tbuckley/cabot-search huggingface dataset:
Central Indiana Hospital for the Insane.
Journal: JAMA (1898)

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
Infusion of Marrow in Mouse and Dog After Thio-Tepa
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
Problems—lower income group
Journal: JAMA (1966)

<h3>Measles</h3> quently figure in the spread of measles to the home. Several studies, including a recent Pittsburgh survey, indicate "at least 80% of pre-school children get measles from an older brother or sister or other school-age contact," Dr. Warren said. F. Robert Freckleton, MD, chief of Immunization Activities in the office of the CDC chief, agreed: "The way measles spreads in a community is primarily among children in the lower grades in school... Then they bring it back home and infect their pre-school siblings." Dr. Freckleton is responsible for administering a federally legislated grants program to assist states and localities in immunizing pre-school children against measles. Eighty-seven project grants are in operation—38 state and territorial, and 49 local health departments "mostly in reasonably large metropolitan areas."
LEPROSY.
Journal: JAMA (1904)

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
FRACTURES
Journal: JAMA (1970)

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
Activity of gemcitabine/5-FU combination in refractory esophagogastric (EG) cancer.
Authors: Elizabeth Won, David H. Ilson, Joanne F. Chou, Marinela Capanu
Journal: Journal of Clinical Oncology (2014)

e15073 Background: Systemic chemotherapy has been demonstrated to improve survival and palliate symptoms in metastatic EG cancer. 2ndline (or more) chemotherapy with best supportive care also improves progression free and overall survival. Single-agent gemcitabine did not show activity in EG cancers (Ann Oncol 11:1161, 2000). Addition of gemcitabine to 5-fluorouracil (5FU) has shown modest activity (Oncology 69:130, 2005). To determine the efficacy and tolerability of gemcitabine with 5FU, we reviewed our experience in patients (pts) with metastatic or advanced EG cancers treated with this regimen. Methods: Retrospective review of MSKCC database for pts with metastatic EG cancer treated with gemcitabine/5FU (or capecitabine) between 1/1/2000 - 12/31/2012. Gemcitabine given at 600-1000mg/m2 day1, day 8 of q21 day cycle or 600-1000mg/m2 q2 weeks. 5FU given at 600-1000m2/m2 IV/48 hrs, with bolus 5FU/Leucovorin (200-400mg/m2 IV) on day 1. Capecitabine most commonly given as 1500-4000mg flat dose daily, in two divided doses, 7 days on/7 days off. Results: Of 146 pts, median age was 60; KPS 70 (50-90); 84% adenocarcinoma, 6% squamous (SCC). Sites of disease: 45% liver; 22% bone, 21% peritoneum. 112(77%) had ≥ 2 sites of disease. Pts were heavily pretreated: 42(29%) 2 prior lines of treatment (tx) for metastatic disease, 37(25%) 3 lines of tx, and 7(5%) 4+ lines of tx. Prior tx: 5FU/platinum (37%); Taxanes (56%); Irinotecan (44%). With gemcitabine, 49(34%) received 5FU and 97(66%) received capecitabine. In 144 evaluable pts, partial response rate was 7%, and stable disease was seen in 33%. Median PFS 1.84 months (95% CI,1.38-2.04) and for adenocarcinoma 2.0 months (95%CI,1.2-2.2) vs 1.2 months (95%CI: 0.9-1.51) for SCC (p =0.068). In the PR group, median PFS was 5.0 months (range 3.7-16.3 mo). Grade 3 toxicity was seen in 19 (13%); 1 pt had Grade 4 toxicity. 3(2%) discontinued treatment due to toxicity. Conclusions: Combination gemcitabine/5FU or capecitabine in metastatic EG cancer may have some limited activity and is well tolerated in a previously treated population. This regimen may be an appropriate palliative option for patients with an intact performance status who have progressed on other regimens. Research supported by Foundation 14.
Molecular Imaging of the Kinetics of Vascular Endothelial Growth Factor Gene Expression in Ischemic Myocardium
Authors: J. C. Wu
Journal: Circulation (2004)

Background-Angiogenic gene therapy is a promising treatment paradigm for patients with ischemic heart disease.In this study, we used micro-positron emission tomography (microPET) to monitor the transgene expression, function, and effects in a whole-body system.Methods and Results-Adenovirus with cytomegalovirus promoter driving an angiogenic gene (vascular endothelial growth factor [VEGF]) linked to a PET reporter gene (herpes simplex virus type 1 mutant thymidine kinase; Ad-CMV-VEGF 121 -CMV-HSV1-sr39tk) was used to transfect rat embryonic cardiomyoblasts in vitro.Expression of both genes correlated strongly (r=0.98;P<0.001).Afterward, rats underwent ligation of the left anterior descending artery followed by injection of 1×10 10 pfu of Ad-CMV-VEGF 121 -CMV-HSV1-sr39tk (study; n=35) or Ad-null (control; n=15) at the peri-infarct region.Noninvasive microPET imaging was used to assess the uptake of 9-(4-[ 18 F]-fluoro-hydroxymethylbutyl)guanine ([ 18 F]-FHBG) PET reporter probe by cells expressing the HSV1-sr39tk PET reporter gene.Cardiac transgene expression peaked at day 1 and declined over the next 2 weeks.Repeat adenoviral injections at day 60 yielded no detectable signal.The in vivo reporter gene expression (% injected dose/g of [ 18 F]-FHBG) correlated well with ex vivo gamma counting (r=0.92),myocardial tissue HSV1-sr39TK enzyme activity (r=0.95), and myocardial tissue VEGF level (r=0.94;P<0.001 for all).The VEGF 121 isoform induced significant increases in capillaries and small blood vessels.However, the level of neovasculature did not translate into significant improvements in functional parameters such as myocardial contractility by echocardiography, perfusion by nitrogen-13 ammonia imaging, and metabolism by [ 18 F]-fluorodeoxyglucose imaging.Conclusions-Taken together, these findings establish the feasibility of molecular imaging for monitoring angiogenic gene expression with a PET reporter gene and probe noninvasively,
Activation of Peroxisome Proliferator-Activated Receptors by Chlorinated Hydrocarbons and Endogenous Steroids
Authors: Yuan-Chun Zhou, David J. Waxman
Journal: Environmental Health Perspectives (1998)

Trichloroethylene (TCE) and related hydrocarbons constitute an important class of environmental pollutants whose adverse effects on liver, kidney, and other tissues may, in part, be mediated by peroxisome proliferator-activated receptors (PPARs), ligand-activated transcription factors belonging to the steroid receptor superfamily.Activation of PPAR induces a dramatic proliferation of peroxisomes in rodent hepatocytes and ultimately leads to hepatocellular carcinoma.To elucidate the role of PPAR in the pathophysiologic effects of TCE and its metabolites, it is important to understand the mechanisms whereby PPAR is activated both by TCE and endogenous peroxisome proliferators.The investigations summarized in this article a) help clarify the mechanism by which TCE and its metabolites induce peroxisome proliferation and b) explore the potential role of the adrenal steroid and anticarcinogen dehydroepiandrosterone 3p-sulfate (DHEA-S) as an endogenous PPAR activator.Transient transfection studies have demonstrated that the TCE metabolites trichloroacetate and dichloroacetate both activate PPARx, a major liver- expressed receptor isoform.TCE itself was inactive when tested over the same concentration range, suggesting that its acidic metabolites mediate the peroxisome proliferative potential of TCE.Although DHEA-S is an active peroxisome proliferator in vivo, this steroid does not stimulate trans-activation of PPARa or of two other PPAR isoforms, y and 6/Nucl, when evaluated in COS-1 cell transfection studies.To test whether PPARa mediates peroxisomal gene induction by DHEA-S in intact animals, DHEA-S has been administered to mice lacking a functional PPARa gene.DHEA- S was thus shown to markedly increase hepatic expression of two microsomal P4504A proteins associated with the peroxisomal proliferative response in wild-type mice.In contrast, DHEA-S did not induce these hepatic proteins in PPARa-deficient mice.Thus, despite its unresponsiveness to steroidal peroxisome proliferators in transfection assays, PPARa is an obligatory mediator of DHEA-S-stimulated hepatic peroxisomal gene induction.DHEA-S, or one of its metabolites, may thus serve as an important endogenous regulator of liver peroxisomal enzyme expression.
BOOK REVIEWS
Authors: DONALD L. TRUMP
Journal: JNCI Journal of the National Cancer Institute (1990)

Journal Article BOOK REVIEWS Get access Cancer Chemotheraphy: Priniciples and Practice . Bruce A. Chabner , Jerry M. Collins , eds. Philadelphia : J. B. Lippincott Co , 1990 , 576 pp. $87.50. DONALD L. TRUMP DONALD L. TRUMP Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 82, Issue 20, 17 October 1990, Page 1644, https://doi.org/10.1093/jnci/82.20.1644 Published: 17 October 1990
Lymph Node Examination Rate, Survival Rate, and Quality of Care in Colon Cancer—Reply
Authors: Sandra L. Wong
Journal: JAMA (2008)

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
S3 Guideline: Sedation for gastrointestinal endoscopy 2008
Authors: A. Riphaus, T. Wehrmann, B. Weber, J. Arnold, U. Beilenhoff, H. Bitter, S. von Delius, D. Domagk, A. Ehlers, S. Faiss, D. Hartmann, W. Heinrichs, M.-L. Hermans, C. Hofmann, S. In der Smitten, M. Jung, G. Kähler, M. Kraus, J. Martin, A. Meining, J. Radke, T. Rösch, H. Seifert, A. Sieg, B. Wigginghaus, I. Kopp
Journal: Endoscopy (2009)

Correction to: S3 Guideline: Sedation for gastrointestinal endoscopy 2008Endoscopy 2009; 41(09): 787-815DOI: 10.1055/s-0029-1215035
Pancreatic Carcinoma
Authors: Lawrence R. McCormack
Journal: JAMA (1977)

The survival of 28 patients with pancreatic cancer was studied following initial detection of this malignant neoplasm by ultrasonic scanning. By ultrasound examination, 24 patients had an abnormality, and 21 had a demonstrable mass. Twenty-seven patients are now deceased, and the overall survival ranged from eight days to 24 months (mean, 6.1 months). The results of this study indicate that diagnosis by ultrasonic scanning had no effect on the survival of patients with pancreatic carcinoma. (<i>JAMA</i>238:240, 1977)
BRITISH MEDICAL ASSOCIATION—SPECIAL RATES.
Journal: JAMA (1897)

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
England and Wales
Authors: Tim Ban=
Journal: BMJ (1923)

General's Statistical Review of England and lVales for 1921.(New Annual Series, No. 1.) Tables, Part II, Civil."This volume, we learn, forms part of the annual series of statistical publications which, under tlle style of the Registrar-General's Statistical Review, will henceforth take the place of the Registrar-General's Annual Report.The change in form and name is governed by the provisions of Section 5 of the Census Act, 1920, which requires the Registrar-General from time to time to collect and publish statistical information regarding the number and condition of the population in the interval between one census and another.The tables for 1921 have been divided into two groups -medical
Abstract 2192: Concurrent Tumor Treating Fields (TTFields) and dexamethasone decrease proliferation and clonogenicity of patient-derived glioblastoma cells <i>in vitro</i>
Authors: Sharon K. Michelhaugh, Sam Kiousis, Sandeep Mittal
Journal: Cancer Research (2019)

Abstract Background: TTFields are FDA-approved for treatment of newly-diagnosed and recurrent glioblastoma and extend progression-free survival and overall survival in newly-diagnosed glioblastoma patients. Dexamethasone is administered perioperatively to GBM patients to reduce tumor-associated edema and increased intracranial pressure. In addition, high dose corticosteroids may be required during TTFields therapy. In this study, a patient-derived GBM cell line from a newly-diagnosed glioblastoma patient was treated in vitro with TTFields ± dexamethasone followed by proliferation and clonogenic assays. Methods: This study was approved by the Institutional Review Board and written consent obtained from the patient. A single-cell suspension was generated from tumor tissues obtained from the newly-diagnosed patient. Cells were cultured in DMEM/F12 media with 10% fetal bovine serum and gentamicin. Prior to TTFields initiation, cells were plated on plastic coverslips (1×104cells/coverslip; n=7-8/group) and incubated overnight. Then, TTFields were applied at 200 kHz with a field intensity of ~1.6 V/cm for 14 days. Cells were treated with TTFields with or without 50 µM dexamethasone. At the end of the TTFields application, proliferation was assessed with XTT assay and cells were harvested and replated for the clonogenic assay (n=3/group). XTT data and clonogenic assay cell counts were analyzed by one-way ANOVA with Tukey’s post-hoc test. Results: In patient-derived glioblastoma cells treated with TTFields and dexamethasone for 14 days, proliferation was significantly decreased compared to the dexamethasone-only and control groups (0.483±0.30; 1.33±0.18; 1.42±0.11, respectively, ANOVA p&amp;lt;0.001). Similarly, cell counts in the clonogenic assay were markedly decreased in the TTFields ± dexamethasone group compared to dexamethasone-only (1184±425.9; 46464±4580; p&amp;lt;0.05). Conclusions: In glioblastoma cells from a newly-diagnosed patient, concurrent TTFields with dexamethasone produced a ~three-fold reduction of proliferation and reduced clonogenicity compared to control groups. Citation Format: Sharon K. Michelhaugh, Sam Kiousis, Sandeep Mittal. Concurrent Tumor Treating Fields (TTFields) and dexamethasone decrease proliferation and clonogenicity of patient-derived glioblastoma cells in vitro [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 2192.
Use of Gamma Globulin Groups Gm(a), Gm(b), and Gm(x) to Clarify Forensic Disputes on Paternity
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 predictors of severe fatigue in solid tumor patients seeking acute care
Authors: R. Valdres, E. Manzullo, C. P. Escalante
Journal: Journal of Clinical Oncology (2004)

8115 Background: Fatigue is the most common symptom of cancer patients and has been described in various populations. Our objectives are to describe solid tumor patients (STP) and clinical factors associated with severe fatigue (defined as worst fatigue in past 24 hours ≥7/10) in an acute care setting and to determine whether certain clinical factors available during the emergency center (EC) visit identify patients with severe fatigue. Methods: A retrospective cohort of 653 STP admitted to the EC from 5/1/01 to 8/15/01 was studied. Data abstracted from the medical record included demographic, clinical and cancer treatment factors. Descriptive statistics, chi-square and “student” t-tests were utilized. In developing a preliminary predictive model, stepwise logistic regression was employed. Results: The mean age was 56 years (range, 19–92); 333 (51%) were female. The most frequent malignancies were breast cancer 119 (18%) and lung cancer 98 (15%). The majority, 345 (53%) had controlled disease. Of the cohort, 277 (58%) had Zubrod performance scores ≥ 2. Half (326) were not currently receiving cancer treatment. Fifty-seven percent (372) had severe fatigue and over half (51%) had both severe fatigue and severe pain. (Table 1) Conclusions: A majority of STP seeking acute care has severe fatigue. This preliminary model identifies clinical factors in STP with severe fatigue in our EC. Model validation is necessary. If validated, some patients may benefit from earlier identification and referral for fatigue management strategies. This may improve their overall quality of life and potentially influence a lower care level with less cost. Author Disclosure Employment or Leadership Consultant or Advisory Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Ortho Biotech Ortho Biotech