tbuckley/cabot-search huggingface dataset:
On Continuity
Authors: Christine A. Sinsky
Journal: Annals of Internal Medicine (2017)

On Being a Doctor17 October 2017On ContinuityChristine A. Sinsky, MDChristine A. Sinsky, MDFrom American Medical Association, Chicago, Illinois.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M17-0303 Audio Reading - “On Continuity” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "On Continuity," by C.A. Sinsky. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Walking into a patient's hospital room the morning after admission and hearing, “Dr. Sinsky, we are so glad you are here!” regularly reminded me, during my first 28 years of practice, of my purpose. I wasn't a better doctor than the physician who admitted that patient. But I was their doctor—I knew their medical and social particulars, their family, their story. They trusted that I would navigate the system; translate other physicians' recommendations; and, when they were released from the hospital, be there in the clinic to carry on. That regular reminder of purpose diminished when my practice became limited ... Author, Article, and Disclosure InformationAffiliations: From American Medical Association, Chicago, Illinois.Corresponding Author: Christine A. Sinsky, MD, American Medical Association, 330 N. Wabash Avenue, Chicago, IL 60611-5885; e-mail, christine.[email protected]org. PreviousarticleNextarticle Advertisement Audio Reading - “On Continuity” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "On Continuity," by C.A. Sinsky. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics Cited byVoices from the Front Lines: An Analysis of Physicians’ Reflective Narratives about Flaws with the ‘System’Voices from the Front Lines: An Analysis of Physicians’ Reflective Narratives about Flaws with the ‘System’ 17 October 2017Volume 167, Issue 8Page: 600KeywordsForecastingHospitalistsInpatientsOutpatient clinicsOutpatientsProgressive diseasesSurgeonsVascular diseasesWalkingWheelchairs ePublished: 17 October 2017 Issue Published: 17 October 2017 Copyright & PermissionsCopyright © 2017 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Abstract 1762: The START domain of the DLC1 tumor suppressor binds phosphatidylserine and two proteins, PLCD1 and Caveolin-1
Authors: Beatriz Sanchez-Solana, Dunrui Wang, Xiaolan Qian, Alex Papageorge, Parthibane Velayoudame, Jairaj Acharya, Douglas R. Lowy
Journal: Cancer Research (2019)

Abstract The tumor suppressor gene DLC1 encodes a multi-domain protein, which includes a Rho-GAP domain (Rho GTPase activating protein domain) that negatively regulates the activity of RhoA, B, and C, and has been hypothesized to be the basis of its tumor suppressor functions. DLC1 also contains a less well characterized START (StAR-related lipid transfer) domain in its C-terminus, whose overall contribution to DLC1 function remains incompletely understood. START domains in other proteins have been shown to bind lipids, but no lipid has yet been identified that binds the DLC1 START domain. In the present study, we attempted to gain further insight into the molecular function and lipid binding properties of the DLC1 START domain. We previously determined that Caveolin-1, the main structural component and marker of caveolae, interacts with the DLC1 START domain, and this interaction contributes to the full tumor suppressor activity of DLC1. In unpublished studies, we additionally identified Phospholipase C delta 1 (PLCD1), which participates in intracellular Ca2+ mobilization, forming a complex with the DLC1 START domain and with Caveolin-1. We have now developed evidence that, in addition to binding Caveolin-1 and PLCD1, the DLC1 START domain binds a lipid, phosphatidylserine (PS), and have identified a colon cancer-associated DLC1-START domain mutant (R947C) that results in a protein deficient in forming a complex with all three binding partners and displays reduced tumor suppressor activity but intact RhoGAP activity. The interaction between the DLC1-START domain and PS can occur independently of PLCD1 and/or Caveolin-1, but PS promotes complex formation between the DLC1 START domain and PLCD1 or Caveolin-1, without altering PLCD1 to Caveolin-1 binding. Biological assays with wild type DLC1 show cooperation between DLC1 and PLCD1 or Caveolin-1 to inhibit cell migration, but no cooperation is observed when all three genes are overexpressed, suggesting that Caveolin-1 and PLCD1 occupy the same migration signaling pathway. Thus, we have identified a biologically relevant complex between DLC1 and three macromolecules (PLCD1, PS and Caveolin-1) that contributes to the full tumor suppressor function of DLC1 independently of its RhoGAP activity, and are testing the hypothesis that PS serves as a linker between the DLC1 START domain and PLCD1 or Caveolin-1. Citation Format: Beatriz Sanchez-Solana, Dunrui Wang, Xiaolan Qian, Alex Papageorge, Parthibane Velayoudame, Jairaj Acharya, Douglas R. Lowy. The START domain of the DLC1 tumor suppressor binds phosphatidylserine and two proteins, PLCD1 and Caveolin-1 [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 1762.
Adrenal cortex in tumors and hypertension
Authors: J. Nichols
Journal: JAMA (1965)

An abundant literature indicates that diverse L clinical conditions and therapy are associated with hypertrophy, or atrophy of the adrenal gland. Weights of uncertain accuracy or a subjective evaluation of a few microscopical preparations, or both, are usually given. Measurements of the gland or its various zones are mentioned in only a few instances. However, conclusions drawn from changes measured in the focal plane of a microscope are inadequate or even misleading. Nichols and Hennigar,<sup>1</sup>converting thickness to mass in a derived sphere, demonstrated, in dogs with pulmonary hypertension, that a 9% increase in peripheral radius of the gland results in a 96% increase in mass of zona glomerulosa, a relationship not obvious in the plane of a microscopical field. This communication will show that the zona glomerulosa has a mass disproportionately larger than indicated by linear measurements and that increases in zona fasciculata, without change in thickness of
Abstract 18051: Mechanical Circulatory Support and Pulmonary Hypertension - An Analysis of United Network of Organ Sharing Registry
Authors: Sandip Zalawadiya, Ugochukwu Egolum, Henry Ooi
Journal: Circulation (2015)

Background: Severe pulmonary hypertension (PH) is a relative contra-indication for heart transplantation (HT) per International Society of Heart and Lung Transplantation guidelines. Limited data exists comparing different types of mechanical circulatory support devices (MCSDs) for post-HT survival across severity categories of PH. Methods: We performed post-hoc analysis of 14,481 patients (age: 53.3± 12 years, 76% males, median follow-up - 4.2 years) undergoing HT after January 1st, 2000 from the United Network of Organ Sharing registry database. Patients were divided into following categories of PH: None (pulmonary vascular resistance (PVR) &lt;2.5 WU or trans-pulmonary gradient (TPG) &lt;13 mmHg), mild to moderate (PVR ≥2.5 WU and &lt;5 WU or TPG≥ 13 mm Hg and &lt;20 mm Hg) and severe (PVR ≥ 5.0 WU or TPG ≥ 20 mm Hg). We also categorized patients based on types of MCSDs as following: None (n=10,142), pulsatile flow (PF) left (n=709), continuous flow (CF) left (n=3,166), biventricular (BiV; n=347) and total artificial heart (TAH;n=117). Post-HT survival was assessed using multivariable Cox proportional hazard analysis across categories of PH and MCSDs. Results: See Figure 1 and 2. Conclusion: For patients without PH, CF left MCSDs offered significantly better post-HT survival compared to other categories of MCSDs; risk of post-transplant mortality among those with PH was comparable between CF left MCSDs and those undergoing direct HT or having PF left MCSDs.
A Textbook for Midwives.
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
Pneumocystic carinii pneumonia in children with cancer. Diagnosis and treatment
Authors: H. D. Johnson
Journal: JAMA (1970)

Pneumocystis carinii<i>pneumonia was diagnosed in 19 children with cancer. The diagnosis was made in 14 children by pulmonary needle aspiration and demonstration of the organism by methenamine silver nitrate stain. Two children had tension pneumothorax and one had postaspiration hemoptysis following needle aspiration, but there was no mortality from the procedure. Seventeen children were treated with pentamidine isethionate; nine recovered. Toxicity to pentamidine consisted of elevated blood urea nitrogen levels and hypoglycemia</i>.
Control of Body Temperature in the Small Newborn Infant by Low Energy Infrared Radiation
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
Clinical activity of ipilimumab plus nivolumab (Ipi/Nivo) in patients (pts) with metastatic non-clear cell renal cell carcinoma (nccRCC).
Authors: Ruby Gupta, Moshe Chaim Ornstein, Anita Gul, Kimberly D Allman, Jessica Ball, Laura S. Wood, Jorge A. Garcia, Dendra VonMerveldt, Hans J. Hammers, Brian I. Rini
Journal: Journal of Clinical Oncology (2019)

659 Background: Ipi/Nivo is a standard of care for pts with metastatic clear cell RCC. The clinical activity of Ipi/Nivo in patients with metastatic nccRCC remains poorly defined. Methods: Metastatic nccRCC pts who were treated with Ipi/Nivo at Cleveland Clinic or UT Southwestern were retrospectively reviewed. Ipi/Nivo was administered as per CHECKMATE 214. Computed tomography imaging was obtained at baseline and every12 weeks to assess disease response per RECIST 1.1 criteria. Baseline pt characteristics, outcome to therapy and adverse effects as per CTCAE v5.0 were collected. Results: Thirteen pts with metastatic nccRCC histology who were treated with Ipi/Nivo were identified. The median age was 60 years (range, 32-81). Non clear cell histologies included adenocarcinoma of renal origin not otherwise specified (2), unclassified (3), papillary (3), chromophobe (3), translocation (1) and medullary histology (1). Nine pts had ECOG PS 0; four pts had ECOG PS 1. Eleven patients were male and two female. IMDC risk group at time of initiation of Ipi/Nivo was favorable (2 pt), intermediate (10 pts) and poor (1 pt). Nine pts received Ipi/ Nivo as first line treatment, three pts received Ipi/Nivo after prior TKI and one pt received Ipi/ Nivo as third line treatment after prior chemotherapy and nivolumab monotherapy. In total, eight pts have thus far undergone restaging scans with three pts demonstrating partial response (PR), one pt demonstrating stable disease (SD) and four pts demonstrating progressive disease (PD). Two pts experienced grade 2 diarrhea, one after 4 cycles and another after 3 cycles of Ipi/Nivo and required prednisone. One pt demonstrated grade 3 hepatotoxicity after 2 cycles of Ipi/Nivo and required prednisone and Mycophenolate Mofetil while another pt demonstrated grade 1 hepatotoxicity after 3 cycles of Ipi/ Nivo requiring prednisone. One pt experienced grade 2 pancreatitis requiring steroids after one dose of Ipi/Nivo. One pt experienced grade 2 fatigue after 1 cycle of Ipi/Nivo requiring prednisone. Conclusions: Ipi/Nivo is feasible and safe in patients with metastatic nccRCC with preliminary evidence of anti-tumor activity. Updated clinical data will be presented.
Durable Responses Achieved with AM0010
Journal: Cancer Discovery (2016)

Abstract In a phase Ib trial, a combination of the experimental immunotherapy AM0010, a PEGylated form of the recombinant human cytokine IL10, and the anti–PD-1 checkpoint inhibitor pembrolizumab was well tolerated and effective at controlling tumors in some patients with advanced renal cell carcinoma, non–small cell lung cancer, and melanoma.
Dental infection with hepatitis B
Authors: S. V. Williams
Journal: JAMA (1975)

We performed a prospective study to assess the risk of patients acquiring infection following routine professional contact with two dentists incubating type B viral hepatitis. Serum samples from patients exposed during the six weeks before onset of hepatitis in the dentists were tested for hepatitis B surface antigen and for antibody to the antigen shortly after illness developed and again six months later. Household members of exposed patients served as a control group. None of the exposed patients or controls became ill with hepatitis, and none developed antigen. Three of the 237 exposed patients developed antibody, as did four of the 245 controls. The difference between exposed patients and controls was not significant. These results do not support the hypothesis that these two dentists transmitted infection to their patients. (<i>JAMA</i>232:1231-1233, 1975)
Abstract 2839: Leveraging gut microbiota networks to impact tumor immunotherapy
Authors: Lata Jayaraman, Jaclyn Sceneay
Journal: Cancer Research (2019)

Abstract The human gut microbiota forms a diverse, dynamic and complex ecosystem that modulates numerous host processes including metabolism, inflammation and cellular and humoral immune responses. Emerging data suggest that the gut microbiota of cancer patients may predict tumor response to immune checkpoint inhibitors (ICI). To better understand how the microbiome may impact response to ICI, we have developed and validated robust tumor models using either conventional mice treated with antibiotics or germ-free (GF) mice. We have confirmed in both models, that mice lacking a diverse microbiome fail to mount an efficient anti-tumor immune response after treatment with anti-PD-1, primarily due to T cell dysfunction. This response to anti-PD-1 can be restored by introduction of a microbiome using fecal microbial transplant (FMT) prepared from stool from healthy donors in GF mice, and is driven by increased tumor-infiltrating lymphocytes (TILs), specifically CD8+ T cells. Importantly, for the first time, we show that the bacterial spore fraction from healthy donor stool can also restore response to anti-PD-1 and increase CD8+ TILs in both conventional mice treated with antibiotics and GF mice. We have also tested cancer patient-derived microbiome samples that are efficacious or non-efficacious in GF mouse models. We have sequenced the input material as well as the engrafted gut microbiota in these mice via 16S rDNA sequencing. Comparison of these sequences has enabled us to develop a “microbiome signature” of response that is being used in the development of a microbiome-based therapy for combination with ICI. Based on these encouraging animal model data we plan to initiate a randomized, placebo-controlled clinical study in patients with advanced metastatic melanoma. The clinical trial will evaluate the impact of an anti-PD-1 checkpoint inhibitor with adjunctive microbiome therapy on patient outcomes. Seres is developing SER-401, a preclinical stage oral microbiome therapy to improve the efficacy and safety of immunotherapy. Our drug discovery strategy combines computational analyses and empirical in vitro, in vivo and ex-vivo screening of strains and consortia to inform selection and drive microbiome drug design. Data from such a comprehensive approach are invaluable for designing compositions of bacteria that form “functional ecological networks” that can impact response to ICI therapy. We believe these data will provide insight into how microbiome drugs can be developed in the setting of immunotherapy to augment the efficacy of ICIs by altering the cancer-immune set point. Citation Format: Lata Jayaraman, Jaclyn Sceneay. Leveraging gut microbiota networks to impact tumor immunotherapy [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 2839.
623 MULTICENTRE RANDOMISED CONTROLLED STUDY COMPARING CARVEDILOL WITH ENDOSCOPIC BAND LIGATION IN THE PREVENTION OF VARICEAL REBLEEDING
Authors: L. Smith, S. Dickson, P.C. Hayes, E.H. Forrest, D.R. Gaya, P.R. Mills, H. Suzuki, D. Young, A.J. Stanley
Journal: Journal of Hepatology (2013)
Junior Hospital Staff Contract
Authors: S. C. Rastogi, E. F. Prah, R. Mathoda, R. Armah-Kwantreng, W. Samarasinghe, D. J. Bateman, N. Wagner, S. Suhasini, K. Padamsee, B. Lipkin, G. Mullen, M. Viswanathan, M. R. Lowe, J. S. Yennu
Journal: BMJ (1975)
a2u-Globulin Nephropathy and Ravens: Do Ravens of a Different Feather Flock Together?
Authors: Felix A. de la Iglesia, Alexander W. Gough, Robert E. Sigler
Journal: Environmental Health Perspectives (1997)

differentiate significant and trivial chemical hazards and to assess likely risks to humans.This latter justification can be illustrated by the following statement: if all chemicals that are mutagenic in vitro were mutagenic and
Cancer Prevention Strategies: Use of Cancer Prevention Research Registries
Authors: Hoda Anton-Culver
Journal: Environmental Health Perspectives (1995)

We present a model to plan a rational strategy for cancer prevention that has two main functions-assessment and intervention.The assessment function includes three main components: to identify populations at high cancer risk, which may be due to their ethnic group, occupational and environmental exposures, family history, cigarette smoking, or other risk factors; to assess exposure to known carcinogens through the general and occupational environments, lifestyle factors, and the home as well as to document known carcinogens using human tissue banks and develop and validate questionnaires to target known risk factors for each of the most common cancers; and to conduct research studies of high-risk populations, including studies on mechanism and genetic testing.The intervention function includes three components: development of population-based intervention programs using the results from the research studies; evaluation of intervention programs; and modification of existing intervention programs and implementation of new ones.The above-proposed prevention strategy depends to a great extent on population-based cancer registries.Existing cancer registries around the United States should be strengthened and other dimensions should be added to their charge to augment their function in prevention research.To convert existing population-based cancer registries, particularly those that serve multiethnic and multicultural populations, into Cancer Prevention Research Registries (CPRRs), three types of data in addition to their existing required data complement should be incorporated.These are exposure information including occupational history, host factors information, and information about family history of cancer and associated conditions.The primary goal of the CPRRs should be to support cancer prevention research in its widest sense.Future research needs must be designed to investigate each of the components of the prevention strategy as well as its integrated performance.Regardless of what we do in the future, we must now promote healthier lifestyles, prevent exposure to known carcinogens, and improve early detection procedures.
Just Words
Authors: Gode Alexander
Journal: JAMA (1966)

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
Collected Perspectives in Cancer Research: 1983–85
Journal: JNCI Journal of the National Cancer Institute (1986)

Collected Perspectives in Cancer Research: 1983–85 Get access JNCI: Journal of the National Cancer Institute, Volume 77, Issue 3, September 1986, Page 836, https://doi.org/10.1093/jnci/77.3.836-a Published: 01 September 1986