tbuckley/cabot-search huggingface dataset:
Epidemiology of hepatic angiosarcoma in the United States: 1964-1974.
Authors: H Falk, J Herbert, S Crowley, K G Ishak, L B Thomas, H Popper, G G Caldwell
Journal: Environmental Health Perspectives (1981)

A nationwide survey of hepatic angiosarcoma (HAS) in the United States during the years 1964 through 1974 identified 168 cases. Of these, 42 cases (25%) were associated with known etiologic factors, such as vinyl chloride monomer exposure during preparation of poly(vinyl chloride), use of Thorotrast in angiography, exposure to inorganic arsenic, and treatment with androgenic-anabolic steroids; 126 cases (75%) are of uncertain etiology. HAS most often affects males (ratio of approximately 3:1), peaks in the sixth and seventh decades of life (somewhat earlier than other sarcomas of the liver) and appears to occur more often in the industrialized Northeast and Midwest (although reporting artifact may be a factor). There is an extraordinary relative risk for poly(vinyl chloride) polymerization workers; there may also be other chemical-industrial associations that require further investigation. Prospective epidemiologic studies of HAS should be considered as a means of identifying other causative factors (e.g., chemicals or drugs) related to HAS.
Isoproterenol induced myocardial necrosis is associated with stress protein synthesis in rat heart and thoracic aorta
Authors: F P WHITE, S R WHITE
Journal: Cardiovascular Research (1986)

Journal Article Isoproterenol induced myocardial necrosis is associated with stress protein synthesis in rat heart and thoracic aorta Get access F P WHITE, F P WHITE From the Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, PulIman. Washington, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar S R WHITE S R WHITE From the Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, PulIman. Washington, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 20, Issue 7, July 1986, Pages 512–515, https://doi.org/10.1093/cvr/20.7.512 Published: 01 July 1986
Conflagration of children in cars.
Authors: D G Gill
Journal: BMJ (1984)

Conflagration of children in carsThis paper reports on the recent deaths of seven Irish preschool children and the burning of seven others while unattended in parked motorcars.Death was from complications of severe extensive burns, from respiratory burns, or from toxic fumes.In every case the accident occurred while the children were playing or waiting in the car with the ignition switched off. Case reportsFourteen children were trapped in conflagrations in 10 cars, resulting in seven deaths and seven burns of varying severity.All ignitions were off at the time of the accident, no electrical faults were found, and no car had a (
The Use of Placebo in Clinical Trials on Bipolar Disorder: A New Approach for an Old Debate
Authors: Eduard Vieta, Xavier Carné
Journal: Psychotherapy and Psychosomatics (2004)

Placebo response is high in bipolar disorder trials. This is a challenge for researchers and an enigma for clinicians. This article will attempt to aid in the comprehension of the ethical questions and methodologies related to the use of placebo in bipolar disorder.A systematic review of the main computerized data bases (Medline, Embase, Psychlit, Current Contents) was carried out, using the following key words: placebo, bipolar disorder, mania, depression, clinical trial.Placebo has a very important role in the study of bipolar disorders. From a methodological point of view, and given the limitations of non-inferiority designs, the use of placebo is necessary to evaluate the sensitivity of the study and ensure that the drug under investigation is really effective. For this reason, several procedures may be used to satisfactorily solve the ethical objections. Placebo response in bipolar disorder trials is more likely to occur in patients who are mildly ill, bipolar II, mixed-episode, first-episode, rapid cycling, atypical, non-psychotic, substance abusers and medically ill. The use of concomitant medication such as benzodiazepines, a high frequency of visits, a high number of treatment groups and sites, fixed-dose designs, and the concomitant use of psychotherapy are likely to increase placebo response.The subject of the use of placebo in psychiatric clinical trials leads to very relevant ethical, methodological and clinical dilemmas. Many reasons support the use of placebo in acute bipolar studies, whereas in maintenance the length of the treatment with placebo makes the decision more difficult. Ethical concerns can be addressed through operational definitions of outcome measures, add-on and discontinuation designs, early escape strategies, and processes designed to make sure that fully informed consent was fairly obtained. There are a number of clinical and methodological variables that are associated with placebo response.
Cost of Containment-Reply
Authors: Bill R. Newsom
Journal: JAMA (1982)

In Reply.—  To the Blue Cross and Blue Shield organization, cost containment is a reality and has been for many years. Historically, Blue Cross and Blue Shield plans have been concerned with the issue of health care costs, and one focus has been manifested in moves to shift demand for the more expensive methods of delivering health care while increasing the supply of more cost-effective services.  More specifically, the Blue Cross and Blue Shield Associations launched an effort to encourage increased subscriber use of ambulatory surgery as a substitute for inpatient surgery where appropriate. We have recommended to the plans that inpatient and outpatient benefits for surgery be comparable—that is, the scope of services covered should be similar for the same procedures, whether performed in an inpatient or outpatient setting. We have also recommended to the plans that communications with physicians, hospital administrators, and other health care providers should be
Limiting Resuscitation: Emerging Policy in the Emergency Medical System
Authors: Greg A. Sachs, Steven H. Miles, Rebekah A. Levin
Journal: Annals of Internal Medicine (1991)

Patients, families, and physicians frequently decide that a hospitalized patient will forgo cardiopulmonary resuscitation and document this decision with a do-not-resuscitate (DNR) order. In community settings (home, nursing home, hospice), these orders may conflict with paramedics' standing orders to provide cardiopulmonary resuscitation whenever it is medically indicated. We did a nationwide telephone survey of state offices for coordination of emergency medical services (EMS) to see how the states deal with this potential conflict. We identified eight states that have specific policies enabling EMS personnel to accept DNR orders for patients being transported by ambulance. State officials identified administrative complexities and legal concerns as the primary barriers to enacting prehospitalization DNR policies. We also identified 21 local EMS systems that have developed policies for accepting orders to withhold life-sustaining treatment. Four types of policy models, characterized according to procedure for validating DNR orders and telephone accessing the EMS system, show that regulatory reform can address policy barriers in the absence of enabling legislation.
Abstract 1052: Dual role of MEK1/2 and MEK5 in the reversal of epithelial-to-mesenchymal transition
Authors: Van T. Hoang, Steven Elliott, Elizabeth C. Martin, Lyndsay V. Rhodes, Henry C. Segar, Hope Burks, Suravi Chakrabarty, Darlene Monlish, Theresa B. Phamduy, Doug Chrisey, Jane E. Cavanaugh, Patrick Flaherty, Bridgette M. Collins-Burow, Matthew E. Burow
Journal: Cancer Research (2014)

Abstract The mitogen-activated protein kinase (MAPK) pathway has well-established roles in cellular processes including proliferation, differentiation, and regulation of cell fate, namely survival and apoptosis. In breast cancer, constitutive activation of the MAPK/extracellular signal-regulated kinases (ERK) pathways have been linked to chemoresistance and metastatic progression through distinct mechanisms including the activation of epithelial-to-mesenchymal transition (EMT). Our previous studies have shown that overexpression of MEK5 promotes EMT markers and induces the progression to a mesenchymal phenotype. Here, we tested the effects of a novel MEK1/2 and MEK5 inhibitor, SC-1-151, and other known MAPK signaling inhibitors (PD184,352 (MEK1/2), AZD6244 (MEK1/2), BIRB796 (p38)) on a panel of mesenchymal and highly metastatic breast cancer cell lines. While the MEK1/2 and p38 inhibitors decreased cell viability across cell lines, only the dual inhibition of MEK1/2 and MEK5 though the use of SC-1-151 demonstrated a change in cell morphology indicative of mesenchymal-to-epithelial transition (MET). Furthermore, the cells exhibited a significant decrease in migration potential following SC-1-151 treatment. Further analysis of the effects of SC-1-151 in the triple-negative breast cancer cell lines revealed an alteration of the genes associated with EMT, notably a decrease in expression of Fra-1, a transcription factor downstream of MAPK. Immuno-compromised mice inoculated with the MDA-MD-231 cell line and treated with SC-1-151 demonstrated decreased tumor volumes compared to vehicle-treated animals at day 30 post cell injection, implicating the role of MEK inhibition on tumorigenesis. These data demonstrate the need for a better understanding of the dual role of MEK1/2 and MEK5 signaling in breast cancer, and suggest that inhibition of the MEK1/2 and MEK5 signaling pathways leads to a decrease in EMT and cell migration. Citation Format: Van T. Hoang, Steven Elliott, Elizabeth C. Martin, Lyndsay V. Rhodes, Henry C. Segar, Hope Burks, Suravi Chakrabarty, Darlene Monlish, Theresa B. Phamduy, Doug Chrisey, Jane E. Cavanaugh, Patrick Flaherty, Bridgette M. Collins-Burow, Matthew E. Burow. Dual role of MEK1/2 and MEK5 in the reversal of epithelial-to-mesenchymal transition. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1052. doi:10.1158/1538-7445.AM2014-1052
Pulmonary Artery Obstruction and Giant Cell Arteritis
Authors: Phillippe Chassagne
Journal: Annals of Internal Medicine (1995)

Letters1 May 1995Pulmonary Artery Obstruction and Giant Cell ArteritisPhillippe Chassagne, Joseph Gligorov, and Stephane DominiquePhillippe ChassagneHopital de Boisguillaume, BP 100, 76233 Boisguillaume, France.Search for more papers by this author, Joseph GligorovHopital de Boisguillaume, BP 100, 76233 Boisguillaume, France.Search for more papers by this author, and Stephane DominiqueHopital de Boisguillaume, BP 100, 76233 Boisguillaume, France.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-122-9-199505010-00020 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Although thrombosis caused by giant cell arteritis may theoretically affect all medium- and large-sized arteries [1, 2], thrombosis of the pulmonary artery is rare [3, 4]. We report a case of pulmonary infarction secondary to segmentary thrombosis of the pulmonary artery in a patient treated for giant cell arteritis. Pneumonia was suspected in an 86-year-old woman who had been successfully treated for 3 months with prednisone for histologically confirmed giant cell arteritis. A chest radiograph showed infiltration of the upper left lobe of the lung with areas of cavitation.Laboratory findings included a leukocyte count of 22 ...References1. Hunder GG, Michet CJ. Giant cell arteritis and polymyalgia rheumatica. Clin Rheum Dis. 1985; 11:471-83. Google Scholar2. Klein RG, Hunder GG, Stanson AW, Sheps SG. Large artery involvement in giant cell (temporal) arteritis. Ann Intern Med. 1975; 83:806-12. Google Scholar3. Bradley JD, Pinals RS, Blumenfeld HB, Poston WM. Giant cell arteritis with pulmonary nodules. Am J Med. 1984; 77:135-40. Google Scholar4. Glover MU, Muniz J, Bessone L, Carta M, Casellas J, Maniscalco BS. Pulmonary artery obstruction due to giant cell arteritis. Chest. 1987; 91:924-5. Google Scholar Author, Article, and Disclosure InformationAffiliations: Hopital de Boisguillaume, BP 100, 76233 Boisguillaume, France. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByDiagnostic value of PET/CT for giant cell arteritis combined with pulmonary embolism presentingToux chronique révélant une maladie de HortonAtteinte respiratoire de la maladie de Horton : 8 observations et revue de la littératureThoracic vasculitis presenting as surgical problemsSymptômes inauguraux de la maladie de Horton sur une série de 260 patientsPulmonary Manifestations of Systemic VasculitidesPULMONARY INVOLVEMENT IN COMMON RHEUMATOLOGIC DISEASES IN THE ELDERLYManifestations pleuropulmonaires des vascularites systémiquesPulmonary Artery Stenosis and Periarteritis Nodosa 1 May 1995Volume 122, Issue 9Page: 732KeywordsAngiographyGiant cellsInfarctionLesionsPulmonary arteriesSteroidsThoraxThrombosisVasculitisWegener granulomatosis Issue Published: 1 May 1995 CopyrightCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
MYCETOMA IN AMERICA
Authors: RICHARD L. SUTTON
Journal: JAMA (1913)

Although mycetoma, or Madura foot, was described by Kaempfer1 in 1712, its occurrence, or rather its recognition, in America is of quite recent date.Of the cases originating in this country, that described by Adami and Fitzpatrick2 is probably the first.Their patient was a French Canadian, 21 years old, a native of Montreal who had never been outside of Canada.Parkes' patient3 had previously resided in India, and in the case described by Kemper and Jameson4 the course of the disease was so rapid and the pain so great that, in the absence of corroborative microscopic evi- dence, a diagnosis of mycetoma may safely be excluded.In the example reported by Hyde and Senn5 the patient was a dental student, 20 years of age, a native and resident of Iowa.Artwine and Lamb's6 case occurred in a Mexican laborer, 45 years old, and Pope and Lamb's7 patient also was a Mexican laborer, aged 27.The fifth, and last, American case that I have been able to find a record of is the one on the study of which Wright" largely based his admirable contributions to the sub¬ ject of niycetoma.The patient was an Italian woman, ' 2<i years of age, on Dr. H. II. A. Beach's service at the Massachusetts (¡encrai Hospital.The two following cases of Madura-foot disease have recently been under observation in Kansas City:Cask 1.-The patient, A. D., laborer, Bingle, aged 24, was an employee of the Missouri Paeilic Kailway Company, and was referred to my associate, Dr. .1. 1'.KanoUy, the company dermatologist.Dr. Kanoky being absent from the city, 1 diag¬ nosed and treated the ease, and am indebted to him for permission to report it.The patient is a native of Padua, Mexico, and formerly resided at Aransus Pass, Texas, lie has never before Buffered from B Bkin disease, and the cutaneous history of his family also is negative.Present Illness.Three years prior to the time of consulta¬ tion, while walking barefooted across a pasture, the patient stopped into a depression, in the soft, ground that had been left by an old mule (rack, and at the same time sustained a slight, punctured wound of the sole of the left foot, beneath the arch.Be thinks that the wound was probably made by a cactus thorn.The lesion gave rise to but little pain or inconvenience, and was almost forgotten until about a month afterward, when a small, hard lump appeared beneath the skin at the site of the injury.The tumor was incised, hut no pus escaped, nnd no foreign body could be discovered.The tumefaction gradually increased, however, until the depression beneath the arch was replaced by a large, boggy swelling.There was little or no associated pain.In the course of about fourteen months, a minute, oval opening appeared near the site of the original wound, and small amounts of "grainy," yellowish pus escaped.Since then, a number of other openings have developed, until, at present, (here are a hundred or more scattered over the sole and sides of the foot.At no time has the pain been severe.A
Ischemia time impacts recurrence of hepatocellular carcinoma after liver transplantation
Authors: Shunji Nagai, Atsushi Yoshida, Marcelo Facciuto, Dilip Moonka, Marwan S. Abouljoud, Myron E. Schwartz, Sander S. Florman
Journal: Hepatology (2014)

Although experimental evidence has indicated that ischemia-reperfusion (I/R) injury of the liver stimulates growth of micrometastases and adhesion of tumor cells, the clinical impact of I/R injury on recurrence of hepatocellular carcinoma (HCC) after liver transplantation (LT) has not been fully investigated. To study this issue, we conducted a retrospective review of the medical records of 391 patients from two transplant centers who underwent LT for HCC. Ischemia times along with other tumor/recipient variables were analyzed as risk factors for recurrence of HCC. Subgroup analysis focused on patients with HCC who had pathologically proven vascular invasion (VI) because of the associated increased risk of micrometastasis. Recurrence occurred in 60 patients (15.3%) with median time to recurrence of 0.9 years (range, 40 days-4.6 years). Cumulative recurrence curves according to cold ischemia time (CIT) at 2-hour intervals and warm ischemia time (WIT) at 10-minute intervals showed that CIT>10 hours and WIT>50 minutes were associated with significantly increased recurrence (P=0.015 and 0.036, respectively). Multivariate Cox's regression analysis identified prolonged cold (>10 hours; P=0.03; hazard ratio [HR]=1.9) and warm (>50 minutes; P=0.003; HR=2.84) ischemia times as independent risk factors for HCC recurrence, along with tumor factors, including poor differentiation, micro- and macrovacular invasion, exceeding Milan criteria, and alpha-fetoprotein>200 ng/mL. Prolonged CIT (P=0.04; HR=2.24) and WIT (P=0.001; HR=5.1) were also significantly associated with early (within 1 year) recurrence. In the subgroup analysis, prolonged CIT (P=0.01; HR=2.6) and WIT (P=0.01; HR=3.23) were independent risk factors for recurrence in patients with VI, whereas there was no association between ischemia times and HCC recurrence in patients with no VI.Reducing ischemia time may be a useful strategy to decrease HCC recurrence after LT, especially in those with other risk factors.
Echocardiographic Assessment of Left Ventricular Diastolic Pressure.
Authors: Lee L. Konecke
Journal: Annals of Internal Medicine (1972)

Meeting Abstracts1 May 1972Echocardiographic Assessment of Left Ventricular Diastolic Pressure.Lee L. Konecke, M.D., Harvey Feigenbaum, M.D., F.A.C.P., Sonia Chang, B. S., Betty Corya, M.D., John L. Fischer, M.D.Lee L. Konecke, M.D.Search for more papers by this author, Harvey Feigenbaum, M.D., F.A.C.P.Search for more papers by this author, Sonia Chang, B. S.Search for more papers by this author, Betty Corya, M.D.Search for more papers by this author, John L. Fischer, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-76-5-865_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptWhether the echocardiographically recorded mitral valve could reflect alterations in left ventricular diastolic pressure was studied. Simultaneous mitral valve echograms and left ventricular pressures were obtained on 36 patients undergoing diagnostic cardiac catheterization. Attention was given to the left ventricular initial diastolic pressure (LVIDP), left ventricular end-diastolic pressure (LVEDP), and the atrial component of the left ventricular pressure (LVa). The echocardiographic measurements included the opening velocity of the mitral valve in early diastole (DE slope) and the interval between the A point, which is the onset of closure of the mitral valve after atrial systole, and the C point, which... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Lee L. Konecke, M.D.; Harvey Feigenbaum, M.D., F.A.C.P.; Sonia Chang, B. S.; Betty Corya, M.D.; John L. Fischer, M.D.Affiliations: Indianapolis, Ind. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRelation of mitral valve closure to the first heart sound in man 1 May 1972Volume 76, Issue 5Page: 865-865KeywordsBlood pressureCatheterizationDiastoleSystole ePublished: 1 December 2008 Issue Published: 1 May 1972 PDF downloadLoading ...
Deficiency of the autologous mixed lymphocyte reaction in patients with primary biliary cirrhosis.
Authors: S P James, C O Elson, J G Waggoner, E A Jones, W Strober
Journal: Journal of Clinical Investigation (1980)

In this study we show that patients with primary biliary cirrhosis (PCB) have a marked deficiency in the ability to generate an autologous mixed lymphocyte reaction (AMLR) but have a normal ability to generate an allogeneic mixed lymphocyte reaction (MLR). This deficiency is not due to differences in the time-course of the proliferative response or to an altered response to variable numbers of stimulator cells. The deficiency was consistently found irrespective of the methods used to isolate autologous stimulator cells. Both responder cells and stimulator cells obtained from patients with PBC were similar to normal cells in their ability to generate an MLR in allogeneic normal human serum. In addition, serum from patients with PBC inhibited the ability of normal lymphocytes to generate both the AMLR and MLR to a similar degree, suggesting that the defect of the AMLR in PBC is not due to a serum factor. It has been shown that the responder cell population in the AMLR contains a subpopulation of cells that mediate suppression. Therefore, it is possible that the deficiency of the AMLR may be related to previously described abnormalities of suppressor function in patients with PBC.