tbuckley/cabot-search huggingface dataset:
Addresses and Other Papers
Journal: JAMA (1905)

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
Using Telemedicine to Treat Opioid Use Disorder in Rural Areas
Authors: Rita Rubin
Journal: JAMA (2019)

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 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
Randomized, blinded, placebo-controlled phase II trial of docetaxel and bavituximab as second-line therapy in locally advanced or metastatic non-squamous non-small cell lung cancer.
Authors: Mikhail Shtivelband, David R. Spigel, David E. Gerber, Minish Mahendra Jain, Olga V. Ponomarova, Davit Giorgadze, Joseph Shan, Kerstin B. Menander, Chandra Prakash Belani
Journal: Journal of Clinical Oncology (2013)

8095 Background: Bavituximab (B) is a monoclonal antibody against phosphatidylserine (PS) with a selective tumor vascular-directed immune response. The purpose of this trial is to evaluate the efficacy and safety of B or placebo (P) combined with docetaxel (D) in patients with locally advanced or metastatic non-squamous NSCLC. Methods: Patients were randomized 1:1:1 to receive 75 mg/m 2 of D every 21 days for up to 6 cycles combined with weekly blinded infusions of P, 1mg/kg B or 3 mg/kg B until disease progression or unacceptable toxicity. Primary efficacy endpoint was overall response rate (ORR). Secondary endpoints included progression free survival (PFS) and overall survival (OS). Safety was evaluated by adverse events (AEs), vital signs, CBC, biochemistry, urinalysis, coagulation, ECG. Post study unblinding, a PK substudy revealed vial coding discrepancies in the P and 1 mg/kg vials. As a result, data from these two groups were pooled to form the control (C) arm in the analysis. Results: Forty-one patients were entered into the 3mg/kg B+D arm and 80 into the control arm. No significant differences were seen in age, gender, ethnicity or disease stage. ECOG 2 was 13% in C and 24% in 3 mg/kg B+D arms. At this analysis, 54% death events have been reported in 3 mg/kg B+D and 71% in C arm. ORR is 17.1%/13.8% and median PFS is 4.5/3.3 months for 3 mg/kg B+D/C. Median OS is 11.7 months for 3 mg/kg B+D and 7.3 months for C. The safety profile for 3 mg/kg B+D was similar to that of C in severity and frequency. No other safety signal was identified. Conclusions: This randomized, placebo-controlled phase 2 trial demonstrated a positive trend favoring 3 mg/kg B+D in ORR, PFS and OS. 3 mg/kg B in combination with D was well tolerated and is the planned dose forPhase 3. Clinical trial information: NCT01138163.
Evaluation of ERK as a therapeutic target in acute myelogenous leukemia
Authors: Ellen Weisberg, Chengcheng Meng, Abigail Case, Martin Sattler, Hong L. Tiv, Prafulla C. Gokhale, Sara Buhrlage, Jinhua Wang, Nathanael Gray, Richard Stone, Suiyang Liu, Shripad V. Bhagwat, Ramon V. Tiu, Sophia Adamia, James D. Griffin
Journal: Leukemia (2019)
Collaborative learning workshops to optimize integration of cancer immunotherapies in the community setting.
Authors: Latha Shivakumar, Tara Perloff, Lorna Lucas
Journal: Journal of Clinical Oncology (2019)

10535 Background: The expanding armamentarium of immunotherapies available to treat patients with cancer poses a challenge to community practitioners. They need guidance around the practical issues that they must navigate to provide immunotherapy safely and effectively in their own communities. Methods: The Association of Community Cancer Centers (ACCC) implemented collaborative learning workshops focused on best practices for implementing cancer immunotherapies in the community setting with respect to care coordination, monitoring and management of immune-related adverse events (irAEs), and access to care. The workshops were held between April and June of 2018 in community cancer centers. A multidisciplinary steering committee including two medical oncologists, an oncology nurse, and an oncology pharmacist, led this initiative. The workshops started with a 45-minute open discussion section where the faculty posed questions to the learners to understand their specific institutional challenges. The faculty took cues from the initial discussion and focused the remainder of the education on addressing the challenges and barriers that were uncovered, rather than merely summarizing recent clinical data. The faculty discussed clinical case scenarios and presented clinical evidence for the various treatment decisions. At the end of the workshop, the instructors collaborate with the learners to draft an action plan for incorporating changes into their practice. Participants were surveyed at 3 and 6 months following participation in the workshop to report on the status of their action plans. Results: After participating in the workshops, almost 100% of the participants reported being confident in their ability to make changes in their practice. The responses of the participants to the post-activity assessment revealed a 11% relative increase in knowledge and competence and the participants were up to 14.7% more likely to receive evidence-based management with immunotherapies based on effect size calculations. At the 3-month follow-up, the participating sites had already implemented over 30% of the action items listed in their plans and at the 6-month follow-up, 100% of the action items drafted by learners were implemented as planned. Conclusions: The collaborative learning workshops were successful in inducing changes in knowledge, competence, and performance among the intended target audience of community oncology practitioners.
Demonstrations of Physical Signs in Clinical Surgery.
Journal: JAMA (1930)

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
On the presence of HLA-SE alleles and ACPA-IgG variable domain glycosylation in the phase preceding the development of rheumatoid arthritis
Authors: Theresa Kissel, Karin Anna van Schie, Lise Hafkenscheid, Anders Lundquist, Heidi Kokkonen, Manfred Wuhrer, Tom WJ Huizinga, Hans Ulrich Scherer, René Toes, Solbritt Rantapää-Dahlqvist
Journal: Annals of the Rheumatic Diseases (2019)

Objective Anti-citrullinated protein antibodies (ACPA) in rheumatoid arthritis (RA) patients display a unique feature defined by the abundant presence of N -linked glycans within the variable domains (V-domains). Recently, we showed that N -glycosylation sites, which are required for the incorporation of V-domain glycans, are introduced following somatic hypermutation. However, it is currently unclear when V-domain glycosylation occurs. Further, it is unknown which factors might trigger the generation of V-domain glycans and whether such glycans are relevant for the transition towards RA. Here, we determined the presence of ACPA-IgG V-domain glycans in paired samples of pre-symptomatic individuals and RA patients. Methods ACPA-IgG V-domain glycosylation was analysed using ultra-high performance liquid chromatography (UHPLC) in paired samples of pre-symptomatic individuals (median interquartile range (IQR) pre-dating time: 5.8 (5.9) years; n=201; 139 ACPA-positive and 62 ACPA-negative) and RA patients (n=99; 94 ACPA-positive and 5 ACPA-negative). Results V-domain glycans on ACPA-IgG were already present up to 15 years before disease in pre-symptomatic individuals and their abundance increased closer to symptom onset. Noteworthy, human leucocyte antigen class II shared epitope (HLA-SE) alleles associated with the presence of V-domain glycans on ACPA-IgG. Conclusion Our observations indicate that somatic hypermutation of ACPA, which results in the incorporation of N -linked glycosylation sites and consequently V-domain glycans, occurs already years before symptom onset in individuals that will develop RA later in life. Moreover, our findings provide first evidence that HLA-SE alleles associate with ACPA-IgG V-domain glycosylation in the pre-disease phase and thereby further refine the connection between HLA-SE and the development of ACPA-positive RA.
Endothelial TGF-β signalling drives vascular inflammation and atherosclerosis
Authors: Pei-Yu Chen, Lingfeng Qin, Guangxin Li, Zheng Wang, James E. Dahlman, Jose Malagon-Lopez, Sharvari Gujja, Nicholas A. Cilfone, Kevin J. Kauffman, Lele Sun, Hongye Sun, Xinbo Zhang, Binod Aryal, Alberto Canfran-Duque, Rebecca Liu, Pascal Kusters, Alfica Sehgal, Yang Jiao, Daniel G. Anderson, Jeffrey Gulcher, Carlos Fernandez-Hernando, Esther Lutgens, Martin A. Schwartz, Jordan S. Pober, Thomas W. Chittenden, George Tellides, Michael Simons
Journal: Nature Metabolism (2019)
Glucocerebrosidase and its relevance to Parkinson disease
Authors: Jenny Do, Cindy McKinney, Pankaj Sharma, Ellen Sidransky
Journal: Molecular Neurodegeneration (2019)

Mutations in GBA1, the gene encoding the lysosomal enzyme glucocerebrosidase, are among the most common known genetic risk factors for the development of Parkinson disease and related synucleinopathies. A great deal is known about GBA1, as mutations in GBA1 are causal for the rare autosomal storage disorder Gaucher disease. Over the past decades, significant progress has been made in understanding the genetics and cell biology of glucocerebrosidase. A least 495 different mutations, found throughout the 11 exons of the gene are reported, including both common and rare variants. Mutations in GBA1 may lead to degradation of the protein, disruptions in lysosomal targeting and diminished performance of the enzyme in the lysosome. Gaucher disease is phenotypically diverse and has both neuronopathic and non-neuronopathic forms. Both patients with Gaucher disease and heterozygous carriers are at increased risk of developing Parkinson disease and Dementia with Lewy Bodies, although our understanding of the mechanism for this association remains incomplete. There appears to be an inverse relationship between glucocerebrosidase and α-synuclein levels, and even patients with sporadic Parkinson disease have decreased glucocerebrosidase. Glucocerebrosidase may interact with α-synuclein to maintain basic cellular functions, or impaired glucocerebrosidase could contribute to Parkinson pathogenesis by disrupting lysosomal homeostasis, enhancing endoplasmic reticulum stress or contributing to mitochondrial impairment. However, the majority of patients with GBA1 mutations never develop parkinsonism, so clearly other risk factors play a role. Treatments for Gaucher disease have been developed that increase visceral glucocerebrosidase levels and decrease lipid storage, although they have yet to properly address the neurological defects associated with impaired glucocerebrosidase. Mouse and induced pluripotent stem cell derived models have improved our understanding of glucocerebrosidase function and the consequences of its deficiency. These models have been used to test novel therapies including chaperone proteins, histone deacetylase inhibitors, and gene therapy approaches that enhance glucocerebrosidase levels and could prove efficacious in the treatment of forms of parkinsonism. Consequently, this rare monogenic disorder, Gaucher disease, provides unique insights directly applicable to our understanding and treatment of Parkinson disease, a common and complex neurodegenerative disorder.
You Should Get Screened for Colon Cancer, Really
Authors: Uri Ladabaum
Journal: JAMA Network Open (2019)

Shivan J. Mehta, MD, MBA, MSHP; Vikranth Induru, MD; David Santos, BA; Catherine Reitz, MPH; Timothy McAuliffe, BA; Charles Orellana, MD; Kevin G. Volpp, MD, PhD; David A. Asch, MD, MBA; Chyke A. Doubeni, MD, MPH
Re-visiting the HLA dogma
Authors: Antoine Roux, Stijn E. Verleden
Journal: European Respiratory Journal (2019)

Unravelling the intricacies of the human leukocyte antigen (HLA) system has been fundamental to our understanding of the immunobiological discrimination of self from non-self. In the context of solid organ transplantation, the allo-immune response is predominantly driven by a varying but inevitable degree of HLA mismatch (classically HLA class I and II molecules) between donor organs and the recipient host. In general, donor–recipient HLA mismatching tends to be maximal for solid organs where prospective HLA matching is not possible due to logistic reasons. This is true for lung transplantation, although rapid screening cellular and antigenic assays at the time of transplantation and thereafter can help detect, mitigate and manage the risks associated with donor-specific antibody production in the recipient. More recently, the newly developed epitope analysis is a significant step forward for ever finer precision deciphering of immunogenic mismatch-driven donor-specific HLA antibody production (DSA) [1] and graft and recipient outcomes [2]. HLA-G may be protective in solid organ transplantation <http://bit.ly/2ZjnPFy>
CD300a inhibits CD16-mediated NK cell effector functions in HIV-1-infected patients
Authors: Joana Vitallé, Iñigo Terrén, Ane Orrantia, Raquel Pérez-Garay, Francesc Vidal, José A. Iribarren, Carmen Rodríguez, Ana M. López Lirola, Enrique Bernal, Olatz Zenarruzabeitia, Francisco Borrego
Journal: Cellular and Molecular Immunology (2019)

2][3] CD300a is a surface receptor highly expressed on NK cells that has the capacity to inhibit NK cell-mediated cytotoxicity in healthy donors. 4The CD300a molecule has been related to several viral infections and is able to diminish the NK cell killing of pseudorabies-infected cells through interactions with its ligands phosphatidylserine and phosphatidylethanolamine. 5 In addition, CD300a expression on B and CD4+ T lymphocytes is altered during HIV-1 infection, and combined antiretroviral therapy (cART) does not restore nonpathological expression levels. 5,6However, the expression and function of CD300a on NK cells during HIV-1 infection is still unknown.We have determined the surface expression of CD300a on different NK cell subsets and the capacity of this receptor to inhibit CD16-induced NK cell effector functions in healthy and HIV-1 infected individuals.As HIV-1 infection modulates CD300a expression on some immune cells, 5,6 we first analyzed the expression of the CD300a receptor on different NK cell subpopulations from healthy donors, untreated HIV-1-infected subjects, and patients on cART by flow cytometry.The samples were provided by the HIV BioBank integrated in the Spanish AIDS Research Network (RIS) (see Supplementary Material).Clinical data from HIV-1-infected patients are shown in Table S1.Three different NK cell subsets were studied: CD56 bright (CD56 ++ NKp80 + ), CD56 dim (CD56 + NKp80 + ), and CD56 neg (CD56 -NKp80 + ) (Fig. S1).When we examined the CD300a expression, no significant differences were observed between the groups, with the exception of CD56 neg NK cells, which displayed a higher frequency of CD300a+ cells in untreated HIV-1 infected patients (Fig. S2).Ongoing HIV replication induces the expansion of a dysfunctional CD56 neg NK cell subset 1,7,8 (Fig. S1).Thus, we suggest that the overexpression of the CD300a inhibitory receptor on the CD56 neg NK cell subset may contribute to the dysfunctionality observed in this expanded population in HIV-1 infected patients, which is partially restored with cART.We also examined CD300a expression on different NK cell subsets selected according to the expression of NKG2A, NKG2C, CD57, and NKp46 (Fig. S3).These receptors are altered during HIV-1 infection, 7,8 and some of them are commonly used to distinguish NK cell maturation stages. 9In general, we observed that different CD300a expression levels were associated with the
Phase I Study of the Novel Enhancer of Zeste Homolog 2 (EZH2) Inhibitor GSK2816126 in Patients with Advanced Hematologic and Solid Tumors
Authors: Timothy A. Yap, Jane N. Winter, Lisa Giulino-Roth, Jemma Longley, Juanita Lopez, Jean-Marie Michot, John P. Leonard, Vincent Ribrag, Michael T. McCabe, Caretha L. Creasy, Melissa Stern, Teodora Pene Dumitrescu, Xiaowei Wang, Steve Frey, Jennifer Carver, Thierry Horner, Choon Oh, Ahmed Khaled, Arindam Dhar, Peter W.M. Johnson
Journal: Clinical Cancer Research (2019)

Enhancer of zeste homolog 2 (EZH2) activity is dysregulated in many cancers.This phase I study determined the safety, maximum-tolerated dose (MTD), pharmacokinetics, and pharmacodynamics of the intravenously administered, highly selective EZH2 inhibitor, GSK2816126, (NCT02082977). Doses of GSK2816126 ranged from 50 to 3,000 mg twice weekly, and GSK2816126 was given 3-weeks-on/1-week-off in 28-day cycles. Eligible patients had solid tumors or B-cell lymphomas with no available standard treatment regimen.Forty-one patients (21 solid tumors, 20 lymphoma) received treatment. All patients experienced ≥1 adverse event (AE). Fatigue [22 of 41 (53.7%)] and nausea [20 of 41 (48.8%)] were the most common toxicity. Twelve (32%) patients experienced a serious AE. Dose-limiting elevated liver transaminases occurred in 2 of 7 patients receiving 3,000 mg of GSK2816126; 2,400 mg was therefore established as the MTD. Following intravenous administration of 50 to 3,000 mg twice weekly, plasma GSK2816126 levels decreased biexponentially, with a mean terminal elimination half-life of approximately 27 hours. GSK2816126 exposure (maximum observed plasma concentration and area under the plasma-time curve) increased in a dose-proportional manner. No change from baseline in H3K27me3 was seen in peripheral blood mononuclear cells. Fourteen of 41 (34%) patients had radiological best response of stable disease, 1 patient with lymphoma achieved a partial response, 21 of 41 (51%) patients had progressive disease, and 5 patients were unevaluable for antitumor response.The MTD of GSK2816126 was established at 2,400 mg, but the dosing method and relatively short half-life limited effective exposure, and modest anticancer activity was observed at tolerable doses.
Prostitution in the United States.
Journal: JAMA (1922)

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
Normal Global Longitudinal Strain
Authors: Nicholas D’Elia, Stefano Caselli, Wojciech Kosmala, Patrizio Lancellotti, Daniel Morris, Denisa Muraru, Masaaki Takeuchi, Annemien van den Bosch, Roderick W.J. van Grootel, Hector Villarraga, Thomas H. Marwick
Journal: JACC. Cardiovascular imaging (2019)