tbuckley/cabot-search huggingface dataset:
JEAN BAPTISTE VAN HELMONT (1577-1644) "PHILOSOPHER THROUGH FIRE"
Journal: JAMA (1965)

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
CONTINUING EVOLUTION OF THE INTERNSHIP AND RESIDENCY
Journal: JAMA (1949)

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
JAMA Reference Directories
Journal: JAMA (1981)

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
Resource and quality information provided by compliance with NCCN hereditary breast cancer guidelines.
Authors: Peter J. Levonian, Jeffrey Landercasper, Choua Vang, Kristen Marcou, Rima Al Hajj, Mohammed Al-Hamadani
Journal: Journal of Clinical Oncology (2013)

5 Background: NCCN provides guidelines for breast cancer genetic risk assessment and testing. Measuring compliance with NCCN Guidelines (NG) can identify quality gaps. Methods: After IRB approval, a retrospective review of a prospective database of breast cancer patients was conducted to measure compliance with NG for genetic counseling and BRCA testing. Entry criteria were breast cancer patients with diagnosis and treatment at our center, during the 3 year period ending 12/31/11. Genetic counselors (GC) used NG and BRCAPRO modeling in all patients. Surgeon and GC pedigree analyses were compared. Results: Surgeons constructed pedigrees in 675 breast cancer patients and referred 42% (286/675) to the GC. The decision to refer was NCCN compliant in 671/675 (99%). The GC corrected the pedigree in 14% (39/286); nearly all due to the GC identifying extra breast or ovarian cancers. The mean BRCAPRO probability in referred patients was 7.2%. Fifty-nine percent (170/286) of patients seen by the GC received a recommendation for BRCA testing. The NG compliance rate for testing was 98% (170/174). Of 174 BRCA tests offered to patients, 74% (128/174) underwent testing. In tested patients, there were 4% BRCA1+, 5% BRCA 2+, and 1% uncertain variants. Total patient charges for 128 tests were $696,000 ($4,000/test). If the threshold for testing was BRCAPRO &gt; 5% or &gt;10%, then 69 ($276,000) and 45 ($180,000) (p&lt;0.001) patient charges would have occurred, and no patient with BRCA + status would have been missed. Conclusions: High rates of NCCN guideline compliance for genetic counseling and testing are achievable. Our GC's improve accuracy of pedigree assessment and demonstrate adherence to NCCN guidelines, resulting in more testing compared to BRCAPRO modeling. The balance between different methods to trigger testing, their sensitivity, and cost deserves more study, but the observational data contained herein provides information for provider and payer stakeholders regarding estimated GC resources and cost of care.
Prospective Evaluation of the Peptide-Bound Collagen Type I Cross-Links N-Telopeptide and C-Telopeptide in Predicting Bone Metastases Status
Authors: Luis Costa, Laurence M. Demers, A. Gouveia-Oliveira, J. Schaller, Eduardo B. Costa, Miguel C. de Moura, Allan Lipton
Journal: Journal of Clinical Oncology (2002)

The objective assessment of bone metastases is currently based on serial changes in skeletal survey. We performed a prospective study to determine whether a correlation exists between the biochemical markers of bone turnover and x-ray evaluation of bone metastases in patients with or without bisphosphonate therapy, and whether bone markers are influenced by extraskeletal disease.Patients with either bone or extraskeletal metastases were consecutively enrolled and World Health Organization response criteria were applied for both bone and extraosseous disease every 3 to 4 months. Serum levels of bone-specific alkaline phosphatase (B-AP) and C-telopeptide (ICTP) and urine levels of N-telopeptide (NTX) were measured monthly. The data were analyzed by generalized estimation equation regression.We studied 97 patients with bone metastases (52 also with extraskeletal metastases) and 26 with extraosseous disease only. Median time on study was 153 days, and 281 objective evaluations (171 in bone) were performed. With bisphosphonates (49 patients receiving pamidronate and three receiving clodronate), percent change from levels without therapy was 47% for NTX (P <.001) and 69% for B-AP (P =.008). With disease progression in bone, percent change from mean levels during stable disease was 152% for NTX (P <.001) and 144% for ICTP (P <.001) regardless of bisphosphonate therapy. NTX had the highest positive predictive value (71%) for the diagnosis of bone metastases progression. Extraskeletal disease had no significant effect on bone markers.Urinary NTX may be a valuable bone marker to assess the antiresorptive effect of bisphosphonate therapy and to evaluate the progression of bone metastases.
Abstract 197: Molecular interactions of Globo H ceramide with translin-associated factor X (TRAX) underlie its proangiogenic activities
Authors: John Yu, Sheng-Hung Wang, Jing-Yan Cheng, Jung-Tung Hung, Chun-Cheng Lin, Fei-Yun Lo, Chien-Wei Lee, Alice L. Yu
Journal: Cancer Research (2019)

Abstract Glycosphingolipids (GSLs) are ubiquitous glycolipids in eukaryotic plasma membranes that consist of a polar glycan chain and a hydrophobic sphingosine- containing ceramide tail. Although GSLs display various diversities and functions, the mechanistic details of GSL interactions with membranous or intracellular components are poorly understood. Globo H ceramide (GHCer), a tumor-associated GSL overexpressed in most types of epithelial cancers, is a potential target of cancer immunotherapy. Previously, we showed that GHCer is shed by cancer cells to mediate immune suppression and promote angiogenesis in the tumor microenvironment. At the cellular level, GHCer from cancer cells binds to translin-associated factor (TRAX), with consequent release of PLCB1 from TRAX to trigger Ca2+ mobilization. Herein, we found that Gb5-ceramide (Gb5Cer), the pentasaccharide precursor of GHCer, could not promote angiogenesis nor Ca2+ mobilization. At the molecular level, ELISA and biacore analysis revealed that GHCer binds to TRAX with a distinct dissociation constant of 4.09×10-8 M, while its precursors, galactosyl-, lactosyl-, Gb4-, and Gb5Cer- showed negligible binding to TRAX. Molecular docking and molecular dynamics indicated that the fucose residue of Globo H is an important contributor to a favorable glycan conformation for interaction with TRAX, consistent with the finding that Gb5Cer had no proangiogenic activities. In addition, GHCer competed with recombinant C-terminus region of phospholipase C β1 (PLCB1) for binding to TRAX, thus providing a molecular mechanism for the proangiogenic effect of GHCer on tumor microenvironment. This study provides the first evidence for interaction of TRAX with a non-protein GSL, deciphered distinct regions of TRAX for interacting with glycan and lipid portions of GHCer, and illustrated the crucial contribution of fucose moiety on GHCer for its interaction with TRAX and angiogenic activity. Citation Format: John Yu, Sheng-Hung Wang, Jing-Yan Cheng, Jung-Tung Hung, Chun-Cheng Lin, Fei-Yun Lo, Chien-Wei Lee, Alice L. Yu. Molecular interactions of Globo H ceramide with translin-associated factor X (TRAX) underlie its proangiogenic activities [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 197.
Correction
Journal: BMJ (1959)

ANY QUESTIONS ?BRILsRN remarkably constant at 650°C., and rises about 500 C. during suction.2The term "tar" is often employed in discussing smoking as if this material were something different from and separable from " smoke."The truth of the mnatter is that the whole of the particulate matter in tobacco smoke can be condensed to a "tar" and that, because of the very small size of the initially formed droplets, it is of remarkably uniform composition.3Because of confusion in the use of the term "tar" it is recommended that the term "smoke condensate" be employed to replace it.Many ideas have been proposed for reducing "harmfulniess " and " injurious products " in tobacco smoke.Several hundred compounds are known to be present4 and some of these are known to have definite biological effects.5 What- ever proposals are made, it is evident from the nature of smoke that successful reduction of the effect of smoking can be achieved only by taking in less smoke.The use of p nholes in the cigarette is one method of doing th.s.
New Names
Journal: JAMA (1963)

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
AUTHORS' REPLY
Authors: P J Wijkstra, E Tenvergert
Journal: Thorax (1994)

REPLY DrThurlbeck objects to our conclusion that the severity of the lesions of the bronchioles and parenchyma assessed by grading techniques in resected lung specimens do not correlate with lung function measurements obtained in the same subjects.We agree that this conclusion is at variance with much that is in the literature and, indeed, re- ported it for that reason.The data we pre- sented make two basic points: (1) that rather extensive emphysematous destruction of the lung can be present in patients who have a normal FEVI, and (2) that a reduction in FEV, did not correlate with increased inflammatory changes in the peripheral airways assessed with current grading systems.This does not mean that we think emphysematous destruction is not important, only that its presence does not explain the decline in FEVI.Similarly, we did not mean to imply that the abnormal peripheral airway function may not eventually be explained by the effects of the inflammatory process in these airways -only that current morphological grading systems do not identify the lesions responsible for the abnormalities in function.We agree with his closing statement that airflow obstruction is a complicated mat- ter in which the different lesions ofthe bronchi (not just chronic bronchitis), bronchioles (not just the Cosio score), and parenchyma (not just emphysema) contribute to the decline in function.Specific responses to the otherpoints raised in his letter follow.The criticism concerning our failure to re- port data on tumour size and stage does not recognise that we have previously reported these data on the first 143 cases entered into our study.'Tumour size, involvement of
Analog Computer in the Physiology Laboratory
Journal: JAMA (1963)

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
Inheritance
Authors: Kristin Lord
Journal: JAMA (2001)

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
Production of Fetal Abnormalities in Rabbits by Imipramine
Journal: JAMA (1963)

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
MAN AND MONKEY
Journal: JAMA (2013)

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
Charcot’s Opinion and Criticism of German Medicine
Journal: JAMA (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 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
Abstract 820: Autoregulation of CGRP Expression via β <sub>2</sub> -Adrenoreceptor Signaling in Intrinsic Cardiac Adrenergic Cells
Authors: Vince Nguyen, Ignatius Gerardo Zarraga, Saurabh Rastogi, Yochai Birnbaum, Barry Uretsky, Ming-He Huang
Journal: Circulation (2007)

Background : Calcitonin gene-related peptide (CGRP) is a neuropeptide with broad salutary cardiovascular effects. Mechanisms underlying cardiac CGRP regulation are poorly understood. The intrinsic cardiac adrenergic (ICA) cell is a novel cardiac neuroendocrine cell that expresses the δ-opioid receptor. We have shown that δ-opioid stimulation of ICA cells induces epinephrine liberation exerting an infarct-size limiting effect via β 2 -adrenoreceptor (β 2 -AR) stimulation. In this study we hypothesize that ICA cells synthesize and release CGRP which is involved in myocardial function and that CGRP gene expression can be autoregulated by epinephrine released from the ICA cell or regulated exogenously via β 2 -AR agonist. Methods and Results : In situ hybridization coupled with immunofluorescent double labeling localized CGRP mRNA expression exclusively to ICA cells in explanted human left ventricular tissue. To determine whether δ-opioid-enhanced epinephrine release from ICA cells autoregulates CGRP gene expression, isolated and cultured (for 2-weeks) adult rat ICA cells were treated with δ-opioid agonist DPDPE (0.1 μM for 1h) in the absence and presence of the β 2 -AR antagonist ICI-118551 (ICI, 10 μM). DPDPE induced 4-fold increase in CGRP mRNA at 6h post DPDPE-treatment by real-time PCR. This effect was abolished in the presence of ICI. To confirm the epinephrine-β 2 -AR signaling pathway, exogenous epinephrine was applied (0.1 μM for 1h) to ICA cells in the absence and presence of ICI (10 μM). Epinephrine induced 16-fold increase in CGRP mRNA levels at 6h post-treatment. This effect was completely abolished in the presence of ICI. To determine whether endogenous CGRP release from ICA cells exerts tonic modulation on myocyte contractile function, we studied the interaction between ICA cells and myocytes in ICA cell-myocyte co-culture model using a ratio fluorescent spectrometer. Application of CGRP-receptor antagonist CGRP 8 –37 (0.2 μM) reduced myocyte [Ca 2+ ]i transients by 30 ± 5%. Conclusion s: ICA cells exclusively express CGRP gene in human and animal hearts. Robust and sustained CGRP gene-expression can be induced via β 2 -AR signaling through autocrine epinephrine positive feedback or pharmacological β 2 -AR stimulation.