tbuckley/cabot-search huggingface dataset:
Palliative care in community hospitals
Authors: J. Holden
Journal: Journal of the Royal Society of Medicine (2005)

Professor Payne and her colleagues (September 2004 JRSM1) conclude that community hospitals represent an under-used resource for palliative care. I surveyed the use of an urban community hospital for each of the years 1987–2004 when I worked in my previous practice of 8000 patients in Haydock, St Helens. During these 17 years we cared for 249 patients who died of malignant disease when at least part of the terminal phase was spent in the community.

The place of death, and numbers (percentage) of these patients was:​was:



Table 1

The place of death, and numbers (percentage) of these patients was:



Although on average only 3 patients died in the community hospital each year, this was a particularly useful option for those without a family able to care for them at home. It also made an important contribution to our aim of keeping as many patients as possible, when this was desired and appropriate, under our care at death. We achieved this for 74% of patients—a percentage that remained constant. This was probably helped by the out-of-hours service being asked to pass any calls for such patients back to a general practitioner from the practice.

One relative has stated his definition of good palliative care: 'the essential concept is that the doctor (or at least the practice) will stay firmly with the patient and relative at their time of need and not desert them'.2 Community hospitals have an essential role in the provision of this and other aspects of primary palliative care, which should be developed further.3
Astrocytic adenosine receptor A2A and Gs-coupled signaling regulate memory
Authors: Anna G Orr, Edward C Hsiao, Max M Wang, Kaitlyn Ho, Daniel H Kim, Xin Wang, Weikun Guo, Jing Kang, Gui-Qiu Yu, Anthony Adame, Nino Devidze, Dena B Dubal, Eliezer Masliah, Bruce R Conklin, Lennart Mucke
Journal: Nature Neuroscience (2015)
Increased activation-induced cell death of high IFN-γ–producing TH1 cells as a mechanism of TH2 predominance in atopic diseases
Authors: Tunc Akkoc, Pieter J.A. de Koning, Beate Rückert, Isil Barlan, Mübeccel Akdis, Cezmi A. Akdis
Journal: Journal of Allergy and Clinical Immunology (2008)
Hexokinase II and VEGF expression in liver tumors: correlation with hypoxia-inducible factor-1α and its significance
Authors: Seiichi Yasuda, Shigeki Arii, Akira Mori, Naoki Isobe, Weige Yang, Hideaki Oe, Akihisa Fujimoto, Yoshikuni Yonenaga, Hiromi Sakashita, Masayuki Imamura
Journal: Journal of Hepatology (2003)
THE NEW TREATMENT OF HERNIA.Read in the Section of Surgery and Anatomy, at the Forty-fourth Annual Meeting of the American Medical Association.
Authors: ALEXANDER DALLAS
Journal: JAMA (1893)

In venturing to call your attention to some new points in the treatment of hernia, I assume that you are all familiar with the methods now in use and the unsatisfactory results obtained by them. With our 3,500,000 of cases of hernia in this country—a ratio of thirty cases to every practicing physician—the great importance of the subject is self-evident. Of this large number, over 80 per cent, are inguinal and my remarks will refer more particularly to that variety. The treatment of hernia may be divided into, first, the palliative; second, the mixed; third, the treatment of strangulated hernia; and fourth, the "radical cure." <i>First, the Palliative</i>.—The palliative or mechanical treatment of hernia includes all measures used to prevent the descent of the hernial protrusion, but more particularly, the employment of trusses of various descriptions. To the general practitioner this is, unquestionably, the most important method of treatment, for
Chronic kidney disease as a global public health problem: Approaches and initiatives – a position statement from Kidney Disease Improving Global Outcomes
Authors: A.S. Levey, R. Atkins, J. Coresh, E.P. Cohen, A.J. Collins, K.-U. Eckardt, M.E. Nahas, B.L. Jaber, M. Jadoul, A. Levin, N.R. Powe, J. Rossert, D.C. Wheeler, N. Lameire, G. Eknoyan
Journal: Kidney International (2007)
The Transcription Factors T-bet and Runx Are Required for the Ontogeny of Pathogenic Interferon-γ-Producing T Helper 17 Cells
Authors: Yan Wang, Jernej Godec, Khadija Ben-Aissa, Kairong Cui, Keji Zhao, Alexandra B. Pucsek, Yun Kyung Lee, Casey T. Weaver, Ryoji Yagi, Vanja Lazarevic
Journal: Immunity (2014)
CALGB 30704 (Alliance): A Randomized Phase II Study to Assess the Efficacy of Pemetrexed or Sunitinib or Pemetrexed Plus Sunitinib in the Second-Line Treatment of Advanced Non–Small-Cell Lung Cancer
Authors: Rebecca S. Heist, Xiaofei Wang, Lydia Hodgson, Gregory A. Otterson, Thomas E. Stinchcombe, Leena Gandhi, Miguel A. Villalona-Calero, Peter Watson, Everett E. Vokes, Mark A. Socinski
Journal: Journal of Thoracic Oncology (2014)
Androgen-induced TOP2B-mediated double-strand breaks and prostate cancer gene rearrangements
Authors: Michael C Haffner, Martin J Aryee, Antoun Toubaji, David M Esopi, Roula Albadine, Bora Gurel, William B Isaacs, G Steven Bova, Wennuan Liu, Jianfeng Xu, Alan K Meeker, George Netto, Angelo M De Marzo, William G Nelson, Srinivasan Yegnasubramanian
Journal: Nature Genetics (2010)
Marked coronary endothelial dysfunction in patients with low high-density lipoprotein and elevated C-reactive protein
Authors: Lukas E. Spieker, Thomas Munzel, Markus Nauck, Winfried Maerz, Wolf Rafflenbeul, Micheal Pieper, Gabor Sutsch, Ricardo Seabra-Gomes, Frank van den Branden, Gerald S. Werner, Michael Haude, Kurt Quitzau, Paul G. Hugenholtz, Thomas F. Luscher
Journal: Journal of the American College of Cardiology (2003)
Dementia as a Moral Harm
Authors: Monique Lanoix
Journal: The American Journal of Bioethics (2007)

"Dementia as a Moral Harm." The American Journal of Bioethics, 7(6), pp. 59–60 Notes 1. I use the masculine to highlight the fact that women, as moral agents, were not equal to men, for Kant. 2. During an instructive discussion of CitationCooley's (2007) article, this point was made by Christie Simpson, assistant professor and ethics co-ordinator of ethics-based collaborations, Department of Bioethics, Dalhousie University.
Morphological and physiological studies on Indian national kabaddi players.
Authors: S K Dey, G L Khanna, M Batra
Journal: British Journal of Sports Medicine (1993)

Twenty-five national kabaddi players (Asiad gold medalists 1990), mean age 27.91 years, who attended a national camp at the Sports Authority of India, Bangalore before the Beijing Asian Games in 1990, were investigated for their physical characteristics, body fat, lean body mass (LBM) and somatotype. The physiological characteristics assessed included back strength, maximum oxygen uptake capacity and anaerobic capacity (oxygen debt) and related cardiorespiratory parameters (oxygen pulse, breathing equivalent, maximum pulmonary ventilation, maximum heart rate). Body fat was calculated from skinfold thicknesses taken at four different sites, using Harpenden skinfold calipers. An exercise test (graded protocol) was performed on a bicycle ergometer (ER-900) using a computerized EOS Sprint (Jaeger, West Germany). The mean(s.d.) percentage body fat (17.56(3.48)) of kabaddi players was found to be higher than normal sedentary people. Their physique was found to be endomorphic mesomorph (3.8-5.2-1.7). Mean(s.d.) back strength, maximum oxygen uptake capacity (VO2max) and oxygen debt were found to be 162.6(18.08) kg, 42.6(4.91) ml kg-1 min-1 and 5.02(1.29) litre respectively. Physical characteristics, percentage body fat, somatotype, maximum oxygen uptake capacity and anaerobic capacity (oxygen debt) and other cardiorespiratory parameters were compared with other national counterparts. Present data are comparable with data for judo, wrestling and weightlifting. Since no such study has been conducted on international counterparts, these data could not be compared. These data may act as a guideline in the selection of future kabaddi players and to attain the physiological status comparable to the present gold medalists.
Extreme Temperatures and Mortality: Assessing Effect Modification by Personal Characteristics and Specific Cause of Death in a Multi-City Case-Only Analysis
Authors: Mercedes Medina-Ramón, Antonella Zanobetti, David Paul Cavanagh, Joel Schwartz
Journal: Environmental Health Perspectives (2006)

Extremes of temperature are associated with short-term increases in daily mortality.We set out to identify subpopulations and mortality causes with increased susceptibility to temperature extremes.We conducted a case-only analysis using daily mortality and hourly weather data from 50 U.S. cities for the period 1989-2000, covering a total of 7,789,655 deaths. We used distributions of daily minimum and maximum temperature in each city to define extremely hot days (>/= 99 th percentile) and extremely cold days (</= 1st percentile) , respectively. For each (hypothesized) effect modifier, a city-specific logistic regression model was fitted and an overall estimate calculated in a subsequent meta-analysis.Older subjects [odds ratio (OR) = 1.020 ; 95% confidence interval (CI) , 1.005-1.034], diabetics (OR = 1.035 ; 95% CI, 1.010-1.062) , blacks (OR = 1.037 ; 95% CI, 1.016-1.059) , and those dying outside a hospital (OR = 1.066 ; 95% CI, 1.036-1.098) were more susceptible to extreme heat, with some differences observed between those dying from a cardiovascular disease and other decedents. Cardiovascular deaths (OR = 1.053 ; 95% CI, 1.036-1.070) , and especially cardiac arrest deaths (OR = 1.137 ; 95% CI, 1.051-1.230) , showed a greater relative increase on extremely cold days, whereas the increase in heat-related mortality was marginally higher for those with coexisting atrial fibrillation (OR = 1.059 ; 95% CI, 0.996-1.125) .In this study we identified several subpopulations and mortality causes particularly susceptible to temperature extremes. This knowledge may contribute to establishing health programs that would better protect the vulnerable.
Efficacy and Safety of Long-Term Prophylaxis with C1 Inhibitor (C1INH) Concentrate in Patients with Hereditary Angioedema (HAE)
Authors: B. Zuraw, P. Busse, M. White, J. Jacobs, W. Lumry, J. Baker, D. Hurewitz, M. Manning, M. Koleilat, R.A. Friedman, R. Wilkinson, W.E. Cartwright, D. Tanner, G. Kohler, G. Gunther
Journal: Journal of Allergy and Clinical Immunology (2008)

C1INH is widely recognized to be the most effective treatment for acute attacks of HAE. With its relatively long half-life, C1INH may also be effective for long-term prophylaxis. This study, therefore, addressed the impact of long-term prophylactic C1INH on HAE swelling frequency. This multi-center study enrolled 22 patients meeting diagnostic criteria for HAE plus a history of at least 2 attacks per month. Subjects were randomized to receive 12 weeks of either C1 inhibitor (Cinryze, Lev Pharmaceuticals) 1000 units 2×/week or placebo (normal saline) 2×/week by intravenous infusion. At the end of 12 weeks all subjects were crossed over. No changes in other prophylactic medications (androgens or antifibrinolytics) was permitted during the entire 24 weeks or the preceding 4 weeks. The number of discrete angioedema attacks and days of swelling during each arm of the study were summed, and the primary endpoint was the number of attacks on C1 inhibitor versus number of attacks on placebo using each subject as his/her own control. The number of attacks during the C1INH treatment phase was significantly less than during the placebo treatment phase (6.1 vs 12.7, p < 0.0001). Secondary endpoints, including days of swelling (10.1 vs 29.6) also showed a significant benefit for the C1INH phase (p < 0.0001). No safety issues were identified. Prophylactic infusion with C1INH decreases the number of attacks experienced by patients with active HAE and may represent an important modality of treatment for some patients.
Increased Vascular Endothelial Growth Factor Expression But Impaired Vascular Endothelial Growth Factor Receptor Signaling in the Myocardium of Type 2 Diabetic Patients With Chronic Coronary Heart Disease
Authors: Ferdinando Carlo Sasso, Daniele Torella, Ornella Carbonara, Georgina M. Ellison, Michele Torella, Michelangelo Scardone, Claudio Marra, Rodolfo Nasti, Raffaele Marfella, Domenico Cozzolino, Ciro Indolfi, Maurizio Cotrufo, Roberto Torella, Teresa Salvatore
Journal: Journal of the American College of Cardiology (2005)
Health authority brick by brick
Authors: J. Warden
Journal: BMJ (1987)

One year ago today (21 November) the forthcoming birth was announced in parliament of the Health Education Authority (HEA).It came into the world on 1 April this year to a distinctly chill welcome from friends of the defunct Health Education Council, which the new authority supplanted.Now a year later the dust has settled and we can begin to see what is emerging from a fusion which, in public relations terms, was so ineptly handled.The new authority is at last up and running as the main health promotion arm of the National Health Service, though it is not yet in top gear.The trauma ofwhat its new chief executive, Dr Spencer Hagard, calls the winter of discontent left its mark.In fact, last November's announcement came at the very moment when the old Health Education Council was on the brink of a reorganisation that had already taken more than two years to plan.It was deeply unsettling.Several key staff resigned, leaving a vacuum of initiative and what is described as an emotional cauldron.It was in these difficult circumstances that Dr Hagard took over last May, after five years as district medical officer in Cambridgeshire.He found an organisation that had been through more turmoil than was apparent from the outside.His remit was to reconstitute the authority as a statutory component of the NHS.The old council, though wholly funded by the Department of Health and Social Security, had a semidetached status.Its demise, which DHSS officials were suspected of manipulating, came because the government needed a health authority within the NHS to take over the education campaign against the acquired immune deficiency syndrome (AIDS).
Reversible Conversion of Immortal Human Cells from Telomerase-Positive to Telomerase-Negative Cells
Authors: Shin-ichi Kumakura, Takeo W. Tsutsui, Junko Yagisawa, J. Carl Barrett, Takeki Tsutsui
Journal: Cancer Research (2005)

Abstract Immortal cell lines and tumors maintain their telomeres via the telomerase pathway or via a telomerase-independent pathway, referred to as alternative lengthening of telomeres (ALT). Here, we show the reversible conversion of the human papillomavirus type 16 E6-induced immortal human fibroblasts E6 Cl 6 from telomerase-positive (Tel+) to telomerase-negative (Tel−) cells. Tel+ cells converted spontaneously to Tel− cells that reverted to Tel+ cells following treatment with trichostatin A (TSA) and/or 5-aza-2′-deoxycytidine (5-AZC), which induced the reversion from complete to partial methylation of the CpG islands of the human telomerase reverse transcriptase (hTERT) promoter in Tel− E6 Cl 6 cells. Tel− E6 Cl 6 cells lacked the phenotypes characteristic of ALT cell lines such as very long and heterogenous telomeres and ALT-associated promyelocytic leukemia nuclear bodies (APB) but grew for &amp;gt;240 population doublings (PD) after they became telomerase negative. The ratios of histone H3 (H3) lysine (K) 9 methylation to each of H3-K4 methylation, H3-K9 acetylation, and H3-K14 acetylation of the chromatin containing the hTERT promoter in Tel− E6 Cl 6 cells and ALT cell lines were greater than those in Tel+ cells and decreased following treatment with TSA and/or 5-AZC, inversely corresponding to telomerase activity. Our findings suggest the possibility that human tumors may be able to reversibly interconvert their telomere maintenance phenotypes by chromatin structure-mediated regulation of hTERT expression.
Reviews and Notes: Pharmacology: Principles of Addiction Medicine
Authors: Robert J. Beidler
Journal: Annals of Internal Medicine (1996)

Literature of Medicine1 April 1996Reviews and Notes: Pharmacology: Principles of Addiction MedicineRobert J. Beidler, DSWRobert J. Beidler, DSWUniversity of Pennsylvania, Philadelphia, PA 19104Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-124-7-199604010-00028 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail NS Miller; ed. Chevy Chase, MD: American Society of Addiction Medicine; 1995. $140.00. Order phone 301-656-3920.Several comprehensive works on addiction have appeared over the years, many in multivolume series. Most have relied on a group of authors to present material on various aspects of addiction. Most have claimed to provide current scientific knowledge and clinical information that would be useful for practitioners. Despite these noble objectives, however, most have been uneven in quality. Principles of Addiction Medicine is more accurate, more comprehensive, and more even in quality than most such works, with the possible exception of the exhaustive, multivolume, ... Author, Article, and Disclosure InformationAffiliations: University of Pennsylvania, Philadelphia, PA 19104 Previousarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1996Volume 124, Issue 7Page: 698KeywordsAlcoholicsAlcoholsChildrenDrug addictionDrugsPharmacologyPopulation statisticsReproducibilityResearch quality assessmentScientists ePublished: 15 August 2000 Issue Published: 1 April 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Digital Foreign Bodies in Spot-Welders
Authors: W. A. B. Reynard, F. Smith
Journal: BMJ (1947)

MEDIBcALJTIOUSL 843 soft tissues of the ulnar side of the hand and of the webs between the fingers, but none on the thenar side.The emphy- sema thus appeared to be confined mainly to the palmar space and its lumbrical extensions.He was treated by local heat, sling immobilization, and a prophylactic course of sulphadiazine, 1 g. by mouth every four hours.Next day the hand remained swollen but was less pain- ful.There were slight pyrexia (99' F.; 37.20 C.) and some redness around the puncture wound.Sulphadiazine and immobilization were therefore continued.The following day the swelling had completely subsided; there was full function and no pain.A further x-ray examination showed a normal soft-tissue shadow, and he returned to work six days after the accident.
Aplastic Anemia Following Exposure to Benzene Hexachloride (Lindane)
Authors: J. Philip Loge
Journal: JAMA (1965)

In two fatal cases of aplastic anemia, there was a prolonged indoor exposure to vaporized benzene hexa-chloride (lindane). The chemical was in pellet form and vaporized by electrical warming of a ceramic jacket. The literature was reviewed and although benzene hexa-chloride has been a suspected toxin before, this is, to our knowledge, the first detailed report of benzene hexa-chloride exposure and aplastic anemia in which other suspicious drugs or chemical agents were not used. These two cases allow only a presumptive conclusion to be made. Further repeated observations by others will be necessary to make historical evidence alone sufficient for an etiologic diagnosis. More specific in vitro and in vivo testing procedures are urgently needed to screen the increasingly complex array of drugs to which most of us are exposed. Only in this way can a precise relationship between cause and effect be made.
The intraportal lymphoid nodule and its environment in chronic active hepatitis C: An immunohistochemical study
Authors: Jean-François Mosnier, Claude Degott, Patrick Marcellin, Dominique Hénin, Serge Erlincer, Jean-Pierre Benhamou
Journal: Hepatology (1993)

Intraportal lymphoid nodules have been observed in liver biopsy specimens from patients with autoimmune liver disease and chronic active hepatitis C. They are characterized by a nodular lymphocyte aggregate with a germinal center. The purpose of this in situ immunophenotyping study was to determine immunohistochemically the phenotype of immunocompetent cells in and around intraportal lymphoid nodules in patients with chronic hepatitis C. For comparison, we also examined lymphoid nodules in patients with autoimmune liver disease. Liver biopsy specimens from 13 unselected patients with CAH and hepatitis C antibodies and from 7 unselected patients with autoimmune liver disease seen during the same period were studied. Sections of snap-frozen specimens were immunostained with monoclonal antibodies directed against different subsets of T cells, B cells, follicular dendritic cells and macrophages. Intraportal lymphoid nodules were observed in 11 of 13 patients with chronic hepatitis C. They appeared as lymphoid follicles with activated B cells in germinal centers surrounded by a follicular dendritic cell network. A mantle zone of B cells was present around the aggregate of activated B cells. A T-cell zone comprising CD4-positive helper T cells, CD8-positive suppressor/cytotoxic T cells and a few CD25-positive activated T cells expressing interleukin-2 receptor was seen at the periphery of the nodules. Human leukocyte antigen DR was expressed by B cells and by T cells, indicating that T cells were activated. The immunocompetent cells observed in piecemeal necrosis were predominantly CD4 helper T cells, whereas those seen in the lobule were predominantly CD8 suppressor/cytotoxic T cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Prion Protein Conformation in a Patient with Sporadic Fatal Insomnia
Authors: James A. Mastrianni, Randal Nixon, Robert Layzer, Glenn C. Telling, Dong Han, Stephen J. DeArmond, Stanley B. Prusiner
Journal: New England Journal of Medicine (1999)

The human prion diseases include Creutzfeldt–Jakob disease, Gerstmann–Straussler–Scheinker disease, fatal familial insomnia, and the recently described new variant of Creutzfeldt–Jakob disease. Much evidence argues that a post-translational, noncovalent modification of prion protein is the fundamental event in the mechanism underlying these diseases.1 The normal cellular isoform of the prion protein (PrPC) is predominantly α-helical, is detergent soluble, and is readily digested by proteases. In contrast, the pathogenic isoform (PrPSc) has a substantially β-sheet structure, is insoluble in nondenaturing detergents, and shows relative resistance to proteolytic digestion.2–4 The protease-resistant core of PrPSc, designated PrP27–30, is usually detectable . . .