tbuckley/cabot-search huggingface dataset:
WHO wants rapid response to emerging threats
Authors: P. Gunby
Journal: JAMA (1996)

AMONG EFFORTS to cope with new and reemerging microbial threats is that of the World Health Organization (WHO), an autonomous unit within the United Nations system with headquarters in Geneva, Switzerland. Last fall, the WHO established a Division of Emerging, Viral, and Bacterial Diseases Surveillance and Control. This division, the WHO claims, "can mobilize rapid response teams of WHO staff and other international experts in response to epidemic threats and place them on the site of the outbreak within 24 hours." Through the WHO's regional offices, the division is trying to strengthen the epidemiologic surveillance and public health laboratories of as many of its 190 member nations as possible. In effect, it is seeking greater international participation in the WHO's network for monitoring antimicrobial resistance, tracking frequent communicable diseases like influenza, and watching for new or reemerging public health threats. <h3>Typical Reemerging Diseases</h3> In addition to dramatic outbreaks such as
Holding Providers Accountable for Health Care Outcomes
Authors: David W. Baker, Mark R. Chassin
Journal: Annals of Internal Medicine (2018)

Letters3 April 2018Holding Providers Accountable for Health Care OutcomesDavid W. Baker, MD, MPH and Mark R. Chassin, MD, MPP, MPHDavid W. Baker, MD, MPHThe Joint Commission, Oakbrook Terrace, Illinois (D.W.B., M.R.C.)Search for more papers by this author and Mark R. Chassin, MD, MPP, MPHThe Joint Commission, Oakbrook Terrace, Illinois (D.W.B., M.R.C.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/L17-0708 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Dr. Korula asks how we should define precision in measuring outcomes. The precision of an outcome is best discussed using traditional epidemiologic methods for determining sensitivity, specificity, and positive and negative predictive value. The harder question is how precise the measurement of an outcome needs to be for an accountability measure. There is no bright line for making a decision, but looking at the frequency distribution of the outcome may be helpful to understand how much random error in measurement may affect provider rankings. If the variation in the outcome across providers is relatively narrow, then the precision ... Author, Article, and Disclosure InformationAffiliations: The Joint Commission, Oakbrook Terrace, Illinois (D.W.B., M.R.C.)Disclosures: Authors have disclosed no conflicts of interest. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M17-0691. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoHolding Providers Accountable for Health Care Outcomes David W. Baker and Mark R. Chassin Holding Providers Accountable for Health Care Outcomes Jacob Korula Metrics 3 April 2018Volume 168, Issue 7Page: 527KeywordsConflicts of interestDecision makingDisclosureEpidemiological methods and statisticsHealth care providersHealth care qualitySpecificity ePublished: 3 April 2018 Issue Published: 3 April 2018 Copyright & PermissionsCopyright © 2018 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Haydn-Quartett
Journal: JAMA (2003)

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
Book Reviews
Authors: Giovanni A. Fava, Nicoleta Sonino, Murray A. Morphy, P. Salmaggi, G.M. Bressa, G. Nicchia, M. Coniglio, P. La Greca, C. Le Grazie, Jerald F. Dirks, Jeffrey Wunder, Robert Kinsman, Joseph McElhinny, Nelson F. Jones, P. Bech, Diane S. Berry, James W. Pennebaker
Journal: Psychotherapy and Psychosomatics (1993)
Heat Shock Protein 70 Gene Transfection Protects Mitochondrial and Ventricular Function Against Ischemia-Reperfusion Injury
Authors: Jay Jayakumar, Ken Suzuki, Ivan A. Sammut, Ryszard T. Smolenski, Mak Khan, Najma Latif, Haitham Abunasra, Bari Murtuza, Mohamed Amrani, Magdi H. Yacoub
Journal: Circulation (2001)

Background Upregulation of heat shock protein 70 (HSP70) is beneficial in cardioprotection against ischemia-reperfusion injury, but the mechanism of action is unclear. We studied the role of HSP70 overexpression through gene therapy on mitochondrial function and ventricular recovery in a protocol that mimics clinical donor heart preservation. Methods and Results Hemagglutinating virus of Japan (HVJ)-liposome technique was used to transfect isolated rat hearts via intracoronary infusion of either the HSP70 gene (HSP group, n=16) or no gene (CON group, n=16), which was heterotopically transplanted into recipient rats. Four days after surgery, hearts were either perfused on a Langendorff apparatus for 30 minutes at 37°C (preischemia studies [n=8/group]) or perfused for 30 minutes at 37°C, cardioplegically arrested for 4 hours at 4°C, and reperfused for 30 minutes at 37°C (postischemia studies [n=8/group]). Western blotting and immunohistochemistry confirmed HSP70 upregulation in the HSP group. Postischemic mitochondrial respiratory control indices (RCIs) were significantly better preserved in HSP than in CON hearts: NAD + -linked RCI values were 9.54±1.1 versus 10.62±0.46 before ischemia (NS) but 7.98±0.69 versus 1.28±0.15 after ischemia ( P &lt;0.05), and FAD-linked RCI values were 6.87±0.88 versus 6.73±0.93 before ischemia (NS) but 4.26±0.41 versus 1.34±0.13 after ischemia ( P &lt;0.05). Postischemic recovery of mechanical function was greater in HSP than in CON hearts: left ventricular developed pressure recovery was 72.4±6.4% versus 59.7±5.3% ( P &lt;0.05), maximum dP/dt recovery was 77.9±6.6% versus 52.3±5.2% ( P &lt;0.05), and minimum dP/dt recovery was 72.4±7.2% versus 54.8±6.9% ( P &lt;0.05). Creatine kinase release in coronary effluent after reperfusion was 0.20±0.04 versus 0.34±0.06 IU · min −1 · g wet wt −1 ( P &lt;0.05) in HSP versus in CON hearts. Conclusions HSP70 upregulation protects mitochondrial function after ischemia-reperfusion injury; this was associated with improved preservation of ventricular function. Protection of mitochondrial function may be important in the development of future cardioprotective strategies.
Helicobacter pylori (clinical)
Authors: Rathbone Thompson, Disease Kng, M Woodward, C Morrison, J Mcmurray, H Tunstall-Pedae, G Lowe, H Dargie, K Mccoll, J Misiewicz, A Harris', K Bardhan', S Levi', H Langworthy'
Journal: Gut (1996)

Gastric Helicobacter pylori colonisation has been linked to coronary heart disease risk and if proven may represent an important treatable risk factor.To further investigate this association 342 consecutive patients with established acute myocardial infarction and 236 population-based controls were analysed serologically for evidence ofH.pylori colonisation.Overall 2061342 (60.2%) of cases were H. pylori positive compared to 132/236 (55.9 ¶/.) of controls (p=0.30).Although controls were significantly younger than patients (56.0 ±13 (SD) years versus 65.1 ± 11.7 years, p<0.001), age stratified odds ratio for myocardial infarction associated with H. pylori seropositivity was 1.05 (95% CI 0.7-1.53,p =0.87) and this remained non-significant (p=0.46) when other risk factors for ischaemic heart disease were taken into account using logistic regression analysis.We conclude that previous H. pylori infection does not increase the risk of acute myocardial infarction.
Demographic and prognostic factors in ampullary adenocarcinoma: A retrospective review of 74 sequential cases undergoing multidisciplinary management between 1997 and 2009.
Authors: Robert de Wilton Marsh, Romy Pandey, David J. Bentrem, Marshall Baker, Xian Ding, Susan Stocker, Eric Brown, Mark Talamonti
Journal: Journal of Clinical Oncology (2012)

e14642 Background: Ampullary adenocarcinoma represents 1% of GI cancers but accounts for almost 30% of Whipple operations at major centers. Prognosis falls between that of pancreatic and duodenal cancer, but demographic and prognostic factors are not well delineated. Methods: Retrospective review, with patient consent, of an IRB approved common surgical database at two academic institutions. This includes all cases operated on for ampullary adenocarcinoma between 1997 and 2009. Demographics and factors with potential relevance for prognosis by literature review were examined via Kaplan Meier and/or Cox models. Results: 74 cases were identified: 50 had conventional and 22 pylorus preserving Whipple procedures with 2 unresectable cases. Demographics: 38 males, 36 females; 64 Caucasian, 6 African American and 4 others; age 23-83, median 63.08 years. Tumor characteristics: Tis -1, T1-10, T2-22, T3-27, T4-12, Unknown-2; N0-35, N1-38, Unknown-1; pre-existing adenomas in 37 (50%). Tumor markers: CEA 2/34 and CA 19-9 16/37 tested were abnormal. Adjuvant therapy given (chemo and/or chemoRT): 33/74. Status: 34 patients alive and 41 deceased with a median follow-up of 22 months. Factors associated with poor outcome: Perineural invasion (PNI) p = 0.02; Pre-existing adenoma p = 0.001; Weight loss of 10 lbs or more p = 0.01; RBC transfusion in the OR p = 0.001. Factors not statistically prognostic: T stage, lymph nodal status, lymphovascular invasion, jaundice, CEA or CA 19-9 values and absence of adjuvant therapy. Pancreaticobiliary versus intestinal subtype was assessed by H and E staining but one third of cases were indeterminate, and while these appeared to have a worse prognosis, IHC will be performed for accurate classification and determination of significance. Conclusions: This dataset describes the demographics of patients treated for ampullary adenocarcinoma over 12 years and identifies PNI, weight loss, pre-existing adenoma and transfusion in the OR as adverse factors. These prognostic factors (and potentially histologic subtype) should be considered in patient care and future study design.
Understanding Costs and Cost-Effectiveness in Critical Care
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

Economic evaluations are increasingly common in the critical care literature, although approaches to their conduct are not standardized. The American Thoracic Society convened a workshop to address methodologic and reporting issues for economic analyses in critical care and to determine how guidelines from the U.S. Public Health Service Panel on Cost-effectiveness in Health and Medicine (PCEHM) were applicable to critical care. We identified several issues that hamper cost-effectiveness analyses (CEAs) in the critically ill. Data on the effectiveness of intensive care unit (ICU) interventions are often lacking; ICU patients are complex, with multiple concurrent problems and interventions; most ICU therapies are only supportive, and therefore may not individually result in improved outcome; accurate cost data are not commonly available and are difficult to obtain; there is no standardized approach for measuring or valuing costs across countries; typical outcomes in ICU studies (e.g., short-term mortality) are not ideal for CEAs while preferred outcomes for CEAs (e.g., long-term quality-adjusted survival) are rarely collected; valuing the importance of appropriate end-of-life care, an important aspect of ICU care, is difficult, and the burden of critical illness on family members is not easily captured in a CEA. Nevertheless, many of these problems are not unique to critical care, and we believe the PCEHM guidelines can be adapted to the critical care setting. We recommend all CEAs in the critically ill include a PCEHM reference case, where the cost-effectiveness ratio is calculated by adopting a societal perspective, estimating long-term costs and quality of life after ICU care, applying a 3% annual discount rate to costs and effects, and conducting multiway sensitivity analyses. Because elements of the reference case, such as long-term costs and quality of life, may only be estimated using modeling and assumptions, we also recommend inclusion of a "data-rich" case, where the cost-effectiveness ratio is generated as closely as possible from data on actual patient outcomes and costs (e.g., hospital costs per hospital survivor). We recommend that investigators conducting a CEA concurrently with a randomized trial make the proposed model available (e.g., via the Internet) before unblinding of trial data to minimize bias. Adopting a standard approach to CEAs of ICU therapies will provide a valid and more transparent evidence base for health care policy with regard to care of the critically ill.
Annals of Surgery, Philadelphia
Journal: JAMA (1969)

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
What Killed the Woman?
Journal: JAMA (1890)

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
Renal function after methoxyflurane and halothane anesthesia
Authors: R. E. Tobey
Journal: JAMA (1973)

A prospective clinical study was conducted to evaluate the renal effects of methoxyflurane and halothane anesthesia over a period of 20 days in healthy young adults undergoing elective surgery. Twenty patients received methoxyflurane and 14 received halothane. No case of renal failure or apparent impaired renal function occurred. There was no significant difference in fluid input, output, or daily weight. The most important difference observed between the two groups was the significantly elevated blood level of inorganic fluoride found postoperatively in the methoxyflurane-treated patients. The mean serum inorganic fluoride value on the first postoperative day was 21.47± 2.47μmol/liter for those patients administered methoxyflurane compared to only 4.74±0.53μmol/liter for the halothane group. There was a significant correlation between the venous blood concentration of methoxyflurane at the end of the operation and the serum inorganic fluoride level on the first postoperative day. Urinary oxalate crystals were seen postoperatively in 90% of cases in the methoxyflurane group compared to 43% in the halothane group.
Expression of insulin-like growth factor II, α-fetoprotein and hepatitis B virus transcripts in human primary liver cancer
Authors: E Cariani
Journal: Hepatology (1991)

Insulin-like growth factor II is a fetal growth factor structurally and functionally related to insulin and insulin-like growth factor I. Its mRNA expression is developmentally regulated in human liver, the reexpression of insulin-like growth factor II fetal transcripts being often observed in primary liver cancer. Insulin-like growth factor II and α-fetoprotein mRNAs were studied in 16 human primary liver cancers, most of which were highly differentiated. Hepatitis B virus transcripts were also analyzed in the tumors from hepatitis B virus chronic carriers. α-Fetoprotein mRNA was detected in only four tumors and in one nontumorous cirrhotic tissue; all these samples also displayed insulin-like growth factor II fetal transcripts. Furthermore, fetal insulin-like growth factor II mRNAs were observed in five tumors and six nontumorous cirrhotic areas not expressing α-fetoprotein mRNA. The presence of hepatitis B virus RNA was only observed in tissues not expressing α-fetoprotein or fetal insulin-like growth factor II mRNA. In conclusion, fetal insulin-like growth factor II transcripts are more frequently observed than α-fetoprotein mRNA in highly differentiated liver cancers and in surrounding cirrhotic areas. The reexpression of fetal insulin-like growth factor II transcripts might then be a marker of early steps of liver cell transformation. (HEPATOLOGY 1991;13:644–649.)
CheckMate 649: A randomized, multicenter, open-label, phase 3 study of nivolumab (nivo) + ipilimumab (ipi) or nivo + chemotherapy (CTX) vs CTX alone in pts with previously untreated advanced (adv) gastric (G) or gastroesophageal junction (GEJ) cancer.
Authors: Markus H. Moehler, Yelena Yuriy Janjigian, Antoine Adenis, Jean-Sebastien Aucoin, Narikazu Boku, Ian Chau, James M. Cleary, Kynan Tadao Feeney, Fabio A. Franke, Guillermo Ariel Mendez, Michael Schenker, Mingshun Li, Erika Hitre, Felix Couture, Michalis Karamouzis, Pierre-Luc Etienne, Jaffer A. Ajani
Journal: Journal of Clinical Oncology (2017)

TPS4132 Background: Pts with adv G/GEJ cancer have an OS of ≈ 1 y, indicating an unmet medical need for new first-line treatments (Tx). Expression of the PD-1 ligands PD-L1/PD-L2 is observed in up to 40% of pts with G/GEJ cancer and is associated with poor prognosis. In a phase 3 study of the PD-1 inhibitor nivo vs placebo in pts with adv CTX-refractory (CTX-R; ≥ 2 lines) G/GEJ cancer, nivo reduced the risk of death by 37% (HR, 0.63; P &lt; 0.0001) and increased the OS rate at 12 mo (27% vs 11%; Kang YK, et al. J Clin Oncol. 2017;35 (suppl 4S) [abstract 2]). In a phase 1/2 study in pts with CTX-R G/GEJ/esophageal cancer (79% ≥ 2 prior Tx lines), nivo 1 mg/kg + ipi 3 mg/kg had a manageable safety profile and resulted in 26% ORR (44% ORR in pts with PD-L1 + tumors), a median OS of 6.9 mo, and a 34% OS rate at 12 mo (Janjigian Y, et al. ASCO, 2016 [abstract 4010]). In the phase 1 CheckMate 012 trial, nivo + CTX had clinical activity and manageable safety in pts with NSCLC (Rizvi NA, et al. J Clin Oncol. 2016;34:2969-2979). These positive results support investigation of nivo, nivo + ipi, and nivo + CTX in earlier lines of Tx for G/GEJ cancer. The open-label, phase 3 CheckMate 649 trial will evaluate nivo + ipi and nivo + CTX vs CTX alone as first-line Tx for pts with adv G/GEJ cancer (NCT02872116). Methods: 1266 pts aged ≥ 18 y with untreated, inoperable adv/metastatic G/GEJ cancer (histologically confirmed adenocarcinoma) regardless of PD-L1 status will be randomized to receive either nivo + ipi, nivo + CTX (capecitabine/oxaliplatin [XELOX] or fluorouracil/leucovorin/oxaliplatin [FOLFOX]), or investigator choice of XELOX or FOLFOX. Tumor tissue for determination of PD-L1 status (Dako assay) must be provided from ≤ 6 mo before study Tx. No prior systemic Tx, including HER2 inhibitors, are allowed. Pts with known HER2 + status, suspected autoimmune disease, grade &gt; 1 peripheral neuropathy, or active infection are excluded. Primary endpoint is OS in pts with PD-L1 + (≥ 1%) tumors. Other endpoints include OS in all pts; PFS and time to symptom deterioration in all pts and in pts with PD-L1 + tumors; and safety. Clinical trial information: NCT02872116.