tbuckley/cabot-search huggingface dataset:
Hepatic Lesion in Systemic Lupus Erythematosus: Cytoplasmic Tubules in Sinusoidal Endothelium
Authors: K. Kovacs
Journal: JAMA (1972)

To the Editor.—  The detection of cytoplasmic microtubules in the glomerular endothelium of patients with systemic lupus erythematosus (SLE) aroused considerable interest recently. These structures are recognizable very frequently in the kidneys of patients with SLE, and although they are not specific or pathognomonic for this disease, their demonstration has some diagnostic value in suspected cases. 1-3 The exact nature of the cytoplasmic microtubules is not known. They were believed to represent myxovirus-like particles suggesting viral cause of the disease. 1 Other authors, however, assume that they are ultrastructural manifestations of endothelial cell injury, due either to viral infection or to some other deleterious mechanism. 2,4   We found cytoplasmic microtubules in the endothelial cells of the liver sinusoids of a 20-year-old woman patient. Her illness, based on the characteristic history, and clinical and laboratory findings, was diagnosed as SLE with hepatic involvement. Liver biopsy was performed with the Menghini needle.
Coronary Thrombolysis with Human Single-Chain, Urokinase-Type Plasminogen Activator (Pro-Urokinase) in Patients with Acute Myocardial Infarction
Authors: FRANS VAN DE WERF
Journal: Annals of Internal Medicine (1986)

Single-chain, urokinase-type plasminogen activator (prourokinase), isolated from the conditioned medium of a human renal adenocarcinoma cell line, was administered to six patients with evolving myocardial infarction of less than 5 hours' duration and angiographically confirmed total occlusion of the infarct-related coronary artery. The agent was infused intravenously at a rate of 40 mg over 60 minutes immediately followed in three patients by intracoronary infusion of 20 mg over 30 minutes. In four of the six patients complete reperfusion was obtained during intravenous administration and in one patient after 20 minutes of intracoronary infusion. One patient did not respond. The infusion caused significant changes in the fibrinogen level and generation of fibrinogen breakdown products in only one patient. Single-chain, urokinase-type plasminogen activator can induce clot-selective coronary thrombolysis in patients with acute myocardial infarction.
Diabetes Drug Is Linked With Bladder Cancer Risk
Authors: Rebecca Voelker
Journal: JAMA (2012)

Efron said the issue is whether researchers and the FDA want to just follow protocols or whether they want to find the true answers to their questions. “In situations where you are really trying to learn something, you should admit there is bias but get the question right.” Others are also calling for changes in policies that permit only intention-totreat analyses. Researchers at the Harvard School of Public Health in Boston argue that there is no guarantee that intention-to-treat analysis can accurately estimate the clinical effectiveness of treatment and recommend that different analytic methods be used to assess findings of all randomized clinical trials with substantial lack of adherence to the intervention by trial participants or loss to follow-up of participants (Hernan MA and Hernandez-Diaz S. Clin Trials. 2012; 9[1]:48-55). Despite such calls for change in assessing clinical data, persuading an agency like the FDA to consider alternative methods to determine whether trial results are rigorous enough to serve as the basis for approving or rejecting a drug will take time, said Carl C. Peck, MD, adjunct professor at UCSF’s Center for Drug Development Science and a former director of the FDA’s Center for Drug Evaluation and Research. TheFDAlikesintention-to-treatdesign because it isconservative, saidPeck,who isalso the founderandchairmanofNDA Partners, a consultancy group for companiesdevelopingdrugsandmedicaldevices.“TheFDAhasthetaskofprotecting thepublichealthbycreatingahighstandardforsafetyandeffectiveness,andthey have another duty laid on them by Congress, and that is consistencyanduniformity,”Pecksaid.“It’sacombinationofall of those thatmakes theFDAveryconservative,riskaverse,andslowtochange.”
Heart rate variability for risk stratification of life-threatening arrhythmias
Authors: Leonard S. Dreifus, Jai B. Agarwal, Elias H. Botvinick, Keith C. Ferdinand, Charles Fisch, John D. Fisher, J.Ward Kennedy, Richard E. Kerber, Charles R. Lambert, Okike N. Okike, Eric N. Prystowsky, Sanjeev V. Saksena, John S. Schroeder, David O. Williams
Journal: Journal of the American College of Cardiology (1993)
THE EFFECT OF ADRENOCORTICOTROPIC HORMONE ON INFLAMMATION DUE TO TUBERCULIN HYPERSENSITIVITY AND TURPENTINE AND ON CIRCULATING ANTIBODY LEVELS
Authors: Charles K. Osgood, Cutting B. Favour
Journal: The Journal of Experimental Medicine (1951)

The treatment with adrenocorticotropic hormone of guinea pigs sensitized with heat-killed tubercle bacilli caused suppression of their skin reactivity to tuberculin. Similar animals treated with saline did not show this change. Normal guinea pigs treated with adrenocorticotropic hormone showed suppression of inflammation, but not necrosis, produced by intracutaneous oil of turpentine. There was slight, but probably not significant, diminution of inflammation during saline administration. Tuberculin complement-fixing antibody titers were not altered by either adrenocorticotropic hormone or saline administration. Adrenocorticotropic hormone produced marked eosinopenia and lymphopenia in guinea pigs.
Rare Genomic Characters Do Not Support Coelomata: Intron Loss/Gain
Authors: S. W. Roy, M. Irimia
Journal: Molecular Biology and Evolution (2008)

Recently, a new phylogenetic method employing intron position sharing across species was proposed and support for a Coelomate clade reported (Zheng et al. 2007. A rigorous analysis of the pattern of intron conservation supports the Coelomata clade of animals. Mol Biol Evol. 24:2583–2592.). Here, we show that the previous analysis depends on: 1) an idiosyncratic definition of "conserved" introns, 2) exclusion of all phylogenetically informative introns present in outgroups, 3) incorrect inference of change along the critical branch, and 4) lack of variation in rates across branches. The method thus seems unlikely to give accurate results. In addition, we address differences in rates of loss across intron sites, which Zheng et al. claimed invalidates our previous analysis that supported Ecdysozoa (Roy and Gilbert. 2005a. Resolution of a deep animal divergence by the pattern of intron conservation. Proc Natl Acad Sci USA. 102:4403–4408.). Instead, we show that our conclusions are likely to be robust to such concerns.
Pulmonary atresia and intact ventricular septum: surgical management based on a revised classification.
Authors: M de Leval, C Bull, J Stark, R H Anderson, J F Taylor, F J Macartney
Journal: Circulation (1982)

Sixty patients with pulmonary atresia and intact ventricular septum (PA:IVS) presenting from 1970 to 1980 are reviewed. Three groups of patient are discussed: those with tripartite right ventricles, those with no trabecular portion to the cavity, and those with neither trabecular nor infundibular portions. The decrease in early mortality for neonates with PA:IVS since 1977 (one death in 15 patients) supports our current management policy of preoperative prostaglandin E1 infusion with transpulmonary valvotomy (for patients with an infundibular cavity) combined with a left modified Blalock-Taussig shunt using a Gore-Tex prosthesis. Tricuspid valve growth, estimated by serial angiograms in 12 patients, was greater if right ventricle-to-pulmonary artery continuity was established. Later definitive repair was attempted in nine patients, with two early deaths; five underwent right ventricular outflow tract reconstruction and four had modified Fontan procedures. Neonates with critical pulmonary stenosis are also discussed. Their neonatal mortality (nine deaths in 20 patients) was similar to that of comparable patients with PA:IVS, but their actuarial survival at 5 years (55%) was superior (36% at 5 years).
Twenty five years of case finding and audit.
Authors: S Kaul
Journal: BMJ (1991)

These skills have in common that thev can be acquired by many reasonably intelligent and empathic people: they are not the exclusive preserve of any one profession and, indeed, may be most economically used by non-professionals.The danger of internecine strife among the caring professions regarding the ownership of these various techniques is great, and the danger of overprofessionalisation of their practice even more so.
Non-small Cell Lung Cancer Induces an Immunosuppressive Phenotype of Dendritic Cells in Tumor Microenvironment by Upregulating B7-H3
Authors: Thomas Schneider, Hans Hoffmann, Hendrik Dienemann, Philipp A. Schnabel, Alexander H. Enk, Sabine Ring, Karsten Mahnke
Journal: Journal of Thoracic Oncology (2011)
Blood pressure controls needed to save on European health bills
Authors: R. Dobson
Journal: BMJ (2002)

Achieving targets on the control of blood pressure in five European countries would save healthcare systems €1.26bn (£790m; $1.25bn).

The failure to achieve targets is resulting in 281 000 unnecessary major cardiovascular events, according to a report on blood pressure control in the United Kingdom, France, Germany, Italy, and Sweden ( Blood Pressure 2002;11:33-45).

The report was produced by the Department of Public Health and Social Sciences, University of Uppsala, Sweden, and …
Commission rejects mass genetic screening at birth
Authors: Clare Dyer
Journal: BMJ (2005)

Genetic profiling of all newborn babies was rejected last week by the United Kingdom's official genetics watchdog, in a report. Screening could help predict what illnesses babies might develop in later life. After the idea was raised by the government's white paper on genetics in 2003, the Human Genetics Commission set up a joint working group with the NHS's National Screening Committee to look at the arguments for and against profiling at birth.

The NHS was unlikely to be able to afford such a programme within the next 20 years and the evidence base is insufficient …
Regimens for Treatment of Lupus Nephritis
Authors: DAVID KAPLAN
Journal: Annals of Internal Medicine (1980)

Letters1 March 1980Regimens for Treatment of Lupus NephritisDAVID KAPLAN, M.D.DAVID KAPLAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-92-3-437_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In his discussion in the National Institutes of Health conference "Systemic Lupus Erythematosus: Evolving Concepts" (1), Dr. Klippel compares several regimens for the treatment of lupus nephritis: unspecified but modest amounts of prednisone with either azathioprine, cyclophosphamide, azathioprine plus cyclophosphamide, or itermittent intravenous cyclophosphamide, and modest amounts of prednisone alone. He concludes that azathioprine plus cyclophosphamide and intravenous cyclophosphamide may "reduce the progression of renal disease" in patients with systemic lupus erythematosus.His data, however, may be organized as in Table 1, which considers only the preservation of renal function and suggests the following conclusions: cytotoxic drugs...References1. KLIPPEL J. Studies in the treatment of lupus nephritis, in DECKER JL. moderator. Systemic lupus erythematosus: evolving concepts. Ann Intern Med. 1979;91:587-604. LinkGoogle Scholar2. KAPLAN D. Treatment of systemic lupus erythematosus. Arthritis Rheum. 1977;20:S175-80. Google Scholar3. ALBERTHADLERROPES DNM. Does corticosteroid therapy affect the course of patients with systemic lupus erythematosus? Arthritis Rheum. 1979;22:945-53. CrossrefMedlineGoogle Scholar1. KLIPPEL J. Studies in the treatment of lupus nephritis, in DECKER JL, moderator. Systemic lupus erythematosus: evolving concepts. Ann Intern Med. 1979;91:587-604. LinkGoogle Scholar2. DONADIOHOLLEYFERGUSONILSTRUP JKRD. Treatment of diffuse proliferative lupus nephritis with prednisone and combined prednisone and cyclophosphamide. N Engl J Med. 1978;299:1151-5. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: DAVID KAPLAN, M.D.Affiliations: State University of New York Downstate Medical Center Brooklyn, NY 11203 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byClinical pharmacology and toxicology of cyclophosphamide: emphasis on use in rheumatic diseasesFortschritte in der Therapie des Lupus erythematodes 1 March 1980Volume 92, Issue 3Page: 437-438KeywordsCyclophosphamideDrugsLupus erythematosusLupus nephritisRenal diseases ePublished: 1 December 2008 Issue Published: 1 March 1980 PDF downloadLoading ...
A5.6 Anti-Carbamylated Protein Antibodies are Present in Mice with Collagen induced Arthritis
Authors: Jeroen Stoop, Bisheng Liu, Jing Shi, Diahann Jansen, Leendert Trouw, Rene Toes
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Objective</h3> Antibodies against citrullinated proteins (ACPA) are a characteristic of rheumatoid arthritis (RA). Carbamylation is a different type of post translational modification, where a Lysine amino acid is converted into a homocitrullin. Recently we identified antibodies binding to carbamylated proteins (anti-CarP) in a subgroup of RA patients. In ACPA negative RA patients anti-CarP antibodies associate with joint damage. The Aim of this study was to determine whether these anti-CarP antibodies are present in animal models of arthritis. <h3>Methods</h3> Collagen induced arthritis (CIA) was induced in DBA/1 (n = 29) and C57Bl/6 (n = 20) mice by immunisation with type II collagen in CFA. Arthritis severity was monitored using a clinical scoring system. Non-immunised animals (n = 9) served as negative controls. After disease onset serum was harvested and antibody levels were determined by ELISA. The specificity of our anti-CarP. ELISA was validated using dotblots. <h3>Results</h3> Whereas no anti-CarP antibodies could be detected in non-immunised DBA/1 mice, anti-CarP total Ig was present in 93% of the arthritic mice. Of those mice 39% had IgG1 and 79% had IgG2a anti-CarP antibodies. Antibodies to citrullinated proteins could not be detected. The levels of mouse collagen-specific IgG2a correlated with the clinical score. However, the levels of the different anti-CarP isotypes did not. Around 60% of the immunised C56Bl/6 mice developed arthritis. Anti-CarP IgG2c could be detected in 55% of those mice and could not be detected in the mice that did not get CIA. Anti-CarP IgG1 was detected in 28% of the arthritic mice. Interestingly, mouse collagen specific IgG2c antibodies were detected in 100% of the immunised C57Bl/6 mice. Dotblot analysis, using carbamylated and non-modified proteins confirmed the ELISA results regarding the specificity of the antibodies for homocitrulline containing proteins. <h3>Conclusions</h3> Mice with CIA have antibodies to carbamylated proteins and their presence associated with disease development. All immunised mice have anti-mouse CII antibodies, indicating that the presence of anti-CarP antibodies could be a disease specific marker for arthritis in mice. Further studies will be required to determine the role of anti-CarP in the pathogenesis of arthritis.
Radioimmunoassay of Human Ligandin
Authors: Morris Sherman, Nathan M. Bass, John A.H. Campbell, Ralph E. Kirsch
Journal: Hepatology (1983)

A sensitive and specific radioimmunoassay for human ligandin has been developed and used to study ligandin release into the serum in acute and chronic hepatitis. Serum ligandin concentrations were elevated in 67 of 68 cases of acute viral hepatitis. Ligandin levels frequently returned to normal within the first 2 weeks of illness. The rapid disappearance of ligandin preceded the return to normal of serum SGOT. In chronic active hepatitis, serum ligandin levels correlated significantly (p &amp;lt; 0.01) with histologic severity of disease. This correlation was not seen with SGOT. Serum ligandin may be useful in monitoring progress and the need for therapy in chronic active hepatitis.
Novel molecular defects of the ?-aminolevulinate dehydratase gene in a patient with inherited acute hepatic porphyria
Authors: Reiko Akagi, Ryo Shimizu, Kazumichi Furuyama, Manfred O. Doss, Shigeru Sassa
Journal: Hepatology (2000)

Cloning and expression of the defective gene for delta-aminolevulinate dehydratase (ALAD) from the second of 2 German patients with ALAD deficiency porphyria (ADP), who had been originally reported by Doss et al. in 1979, were performed. Cloning of cDNAs for the defective ALAD were performed using Epstein-Barr virus (EBV)-transformed lymphoblastoid cells of the proband, and nucleotide sequences of cloned cDNA were determined. Two separate mutations of ALAD cDNA were identified in each ALAD allele. One was G457A, termed "H1," resulting in V153M substitution, while the other was a deletion of 2 sequential bases at T(818) and C(819), termed "H2," resulting in a frame shift with a premature stop codon at the amino acid position of 294. Using allele-specific oligonucleotide hybridization, the mother of the proband was shown to have an H1 defect, while using genomic DNA analysis, the father was shown to have an H2 defect. Expression of H1 cDNA in Chinese hamster ovary cells produced an ALAD protein with only a partial activity (10.65% +/- 1.80% of the normal), while H2 cDNA encoded no significant protein. These data thus demonstrate that the proband was associated with 2 novel molecular defects of the ALAD gene, 1 in each allele, and account for the extremely low ALAD activity in his erythrocytes ( approximately 1% of normal).
Soluble CD23 (sCD23) serum levels and lymphocyte subpopulations in peripheral blood in rhinitis and extrinsic and intrinsic asthma
Authors: I. Sánchez‐Guerrero, M. D. Albaladejo, A. M. García‐Alonso, M. Muro, J. Hernández, M. R. Alvarez
Journal: Allergy (1994)

To determine serum levels of IgE and sCD23 and lymphocyte subpopulations, we studied 37 control subjects and 84 patients (27 with allergic rhinitis, 27 with extrinsic asthma, and 30 with intrinsic asthma). A rise in surface CD23 on B and monocyte cells and sCD23 serum levels was exhibited by patients with rhinitis and extrinsic asthma. Unexpectedly, in intrinsic asthmatic patients, high CD23 expression on monocytes and high sCD23 levels were seen that did not result in IgE production. It appears that CD23, in its soluble form, could be a good disease marker, especially in asthma. Atopic patients yielded a significantly lower proportion of CD4+ T cells than intrinsic asthmatic patients and normal persons. Otherwise, CD4+CD29+CD45RA- and CD4+CD29-CD45RA T-cell subsets were significantly decreased in all patient groups.
Stab Wounds Associated With Terrorist Activities in Israel
Authors: J. Hanoch, E. Feigin, A. Pikarsky, C. Kugel, A. Rivkind
Journal: JAMA (1996)

To describe injuries resulting from terrorist-associated knife stabbings.Retrospective case series.Israel (population 5.5 million).Israeli victims (N=154) of knife stabbings on nationalistic basis (the intifada) between July 1987 and April 1994.A total of 125 men and 29 women sustained stab wounds associated with terrorist activities. The median age was 28 years (range, 12-92 years), and 99 victims were aged 18 to 35 years. Seventy percent (108 patients) of the stabbing events occurred between 7 AM and 11 AM. The 154 victims sustained a total of 327 stab wounds, the median number of injuries was 2 per person (range, 1-28), and 68 individuals (44%) sustained more than 1 stab wound. The chest was the most commonly involved site (146 wounds), with the right posterior chest stabbed in 71 patients. The knife penetrated the heart in 20 patients and penetrated the peritoneal cavity in 29 patients. Overall, 29 patients (19%) had superficial injuries, 86 (56%) had internal organ injuries that mandated operative interventions, and 39 died (overall mortality, 25.3%).Unlike other civilian stabbings, wounds resulting from terrorist-associated stabbings represent severe and highly lethal injuries.
Re: Umberto Capitanio, Shahrokh F. Shariat, Hendrik Isbarn, et al. Comparison of Oncologic Outcomes for Open and Laparoscopic Nephroureterectomy: A Multi-Institutional Analysis of 1249 Cases. Eur Urol 2009;56:1–9
Authors: Joan Palou, Óscar Rodríguez, Noel Clarke
Journal: European Urology (2009)
Excretion of verapamil in human milk
Authors: M de Swiet
Journal: BMJ (1984)

At the neuromuscular junction, the acetylcholine receptor (AChR) is specifically clustered in the postsynaptic membrane via interactions with rapsyn and other scaffolding proteins. However, it remains unclear where these proteins bind on the AChR and how the interactions are regulated. Here, we define a phosphorylation-dependent binding site on the receptor that mediates agrin-induced clustering. Using chimeric proteins in which CD4 is fused to the large intracellular loop of each of the AChR subunits we found that agrin induced clustering of only chimeras containing the β subunit loop. By making deletions in the β loop we defined a 20 amino-acid sequence that is sufficient for clustering. The sequence contains a conserved tyrosine (Y390) whose phosphorylation is induced by agrin and whose mutation abolished clustering of β loop chimeras and their ability to inhibit agrin-induced clustering of the endogenous AChR. Phosphorylation of the AChR β subunit is correlated with increased rapsyn/AChR binding, suggesting that the effect of βY390 phosphorylation on clustering is mediated by rapsyn. Indeed, we found that rapsyn associated with CD4-β loop chimeras in a phosphorylation-dependent manner, and that agrin increased the ratio of rapsyn binding to wild type AChR but not to AChR-β<sup>3F/3F</sup>, which lacks β loop tyrosine phosphorylation sites. Together, these findings suggest that agrin-induced phosphorylation of the β subunit motif increases the stoichiometry of rapsyn binding to the AChR, thereby helping to stably cluster the receptor and anchor it at high density in the postsynaptic membrane.
European agency approves use of fluoxetine for children and teens
Authors: Lynn Eaton
Journal: BMJ (2006)

The European Medicines Agency has approved the use of fluoxetine (Prozac) for children aged 8 years or more and teenagers who have moderate to severe depression—but only where psychological therapies alone have failed.

The decision is in line with existing guidelines for England and Wales. Initially France had rejected the use of the drug in children and adolescents on the basis of unresolved concerns …
Urine PGE-M: A Metabolite of Prostaglandin E2 as a Potential Biomarker of Advanced Colorectal Neoplasia
Authors: J. Chad Johnson, Carl R. Schmidt, Martha J. Shrubsole, D. Dean Billheimer, Prashant R. Joshi, Jason D. Morrow, Martin J. Heslin, M. Kay Washington, Reid M. Ness, Wei Zheng, David A. Schwartz, Robert J. Coffey, R. Daniel Beauchamp, Nipun B. Merchant
Journal: Clinical Gastroenterology and Hepatology (2006)