tbuckley/cabot-search huggingface dataset:
The Rapid Rise in Investment in Psychedelics—Cart Before the Horse
Authors: Joshua Phelps, Ravi N. Shah, Jeffrey A. Lieberman
Journal: JAMA Psychiatry (2022)

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 Psychiatry 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 Psychiatry journal
COVID-19 and myocardial infarction – Authors' reply
Authors: Ioannis Katsoularis, Osvaldo Fonseca-Rodríguez, Paddy Farrington, Krister Lindmark, Anne-Marie Fors Connolly
Journal: The Lancet (2021)

of ischaemic stroke, which shares some of the same pathophysiological features as myocardial infarction.Furthermore, the increase in the risk of myocardial infarction was of the same magnitude as for ischaemic stroke, for which the risk of inaccurate diagnosis codification was low.Therefore, the case of a connection between COVID19 and cardiovascular events is strengthened.We declare no competing interests.
Cancer Chemotherapy
Authors: Mary E. Costanza
Journal: JAMA (1980)

This third and welcome edition of<i>Cancer Chemotherapy</i>is a useful, well-written, and succinct review of modern day chemotherapy. It contains a brief, clear account of the basic theory underlying the pharmacologic principles of chemotherapy. An extended section describes specific properties, such as mechanism of action, metabolism, toxicity, and administration, for each of the more commonly used drugs. Chapters on each of the organ cancers follow. Most are focused exclusively on chemotherapeutic interventions. Some are more generalized, with brief discussions including rules for staging workup and indications for other modalities of treatment. The notably complex section on testicular carcinoma is particularly well done. It deals with interdisciplinary maneuvers, and includes the latest successful combination chemotherapy regimens for advanced stages. The section on breast cancer is good, but, perhaps because of my own interest in the subject, I think it a little short on some of the major controversial issues that
Artificial Intelligence–Assisted Amphiregulin and Epiregulin IHC Predicts Panitumumab Benefit in <i>RAS</i> Wild-Type Metastatic Colorectal Cancer
Authors: Christopher J.M. Williams, Jenny F. Seligmann, Faye Elliott, Michael Shires, Susan D. Richman, Sarah Brown, Liping Zhang, Shalini Singh, Judith Pugh, Xiao-Meng Xu, Andrea Muranyi, Christoph Guetter, Auranuch Lorsakul, Uday Kurkure, Zuo Zhao, Jim Martin, Xingwei Wang, Kien Nguyen, Wen-Wei Liu, Dongyao Yan, Nicholas P. West, Jennifer H. Barrett, Michael Barnes, Isaac Bai, Matthew T. Seymour, Philip Quirke, Kandavel Shanmugam
Journal: Clinical Cancer Research (2021)

High tumor mRNA levels of the EGFR ligands amphiregulin (AREG) and epiregulin (EREG) are associated with anti-EGFR agent response in metastatic colorectal cancer (mCRC). However, ligand RNA assays have not been adopted into routine practice due to issues with analytic precision and practicality. We investigated whether AREG/EREG IHC could predict benefit from the anti-EGFR agent panitumumab.Artificial intelligence algorithms were developed to assess AREG/EREG IHC in 274 patients from the PICCOLO trial of irinotecan with or without panitumumab (Ir vs. IrPan) in RAS wild-type mCRC. The primary endpoint was progression-free survival (PFS). Secondary endpoints were RECIST response rate (RR) and overall survival (OS). Models were repeated adjusting separately for BRAF mutation status and primary tumor location (PTL).High ligand expression was associated with significant PFS benefit from IrPan compared with Ir [8.0 vs. 3.2 months; HR, 0.54; 95% confidence interval (CI), 0.37-0.79; P = 0.001]; whereas low ligand expression was not (3.4 vs. 4.4 months; HR, 1.05; 95% CI, 0.74-1.49; P = 0.78). The ligand-treatment interaction was significant (Pinteraction = 0.02) and remained significant after adjustment for BRAF-mutation status and PTL. Likewise, RECIST RR was significantly improved in patients with high ligand expression (IrPan vs. Ir: 48% vs. 6%; P < 0.0001) but not those with low ligand expression (25% vs. 14%; P = 0.10; Pinteraction = 0.01). The effect on OS was similar but not statistically significant.AREG/EREG IHC identified patients who benefitted from the addition of panitumumab to irinotecan chemotherapy. IHC is a practicable assay that may be of use in routine practice.
Cancer Commons’ virtual tumor board program: A patient-centric advisory panel and real-world data registry.
Authors: Lola Rahib, David Kuang-Fu Chang, Davendra Sohal, Conan Grant Kinsey, Deborah Christensen, Mark Shapiro, Fatima Zelada-Arenas, Andrew Scott Paulson, Muhammad Shaalan Beg
Journal: Journal of Clinical Oncology (2022)

527 Background: We initiated a nationwide Virtual Tumor Board (VTB) program for pancreatic cancer (PC) patients (pts). The VTB consists of oncology experts and serves as an advisory panel by providing information on treatment (Tx) options based on a comprehensive review of patients’ oncologic history. Personalized Tx options and their rationales are provided and outcomes tracked in a prospective registry (XCELSIOR). Methods: PC pts who participated in XCELSIOR shared access to their full medical records, which were collected, processed, and abstracted. The panel reviewed cases asynchronously through an interactive platform followed by a VTB which was held weekly through videoconferencing. Tx options were summarized into a written report and provided to patients and their physicians. Outcomes and quality of life are tracked longitudinally through an IRB-approved 21CFR11 compliant observational registry (XCELSIOR). Results: From 9/2020 to 8/2021, the VTB reviewed 79 unique cases; 56% were male; median age at diagnosis was 66 (50-87). At the time of VTB, 68 (87%) had metastatic disease and 8 (10%) had locally advanced disease. Median prior therapy lines was 2 (0-9), with 26 (35%), 24 (32%), 6 (8%), and 19 (25%) pts having received 1, 2, 3 and 4+ lines of therapy, respectively. Median time from diagnosis for pts presenting after 1, 2, and 3+ lines of prior Tx was 9.5, 11, and 17.5 months, respectively. First-line Tx was FOLFIRINOX in 40 (53%) pts and gemcitabine/nab-paclitaxel in 22 (29%) pts. At the time of VTB, 32 (37%) of patients had stable disease, 23 (26%) had disease progression, 18 (21%) had recently started a new Tx, 7 (8%) were responding to Tx, 3 (3%) had stable disease on imaging but rising CA 19-9, and 4 (4%) were others. Prior to VTB, 69 (87%) pts had molecular profiling results available. Collectively the VTB provided 375 Tx and diagnostic (NGS, imaging, etc.) options with a median of 4 (1-12) options per patient. As of 9/8/2021, 87 VTB reports were provided. Of 25 instances of ‘no Tx decision’, 10 (40%) are deceased, 10 (40%) are stable, and 5 (10%) had other reasons. Of the 25 people who started a subsequent Tx, 14 (56%) were identified by the VTB. These included 9 (64%) FDA-approved, 3 (21%) off-label, and 2 (14%) on-trial Tx. Tx not identified by the VTB included 3 (33%) FDA-approved, 2 (22%) off-label, 2 (22%) on-trial, and 2 (22%) local Tx. Conclusions: We present our experience of utilizing a platform for patients to receive a virtual tumor board review and utilize an IRB-approved registry as a learning system. Early data indicate successes in identifying treatment and clinical trial opportunities. Future steps include streamlining communication with primary oncologists and enhancing access to treatments. NCT03793088.
A Treacherous Course
Authors: Jessica Little, Anand Vaidya, Nikolaus Jilg, Emily S. Lau, Meghan A. Baker
Journal: New England Journal of Medicine (2021)

A 33-year-old man presented to the emergency department in September 2019 with vomiting, abdominal pain, and fever. One month before presentation, he attempted to emigrate from Mexico to the United States. At that time, he was apprehended and sent to a detention center in Texas. He was subsequently deported to Mexico. He made a second attempt to emigrate 2 weeks before presentation, traveling on foot through Mexico and crossing the border by swimming across the Rio . . .
Differential Kinase Activity Across Prostate Tumor Compartments Defines Sensitivity to Target Inhibition
Authors: Nezihi Murat Karabacak, Yu Zheng, Taronish D. Dubash, Risa Burr, Douglas S. Micalizzi, Ben S. Wittner, Maoxuan Lin, Devon F. Wiley, Valentine Comaills, Erin Emmons, Kira L. Niederhoffer, Uyen Ho, Jacob Ukleja, Dante Che, Hannah Stowe, Linda T. Nieman, Wilhelm Haas, Shannon L. Stott, Michael S. Lawrence, David T. Ting, David T. Miyamoto, Daniel A. Haber, Mehmet Toner, Shyamala Maheswaran
Journal: Cancer Research (2022)

Cancer therapy often results in heterogeneous responses in different metastatic lesions in the same patient. Inter- and intratumor heterogeneity in signaling within various tumor compartments and its impact on therapy are not well characterized due to the limited sensitivity of single-cell proteomic approaches. To overcome this barrier, we applied single-cell mass cytometry with a customized 26-antibody panel to PTEN-deleted orthotopic prostate cancer xenograft models to measure the evolution of kinase activities in different tumor compartments during metastasis or drug treatment. Compared with primary tumors and circulating tumor cells (CTC), bone metastases, but not lung and liver metastases, exhibited elevated PI3K/mTOR signaling and overexpressed receptor tyrosine kinases (RTK) including c-MET protein. Suppression of c-MET impaired tumor growth in the bone. Intratumoral heterogeneity within tumor compartments also arose from highly proliferative EpCAM-high epithelial cells with increased PI3K and mTOR kinase activities coexisting with poorly proliferating EpCAM-low mesenchymal populations with reduced kinase activities; these findings were recapitulated in epithelial and mesenchymal CTC populations in patients with metastatic prostate and breast cancer. Increased kinase activity in EpCAM-high cells rendered them more sensitive to PI3K/mTOR inhibition, and drug-resistant EpCAM-low populations with reduced kinase activity emerged over time. Taken together, single-cell proteomics indicate that microenvironment- and cell state-dependent activation of kinase networks create heterogeneity and differential drug sensitivity among and within tumor populations across different sites, defining a new paradigm of drug responses to kinase inhibitors.
Relevance of using caspase-3 detection versus TUNEL-test in studies of vascular cell apoptosis Randolph Hutter, Merce Roque, Bernhard Sauter, John T. Fallon, Carlos Cordon-Cardo, Valentin Fuster, Juan Jose Badimon. Cardiovascular Institute. Mount Sinai School of Medicine, New York, NY
Journal: Journal of the American College of Cardiology (2001)
FACIAL PAIN
Authors: C J McGEE, W D LUXMORE
Journal: Annals of Internal Medicine (1949)

Article1 May 1949FACIAL PAINCHAS. J. MCGEE, M.D., WILLIAM D. LUXMORE, D.D.S.CHAS. J. MCGEE, M.D.Search for more papers by this author, WILLIAM D. LUXMORE, D.D.S.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-30-5-914 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptFor some time we have been amazed at some of the unusual concomitants of dental disorders, especially with reference to the cause of pain so frequently seen in and around the face. The subject has been copiously reviewed as "Atypical Face Pain" by McElin and Horton,1and Glaser,2, 3, 4to whose papers and bibliographies one is referred. These authors have in the main dealt with the pathways by which pain is referred, and have attempted to treat the pain by an attack on the pathway, while Kelly and Langheinz5appear to have made a step in attacking the cause...Bibliography1. MCELINHORTON TWBT: Atypical face pain: a statistical consideration of 66 cases, Ann. Int. Med., 1947, xxxi, 749-768. Google Scholar2. GLASER MA: Atypical neuralgia, so called: a critical analysis of 143 cases, Arch. Neurol. and Psychiat., 1928, xx, 537-558. CrossrefGoogle Scholar3. GLASERBEERMAN MAHM: Atypical facial neuralgia: an analysis of 200 cases, Arch. Int. Med., 1938, lxi, 172-183. CrossrefGoogle Scholar4. GLASER MA: Atypical facial neuralgia: diagnosis, cause, and treatment, Arch. Int. Med., 1940, lxv, 340-367. CrossrefGoogle Scholar5. KELLYLANGHEINZ WJHW: Dental treatment of trismus, tinnitus, otalgia and obscure neuralgias, Arch. Otolaryng., 1947, xlv, 191-204. CrossrefGoogle Scholar6. LUXMORE WD: Peridental atrophy, Mid-West Homeopathic News Jr., 1931, iv, 307-309. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication April 10, 1948.†Formerly Fellow in Medicine, Northwestern University, Chicago, Illinois. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1949Volume 30, Issue 5Page: 914-918 ePublished: 1 December 2008 Issue Published: 1 May 1949 PDF downloadLoading ...
Table of Contents
Authors: Corey Georgesen, Lindy Fox, Joanna Harp, Warren Heymann, Hidemi Nakagawa, Osamu Nemoto, Atsuyuki Igarashi, Hidehisa Saeki, Hironobu Kaino, Takeshi Nagata, Cheng Quan, Xiao-Ying Chen, Xia Li, Feng Xue, Li-Hong Chen, Na Liu, Bo Wang, Lan-Qi Wang, Xiao-Pan Wang, Hui Yang, Jie Zheng, Saud Aleissa, Cristian Navarrete-Dechent, Miguel Cordova, Aditi Sahu, Stephen Dusza, William Drph, Anthony Phillips, Erica Rossi, Kishwer Lee, Shiri Nawrocki, Jisun Cha, Fahimeh Abdollahimajd, Nasim Niknezhad, Reza Haghighatkhah, Nastaran Namazi, Nakisa Niknejad, Atefeh Talebi, Veronika Teusch, Wibke Uller, Florentine Manger, Katharina Vill, Armin Piehler, Rene´m€ Uller-Wille, Holger Goessman, Simone Hammer, Walter Wohlgemuth, Robert Micheletti, Peter Chansky, Paul Haun, John Seykora, Jennifer Dekerlegand, Laith Sultan, Susan Schultz, Chandra Sehgal, Joseph Sobanko, Mika Tabata, Sara Choi, Kelsey Hirotsu, Bernice Kwong, Teo Soleymani
Journal: Journal of the American Academy of Dermatology (2020)
Javits Center
Authors: JoAnne Burger
Journal: JAMA (2021)

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 HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 2022 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 journal
Abstract 43: A20 Plays as a Regulator in Tnfα-induced Injury of Human Umbilical Vein Endothelial Cells Through Tak1-dependent Pathway
Authors: Lei Li, Jiafeng Lin, Maoping Chu, Kangting Ji, Lianpin Wu
Journal: Circulation Research (2017)

A20, a negative regulator of nuclear factor κB signaling, has been shown to attenuate atherosclerotic events. Transforming growth factor beta-activated kinase 1 (TAK1) plays a critical role in TNFα-induced atherosclerosis via endothelial nitric oxide (NO) synthase (eNOS) uncoupling and NO reduction. Aims: In the study, we investigated the hypothesis that A20 protected endothelial cells induced by TNFα through modulating eNOS activity and TAK1 signalling. Human umbilical vein endothelial cells (HUVECs) were stimulated by TNFα. The impact of A20 on cell apoptosis, eNOS expression and NO production and related TAK1 pathway were detected. Both eNOS and NO production were remarkably reduced, TAK1and p38 MAPK phosphorylation, HUVECs apoptosis increased after TNFα stimulation for 2 hrs, all of which were effectively attenuated by A20 over-expression. Inhibition of A20 significantly activated TAK1, p38 MAPK phosphorylation, and cell apoptosis, but eNOS expression, NO production decreased. Furthermore, p38 MAPK expression was suppressed by A20 over-expression, but re-enhanced by inhibiting A20 or activation of TAK1. Furtherly, TNFα-induced suppression of eNOS and NO production were largely prevented by silencing p38 MAPK. Collectively, our results suggested that A20-mediated TAK1 inactivation suppresses p38 MAPK and regulated MAPK/eNOS pathway, which contributes to endothelial cell survival and function preservation.
Necropsy Percentage.
Journal: JAMA (1926)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
The effect of the interleukin-6 -174G&gt;C Promoter gene polymorphism on endothelial function David J. Brull, Paul Leeson, Michael Mullen, Marcello deDivitis, Hugh E. Montgomery, John E. Deanfield, Steve E. Humphries. Royal Free and University College London Medical School, London, United Kingdom, Great Ormond Street Hospital, London, United Kingdom
Journal: Journal of the American College of Cardiology (2001)
Medical Error
Journal: JAMA (2006)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
VIENNA
Journal: JAMA (1933)

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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Triple Therapy to Outwit the <i>BRAF</i> Oncogene
Authors: Chao Zhang, Gideon Bollag
Journal: Cancer Discovery (2021)

BRAF-mutant cancers have been knocked down by BRAF and MEK inhibitor combos, yet the cancers always find a way to get back up. Adding a third medicine, namely, a dimer-selective BRAF inhibitor, can knock down longer and better.See related article by Adamopoulos et al., p. 1716.