tbuckley/cabot-search huggingface dataset:
Quarterly J Experimental Physiology, Edinburgh
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
Evaluation of Dr. John Eager Howard's contributions to medicine
Authors: S. P. Asper
Journal: JAMA (1969)

Most physicians possess a number of attributes in common. They have scientific competence, empathy for the sick, and willingness to spend long hours at their work. Physicians differ widely, however, in degrees of ability, some showing talents in one direction and some in others. Rare indeed is the physician whose intellect, talents, and diligence complement each other in ways to create a life of unique productivity. Such a physician is the Passano Foundation laureate for 1968, John Eager Howard, MD, of Baltimore, professor of medicine at Johns Hopkins and the 28th scientist to receive this distinguished honor. The Passano Award itself is simply recognition by the foundation and by the community that there is one among us whose scientific contributions are meritorious, whose leadership in the profession has been effective, and whose way of life is such that many might wish to emulate it. As notable as this award may
Ian Macalister
Journal: BMJ (2006)

British family planning doctor whose assisted suicide in a Swiss clinic refuelled UK euthanasia debate Anne Turner's final trip to continental Europe was one she resented having to make.She loved travelling to Europe, often for the opera.But having decided to kill herself, she felt frustrated at the need to leave the comfort of her cosy bungalow in Bath.However, with typical self assurance, Dr Turner made precise plans.She would die in Switzerland on 24 January 2006, the day before her 67th birthday.Events early in the childhood of the woman dubbed "Boadicea" by a friend can probably be credited for the independence and strength of character that she exhibited throughout her life.Just 18 months after her birth in Harrogate in 1939, she was evacuated, with her sister, from war torn Europe to Vancouver in Canada.She only just made it.A German U boat sank the vessel behind the one in which she was travelling and such evacuations promptly ceased.But having safely reached North America, she enjoyed living with cousins and a grandmother.In 1945 however, she returned to Westerham, Kent, in England and to parents she didn't know-and to the austere, postwar landscape.She would later joke that it felt as if she had been evacuated to the United Kingdom rather than returned home.After her carefree existence in Canada, the grey skies, food rations, and lack of central heating did not endear her to her native land.Her father, a civil servant, and her mother, a local councillor, were strict and somewhat distant parents.So being packed off to boarding school in 1952 seemed more like a release than a frightening trip into the unknown.Shortly after leaving school a lifethreatening adder bite provided a first glimpse of her mortality.Her response was not fear but curiosity.And from this near-death experience she decided that dying was as easy as going to sleep.In 1958 she went to St Thomas' to study medicine.On the first day she met her future husband, Jack Turner.After qualifying, they worked in the south of England before settling in Bath, where they found jobs in general practice and began a family.Anne Turner soon developed an interest in family planning, and was to play a key role
The Canteen.
Authors: T. D. Crothers
Journal: JAMA (1901)

result, and in two others with one in five.In thirty cases of death followed by an autopsy, the clinical and bacteriological diagnosis was confirmed by the autopsy.Out of 36 deaths the sero-diagnosis was positive in 35 cases, in the thirty-sixth case it was hardly perceptible with a 1 in 0 solution.As a means of diagnosis this method is excellent, as applied to 289 patients forty hours after admission, it was positive in 215 cases.Dr. Tobiosen examined also a certain number of other
Abstract O-3: A β1-Adrenergic Receptor/β-Arrestin1-Regulatable MicroRNA, MiR-150 Protects the Mouse Heart from Ischemic Injury by Repressing Pro-apoptotic Egr2 and P2x7r
Authors: Il-man Kim, Yaoping Tang, Yongchao Wang, Kyoung-mi Park, Qiuping Hu
Journal: Circulation Research (2014)

MicroRNA (miR)-150 is down-regulated in patients with acute myocardial infarction (AMI), atrial fibrillation, dilated and ischemic cardiomyopathy as well as in various mouse heart failure (HF) models. Circulating miR-150 has been recently proposed as a better biomarker of HF than clinically used markers such as brain natriuretic peptide. We recently showed that β-arrestin1-biased β1-adrenergic receptor (β1AR) cardioprotective signaling activated by the β-arrestin-biased β-blocker, carvedilol (Carv) stimulates the processing of miR-150 in the heart (see figure A). However, the potential role of miR-150 in ischemic injury and HF is unknown. Here, we show that genetic deletion of miR-150 in mice causes abnormalities in cardiac structural and functional remodeling after MI. The cardioprotective roles of miR-150 during ischemic injury were attributed to repression of the pro-apoptotic genes egr2 (zinc binding transcription factor induced by ischemia) and p2x7r (pro-inflammatory ATP receptor) [see figure B]. These findings reveal a pivotal role for miR-150 as a regulator of cardiomyocyte survival during cardiac injury. In conclusion, our study will help to stratify HF patients that may respond better to β-arrestin-biased β-blockers, which is guided by circulating levels of miR-150.
Irinotecan Plus Gemcitabine Induces Both Radiographic and CA 19-9 Tumor Marker Responses in Patients With Previously Untreated Advanced Pancreatic Cancer
Authors: Caio Max S. Rocha Lima, Diane Savarese, Howard Bruckner, Arkadiusz Dudek, John Eckardt, John Hainsworth, Furhan Yunus, Eric Lester, William Miller, Wayne Saville, Gary L. Elfring, Paula K. Locker, Linda D. Compton, Langdon L. Miller, Mark R. Green
Journal: Journal of Clinical Oncology (2002)

PURPOSE: This phase II, multicenter, open-label, single-arm study evaluated the efficacy and safety of irinotecan and gemcitabine as combination chemotherapy for previously untreated patients with unresectable or metastatic pancreatic cancer. PATIENTS AND METHODS: Patients received repeated 21-day cycles at starting doses of gemcitabine 1,000 mg/m 2 over 30 minutes followed immediately by irinotecan 100 mg/m 2 over 90 minutes, both given intravenously on days 1 and 8. Patients were evaluated for objective tumor response, changes in the serum tumor marker CA 19-9, time to tumor progression (TTP), survival, and safety. RESULTS: Forty-five patients were treated. Eleven patients (24%) had 50% or greater reductions in tumor area. These were confirmed one cycle later in nine patients (response rate, 20%; 95% confidence interval, 8% to 32%). Among 44 patients with baseline CA 19-9 determinations, CA 19-9 decreased during therapy in 22 patients (50%) and was reduced by 50% or more in 13 patients (30%). Median TTP was 2.8 months (range, 0.3 to 10.8 months). There were significant (P &lt; .001) correlations between proportional changes in CA 19-9 and radiographic changes in tumor area with regard to extent of change (r = .67), timing of minimum on-study values (r = .85), and tumor progression (r = .89). Median survival was 5.7 months (range, 0.4 to 19.4+ months), and the 1-year survival rate was 27%. Severe toxicities were uncommon and primarily limited to grade 4 neutropenia (2%), grade 4 vomiting (2%), and grade 3 diarrhea (7%). CONCLUSION: Irinotecan/gemcitabine is a new combination that offers encouraging activity in terms of radiographic and CA 19-9 response and notable 1-year survival in pancreatic cancer. The regimen was well tolerated, with minimal grade 3 and 4 toxicities and excellent maintenance of planned dose-intensity.
Outbreak of Pharyngoconjunctival Fever at a Summer Camp—North Carolina, 1991
Journal: JAMA (1992)

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
Contents
Authors: S Sarkar, Z Jiang, D Evon, A Wahed, J Hoofnagle, R Brown, E Verna, M Pereira, H Tilson, C Aguilar, C.-S Leu, M Buti, E Fagan, L Pham, H Ngo, Y.-S Lim, S Hwang, V Reichenbach, G Ferna ´ndez-Varo, G Casals, D Oro, J Ros, P Melgar-Lesmes, R Weiskirchen, M Morales-Ruiz, W Jime ´nez, Q Lai, A Avolio, J Lerut, G Singh, S Chan, P Berloco, G Tisone, S Agnes, K Chok, W Sharr, M Rossi, T Manzia, C Lo, J Guerrero, R Teruel, C Martı ´nez, I Arcas, I Martı ´nez-Martı ´nez, M De La Morena-Barrio, V Vicente, J Corral
Journal: Journal of Hepatology (2012)
Phase I/II study of erlotinib and temsirolimus for patients with recurrent malignant gliomas (MG) (NABTC 04–02)
Authors: S. M. Chang, J. Kuhn, K. Lamborn, T. Cloughesy, I. Robins, F. Lieberman, A. Yung, J. Dancey, M. Prados, P. Wen
Journal: Journal of Clinical Oncology (2009)

2004 Background: Glioblastomas (GBM) frequently have EGFR amplification/mutations and inactivation of PTEN. Although single agent EGFR and mTOR inhibitors have limited activity, combinations of these agents may be more effective. Methods: The North American Brain Tumor Consortium conducted a phase I/II study of the EGFR inhibitor erlotinib in combination with the mTOR inhibitor temsirolimus in recurrent MG. Eligibility criteria were histologically proven GBM and anaplastic gliomas (AG), radiologic progression, &gt;18 years old, KPS &gt;60, adequate bone marrow and organ function. There was no limit on the number of prior relapses for phase I and no more than two prior relapses for phase II. Patients must not be receiving enzyme-inducing antiepileptic drugs. The dose of erlotinib was 150 mg/d in phase I and titrated up to maximum of 200mg/d in phase II depending on tolerability. Patients initially received temsirolimus 50 mg i.v. once weekly and the dose adjusted based on toxicities. Escalation was performed in groups of three. MTD was defined as the dose with 1/6 or fewer patients with dose-limiting toxicities (DLTs). Primary endpoint for the phase II component was PFS6. Results: In phase I, 22 patients were enrolled (15 GBM; 7 AG). Median age was 54 years (26–74); median KPS 90 (70–100); median prior relapses 1 (0–3). The MTD was determined to be 150 mg of erlotinib daily combined with 15 mg of temsirolimus weekly. DLTs were rash, mucositis, and liver function abnormalities. Pharmacokinetic data were similar to that for single agent erlotinib and temsirolimus; there was no interaction between the two drugs. AUC accumulation ratios between cycle 1 and 2 for erlotinib and OSI-420 were 3.6 and 4.6, respectively. In phase II, there were 56 patients (including 12 phase I patients treated at the MTD): 40 GBM; 16 AG, median age 47 years (20–72); median KPS 90 (range 60–100), median prior relapses 1 (range 1–3). Six patients discontinued therapy as a result of toxicities. For GBM patients, there was no PR, 30% SD, and PFS6 was 12.5%. For AG patients there was 12.5% PR, 12.5% SD, and PFS6 was 6.25%. Conclusions: The combination of erlotinib and temsirolimus was associated with a higher than expected incidence of toxicities and had minimal activity in recurrent MG. [Table: see text]
Still's disease in a 70-year-old woman
Authors: L. A. Steffe
Journal: JAMA (1983)

IN 1971, Bywaters<sup>1</sup>reported adultonset Still's disease in 14 patients older than 16 years. The usual clinical picture is that of a young adult with high spiking fever, malaise, a maculopapular rash, and any of numerous associated findings. Laboratory abnormalities are nonspecific. Systemic manifestations often precede the development of arthritis by years, making this a diagnosis to be considered when evaluating fever of undetermined origin. <h3>Report of a Case</h3> A 70-year-old woman was referred to the Medical College of Virginia, Richmond, in June 1980 for further evaluation of an episodic fever of undetermined origin. The fever had been present for two years and had led to five hospital admissions. The patient had previously been treated for right-calf thrombophlebitis, daily fevers, and dry, hacking cough. In October 1978, severe anterior pleuritic chest pain developed. Pleurocentesis yielded 60 mL of yellow, cloudy fluid found to be exudative (WBC count, 15,300/cu mm,
Influence of the Royal College of Radiologists' guidelines on hospital practice: a multicentre study. Royal College of Radiologists Working Party.
Authors: P Bourdillon, P Camm, A Cohen, E Davies, W Ennis, K Evans, P Hacking, M Lavelle, J Laws, M Mcnulty, C Roberts, G Roberts, G Row, R Sutherland, J Williams, Ox3 7lf, Henriet Nienhuis, Michael Goldacre, Valerie Seagroatt, Martin Vessey
Journal: BMJ (1992)

OBJECTIVE--To measure the effect on hospital radiology referral practice of introducing a strategy for change involving guidelines of good practice, monitoring, and peer review. DESIGN--Prospective data collection over a continuous 21-24 month period at each centre some time between January 1987 and December 1990. SETTING--Five district general hospitals and one district health authority. SUBJECTS--314,663 inpatient discharges, deaths, and day cases and 1,706,781 outpatient attendances under the care of 722 consultants from 25 clinical specialties. MAIN OUTCOME MEASURES--Number of referrals for x ray examination per 100 inpatient discharges, deaths, and day cases and per 100 new outpatient attenders. RESULTS--Most doctors were prepared to accept standards of clinical practice set by peers and also the monitoring and review of their practice with respect to these standards by local colleagues. 18% of firms were identified before guidelines were instituted as having persistently high referral rates. Appreciable, and often dramatic reductions in referral rates for individual x ray examinations were recorded by a substantial number of firms in every centre and in every specialty after guidelines were instituted. The major part of this reduction was achieved by some of the firms whose initial practice did not meet "high referral" criteria. Important variations in compliance with agreed standards of good practice were observed. CONCLUSIONS--The study offers strong experimental evidence to support a recent suggestion that at least a fifth of radiological examinations carried out in NHS hospitals are clinically unhelpful. The problem of how to assure compliance with agreed standards of practice needs to be resolved. Until this happens medical audit alone is unlikely to translate good practice into common practice.
Epidemiology of Ultraviolet-DNA Repair Capacity and Human Cancer
Authors: Lawrence Grossman
Journal: Environmental Health Perspectives (1997)

The following conclusions are derived from an epidemiological study.Reduced repair of ultraviolet (UV)-induced DNA damage contributes directly to basal cell carcinoma (BCC) in individuals with prior sunlight overexposure.A family history of BCC is a predictor of low DNA repair.Repair of UV-damaged DNA declines at a fixed rate of approximately 1 % per annum in noncancerous controls.The DNA repair differences between young BCC cases and their controls disappear as they age.Hence, BCC, in terms of DNA repair, is a premature aging disease.The persistence of photochemical damage because of reduced repair results in point mutations in the p53 gene and allelic loss of the nevoid BCC gene (Gorlin's syndrome) located on chromosome 9q.The fact that environmental vulnerability is gender oriented implicates hormones in regulating DNA repair.Xeroderma pigmentosum appears to be a valid paradigm for the role of DNA repair in BCC in the general population.
Dose Assessment Analogies
Authors: Bo Lindell
Journal: Environmental Health Perspectives (1978)

Assessments of radiation detriment are based on the absorbed dose in the organs and tissues of interest, assuming a linear, nonthreshold dose--response relationship for the induction of cancer or genetic effects at low doses. Similar assessments may be made for nonradioactive, mutagenic, or carcinogenic substances, in which case the time integral of the local tissue concentration of the substance may be the quantity which would correspond to the radiation dose. It can be shown that the assessment then involves calculations which are very similar to those made in the assessment of radiation detriment. It is suggested that an attempt should be made to make such assessments for nonradioactive pollutants, in order to provide a more appropriate basis for comparisons with radiation detriments. In the assessment of the detriment from inhaled substances, the overall collective intake commitment is simply the total amount of each substance ever to be inhaled, irrespective of when or where. This quantity might be assumed to be proportional to the total detriment in form of lung cancer.
Being Human Available
Journal: JAMA (2004)

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
Einführung in die pathologische Histologie der wichtigsten Pulpa- und Kiefererkrankungen sowie der hauptsächlichsten Tumoren der Mundhöhle.
Journal: JAMA (1931)

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
HIV protease inhibitors promote atherosclerotic lesion formation independent of dyslipidemia by increasing CD36-dependent cholesteryl ester accumulation in macrophages
Authors: James Dressman, Jeanie Kincer, Sergey V. Matveev, Ling Guo, Richard N. Greenberg, Theresa Guerin, David Meade, Xiang-An Li, Weifei Zhu, Annette Uittenbogaard, Melinda E. Wilson, Eric J. Smart
Journal: Journal of Clinical Investigation (2003)

Protease inhibitors decrease the viral load in HIV patients, however the patients develop hypertriglyceridemia, hypercholesterolemia, and atherosclerosis. It has been assumed that protease inhibitor–dependent increases in atherosclerosis are secondary to the dyslipidemia. Incubation of THP-1 cells or human PBMCs with protease inhibitors caused upregulation of CD36 and the accumulation of cholesteryl esters. The use of CD36-blocking antibodies, a CD36 morpholino, and monocytes isolated from CD36 null mice demonstrated that protease inhibitor–induced increases in cholesteryl esters were dependent on CD36 upregulation. These data led to the hypothesis that protease inhibitors induce foam cell formation and consequently atherosclerosis by upregulating CD36 and cholesteryl ester accumulation independent of dyslipidemia. Studies with LDL receptor null mice demonstrated that low doses of protease inhibitors induce an increase in the level of CD36 and cholesteryl ester in peritoneal macrophages and the development of atherosclerosis without altering plasma lipids. Furthermore, the lack of CD36 protected the animals from protease inhibitor–induced atherosclerosis. Finally, ritonavir increased PPAR-γ and CD36 mRNA levels in a PKC- and PPAR-γ–dependent manner. We conclude that protease inhibitors contribute to the formation of atherosclerosis by promoting the upregulation of CD36 and the subsequent accumulation of sterol in macrophages.