in patients (pts) with BRCA+ metastatic breast cancer. We previously reported a window trial with median 88% tumor volume reduction after 2 months for early stage breast cancer. This study expanded to evaluate the pathologic response of TALA alone x 6 months in BRCA+ pts and operable breast cancer. Methods: The study was approved by the Institutional Review Board. Eligibility included ≥ 1 cm tumor and BRCA+. HER2+ tumors were excluded. Twenty pts underwent a pre-treatment biopsy, 6 months of once daily oral TALA (1 mg), followed by definitive surgery. Pts received adjuvant therapy at physician’s discretion. Endpoint was residual cancer burden (RCB). With 20 patients, the RCB0 + RCB1 response rate can be estimated with a 95% confidence interval with half width < 20%. Results: All 20 planned pts have enrolled from 08/2016-09/2017: median age = 38 (range 23-58); BRCA1+ = 16 and BRCA2+ = 4; 17 patients had triple negative breast cancer (TNBC, ER/PR < 10%) and 3 had hormone+ disease; Clinical stage I = 5, stage II = 12, Stage III = 3 including 1 patient with inflammatory breast carcinoma (IBC) and 1 with metaplastic chondrosarcomatous carcinoma (MpBC). One pt chose to receive chemotherapy prior to surgery so no RCB obtained. To date 18 pts have completed TALA and 17 surgery. This report will be updated with the final 2 patients scheduled for surgery in 03/2018. RCB0 = 9 (including the 1 pt with IBC and 1 pt with MpBC, 8 pts had TNBC and 1 with ER+ invasive lobular). RCBI = 1; RCB II = 5, RCBIII = 2. RCB0/1 rate = 10/17 = 59%, 95% CI = (36%, 78%). There was 1 grade 4 toxicity of thrombocytopenia. Grade 3 toxicities included: anemia = 8; neutropenia = 3, UTI = 1. Most common grade 1/2 toxicities included: nausea, fatigue, neutropenia, alopecia, dizziness and dyspnea. Toxicities were managed by dose reduction and transfusions. Nine pts required dose reduction. Conclusions: Single agent oral TALA once daily given preoperatively without chemotherapy produced significant pathologic complete responses with manageable toxicity. This pilot trial exceeded our expectations and is novel to demonstrate RCB0 in TNBC by a single targeted therapy. These results warrants a larger study for this pt population. Clinical trial information: NCT02282345.
Proprioception from a neurally controlled lower-extremity prosthesis
Authors: Tyler R. Clites, Matthew J. Carty, Jessica B. Ullauri, Matthew E. Carney, Luke M. Mooney, Jean-François Duval, Shriya S. Srinivasan, Hugh. M. Herr
Journal: Science Translational Medicine (2018)

An agonist-antagonist myoneural interface in a subject with a transtibial amputation improves prosthetic control.