tbuckley/cabot-search huggingface dataset:
The United States Needs a Health System Like Other Countries
Authors: William A. Glaser
Journal: JAMA (1993)

Every developed country except the United States has a comprehensive health system for coverage, service provision, and finance. Social policy in the United States once was guided by thinkers who realized this, and the Social Security system--complete except for health insurance--resulted. The climate of thinking changed, and health policy for some time has been dominated by classical economists who argue that free competitive markets will solve all problems. They justify their arguments by claiming that the only alternative is full government takeovers of service and financing, as in Canada. While this debate has dragged along, problems in the United States have become grave. Instead of reviving the institutional economics and social policies that once served the United States well, the Clinton administration has turned policy over to devotees of managed competition. But the problem is how to organize the country, and national health insurance--easily observed in other countries--is superior to the current chaos and free-market utopias in the United States. Important aims would be achieved, such as expanding coverage, obtaining stable revenue, and containing costs. Important political barriers can be overcome, such as resistance by small business. Such a health system includes machinery for setting goals and implementing results, involving collaboration among providers, payers, and government.
The sarcoplasmic reticulum as the primary target of reperfusion protection
Authors: H PIPER, S KASSECKERT, Y ABDALLAH
Journal: Cardiovascular Research (2006)

Prolonged myocardial ischemia leads to the loss of viable tissue in the heart, even if the ischemic episode is eventually ended by reperfusion. As we now know today, the extent of infarct is only partially due to the ischemic injury. Another part of tissue loss is due to death signals generated at the time of and by the specific circumstances of reperfusion, a phenomenon termed “reperfusion injury” [1,2]. The existence of reperfusion injury has been revealed by successful attempts to interfere with such causes at the time of reperfusion and limit, thereby, the extent of final tissue loss. Reperfusion injury is initiated within the first minutes of reperfusion. This is why these minutes represent a valuable “window of opportunity” for myocardial protection. One of the most recent strategies to interfere within that time window is postconditioning, i.e. the repetitive application of brief bouts of ischemia within the first minutes of reperfusion [3]. This protocol is so promising because it has brought reperfusion protection to the clinical arena and reperfusion injury to the broad attention of clinical cardiologists.

The nature of the death signals activated during the first minutes of reperfusion is still a matter of debate. Opinions are also divided on whether the ensuing cell loss is due to necrosis or apoptosis. Cell damage in reperfused myocardium exhibits a peculiar histological appearance. It is characterized by hypercontracted sarcomeres (“contraction bands”) and frequent sarcolemmal ruptures that gave rise to the term “contraction band necrosis” [4,5]. The histological picture has led to a hypothesis on the pathogenesis of acute reperfusion injury. According to this hypothesis, it is an uncontrolled activation of the contractile machinery in myocardial cells upon reperfusion that produces the final, decisive blow to cardiomyocytes already weakened by the ischemic history and ends their fate by disruption …
Hypokalemia in Leukemia
Authors: JEFFREY R. FISHER
Journal: Annals of Internal Medicine (1977)

Comments and Corrections1 March 1977Hypokalemia in LeukemiaJEFFREY R. FISHER, M.D.JEFFREY R. FISHER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-86-3-363 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Mir and associates (1) have reported on the frequent association of hypokalemia and acute myeloid leukemia with unexplained renal potassium (K) loss. In a subsequent letter Yeung and Trowbridge (2) noted the prevalence of low serum K in chronic granulocytic leukemia. Both groups of authors review the possible causes of hypokalemia in acute leukemia, but make no mention of direct renal involvement by the leukemic process as a potential cause. Renal leukemic infiltrates are frequently seen at postmortem examination (3) but hypokalemia has not been reported in acute lymphoblastic leukemia. During the past year we have seen...References1. MIRBRABINTANG MBO: Hypokalemia in acute myeloid leukemia. Ann Intern Med 82:54-57, 1975 LinkGoogle Scholar2. YEUNGTROWBRIDGE KA: Chronic granulocytic leukemia: hypokalemia in acute blastic crisis. Ann Intern Med 85:533-534, 1976 LinkGoogle Scholar3. BOGGSWINTROBECARTWRIGHT DMG: The acute leukemics. Medicine 41:163-225, 1962 CrossrefMedlineGoogle Scholar4. FREIFRITZPRICE ERE: Renal and hepatic enlargement in acute leukemia. Cancer 16:1089-1092, 1963 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySpurious Hypokalemia in Myeloproliferative Disorders 1 March 1977Volume 86, Issue 3Page: 363-364KeywordsAcute myeloid leukemiaAutopsyPotassiumPrecursor cells ePublished: 1 December 2008 Issue Published: 1 March 1977 PDF downloadLoading ...
Quantitative ultrastructural studies of gall bladder epithelium in gall stone free subjects and patients with gall stones.
Authors: S Sahlin, J Ahlberg, K Einarsson, R Henriksson, A Danielsson
Journal: Gut (1990)

The present study aimed at a further evaluation of the role of glycoproteins in the formation of cholesterol gall stones in man. An electron microscopic morphometric study of the gall bladder epithelium was performed in six gall stone free subjects and 12 gall stone patients. Six of the gall stone patients were treated with ursodeoxycholic acid three weeks before cholecystectomy. The number and the volume density of the mucin containing secretory granules, were not significantly increased in gall stone patients compared with gall stone free subjects. Treatment with ursodeoxycholic acid did not affect the number or volume density of the secretory granules. Thus, these results do not give evidence for that the degree of cholesterol saturation influences mucin content in the gall bladder wall of man. A major new finding was that gall stone patients had a markedly reduced total lysosome area and volume density of lysosomes compared with gall stone free subjects, a finding which may be related to a decreased intracellular degradation of protein and/or mucin.
Integrative genetic and metabolite profiling analysis suggests altered phosphatidylcholine metabolism in asthma
Authors: J. S. Ried, H. Baurecht, F. Stückler, J. Krumsiek, C. Gieger, J. Heinrich, M. Kabesch, C. Prehn, A. Peters, E. Rodriguez, H. Schulz, K. Strauch, K. Suhre, R. Wang‐Sattler, H.‐E. Wichmann, F. J. Theis, T. Illig, J. Adamski, S. Weidinger
Journal: Allergy (2013)

Abstract Background Genome‐wide association studies (GWAS) have identified many risk loci for asthma, but effect sizes are small, and in most cases, the biological mechanisms are unclear. Targeted metabolite quantification that provides information about a whole range of pathways of intermediary metabolism can help to identify biomarkers and investigate disease mechanisms. Combining genetic and metabolic information can aid in characterizing genetic association signals with high resolution. This work aimed to investigate the interrelation of current asthma, candidate asthma risk alleles and a panel of metabolites. Methods We investigated 151 metabolites, quantified by targeted mass spectrometry, in fasting serum of asthmatic and nonasthmatic individuals from the population‐based KORA F4 study ( N = 2925). In addition, we analysed effects of single‐nucleotide polymorphisms (SNPs) at 24 asthma risk loci on these metabolites. Results Increased levels of various phosphatidylcholines and decreased levels of various lyso‐phosphatidylcholines were associated with asthma. Likewise, asthma risk alleles from the PDED3 and MED24 genes at the asthma susceptibility locus 17q21 were associated with increased concentrations of various phosphatidylcholines with consistent effect directions. Conclusions Our study demonstrated the potential of metabolomics to infer asthma‐related biomarkers by the identification of potentially deregulated phospholipids that associate with asthma and asthma risk alleles.
Floctafenine and Coma in Cirrhosis
Authors: PAOLO PASQUA
Journal: Annals of Internal Medicine (1982)

Letters and Corrections1 February 1982Floctafenine and Coma in CirrhosisPAOLO PASQUA, ANTONIO CRAXI, LUIGI PAGLIARAPAOLO PASQUASearch for more papers by this author, ANTONIO CRAXISearch for more papers by this author, LUIGI PAGLIARASearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-96-2-253_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Floctafenine (idarac), a nonnarcotic analgesic of the hydroxyquinoline group, is used widely because of its minimal untoward side effects, even in high-risk patients. In particular, no sleep-inducing effect has been reported from animal or human studies (1, 2). In our department, in which mainly patients with chronic liver diseases are seen, it has therefore been used as a safe first-choice analgesic. We have recently studied an episode of coma in a cirrhotic patient in which floctafenine could be causally involved.A 53-year-old alcoholic patient with cirrhosis, chronic pancreatitis, and duodenal ulcer was admitted to our department because...References1. GLOMOTCHEVALIERYANNIER RBB. Toxicological studies on floctafenine. Toxicol Appl Pharmacol. 1976;36:173-85. CrossrefMedlineGoogle Scholar2. PETERFALVIDERAEDTBENZONI MRJ. Floctafenine, a new non-narcotic analgesic. Arch Int Pharmacodyn Ther. 1975;216 (1):97-112. MedlineGoogle Scholar3. SCHENTAGCALLERIROSECERRADE GLOPPERBERNHARD JGJFEH. Pharmacokinetic and clinical studies in patients with cimetidine-associated mental confusion. Lancet. 1979;1:177-81. CrossrefMedlineGoogle Scholar4. KIMELBLATTCERRACALLERIBERGMCMILLENSCHENTAG BFGMMJ. Dose and serum concentration relationships in cimetidine-associated mental confusion. Gastroenterology. 1980;78:791-5. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: PAOLO PASQUA; ANTONIO CRAXI; LUIGI PAGLIARAAffiliations: Universita Degli Studi di Palermo Palermo 90146 Italy PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byFloctafenineNON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs)FloctafenineHEPATOTOXICITY OF ANALGESICS AND ANTI-INFLAMMATORY AGENTSAnti-inflammatory analgesics and drugs used in rheumatoid arthritis and gout 1 February 1982Volume 96, Issue 2Page: 253-253KeywordsAlcoholicsAnalgesicsChronic liver diseaseChronic pancreatitisCirrhosisComaDuodenal ulcers ePublished: 1 December 2008 Issue Published: 1 February 1982 PDF downloadLoading ...
Protective effect of human leukocyte antigen B27 in hepatitis C virus infection requires the presence of a genotype-specific immunodominant CD8+ T-cell epitope
Authors: Christoph Neumann-Haefelin, Jörg Timm, Julia Schmidt, Nadine Kersting, Karen Fitzmaurice, Cesar Oniangue-Ndza, Michael N. Kemper, Isla Humphreys, Susan McKiernan, Dermot Kelleher, Volker Lohmann, Paul Bowness, Daniela Huzly, Hugo R. Rosen, Arthur Y. Kim, Georg M. Lauer, Todd M. Allen, Eleanor Barnes, Michael Roggendorf, Hubert E. Blum, Robert Thimme
Journal: Hepatology (2009)

Human leukocyte antigen B27 (HLA-B27) is associated with protection in human immunodeficiency virus (HIV) and hepatitis C virus (HCV) infection. This protective role is linked to single immunodominant HLA-B27-restricted CD8+ T-cell epitopes in both infections. In order to define the relative contribution of a specific HLA-B27-restricted epitope to the natural course of HCV infection, we compared the biological impact of the highly conserved HCV genotype 1 epitope, for which the protective role has been described, with the corresponding region in genotype 3 that differs in its sequence by three amino acid residues. The genotype 3a peptide was not recognized by CD8+ T cells specific for the genotype 1 peptide. Furthermore, patients with acute or chronic infection with HCV genotype 3a did not mount T-cell responses to this epitope region, and their autologous viral sequences showed no evidence of T-cell pressure. Finally, we found a significantly higher frequency of HLA-B27 positivity in patients with chronic HCV genotype 3a infection compared to genotype 1 infection, indicating that there is no protection by HLA-B27 in HCV genotype 3 infection. Conclusion: Our data indicate that the protective effect of HLA-B27 is limited to HCV genotype 1 infection and does not expand to other genotypes such as genotype 3a. This can most likely be explained by intergenotype sequence diversity leading to the loss of the immunodominant HLA-B27 epitope in viral strains other than genotype 1. Our results underline the central role of a single HLA-B27-restricted epitope-specific CD8+ T-cell response in mediating protection in HCV genotype 1 infection. (Hepatology 2010;51:54–62.)
Counts of activated blood eosinophils for monitoring asthma
Authors: J. Hed, G. Halldén
Journal: Allergy (1993)

The FOG method is a new cell membrane permeabilization technique which makes it possible to identify the eosinophils in unseparated peripheral blood and allows analyses of both surface and intracellular antigens by flow cytometry. This technique has been adapted to analyse eosinophil activity in peripheral blood from asthmatic patients by measuring the expression of the EG2-epitope on intracellular ECP.
ACUTE ABDOMINAL SYMPTOMS IN TYPHOID FEVER FROM INFLAMED MESENTERIC GLANDS, SIMULATING INTESTINAL PERFORATION AND OTHER ACUTE ABDOMINAL CONDITIONS. TWQ ILLUSTRATIVE CASES.
Authors: RUSSELL STURGIS ROWLAND
Journal: JAMA (1906)

Acute abdominal symptoms in typhoid fever have recently attracted considerable interest because of the importance of early diagnosis in intestinal perforation.<sup>1</sup> The literature is becoming filled with records of cases containing additions to our knowledge of diagnosis and treatment.<sup>2</sup>These studies have shown the varied symptomatology of intestinal perforation and have demonstrated that exploratory laparotomy for diagnostic purposes is more conservative than waiting, in doubtful cases. As a result, an increasing number of patients have been operated on in whom no perforation was found. Almost every surgeon of experience has had one or more of these cases.<sup>3</sup> I wish to relate the histories of two typhoid fever patients who had such pronounced abdominal symptoms that in one intestinal perforation was suspected, and in the other a complex of abdominal conditions—appendi-appendicitis, tuberculous peritonitis or typhoid fever complicated by one of these conditions. Laparotomy was performed in both instances,
MPs are to investigate need for drug companies to share clinical trial data
Authors: G. Iacobucci
Journal: BMJ (2012)

MPs are set to investigate drug companies’ sharing of clinical trial data, after mounting pressure on the issue, the chairman of the health select committee has announced.

In a discussion panel at the NHS Alliance’s conference in Bournemouth today, the committee’s chairman, Stephen Dorrell, confirmed that MPs would examine the issue as a matter of priority within the next 12 months.

The announcement came after the BMJ recently launched its open data campaign, which aims to achieve “appropriate and necessary independent scrutiny of data from clinical trials” and to “highlight the problems caused by lack of access to data.”1

In September this year the doctor and science writer Ben Goldacre published Bad Pharma …
Splenic lymphoma with circulating villous lymphocytes: Report of seven cases and review of the literature
Authors: Tsieh Sun, Myron Susin, Judith Brody, Klaus Dittmar, Saul Teichberg, Robert Weiner, Jen H. Lin, Norbert Felber
Journal: American Journal of Hematology (1994)

Abstract Splenic lymphoma with villous lymphocytes (SLVL) is a relatively new entity with only a few reports published. We report seven cases of SLVL with detailed clinicopathologic and comprehensive immunophenotypic studies to further characterize this lymphoma, which is frequently confused with hairy cell leukemia and other low‐grade B‐cell lymphoid neoplasms. The diagnostic criteria we used include 1) prominent splenomegaly, 2) insignificant or no lymphadenopathy, 3) lymphocytosis without leukopenia, 4) presence of circulating villous lymphocytes, 5) characteristic cytologic and histologic features, and 6) specific phenotypic and cytochemical findings. Our studies show that SLVL does not represent a pure entity but rather a morphologically heterogeneous group of low‐grade lymphomas with various cytologlc and histologic features. Although immunophenotyping is helpful in differential diagnosis, multiparameter studies are necessary to confirm the diagnosis. In our series, only two patients died of SLVL, who probably developed transformation to a higher‐grade lymphoma. © 1994 Wiley‐Liss, Inc.
Out-of-Hospital Mortality Among Patients Receiving Methadone for Noncancer Pain
Authors: Wayne A. Ray, Cecilia P. Chung, Katherine T. Murray, William O. Cooper, Kathi Hall, C. Michael Stein
Journal: JAMA Internal Medicine (2015)

Growing methadone use in pain management has raised concerns regarding its safety relative to other long-acting opioids. Methadone hydrochloride may increase the risk for lethal respiratory depression related to accidental overdose and life-threatening ventricular arrhythmias.
SAFETY OF RETROGRADE RECANALIZATIONS TO CHRONIC TOTAL OCCLUSION VIA TRANSSEPTAL PATHWAYS WITH USE OF A NOVEL METAL-CATHETER ANALYZED BY ECHOCARDIOGRAPHY
Authors: Takimura Hideyuki, Toshiya Muramatsu, Reiko Tsukahara, Yoshiaki Ito, Tsuyoshi Sakai, Hiroshi Ishimori, Keisuke Hirano, Masatsugu Nakano, Masahiro Yamawaki, Shinya Sasaki, Motoharu Araki, Yasunari Sakamoto, Ikki Komatsu, Takuro Takama
Journal: Journal of the American College of Cardiology (2011)
STAT6 Transcription Factor Is a Facilitator of the Nuclear Receptor PPARγ-Regulated Gene Expression in Macrophages and Dendritic Cells
Authors: Attila Szanto, Balint L. Balint, Zsuzsanna S. Nagy, Endre Barta, Balazs Dezso, Attila Pap, Lajos Szeles, Szilard Poliska, Melinda Oros, Ronald M. Evans, Yaacov Barak, John Schwabe, Laszlo Nagy
Journal: Immunity (2010)

Peroxisome proliferator-activated receptor γ (PPARγ) is a lipid-activated transcription factor regulating lipid metabolism and inflammatory response in macrophages and dendritic cells (DCs). These immune cells exposed to distinct inflammatory milieu show cell type specification as a result of altered gene expression. We demonstrate here a mechanism how inflammatory molecules modulate PPARγ signaling in distinct subsets of cells. Proinflammatory molecules inhibited whereas interleukin-4 (IL-4) stimulated PPARγ activity in macrophages and DCs. Furthermore, IL-4 signaling augmented PPARγ activity through an interaction between PPARγ and signal transducer and activators of transcription 6 (STAT6) on promoters of PPARγ target genes, including FABP4. Thus, STAT6 acts as a facilitating factor for PPARγ by promoting DNA binding and consequently increasing the number of regulated genes and the magnitude of responses. This interaction, underpinning cell type-specific responses, represents a unique way of controlling nuclear receptor signaling by inflammatory molecules in immune cells.
Antiretroviral Agents and Prevention of Malaria in HIV-Infected Ugandan Children
Authors: Jane Achan, Abel Kakuru, Gloria Ikilezi, Theodore Ruel, Tamara D. Clark, Christian Nsanzabana, Edwin Charlebois, Francesca Aweeka, Grant Dorsey, Philip J. Rosenthal, Diane Havlir, Moses R. Kamya
Journal: New England Journal of Medicine (2012)

Human immunodeficiency virus (HIV) protease inhibitors show activity against Plasmodium falciparum in vitro. We hypothesized that the incidence of malaria in HIV-infected children would be lower among children receiving lopinavir–ritonavir–based antiretroviral therapy (ART) than among those receiving nonnucleoside reverse-transcriptase inhibitor (NNRTI)–based ART.
Infection with GB Virus C and Reduced Mortality among HIV-Infected Patients
Authors: Hans L. Tillmann, Hans Heiken, Adriana Knapik-Botor, Stefan Heringlake, Johann Ockenga, Judith C. Wilber, Bernd Goergen, Jill Detmer, Martin McMorrow, Matthias Stoll, Reinhold E. Schmidt, Michael P. Manns
Journal: New England Journal of Medicine (2001)

The flavivirus GB virus C (GBV-C, also designated hepatitis G virus) was identified in a search for hepatitis viruses, but no disease is currently known to be associated with it. We investigated the relation between coinfection with GBV-C and the long-term outcome in patients infected with the human immunodeficiency virus (HIV).
Uni-, Bi-, Tri-, and Quadricuspid Aortic Valves
Authors: Matthias R Schulze, Ruth H Strasser
Journal: New England Journal of Medicine (2006)

A 47-year-old woman presented with left-sided chest pain and minimal dyspnea on exertion. Echocardiography showed a quadricuspid aortic valve. Tricuspid, bicuspid, and unicuspid aortic valves are also shown.
1028-171 Fasting blood glucose: An underestimated risk factor for subclinical coronary atherosclerosis
Authors: Khurram Nasir, Roger S Blumenthal, Joel B Braunstein, Romeu Meneghello, Jose A Maluf, Wendy S Post, Matthew J Budoff, Raul D Santos
Journal: Journal of the American College of Cardiology (2004)
Sudden Heart Failure in a 30-Year-Old Woman
Authors: Robert J. Cihak
Journal: JAMA (1970)

Dr. Edward H. Eliscu: This 30-year-old Negro woman was admitted to another hospital on Dec 6, 1968. She had been in good health until the day before admission when she experienced sudden onset of bounding pulses in her neck while climbing stairs; this was followed by dyspnea and precordial pain. There was no history of rheumatic fever or of recent fever, chills, trauma, or dental work. Physical examination at that time revealed a temperature of 101 F (38.3 C), blood pressure 110/60 mm Hg, and a rumbling, continuous murmur at the lower left sternal border. She remained febrile, despite treatment with several antibiotics. Hematocrit value dropped from 42% at the time of admission to 26%, with reticulocytes accounting for 8% of the erythrocytes. <h3>Discussion</h3> Dr. Laurence L. Robbins: Dr. Forrester, do you have any ideas about this case? Dr. Deborah M. Forrester: At the time of the examination in March