tbuckley/cabot-search huggingface dataset:
A phase 1/2 study of a novel IL-2 cytokine, NKTR-214, and nivolumab in patients with select locally advanced or metastatic solid tumors.
Authors: Adi Diab, Nizar M. Tannir, Chantale Bernatchez, Cara L. Haymaker, Salah E Bentebibel, Brendan D. Curti, Michael K.K. Wong, Ivan Gergel, Mary Ann Tagliaferri, Jonathan Zalevsky, Ute Hoch, Sandra Aung, Michael Imperiale, Daniel C. Cho, Scott S. Tykodi, Igor Puzanov, Harriet M. Kluger, Michael E. Hurwitz, Patrick Hwu, Mario Sznol
Journal: Journal of Clinical Oncology (2017)

e14040 Background: NKTR-214 is a CD-122-biased agonist that targets the IL-2 pathway and is designed to provide sustained signaling through the heterodimeric IL-2 receptor pathway (IL-2Rβɣ) to preferentially activate and expand NK and effector CD8+ T cells over T regulatory cells within the tumor microenvironment. In a phase 1 monotherapy trial, pts treated with NKTR-214 demonstrated a substantial increase in CD8+ T and NK cells within the tumor microenvironment even when pretreated with multiple prior immunotherapeutic agents (abstract submitted). Based on this biomarker data and a favorable safety profile, a trial combining NKTR-214 and nivolumab was initiated. Methods: This is an on-going phase 1/2 study of NKTR-214 plus nivolumab in Pts with either melanoma (Mel), NSCLC, renal, bladder, or TNBC. Pts who are immunotherapy naïve or checkpoint therapy relapse/refractory are being studied separately. NKTR-214 and nivolumab are administered IV on a q2w or q3w schedule. Cohort 1 received NKTR-214 0.006 mg/kg q3w with nivolumab 240 mg q2w. Blood and tumor tissue were collected to measure immune activation using flow cytometry, immunohistochemistry, T cell clonality and gene expression analyses. Results: As of February 7, 2017, 5 Pts have been treated with the combination and all Pts were naïve to checkpoint inhibitors. There have been no dose limiting toxicities, no drug-related or immune related grade 3-5 adverse events (TRAEs) and no Pts have discontinued treatment. The most common TRAEs were pruritis and rash. Radiographic scans were available for 2 Pts. On treatment, Pt 1 with Mel had a mixed radiographic response at 1st scan, a ~40% decrease in LDH and a robust tumor immune cell infiltrate at week 3 the majority being newly proliferating CD8+ T cells expressing PD-1. Pt 2 with Mel had an unconfirmed complete response per RECIST 1.1 after 6 weeks of treatment; follow up tumor response data will be presented. Conclusions: Preliminary data demonstrate that NKTR-214 and nivolumab combination therapy is well tolerated with early evidence of clinical activity. Updated safety, pharmacokinetics, tumor response and biomarker data will be presented. Clinical trial information: NCT02983045.
Heart Rate and Outcomes in Hospitalized Patients With Heart Failure With Preserved Ejection Fraction
Authors: Phillip H. Lam, Daniel J. Dooley, Prakash Deedwania, Steven N. Singh, Deepak L. Bhatt, Charity J. Morgan, Javed Butler, Selma F. Mohammed, Wen-Chih Wu, Gurusher Panjrath, Michael R. Zile, Michel White, Cherinne Arundel, Thomas E. Love, Marc R. Blackman, Richard M. Allman, Wilbert S. Aronow, Stefan D. Anker, Gregg C. Fonarow, Ali Ahmed
Journal: Journal of the American College of Cardiology (2017)
Molecular imaging with 18F-fluoroestradiol (18F-FES) to assess intra-patient heterogeneity in metastatic breast cancer (MBC): A European TRANSCAN program
Authors: A. Gennari, E. Brain, O. Nanni, E. Muñoz Couselo, N. Harbeck, R. Geiss, A. Rocca, J. Cortés, T. Degenhardt, A. Piccardo, J-L. Albérini, F. Matteucci, A. Decensi, D.S. Corradengo, D. Andreis, D. Marra, G. Gebhart, C. Brambati, D. Amadori, P. Bruzzi
Journal: Annals of Oncology (2017)
A Novel Clinical Score to Assess Seizure Risk
Authors: Barry M. Czeisler, Jan Claassen
Journal: JAMA Neurology (2017)

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 Neurology 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 Neurology journal
68Ga-PSMA-PET/CT as a changing practice tool in biochemically recurrent prostate cancer
Authors: P.M. Domingues, T. Abreu, M.B. Siqueira, G. Marinho, D. Rosa, H. Cottas, L.H. Araujo, D. Herchenhorn, F.A. Peixoto
Journal: Annals of Oncology (2017)
MNK1/2 inhibition limits oncogenicity and metastasis of KIT-mutant melanoma
Authors: Yao Zhan, Jun Guo, William Yang, Christophe Goncalves, Tomasz Rzymski, Agnieszka Dreas, Eliza Żyłkiewicz, Maciej Mikulski, Krzysztof Brzózka, Aniela Golas, Yan Kong, Meng Ma, Fan Huang, Bonnie Huor, Qianyu Guo, Sabrina Daniela da Silva, Jose Torres, Yutian Cai, Ivan Topisirovic, Jie Su, Krikor Bijian, Moulay A. Alaoui-Jamali, Sidong Huang, Fabrice Journe, Ghanem E. Ghanem, Wilson H. Miller, Sonia V. del Rincón
Journal: Journal of Clinical Investigation (2017)

Melanoma can be stratified into unique subtypes based on distinct pathologies. The acral/mucosal melanoma subtype is characterized by aberrant and constitutive activation of the proto-oncogene receptor tyrosine kinase C-KIT, which drives tumorigenesis. Treatment of these melanoma patients with C-KIT inhibitors has proven challenging, prompting us to investigate the downstream effectors of the C-KIT receptor. We determined that C-KIT stimulates MAP kinase-interacting serine/threonine kinases 1 and 2 (MNK1/2), which phosphorylate eukaryotic translation initiation factor 4E (eIF4E) and render it oncogenic. Depletion of MNK1/2 in melanoma cells with oncogenic C-KIT inhibited cell migration and mRNA translation of the transcriptional repressor SNAI1 and the cell cycle gene CCNE1. This suggested that blocking MNK1/2 activity may inhibit tumor progression, at least in part, by blocking translation initiation of mRNAs encoding cell migration proteins. Moreover, we developed an MNK1/2 inhibitor (SEL201), and found that SEL201-treated KIT-mutant melanoma cells had lower oncogenicity and reduced metastatic ability. Clinically, tumors from melanoma patients harboring KIT mutations displayed a marked increase in MNK1 and phospho-eIF4E. Thus, our studies indicate that blocking MNK1/2 exerts potent antimelanoma effects and support blocking MNK1/2 as a potential strategy to treat patients positive for KIT mutations.
First FDA Approval Agnostic of Cancer Site — When a Biomarker Defines the Indication
Authors: Steven Lemery, Patricia Keegan, Richard Pazdur
Journal: New England Journal of Medicine (2017)

In May 2017, the FDA approved pembrolizumab, a programmed death 1 inhibitor, for adult and pediatric patients with unresectable or metastatic, microsatellite-instability–high or mismatch-repair–deficient solid tumors, regardless of tumor site or histology.
Staphylococcus aureus meticillino-resistente: verso una risposta coordinata a una sfida continua
Authors: M J Struelens, O Denis
Journal: Eurosurveillance (2000)

Lo Staphylococcus aureus meticillino-resistente (MRSA) rappresenta una seria sfida per la sanita pubblica in molte istituzioni sanitarie in tutto il mondo. E' una causa comune di epidemie di infezioni crociate ed e diventato endemico in molte regioni dove contribuisce alla morbosita, alla mortalita, e ai costi dell'assistenza associata alle infezioni ospedaliere. Il recente progetto EARSS (European Antimicrobial Resistance Surveillance System) ha fornito dati che suggeriscono che, in Europa, la meticillino-resistenza tra gli S. aureus isolati da sangue e piu comune nei paesi dell'Europa meridionale che in quelli settentrionali (1).
High chemopreventive and therapeutic efficacy of Id1 inhibition in KRAS-mutant (KM) adenocarcinoma (AD) non-small cell lung cancer (NSCLC)
Authors: M. Roman Moreno, S. Vicent, I. Lopez, I. Baraibar Argota, E. Fraile, I. Gil Bazo
Journal: Annals of Oncology (2017)
Association of Public Health Initiatives With Outcomes for Out-of-Hospital Cardiac Arrest at Home and in Public Locations
Authors: Christopher B. Fordyce, Carolina M. Hansen, Kristian Kragholm, Matthew E. Dupre, James G. Jollis, Mayme L. Roettig, Lance B. Becker, Steen M. Hansen, Tomoya T. Hinohara, Claire C. Corbett, Lisa Monk, R. Darrell Nelson, David A. Pearson, Clark Tyson, Sean van Diepen, Monique L. Anderson, Bryan McNally, Christopher B. Granger
Journal: JAMA Cardiology (2017)

Little is known about the influence of comprehensive public health initiatives according to out-of-hospital cardiac arrest (OHCA) location, particularly at home, where resuscitation efforts and outcomes have historically been poor.
ATF4-Induced Metabolic Reprograming Is a Synthetic Vulnerability of the p62-Deficient Tumor Stroma
Authors: Juan F. Linares, Thekla Cordes, Angeles Duran, Miguel Reina-Campos, Tania Valencia, Christopher S. Ahn, Elias A. Castilla, Jorge Moscat, Christian M. Metallo, Maria T. Diaz-Meco
Journal: Cell Metabolism (2017)
Myeloid Notch1 deficiency activates the RhoA/ROCK pathway and aggravates hepatocellular damage in mouse ischemic livers
Authors: Ling Lu, Shi Yue, Longfeng Jiang, Changyong Li, Qiang Zhu, Michael Ke, Hao Lu, Xuehao Wang, Ronald W. Busuttil, Qi‐Long Ying, Jerzy W. Kupiec‐Weglinski, Bibo Ke
Journal: Hepatology (2017)

Notch signaling plays an emerging role in the regulation of immune cell development and function during inflammatory response. Activation of the ras homolog gene family member A/Rho‐associated protein kinase (ROCK) pathway promotes leukocyte accumulation in tissue injury. However, it remains unknown whether Notch signaling regulates ras homolog gene family member A/ROCK–mediated immune responses in liver ischemia and reperfusion (IR) injury. This study investigated intracellular signaling pathways regulated by Notch receptors in the IR‐stressed liver and in vitro . In a mouse model of IR‐induced liver inflammatory injury, we found that mice with myeloid‐specific Notch1 knockout showed aggravated hepatocellular damage, with increased serum alanine aminotransferase levels, hepatocellular apoptosis, macrophage/neutrophil trafficking, and proinflammatory mediators compared to Notch1‐proficient controls. Unlike in the controls, myeloid Notch1 ablation diminished hairy and enhancer of split‐1 (Hes1) and augmented c‐Jun N‐terminal kinase (JNK)/stress‐activated protein kinase–associated protein 1 (JSAP1), JNK, ROCK1, and phosphatase and tensin homolog (PTEN) activation in ischemic livers. Disruption of JSAP1 in myeloid‐specific Notch1 knockout livers improved hepatocellular function and reduced JNK, ROCK1, PTEN, and toll‐like receptor 4 activation. Moreover, ROCK1 knockdown inhibited PTEN and promoted Akt, leading to depressed toll‐like receptor 4. In parallel in vitro studies, transfection of lentivirus‐expressing Notch1 intracellular domain promoted Hes1 and inhibited JSAP1 in lipopolysaccharide‐stimulated bone marrow–derived macrophages. Hes1 deletion enhanced JSAP1/JNK activation, whereas clustered regularly interspaced short palindromic repeats/CRISPR‐associated protein 9–mediated JSAP1 knockout diminished ROCK1/PTEN and toll‐like receptor 4 signaling. Conclusion: Myeloid Notch1 deficiency activates the ras homolog gene family member A/ROCK pathway and exacerbates hepatocellular injury by inhibiting transcriptional repressor Hes1 and inducing scaffold protein JSAP1 in IR‐triggered liver inflammation; our findings underscore the crucial role of the Notch–Hes1 axis as a novel regulator of innate immunity‐mediated inflammation and imply the therapeutic potential for the management of organ IR injury in transplant recipients. (H epatology 2018;67:1041–1055)
Glycated Apolipoprotein A-IV Induces Atherogenesis in Patients With CAD in Type 2 Diabetes
Authors: Yang Dai, Ying Shen, Qing Run Li, Feng Hua Ding, Xiao Qun Wang, Hong Juan Liu, Xiao Xiang Yan, Ling Jie Wang, Ke Yang, Hai Bo Wang, Qiu Jing Chen, Wei Feng Shen, Rui Yan Zhang, Lin Lu
Journal: Journal of the American College of Cardiology (2017)
<i>Notes from the Field</i>: Multiple Cases of Seoul Virus Infection in a Household with Infected Pet Rats — Tennessee, December 2016–April 2017
Authors: Mary-Margaret A. Fill, Heather Mullins, Andrew Stephen May, Heather Henderson, Shelley M. Brown, Cheng-Feng Chiang, Nishi R. Patel, John D. Klena, Annabelle de St. Maurice, Barbara Knust, Stuart T. Nichol, John R. Dunn, William Schaffner, Timothy F. Jones
Journal: MMWR Morbidity and Mortality Weekly Report (2017)
Multicenter, phase III, open-label, randomized study in relapsed/refractory CLL to evaluate the benefit of GDC-0199 (ABT-199) plus rituximab compared with bendamustine plus rituximab.
Authors: Mehrdad Mobasher, Jane Huang, Rebecca L. Elstrom, Mostafa Elhamy, Coen Bernaards, Michael J. Hallek, Peter Hillmen, Arnon Philip Kater, Thomas J. Kipps, John Francis Seymour
Journal: Journal of Clinical Oncology (2014)

TPS7120^ Background: Response rate to initial treatment of CLL is high, but relapsed/refractory (R/R) CLL may be characterized by resistance to chemotherapy. Bendamustine and rituximab (B+R), commonly used to treat patients with relapsed CLL, has shown an overall response rate (ORR) of 59% and median progression-free survival (PFS) of 15.2 mo. Despite progress, CLL remains incurable, and new treatments are needed to improve outcomes. Universal overexpression of Bcl-2, an anti-apoptotic protein, and dysregulation of the intrinsic apoptotic pathway in CLL likely contributes to chemotherapy resistance. GDC-0199/ABT-199 (199), a selective, potent, orally bioavailable Bcl-2 inhibitor, has shown preliminary anti-tumor activity, including complete remissions, in R/R CLL. This study will compare 199+R vs B+R to determine if 199+R provides a more effective and tolerable treatment strategy for R/R CLL, providing a chemotherapy-free regimen. Methods: Approximately 370 patients will be enrolled at approximately 150 sites in North America, Europe and Asia Pacific, and randomized 1:1 to receive 199+R (Arm A) or B+R (Arm B). In both arms, R treatment will consist of infusions on Day 1 of each 28-day cycle for 6 cycles (Cycle 1: 375mg/m2; Cycles 2-6: 500mg/m2). In Arm A, after an initial ramp-up period, patients will receive 400mg of 199 daily. After completion of 199+R, 199 will be continued until disease progression or for a maximum of 2 years. In Arm B, bendamustine will be infused (70mg/m2) on Days 1 and 2 of each 28-day cycle for 6 cycles. Patients in both arms will be followed until disease progression. Key eligibility criteria include a diagnosis of R/R CLL; previously treatment with 1-3 lines of therapy; ECOG PS ≤1; and adequate marrow function. The primary outcome is investigator-assessed PFS (time from randomization until disease progression or death from any cause). Secondary outcomes include ORR, adverse events, and patient-reported outcomes. The study opened in Dec 2013; primary estimated completion is Aug 2020. Clinical trial information: NCT02005471.
Cost-effectiveness of nivolumab+ipilimumab in first-line treatment of advanced melanoma: Analysis using 28-month overall survival from CheckMate 067
Authors: J. Sabater, T. Baker, V. Paly, K. Gupte-Singh, M. Lorenzi, A. Jeffers, H. Beyhaghi, S. Kotapati, S. Rao, A. Briggs
Journal: Annals of Oncology (2017)
GW28-e0756 New and Definitive Marker Confirming the Optimal Status in the Treatment of Heart Failure with Preserved Ejection Fraction
Authors: Thach Nguyen, Khanh Duong, Luong Ngoc Tuyet Nhi, Nguyen Minh Tri Nhan, Luong Thanh Phuoc, Gianluca Rigatelli
Journal: Journal of the American College of Cardiology (2017)
Abstract 15090: Impact of Disclosure of Genetic Risk for Coronary Heart Disease on Physician Attitudes and Decision-Making: The MI-GENES Study
Authors: Sherry-Ann Brown, Hayan Jouni, Iftikhar Kullo
Journal: Circulation (2016)

Introduction:  Whether electronic health record (EHR)-based disclosure of genetic risk of coronary heart disease (CHD) influences physician decision-making and attitudes toward clinical use of genomic information is unknown.   Hypothesis:  We hypothesized that receipt of a multi-locus CHD genetic risk score (GRS) for a patient would lead to positive physician attitudes regarding incorporation of genomic information in clinical practice and assist with clinical decision-making.   Methods:  The MI-GENES trial randomized patients aged 45-65 years (n=203) at intermediate risk for CHD to receive conventional risk scores (‘CRS encounters’) or CRS plus a 28-variant GRS (‘GRS encounters’). Risk was disclosed using an EHR-based decision aid, along with genetic counseling and physician discussion. All study physicians had both CRS and GRS encounters. A survey was completed by study physicians following risk disclosure encounters. Data were analyzed using logistic regression and expressed as odds ratio (OR) with 95% confidence intervals. For responses with low frequency, data were analyzed using Fisher’s exact test, and p-values were reported.   Results:  Academic faculty cardiologists (n=4) and internists (n=2) participated in the disclosure of GRS/CRS risk to patients. Following GRS encounters, physicians were more likely to report that they would use the genetic risk score if it becomes available in the future (100% versus 83%, p=0.0001), and to recommend CHD genetic testing to family members if available in the future (OR 16.38 (4.67-103.89), p=   Conclusions:  Availability of a multi-locus GRS for CHD associated with positive physician attitudes toward incorporation of genomic information in clinical practice and assisted with clinical decision-making in precision medicine.
Retrospective analysis of glioblastoma multiforme (GBM) patients treated initially with BCNU compared to temozolomide (TMZ) with concomitant radiation therapy
Authors: M. Vinjamuri, R. Adumala, R. Altaha, J. Hobbs, E. Crowell
Journal: Journal of Clinical Oncology (2007)

2071 Background: TMZ and radiation as initial treatment has become the standard of care for GBM. There are no randomized studies comparing TMZ to BCNU in GBM. Methods: We did a retrospective analysis of all 100 GBM patients (pts) diagnosed by our pathology department in the last 10 years. 20 pts were excluded, in 12 pts no chemotherapy was given and there was no data available for 8 pts. BCNU treatment was given in earlier years than TMZ generally. Overall survival (OS), progression free survival (PFS) and four prognostic factors were compared between BCNU and TMZ treated groups. Results: Results show that there is no significant difference in OS and PFS between the two groups. Survival curves were superimposable. This is despite the fact that tumor size and ECOG performance status were worse, though not significantly so in the BCNU group. Age was the only variable that correlated with survival. After correcting for age there was still no difference in PFS and OS between the BCNU and TMZ group. Conclusions: Our study fails to shows superiority of TMZ over BCNU despite the fact that the BCNU group had worse prognostic factors. A randomized comparison of these two agents seems justifiable. [Table: see text] No significant financial relationships to disclose.
Veliparib with temozolomide or carboplatin/paclitaxel versus placebo with carboplatin/paclitaxel in patients with BRCA1/2 locally recurrent/metastatic breast cancer: randomized phase II study
Authors: H.S. Han, V. Diéras, M. Robson, M. Palácová, P.K. Marcom, A. Jager, I. Bondarenko, D. Citrin, M. Campone, M.L. Telli, S.M. Domchek, M. Friedlander, B. Kaufman, J.E. Garber, Y. Shparyk, E. Chmielowska, E.H. Jakobsen, V. Kaklamani, W. Gradishar, C.K. Ratajczak, C. Nickner, Q. Qin, J. Qian, S.P. Shepherd, S.J. Isakoff, S. Puhalla
Journal: Annals of Oncology (2017)
Retraction Note to: Extranuclear ERα is associated with regression of T47D PKCα-overexpressing, tamoxifen-resistant breast cancer
Authors: Bethany Perez White, Mary Ellen Molloy, Huiping Zhao, Yiyun Zhang, Debra A. Tonetti
Journal: Molecular Cancer (2017)

Prior to the introduction of tamoxifen, high dose estradiol was used to treat breast cancer patients with similar efficacy as tamoxifen, albeit with some undesirable side effects. There is renewed interest to utilize estradiol to treat endocrine resistant breast cancers, especially since findings from several preclinical models and clinical trials indicate that estradiol may be a rational second-line therapy in patients exhibiting resistance to tamoxifen and/or aromatase inhibitors. We and others reported that breast cancer patients bearing protein kinase C alpha (PKCα)- expressing tumors exhibit endocrine resistance and tumor aggressiveness. Our T47D:A18/PKCα preclinical model is tamoxifen-resistant, hormone-independent, yet is inhibited by 17β-estradiol (E2) in vivo. We previously reported that E2-induced T47D:A18/PKCα tumor regression requires extranuclear ERα and interaction with the extracellular matrix. T47D:A18/PKCα cells were grown in vitro using two-dimensional (2D) cell culture, three-dimensional (3D) Matrigel and in vivo by establishing xenografts in athymic mice. Immunofluoresence confocal microscopy and co-localization were applied to determine estrogen receptor alpha (ERα) subcellular localization. Co-immunoprecipitation and western blot were used to examine interaction of ERα with caveolin-1. We report that although T47D:A18/PKCα cells are cross-resistant to raloxifene in cell culture and in Matrigel, raloxifene induces regression of tamoxifen-resistant tumors. ERα rapidly translocates to extranuclear sites during T47D:A18/PKCα tumor regression in response to both raloxifene and E2, whereas ERα is primarily localized in the nucleus in proliferating tumors. E2 treatment induced complete tumor regression whereas cessation of raloxifene treatment resulted in tumor regrowth accompanied by re-localization of ERα to the nucleus. T47D:A18/neo tumors that do not overexpress PKCα maintain ERα in the nucleus during tamoxifen-mediated regression. An association between ERα and caveolin-1 increases in tumors regressing in response to E2. Extranuclear ERα plays a role in the regression of PKCα-overexpressing tamoxifen-resistant tumors. These studies underline the unique role of extranuclear ERα in E2- and raloxifene-induced tumor regression that may have implications for treatment of endocrine-resistant PKCα-expressing tumors encountered in the clinic.
Pathogenetic insights from quantification of the cerebriform connective tissue nevus in Proteus syndrome
Authors: Neera R. Nathan, Rachna Patel, Molly M. Crenshaw, Marjorie J. Lindhurst, Cara Olsen, Leslie G. Biesecker, Kim M. Keppler-Noreuil, Thomas N. Darling
Journal: Journal of the American Academy of Dermatology (2017)
Mechanotransduction of human pluripotent stem cells cultivated on tunable cell-derived extracellular matrix
Authors: In Gul Kim, Chang-Hyun Gil, Joseph Seo, Soon-Jung Park, Ramesh Subbiah, Taek-Hee Jung, Jong Soo Kim, Young-Hoon Jeong, Hyung-Min Chung, Jong Ho Lee, Man Ryul Lee, Sung-Hwan Moon, Kwideok Park
Journal: Biomaterials (2017)
GW28-e0689 Updating 10-year atherosclerotic cardiovascular risk assessment equation for Chinese adults
Authors: Miao Wang, Jing Liu, Wei Wang, Jun Liu, Jiayi Sun, Yue Qi, Ying Wang, Yongchen Hao, Lanping Qin, Mengge Zhou, Shen Gao, Dong Zhao
Journal: Journal of the American College of Cardiology (2017)