tbuckley/cabot-search huggingface dataset:
Sweden bans privatisation of hospitals
Authors: Jane Burgermeister
Journal: BMJ (2004)

The Swedish coalition government has banned the privatisation of hospitals, amid fears that the expansion of private health care could destroy the principle of a fair and free public health service.

Health minister Lars Engqvist, a Social Democrat, said that new legislation would end the practise of private patients “buying their way past” hospital waiting lists. Provincial authorities, which are responsible in Sweden for the local healthcare system, will not be allowed in future to hand over the running of a hospital to a profit making company.

The ban comes after two provincial authorities, both controlled by centre right parties, began to privatise state …
Abstract 2508: Ammonia as a Biochemical Marker of Neurological Outcome in Patients With Out-of -hospital Cardiac Arrest Who Were Terared With Hypothermia
Authors: Asuka Kasai, Ken Nagao, Kimio Kikushima, Kazuhiro Watanabe, Takeo Mukoyama, Yoshitaru Tominaga, Katsusige Tada, Mitsuru Ishii, Nobutaka Chiba, Taketomo Soga, Kei Nishikawa
Journal: Circulation (2009)
Paget's disease of the scrotum: a case exhibiting positive prostate-specific antigen staining and associated prostatic adenocarcinoma
Authors: None Allan, None Mclaren, None Aldridge
Journal: British Journal of Dermatology (1998)

A 75-year-old man with carcinoma of the prostate presented with a pruritic, erythematous plaque involving the scrotal skin. Histological examination revealed extramammary Paget's disease. The intraepidermal tumour cells expressed prostate-specific antigen in keeping with a prostatic origin.
Dementia in an American-Chinese nursing home population
Authors: M Serby, J C Chou, E H Franssen
Journal: American Journal of Psychiatry (1987)

Of 58 demented residents in an American-Chinese nursing home, 44 (75.9%) had multi-infarct dementia, seven (12.1%) had possible Alzheimer's disease, four (6.9%) had other dementias, and three 5.2% had unknown disorders. Alzheimer's disease was relatively less prevalent than in U.S. nursing homes overall.
THE ROLE OF THE INTERNIST IN RESTORATIVE SERVICES FOR THE AGED
Authors: S D POMRINSE
Journal: Annals of Internal Medicine (1957)

Article1 November 1957THE ROLE OF THE INTERNIST IN RESTORATIVE SERVICES FOR THE AGEDS. D. POMRINSE, M.D.S. D. POMRINSE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-47-5-900 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIn this discussion I shall use the termrestorative servicesrather thanrehabilitationto identify services provided by the physician and other professional and technical personnel in allied medical fields to improve or at least to maintain the physical and functional capacity of a patient. The termrestorative servicesseems more appropriate thanrehabilitation, since the latter generally implies vocational goals, and obviously we are less likely to be concerned with them when dealing with older persons. My discussion will therefore be concerned with a dynamic medical program for restoring maximal possible function in an older patient. Primary emphasis will...Bibliography1. PerrottSmithPennellAltenderfer GSLMMYME: Care of the long term patient, Source Book on Size and Characteristics of the Problem, Public Health Service Publication No. 344, U. S. Department of Health, Education and Welfare, Public Health Service, 1954, U. S. Government Printing Office, Washington 25, D. C. Google Scholar2. Special Health Services Fact Book, U. S. Department of Health, Education and Welfare, Public Health Service. (Not available for general distribution.) Google Scholar3. Guides to Action on Chronic Illness, 1956, National Health Council, New York, N. Y. Google Scholar4. Dacso MM: Clinical problems in geriatric rehabilitation, Geriatrics 8: 179-185 (Apr.) 1953. MedlineGoogle Scholar5. Buchanan J: Rapid mobilization of cerebrovascular accident patients, Arch. Physical Med. and Rehabil. 37: 150-151 (Mar.) 1956. MedlineGoogle Scholar6. FerderberHammel MG: An effective comprehensive program for geriatric patients, J. A. M. A. 157: 407-413 (Jan. 29) 1955. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Washington, D. C.*From the Symposium on Rehabilitation, presented at the Thirty-eighth Annual Session of The American College of Physicians, Boston, Massachusetts, April 11, 1957.From the Division of Special Health Services, Department of Health, Education, and Welfare, Washington, D. C.Requests for reprints should be addressed to S. D. Pomrinse, M.D., Medical Director, Chief, Health of the Aged, Chronic Disease Program, Division of Special Health Services, Department of Health, Education, and Welfare, Washington 25, D. C. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 November 1957Volume 47, Issue 5Page: 900-903KeywordsAllied health care professionalsMedical educationMedical services ePublished: 1 December 2008 Issue Published: 1 November 1957 PDF downloadLoading ...
Abstract #5671: Identification of glioma-released factors attracting and reprogramming brain macrophages into invasion promoting cells
Authors: Bozena Kaminska, Pawel Wisniewski, Aleksandra Ellert-Miklaszewska, Maciej Lipko, Michal Dabrowski
Journal: Cancer Research (2009)

Tumor-associated macrophages represent the major component of the stroma of many tumors, including gliomas, and their high content correlates with malignancy and poor patient prognosis. These macrophages express protumoral functions, including promotion of angiogenesis, matrix remodelling and suppression of adaptive immunity. Molecular mechanisms underlying accumulation and activation of tumor-associated macrophages are unknown. We demonstrated that glioma-derived soluble factors convert cultured brain macrophages into amoeboid cells which support glioma invasion, while attenuating inflammatory responses. Analyzing global gene expression and signaling pathways, we demonstrate that glioma-derived factors induce an alternative, non-immune activation of brain macrophages. While inflammatory (endotoxin) treatment involves activation of MAPK, NF\#954;B and STAT1 signaling pathways, glioma-derived factors induced Integrin-linked and TGF\#946; signaling. Increased phosphorylation of kinases FAK, Akt, MAPK and STAT3/5 were followed by release of anti-inflammatory cytokines and metalloproteinases stimulating invasiveness of glioma cells. Glioma-derived factors strongly stimulated motility and phagocytic properties of macrophages. Computational analysis of microarray data revealed that the most discriminative feature is a lack of interferon response genes in glioma-exposed macrophages. To identify glioma-derived factors stimulating brain macrophages, glioma conditioned medium was fractionated by HPLC, analyzed functionally and by mass-spectrometry in search for activating factors. This approach led to identification of Osteopontin and Lactadherin, two proteins sharing RGD motif and known to interact with integrins. Interference with integrin binding using RGD-containing peptide or siRNA mediated silencing osteopontin and/or lactadherin expression abolished glioma-induced transformation of macrophages, and downstream signal transduction. Our findings demonstrate that gliomas attract brain macrophages and employ specific signals to transform them into tumor-supportive cells. We show for the first time signals and mechanisms responsible for \#8220;re-education\#8221; of macrophages into tumor supportive cells and provide evidence that glioma-macrophage interactions are a potential target of anti-tumor therapy.   Citation Information:  In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr 5671.
Abstract 1643: Prognostic Value of Ankle Brachial Index in Asymptomatic Peripheral Arterial Disease Patients With Prior Coronary or Cerebrovascular Disease
Authors: Luis Manzano, Javier Moreno-Palomares, Eduardo Rovira-Daudi, Aquilino Sanchez-Purificacion, Manuel A Suarez-Tembra, Eva Estirado-Cabo, Francisco J Del Valle-Gutierrez, Angel Sanchez-Rodriguez, Francisco J Conde-Garcia, Miguel A Rico-Corral, Juan de Dios Estrella-Cazalla, Joaquin Anton-Martinez
Journal: Circulation (2009)
Outcomes of acute leukemia patients transplanted with naive T cell–depleted stem cell grafts
Authors: Marie Bleakley, Shelly Heimfeld, Keith R. Loeb, Lori A. Jones, Colette Chaney, Stuart Seropian, Ted A. Gooley, Franziska Sommermeyer, Stanley R. Riddell, Warren D. Shlomchik
Journal: Journal of Clinical Investigation (2015)

BACKGROUND. Graft-versus-host disease (GVHD) is a major cause of morbidity and mortality following allogeneic hematopoietic stem cell transplantation (HCT). In mice, naive T cells (TN) cause more severe GVHD than memory T cells (TM). We hypothesized that selective depletion of TN from human allogeneic peripheral blood stem cell (PBSC) grafts would reduce GVHD and provide sufficient numbers of hematopoietic stem cells and TM to permit hematopoietic engraftment and the transfer of pathogen-specific T cells from donor to recipient, respectively.
Efforts Needed to Foster Participation of Blacks in Stroke Studies
Authors: Mike Mitka
Journal: JAMA (2004)

SAN DIEGO—Blacks are disproportionately affected by stroke and researchers do not fully understand why. That a better understanding of why blacks are more likely to experience and die of stroke is needed is underscored by sobering figures on the impact of the disease on the black community. But getting the answers requires a concerted effort to recruit black participants in stroke research—an effort stymied, in part, by a clash of cultures between historically “ivory tower” researchers and a subject population leery of being experimented upon. Black men experience stroke at the rate of 87 per 100000 vs 59 per 100000 for white men, according to the American Heart Association; among black women, the incidence of stroke is 78 per 100000 vs 58 per 100000 for white women. Blacks younger than 65 years have a twoto four-fold greater risk of ischemic stroke compared with their white counterparts. Blacks also are more likely to die of stroke and develop hypertension earlier in life with greater severity than whites. Studies suggest that the disparity is caused by a variety of physiological, socioeconomic, and cultural factors, but the research community has been slow to embrace research that will better define those factors. Although the National Institutes of Health mandated in 1993 that the clinical research it funds should include proportionate representation of patients by racial and ethnic group, most studies involving stroke research have enrolled too few blacks to obtain definitive clinical answers. But this situation is finally changing. Just last year, researchers published the first major multicenter, randomized prospective, clinical trial that tried to answer clinical questions specifically regarding blacks and stroke ( JAMA. 2003;289:2947-2957). At the American Stroke Association’s International Stroke Conference held in San Diego last month, researchers from that groundbreaking study, the African
Abstract 2990: Notch1 monoclonal antibody inhibits tumor growth and modulates angiogenesis
Authors: Heidi Okamura, Theresa Proia, Alisa Bell, Qing Liu, Zakir Siddiquee, Jie Lin, Jeno Gyuris
Journal: Cancer Research (2014)

Abstract AVEO Oncology has developed a series of inducible mouse models of cancer, which through the preservation of critical tumor/stromal interactions, facilitate identification of cell-surface and secreted proteins that represent viable targets for therapeutic antibodies and other biologics. Functional genetic screens performed in vivo in these models identified the Notch pathway as a critical regulator of tumor maintenance. This finding was consistent with emerging evidence that activation of Notch signaling via receptor point mutation, receptor amplification, and elevated receptor and ligand expression, plays a key role in various human cancers. Moreover, the Notch pathway controls diverse aspects of tumorigenesis and tumor maintenance, regulating tumor autonomous processes and interactions with the microenvironment, including angiogenesis. To further understand the role of the Notch pathway in tumor maintenance, and to assess the therapeutic potential of targeting the Notch pathway in cancer, we have generated monoclonal antibodies that inhibit the Notch1 receptor. Characterization of monoclonal antibodies targeting Notch1 through cell-based and biochemical studies demonstrated that the Notch1 monoclonal antibody bound with high affinity and high specificity to the Notch1 receptor, prevented ligand-mediated activation of the target receptor, and specifically repressed Notch-dependent signaling with high potency. Significantly, specific inhibition by the Notch1 monoclonal antibody did not result in the dose-limiting gut toxicity observed with Notch1 mAb resulted in tumor inhibition that was accompanied by increased vascular density, inhibition of Notch target gene expression, and increased expression of angiogenesis-related genes, consistent with expected changes resulting from Notch1/Dll4 pathway inhibition. In addition, several tumor models treated in combination with Notch1 mAb and an investigational VEGF pathway inhibitor, tivozanib, demonstrated increased tumor inhibition compared to either agent alone. Interestingly, combination treatment resulted in decreased vascular density and downregulated expression of angiogenesis genes, similar to treatment with VEGF inhibitor alone. Collectively, our work suggests that combination therapy of Notch1 antibodies with VEGF inhibitors should be evaluated as a potential viable therapeutic option for VEGF-resistant tumors. Citation Format: Heidi Okamura, Theresa Proia, Alisa Bell, Qing Liu, Zakir Siddiquee, Jie Lin, Jeno Gyuris. Notch1 monoclonal antibody inhibits tumor growth and modulates angiogenesis. [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 2990. doi:10.1158/1538-7445.AM2014-2990
Cancer Chemotherapy Reports
Authors: M.D. Jerome B. Block
Journal: CA A Cancer Journal for Clinicians (1973)

surprises lineitscourse.Thewell appreciated vistas are Chemothera viewed once more, but anoccasional turninthepath offers Re orts something new.Forthose ofuswhomust look back before p welookforward, there areseveral articles ontheuse ofan imidazole carboxamide derivative in human cancers.
Height and risk of cancer
Authors: M. McCarthy, D. J Gunnell, G. D. Smith, J. M P Holly, S. Frankel, M. Shipley, D. A Leon
Journal: BMJ (1999)

Editor—In two separate cohort studies Gunnell et al1 and Davey Smith et al2 found an association between height and non-smoking related cancers. An accompanying editorial indicates that causality for this association is supported by studies in animals.3 None of the articles, however, examines the possibility of bias from survival selection in the cohort studies.

Cancer and heart disease are the main causes of death in old age but the mean age of death for heart disease is younger than for cancer. Heart disease is strongly associated with smoking and also with short stature. Is it possible that there is selective survival of taller people because shorter people die earlier from heart disease? This hypothesis is strengthened by the lack of association with smoking related cancers: smoking would be expected to cause heart disease first.

A test of this hypothesis would be to compare at the same mean age the heights of people with heart disease with the heights of people who had died from cancer. Did the referee ask for this? The two papers would be strengthened if the issue could be addressed.
Cardiac iron overload in sickle‐cell disease
Authors: Antonella Meloni, Mammen Puliyel, Alessia Pepe, Vasili Berdoukas, Thomas D. Coates, John C. Wood
Journal: American Journal of Hematology (2014)

Chronically transfused sickle cell disease (SCD) patients have lower risk of myocardial iron overload (MIO) than comparably transfused thalassemia major (TM) patients. However, cardioprotection is incomplete. We present the clinical characteristics of six patients who have prospectively developed MIO, to identify potential risk factors for cardiac iron accumulation. From 2002 to 2011, cardiac, hepatic, and pancreatic iron overload were assessed by R 2 and R 2 * magnetic resonance imaging techniques in 201 chronic transfused SCD patients as part of their clinical care. At the time, they developed MIO, five of six patients had been on chronic transfusion for more than 11 years; only one was on exchange transfusion. The time to MIO was correlated with reticulocyte and hemoglobin S percentages. All patients had qualitatively poor chelation compliance (&lt;50%). All patients had serum ferritin levels &gt;4600 ng/ml and liver iron concentration &gt;22 mg/g. Pancreatic R 2 * was &gt;100 Hz in every patient studied (5/6). Cardiac iron rose proportionally to pancreas R 2 *, with all patients having pancreas R 2 *&gt;100 Hz when cardiac iron was present. MIO had a threshold relationship with liver iron that was higher than observed in TM patients. In conclusion, MIO occurs in a small percentage of chronically transfused SCD patients and is only associated with exceptionally poor control of total body iron stores. Duration of chronic transfusion is clearly important but other factors, such as levels of effective erythropoiesis, appear to contribute to cardiac risk. Pancreas R 2 * can serve as a valuable screening tool for cardiac iron in SCD patients. Am. J. Hematol. 89:678–683, 2014. © 2014 Wiley Periodicals, Inc.
Defective humoral responses and extensive intravascular apoptosis are associated with fatal outcome in Ebola virus-infected patients
Authors: Sylvain Baize, Eric M. Leroy, M.-C. Georges-Courbot, Monique Capron, Joseph Lansoud-Soukate, Patrice Debré, Susan P. Fisher-Hoch, Joseph B. McCormick, Alain J. Georges
Journal: Nature Medicine (1999)
Abstract 8134: Differences in Electrocardiographic Findings Between Takotsubo Cardiomyopathy and Reperfused Non-Q-Wave Anterior Acute Myocardial Infarction
Authors: Masami Kosuge, Toshiaki Ebina, Kiyoshi Hibi, Kengo Tsukahara, Noriaki Iwahashi, Mitsuaki Endo, Nobuhiko Maejima, Satoshi Morita, Kazuaki Uchino, Toshiyuki Ishikawa, Satoshi Umemura, Kazuo Kimura
Journal: Circulation (2011)

Background: In takotsubo cardiomyopathy (TC), left ventricular dysfunction dramatically improves in a short time, and negative T waves (Neg T) with QT interval prolongation commonly appear, suggesting viable but sympathetically denervated myocardium. However, these findings are often observed in reperfused non-Q-wave anterior acute myocardial infarction (ant AMI). Methods: We compared 34 patients with TC and 237 with non-Q-wave ant AMI in whom occlusion followed by TIMI 3 flow of the left anterior descending coronary artery were documented by emergency coronary angiography. All patients were admitted within 6 h after symptom onset. After admission, ECGs with the greatest amplitude of Neg T (mean 2 days later) were analyzed. Results: As compared with patients with non-Q-wave ant AMI, those with TC were older (70±11 vs 61±11 years, p&lt;0.01), more likely to be women (85% vs 21%, p&lt;0.01), and had a lower peak creatine kinase level (289±298 vs 1505±921 mU/ml, p&lt;0.01) despite a lower left ventricular ejection fraction on admission (41±10% vs 52±10%, p&lt;0.01). TC was associated with a longer maximal QTc interval (642±93 vs 586±81 ms, p&lt;0.01), a greater amplitude of maximal Neg T (10±4 vs 8±5 mm. p&lt;0.05), and a greater number of leads with Neg T ≥1.0 mm (10±1 vs 6±2, p&lt;0.01). Distribution of Neg T is shown in Figure, using the Cabrera sequence to display limb leads. In TC, Neg T was always observed in leads -aVR and V4-6, whereas Neg T was rare in lead V1. Neg T in lead -aVR (i.e., positive T wave in lead aVR) combined with no Neg T in lead V1 identified TC with 94% sensitivity, 95% specificity, and 94% accuracy, which was the highest diagnostic accuracy. Conclusions: As compared with non-Q-wave ant AMI, negative T waves appear more frequently and broadly in TC, suggesting that TC might be associated with more extensive viable but denervated myocardium. The combination of positive T wave in lead aVR and no negative Twave in lead V1 simply but accurately differentiates TC from non-Q-wave ant AMI.
Newly Developed Barrett’s Esophagus after Subtotal Esophagectomy
Authors: D Franchimont, A Covas, C Brasseur, J-L Van Laethem, I El-Nakadi, J Devière
Journal: Endoscopy (2003)

More detailed information regarding the early mucosal events that lead to intestinal metaplasia would be very beneficial for understanding the pathogenesis of Barrett's esophagus (BE). Gastroesophageal reflux and duodenogastroesophageal reflux play a major role in the pathogenesis of Barrett's esophagus. The aim of this study was to investigate the prevalence of newly developed BE in patients who had previously undergone a subtotal esophagectomy - a clinical condition characterized by the absence of a lower esophageal sphincter and massive gastroesophageal reflux.A retrospective examination was carried out on all patients who underwent subtotal esophagectomy (n = 87) listed in our institution's computer files from 1995 to 2000. Twenty-one patients were excluded due to missing data or no upper gastrointestinal endoscopy after surgery.Based on the Savary-Miller classification, 47 patients developed either type I (n = 2), II (n = 8), III (n = 11) or IV (n = 26) esophagitis after surgery. Newly developed BE was observed in nine patients (13.5 %) after subtotal esophagectomy (median time to diagnosis: 489 days, range 43 - 1172). None of the patients had persistent BE immediately after surgery, and two of the patients with newly developed BE had had no history of BE before surgery or at the time of surgery. Proton-pump inhibitor therapy after surgery and neoadjuvant chemotherapy did not appear to influence the development of BE after subtotal esophagectomy.Newly developed BE after subtotal esophagectomy may provide further insights into the early mucosal events that lead to intestinal metaplasia and into the roles of gastroesophageal and duodenoesophageal reflux in the pathogenesis of BE.