tbuckley/cabot-search huggingface dataset:
Compression-Decompression CPR: The Biomotor
Authors: Sam I. Lerman
Journal: JAMA (1994)

<h3>To the Editor.</h3> —An Editorial<sup>1</sup>in<i>JAMA</i>discusses the premature termination by the Food and Drug Administration (FDA) of trials of compression-decompression cardiopulmonary resuscitation (CPR), because of lack of informed consent. The addition of a suction phase to conventional CPR is a trivial, innocuous detail that should not require consent. The developers of the Ambu<sup>2</sup>device must certainly have tried its suction on willing volunteers and shown that its worst effect might be minor ecchymoses. In any case, the use of alternate pressure and suction for CPR is described in the August 5,1939,<i>Wiener Medizinische Wochenschrift</i>by Dr Rudolph Eisenmenger, Facharzt für physikalische Therapie, Vienna, Austria. His device, which he called a Biomotor, was a cuirass ventilator that applied alternate positive and negative air pressure to the torso, and was used extensively throughout Europe for mine rescue and other victims of asphyxia as well as polio. He urged
Cytokinetically quiescent (G0/G1) human multiple myeloma cells are susceptible to simultaneous inhibition of Chk1 and MEK1/2
Authors: Xin-Yan Pei, Yun Dai, Leena E. Youssefian, Shuang Chen, Wesley W. Bodie, Yukie Takabatake, Jessica Felthousen, Jorge A. Almenara, Lora B. Kramer, Paul Dent, Steven Grant
Journal: Blood (2011)
The effect of swimming on patients with ischemic heart disease.
Authors: S Magder, D Linnarsson, L Gullstrand
Journal: Circulation (1981)

Swimming is frequently recommended for cardiac rehabilitation, but little is known of its physiologic consequences in ischemic heart disease. Eight males who had had a myocardial infarction 8-17 months before the study were exercised to exhaustion or angina with 10 W/min-1 ramp on a cycle ergometer in sitting and supine positions. Oxygen uptake (VO2) was continuously measured to monitor the physiologic power requirement. All eight patients were taking beta blockers and four were taking digoxin. During sitting cycling, angina occurred in four and ST depression in five; during supine cycling, angina occurred in five and ST depression in six. VO2 was then measured while they swam at their own comfortable speed (mean 0.43 m/sec-1) in a swimming flume at water temperatures of 25.5 degrees C and 18 degrees C. In six, the water speed was gradually increased until they were limited by symptoms. Comfortable swimming at 25.5 degrees C was 87% (1.28 1/min-1) and at 18 degrees C 89% (1.30 1/min-1) of sitting peak VO2, while heart rates were 92% and 91% respectively. The mean peak VO2 and heart rate did not differ significantly between bicycle and swim tests (peak VO2 sitting 1.49 +/- 0.23, supine 1.42 +/- 0.24, 25.5 degrees C 1.60 +/- 0.17, 18 degrees C 1.52 +/- 0.19 1/min-1). Only two patients reported angina while swimming in warm water and one in cold water, although ST depression occurred in six in both swims. The subjective comfort and large muscle groups involved make swimming a good exercise, but the high relative energy cost and failure to identify ischemic symptoms indicate caution in cardiac patients, especially if their swimming skills are poor.
Effect on prescribing of the limited list in a computerised group practice.
Authors: W G Irwin, K A Mills, K Steele
Journal: BMJ (1986)

The prescribing of drugs in the therapeutic classes that are affected by the government9s limited list was investigated in a computerised group practice of just over 3,000 patients. Prescribable drugs in categories that are affected by the list were identified for two consecutive six month periods before and one six month period after the introduction of the list. A significant decrease in the prescribing of cough and cold remedies, vitamins, and antacids occurred after the list was introduced, whereas no change occurred in the prescribing of laxatives, benzodiazepines, or analgesics. The prescribing of iron and penicillin increased significantly after the list was introduced, whereas the use of H2 antagonists and non-steroidal anti-inflammatory drugs showed no significant change.
Does Postoperative Irradiation Improve Survival in Lung Cancer?
Authors: Evan Sherrah-Davies
Journal: JAMA (1966)

The treatment of carcinoma of the lung is unrewarding, because the majority of cases, when first seen, are too advanced for anything more than palliative treatment to be possible. An overall fiveyear cure rate of the order of 3% is realistic, and surgery, which holds undisputed priority as the treatment of choice for the apparently "early" case, fails to cure once the disease has spread beyond surgically removable tissues. Most surgeons remove obvious mediastinal glands, and some attempt a routine "radical" mediastinal dissection, but a true block-dissection, as done for cervical nodes, is impossible for anatomical reasons, and once mediastinal nodes are involved, survival rates drop sharply. It is reasonable to suggest, therefore, that postoperative radiation to the mediastinum may help to improve survival rates by dealing with local cancer which is inaccessible to the knife. Theorizing about this, however, does not invite optimism. First, it is well-known that a
Equipping all citizens with the skills and equipment to be lifesavers
Authors: A. S. Lockey, D. Pitcher
Journal: BMJ (2013)

We agree with Malhotra and Rakhit that improved levels of bystander cardiopulmonary resuscitation (CPR) and reduced times to defibrillation for all victims of cardiac arrest are vital.1

The Resuscitation Council (UK) and British Heart Foundation (BHF) are jointly funding a research database to identify best practice and improve patient outcomes for those who experience pre-hospital cardiac arrest.2 …
Growth-hormone–induced signal transducer and activator of transcription 5 signaling causes gigantism, inflammation, and premature death but protects mice from aggressive liver cancer
Authors: Katrin Friedbichler, Madeleine Themanns, Kristina M. Mueller, Michaela Schlederer, Jan-Wilhelm Kornfeld, Luigi M. Terracciano, Andrey V. Kozlov, Susanne Haindl, Lukas Kenner, Thomas Kolbe, Mathias Mueller, Kenneth J. Snibson, Markus H. Heim, Richard Moriggl
Journal: Hepatology (2011)

Persistently high levels of growth hormone (GH) can cause liver cancer. GH activates multiple signal-transduction pathways, among them janus kinase (JAK) 2-signal transducer and activator of transcription (STAT) 5 (signal transducer and activator of transcription 5). Both hyperactivation and deletion of STAT5 in hepatocytes have been implicated in the development of hepatocellular carcinoma (HCC); nevertheless, the role of STAT5 in the development of HCC as a result of high GH levels remains enigmatic. Thus, we crossed a mouse model of gigantism and inflammatory liver cancer caused by hyperactivated GH signaling (GHtg) to mice with hepatic deletion of STAT5 (STAT5Δhep). Unlike GHtg mice, GHtgSTAT5Δhep animals did not display gigantism. Moreover, the premature mortality, which was associated with chronic inflammation, as well as the pathologic alterations of hepatocytes observed in GHtg mice, were not observed in GHtg animals lacking STAT5. Strikingly, loss of hepatic STAT5 proteins led to enhanced HCC development in GHtg mice. Despite reduced chronic inflammation, GHtgSTAT5Δhep mice displayed earlier and more advanced HCC than GHtg animals. This may be attributed to the combination of increased peripheral lipolysis, hepatic lipid synthesis, loss of hepatoprotective mediators accompanied by aberrant activation of tumor-promoting c-JUN and STAT3 signaling cascades, and accumulation of DNA damage secondary to loss of cell-cycle control. Thus, HCC was never observed in STAT5Δhep mice. Conclusion : As a result of their hepatoprotective functions, STAT5 proteins prevent progressive fatty liver disease and the formation of aggressive HCC in the setting of hyperactivated GH signaling. At the same time, they play a key role in controlling systemic inflammation and regulating organ and body size.
The Case Against Assisted Suicide: For the Right to End-of-Life Care
Authors: E. J. Emanuel
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 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
Diagnosis of Chronic Night Cough
Authors: Kenneth M. Frankel
Journal: JAMA (1979)

<h3>To the Editor.—</h3> The answer to the question by Franklin Drucker, MD (241:2082, 1979), regarding the diagnosis and treatment of chronic night cough seems incomplete. Consideration should be given to ruling out tracheobronchial aspiration as a presenting manifestation of esophageal disease. Aspiration from pharyngeal or gastroesophageal contents may be the irritant triggering the cough reflex. Not infrequently, nocturnal regurgitation and aspiration may be the most prominent symptoms of a Zenker's pharyngoesophageal diverticulum. A fairly frequent occurrence is the development of pulmonary complications in the presence of exceedingly minor or no esophageal symptoms; thus, the presence of the diverticulum may not be recognized for a considerable period. In addition, regurgitation of gastric contents secondary to gastroesophageal reflux, with or without hiatal hernia, may result in repeated episodes of pulmonary aspiration. Recent reports suggest that as many as 50% of the patients with gastroesophageal reflux may have evidence of respiratory involvement and
Cryoprecipitation of an anti-Pr2 monoclonal IgM cold agglutinin in the presence of GM3 ganglioside.
Authors: P Yeni, M L Harpin, B Habibi, A Billecocq, M J Morelec, J P Clauvel, F Danon, N Baumann, J C Brouet
Journal: Journal of Clinical Investigation (1984)

The mechanism of cryoprecipitation of a monoclonal IgM kappa cryoglobulin (Mou) with a cold agglutinin activity of Pr2 specificity has been studied. By immunodiffusion this cryoglobulin reacted (by its Fab' fragment) with micellar GM3, a ganglioside bearing the Pr2 antigenic determinant. In contrast to previous reports that indicated a possible temperature dependent self-association of IgM molecules via an immunological interaction leading to cold precipitation, we could not detect any affinity of this cryoglobulin for IgM when we used passive hemagglutination or an indirect enzyme-linked immunosorbent assay (ELISA). However, a GM3-like ganglioside could be extracted, by drastic methods, from the cryoglobulin studied at 22 degrees C, whereas no GM3 was extracted from two control cryoglobulins. Some minor gangliosides (representing less than 25% of total amount of bound gangliosides) were also extracted from Mou cryoglobulin and these gangliosides were shown to crossreact with GM3, as they specifically bind to Mou cryoglobulin by ELISA. After cryoprecipitation the serum still contained a monoclonal anti-Pr2 IgM kappa. A GM3-like ganglioside could be extracted from this purified IgM, and cryoprecipitability could be induced by the addition of a minute amount of micellar GM3. These results suggest that Mou cryoglobulin circulates as an immune complex and that cryoprecipitation may depend on unique IgM-GM3 (or IgM-GM3 cross-reacting gangliosides) complexes.
Chloroquine Inhibits Autophagy to Potentiate Antiestrogen Responsiveness in ER+ Breast Cancer
Authors: Katherine L. Cook, Anni Wärri, David R. Soto-Pantoja, Pamela AG. Clarke, M. Idalia Cruz, Alan Zwart, Robert Clarke
Journal: Clinical Cancer Research (2014)

Estrogen receptor-α (ERα)-targeted therapies including tamoxifen (TAM) or Faslodex (ICI) are used to treat ER(+) breast cancers. Up to 50% of tumors will acquire resistance to these interventions. Autophagy has been implicated as a major driver of antiestrogen resistance. We have explored the ability of hydroxychloroquine (HCQ), which inhibits autophagy, to affect antiestrogen responsiveness.TAM-resistant MCF7-RR and ICI-resistant/TAM cross-resistant LCC9 ER(+) breast cancer cells were injected into mammary fat pads of female athymic mice and treated with TAM and/or ICI in combination with oral low-dose HCQ.We show that HCQ can increase antiestrogen responsiveness in MCF7-RR and LCC9 cells and tumors, likely through the inhibition of autophagy. However, the combination of ICI+HCQ was less effective than HCQ alone in vivo, unlike the TAM+HCQ combination. Antiestrogen treatment stimulated angiogenesis in tumors but did not prevent HCQ effectiveness. The lower efficacy of ICI+HCQ was associated with ICI effects on cell-mediated immunity within the tumor microenvironment. The mouse chemokine KC (CXCL1) and IFNγ were differentially regulated by both TAM and ICI treatments, suggesting a possible effect on macrophage development/activity. Consistent with these observations, TAM+HCQ treatment increased tumor CD68(+) cells infiltration, whereas ICI and ICI+HCQ reduced peripheral tumor macrophage content. Moreover, macrophage elimination of breast cancer target cells in vitro was reduced following exposure to ICI.HCQ restores antiestrogen sensitivity to resistant tumors. Moreover, the beneficial combination of TAM+HCQ suggests a positive outcome for ongoing neoadjuvant clinical trials using this combination for the treatment of ER(+) ductal carcinoma in situ lesions.
Graphene Oxide: Purified Graphene Oxide Dispersions Lack In Vitro Cytotoxicity and In Vivo Pathogenicity (Adv. Healthcare Mater. 3/2013)
Authors: Hanene Ali‐Boucetta, Dimitrios Bitounis, Rahul Raveendran‐Nair, Ania Servant, Jeroen Van den Bossche, Kostas Kostarelos
Journal: Advanced Healthcare Materials (2013)

Preparation of a high dispersibility graphene oxide (GO) that can be reliably used in biological investigations is reported by Kostas Kostarelos and co-workers on page 433. Exposure of cells and tissue to the graphene oxide indicated a lack of cytotoxic responses in human cell cultures (in vitro) and after injection to living animals (in vivo).
Chernobyl's Legacy
Authors: Joan Stephenson
Journal: JAMA (2001)

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
Predicting Life Expectancy in Heart Failure
Authors: Clyde W. Yancy
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 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
Many groups offer AIDS information, support
Authors: Marsha F. Goldsmith
Journal: JAMA (1985)

Homosexual and bisexual men, who account for approximately 75% of reported AIDS cases in this country, were the first—and remain among the most active—organizers of resource centers for information, counseling, and support for persons who are in high-risk groups for AIDS. Such centers deal not only with persons at risk but with those who may have been diagnosed with AIDS or AIDS-related complex, or who are suffering severe psychological stress from what has been called "fear of AIDS." These service organizations are ready and willing to help anyone who wants or needs to learn more concerning what is known about AIDS. Several of the local organizations, such as the Howard Brown Memorial Clinic in Chicago (hot line number 1-800-AID-AIDS), offer medical services for patients with other sexually transmitted diseases (STDs) as well. All of the AIDS resource groups can supply the names of physicians knowledgeable in this area of medical
No Benefit From Defibrillation Threshold Testing in the SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial)
Authors: Joseph A. Blatt, Jeanne E. Poole, George W. Johnson, David J. Callans, Merritt H. Raitt, Ramakota K. Reddy, Francis E. Marchlinski, Raymond Yee, Thomas Guarnieri, Mario Talajic, David J. Wilber, Jill Anderson, Kiyon Chung, Wai Shun Wong, Daniel B. Mark, Kerry L. Lee, Gust H. Bardy
Journal: Journal of the American College of Cardiology (2008)
Intracranial Hemorrhage: Cerebral Amyloid Angiopathy or Nasal Decongestants?-Reply
Authors: Thomas Mirsen
Journal: JAMA (1990)

<h3>In Reply.—</h3> I am grateful to Dr Weintraub for addressing the relationship of nasal decongestants, chiefly phenylpropanolamine, to stroke and intracranial hemorrhage. The association between nasal decongestants and cerebral hemorrhage in the patient under consideration indeed implies a causal connection. Such a link is firmest when there exists definite evidence of vasculitis, or when the subject is a young person free of recognized risk factors for cerebrovascular disease. In this instance, however, the patient was old enough at presentation to harbor cerebral amyloid angiopathy (CAA). Although CAA is relatively uncommon in persons between 60 and 70 years old,<sup>1</sup>one of the 11 examples of cerebral hemorrhage due to CAA described by Gilbert and Vinters<sup>2</sup>closely resembles the case under discussion. This was a 61-year-old woman free of dementia with a large occipital hemorrage leading to death, who on pathological analysis proved to have CAA. The subsequent clinical course
Interest in Neurologic Manifestations of Sickle-Cell Disease
Authors: TERKASA LUNO
Journal: Annals of Internal Medicine (1982)

Letters and Corrections1 February 1982Interest in Neurologic Manifestations of Sickle-Cell DiseaseTERKASA LUNO, M.D.TERKASA LUNO, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-96-2-260_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We have a specialized interest in the neurologic manifestations of sickle-cell disease. We are interested in receiving bibliographic summaries of the work of others interested in this clinical problem and, eventually, in making personal contact with them and working out an arrangement for a year of university study abroad.... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University Clinics B.P. 825 Kinshasa XI; Republic of Zaire PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1982Volume 96, Issue 2Page: 260-260 Issue Published: 1 February 1982 PDF downloadLoading ...
Abstract 2820: The mechanism of mesenchymal-to-epithelial transition driven by hepatocytes in prostate cancer.
Authors: Bo Ma, Alan Wells
Journal: Cancer Research (2013)

Abstract Metastasis of prostate cancer (PCa) almost always leads inexorably to death, but little is known about how cancer cells seed ectopic sites and survive in these inhospitable sites. Our lab has previously shown that carcinoma cells undergo a phenotypic change driven by the metastatic microenvironment, to attain an, at least partial mesenchymal (like)-to-epithelial reverting transition (MET/MErT). This phenotypic plasticity, marked by E-cadherin re-expression, plays a key role in metastatic breast and prostate cancer cell survival in vitro and is though to occur after seeding in the ectopic sites and subsequent treatment with chemotherapeutics. In this study we are seeking the pathway(s) involved in the mesenchymal to epithelial transition and subsequent cell survival. By using hepatocytes co-cultured with prostate cancer cells (DU145 or PC3) we found MET PCa cells displayed more resistance to chemotherapeutics, cell death inducing cytokines, or a combination of both. Moreover, E-cadherin knockdown in PCa cells abolished this survival advantage conferred by hepatocytes. This indicated the key role of E-cadherin in hepatocyted driven PCa cells survival. We focused next on the feedback pathways activated by E-cadherin homotypic binding, the MAP kinases. Our data showed that p38 MAPK regulated E-cadherin expression during DU145 cells MET driven by hepatocytes. By using immunofluorescence, the level of phosphor-p38 was much lower in DU145 cells co-cultured with hepatocytes, and the p38 was only detected in the nucleus, which suggested that hepatocytes suppressed p38 MAPK activity in DU145 cells. When co-cultured with hepatocytes, p38α knockdown DU145 displayed much higher levels of E-cadherin, especially in the rim of cells. Additionally, both p38 inhibitor SB202580 and p38α siRNA transfected cells expressed higher E-cadherin than control in DU145. Taken together, hepatocytes regulate PCa cells to undergo MET via suppressing p38 MAPK activity in the cancer cells. Citation Format: Bo Ma, Alan Wells. The mechanism of mesenchymal-to-epithelial transition driven by hepatocytes in prostate cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2820. doi:10.1158/1538-7445.AM2013-2820
Decay-accelerating factor expression in the rat kidney is restricted to the apical surface of podocytes
Authors: Lihua Bao, O. Brad Spiller, Patricia L. St. John, Mark Haas, Bradley K. Hack, Guohui Ren, Patrick N. Cunningham, Mona Doshi, Dale R. Abrahamson, B. Paul Morgan, Richard J. Quigg
Journal: Kidney International (2002)