tbuckley/cabot-search huggingface dataset:
Abstract 18608: Ventricular Myocarditis Coincides With Atrial Myocarditis in Patients
Authors: Paul Krijnen, Mark Begieneman, Liza Rijvers, Bela Kubat, Walter Paulus, Lawrence Roozendaal, Albert Van Rossum, Hans Niessen
Journal: Circulation (2014)

Introduction: Studies on the role of inflammatory cells in myocarditis focus mainly on the ventricles. However, little is known about inflammatory cell infiltration of the atria in patients with diagnosed myocarditis. A common complication in myocarditis is atrial fibrillation (AF), which is associated with inflammation of the atria. Therefore, we quantified inflammatory cells both in the ventricles and the atria of patients with lymphocytic myocarditis and catecholamine myocarditis. Methods: From post-mortem obtained hearts of lymphocytic myocarditis patients (n=5), catecholamine myocarditis patients (n=5) and control patients (n=5), tissue slides of the left and right ventricles and left and right atria were stained with antibodies identifying neutrophils, lymphocytes and macrophages. These cells were subsequently quantified in atrial and ventricular myocardium and in the atrial adipose tissue. Results: The number of macrophages were significantly increased in the myocardium of the atria and the ventric...
17-allylamino-17-demethoxygeldanamycin disrupts SYT-SSX-β-catenin interaction in synovial sarcoma
Authors: Jefferson Terry, Torsten O. Nielsen
Journal: Clinical Cancer Research (2006)

B32   The Hsp90 chaperone inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG) is effective against synovial sarcoma (SS)  in vitro ; this study tested if its mechanism of action involves destabilization of the disease-defining fusion oncoprotein SYT-SSX and its interaction with β-catenin. SS has a poor prognosis overall as it typically exhibits little response to conventional chemotherapy; drugs that specifically target the aberrations that underlie SS pathogenesis are likely to be more effective. Although its role in pathogenesis is incompletely understood, SYT-SSX is an attractive therapeutic target because it is ubiquitous in SS, its expression in non-malignant cell lines has been shown to be oncogenic, and β-catenin-SYT-SSX interaction in the nucleus increases nuclear β-catenin levels and enhances β-catenin-mediated transcription, demonstrating a link between SYT-SSX and the cell cycle machinery. Accordingly, relatively high levels of nuclear-localized β-catenin can be demonstrated in a significant proportion of SS cases; this likely plays a role in SS pathogenesis and methods to disrupt the SYT-SSX-β-catenin interaction may lead to the development of effective clinical therapies. 17-AAG destabilizes fusion oncoproteins in other cancers, suggesting it may also destabilize SYT-SSX, and by extension result in decreased nuclear β-catenin and β-catenin-mediated signaling. To examine this possibility, the effects of 17-AAG on the subcellular localization of β-catenin, total cellular levels of SYT-SSX and β-catenin and levels of β-catenin-mediated transcription from both exogenous and endogenous sources were examined in two SS cell line models, SYO-1 and Fuji. This study found that 17-AAG disrupts the interaction between β-catenin and SYT-SSX, promotes redistribution of β-catenin from the nucleus to the cell membrane and decreases levels of β-catenin-mediated transcription in both cell line models. These effects were not associated with degradation of SYT-SSX itself, however, suggesting that 17-AAG inhibits formation of the β-catenin-SYT-SSX complex by destabilizing unidentified intermediary binding partner(s), or by affecting post-translational modification(s) of β-catenin or SYT-SSX required for interaction. This study demonstrates that the clinically-applicable drug 17-AAG disrupts a connection between the SS-defining fusion protein SYT-SSX and the cell cycle machinery and presents additional evidence for SYT-SSX and β-catenin as valid therapeutic targets in SS.
Immunotherapy with Hymenoptera venoms
Authors: J. Bousquet, U. R. Müller, S Dreborg, R. Jarisch, H.‐J. Malling, H. Mosbech, R. Urbanek, L. Youlten
Journal: Allergy (1987)

Immunotherapy with Hymenoptera venoms is widely used throughout the world and is accepted as an effective treatment for most patients with Hymenoptera venom allergy. There are, however, still some unresolved problems with this form of treatment. At present there is no definite test which makes it possible to identify patients at risk ‐ and thus candidates for immunotherapy ‐ unequivocally. On the basis of prospective studies on the natural history of Hymenoptera allergy, venom immunotherapy is indicated in adults with severe systemic anaphylaxis. It is usually not necessary in patients with large local reactions only. Children with mild systemic reactions, e.g. urticaria, will need immunotherapy only in case of repeated reactions and/or a high risk of re‐exposure. The selection of venoms for immunotherapy may lead to some confusion owing to common antigenic determinants shared by venoms of various Hymenoptera species. Many different regimens for immunotherapy have been proposed. At present, the three main are: rush, stepwise or clustered and classical. The maintenance dose of 100 μg usually protects from life‐threatening reactions. However, in some patients 200 μg are necessary for complete protection. The usual interval between maintenance injections is 4 to 6 weeks. In many patients a strong increase of venom specific serum IgG‐antibodies usually parallels clinical protection induced by venom immunotherapy, although many exceptions have been reported. Allergic side effects of venom immunotherapy are not rare, especially with honey bee venom and during the initial phase of dose increase. The question of the duration of venom immunotherapy is handled differently: although some authors recommend treatment for life, most suggest treating patients until skin tests and RAST become negative.
A memorable patient: He was going to die anyway
Authors: J. Goldin
Journal: BMJ (1999)

He was memorable and yet I cannot remember much about him. Mid-30s, perhaps, slim, unkempt with a somewhat haunted look about him, sitting up in his hospital bed wearing pyjamas, staring ahead. Whereas other patients on the ward had visitors, nurses busying themselves around their beds, this man seemed to have an invisible barrier around him, which was rarely crossed. He was the man who had drunk paraquat and was going to die in a few days.

He did not …
Risk of second primary <i>in situ</i> and invasive melanoma in a Dutch population‐based cohort: 1989–2008
Authors: R.J.T. van der Leest, L. Liu, J.W.W. Coebergh, H.A.M. Neumann, W.J. Mooi, T. Nijsten, E. de Vries
Journal: British Journal of Dermatology (2012)

Patients with melanoma are at increased risk of developing a subsequent melanoma.To estimate the risks of developing a second primary in situ or invasive cutaneous melanoma after a first melanoma, between 1989 and 2008.Patients were followed until diagnosis of a second melanoma, date of death or end of study. Cumulative risks, standardized incidence ratio (SIR, observed second melanomas divided by background age-, calendar- and sex-specific incidence rates of melanoma, as recorded in the Netherlands Cancer Registry) and absolute excess risk (AER, observed minus expected per 10 000 person-years) of second melanomas were calculated.In total, 10 765 patients with in situ melanoma and 46 700 with invasive melanoma were included. The cumulative risks of a second invasive melanoma after a first in situ or invasive melanoma at 20 years of follow-up were 6·2% and 5·0%, respectively. The relative risk of developing any melanoma (in situ or invasive) after any first melanoma (measured as SIR) varied from 12·4-fold [invasive after invasive melanoma; 95% confidence interval (CI) = 11·6-13·2] to 26·4-fold (in situ after in situ melanoma; 95% CI = 22·6-30·7) increase compared with the general population. SIRs and AERs remained elevated up to 20 years after the first melanoma.This study shows significantly increased long-term risks (both relative and absolute) of developing a second invasive melanoma after a first melanoma (invasive and in situ), and might serve as a basis for follow-up guidelines.
Appropriate electrophysiologic study and treatment of patients with the Wolff-Parkinson-White syndrome
Authors: Albert L. Waldo, Masood Akhtar, David G. Benditt, Pedro Brugada, A.John Camm, John J. Gallagher, Paul C. Gillette, George J. Klein, Samuel Levy, Melvin M. Scheinman, Hein J.J. Wellens, Douglas P. Zipes
Journal: Journal of the American College of Cardiology (1988)
Serotonin induces melanogenesis via serotonin receptor 2A
Authors: H.J. Lee, M.K. Park, S.Y. Kim, H.Y. Park Choo, A.Y. Lee, C.H. Lee
Journal: British Journal of Dermatology (2011)

Serotonin (5-hydroxytryptamine, 5-HT) levels are increased by light exposure but the role and mechanism of 5-HT in the pigmentation of skin cells are unclear.To clarify the effect of 5-HT on melanogenesis and to determine the 5-HT receptor subtype involved.B16F10, SK-MEL-2 and Melan-A cells were cultured in Dulbecco's modified Eagle's medium with low fetal bovine serum. The three cell lines were treated with various concentrations of 5-HT, and 5-HT receptor agonists and antagonists. The involvement of the 5-HT receptor 2A (5-HTR2A) was examined by gene silencing and use of 5-HTR2A antagonists.5-HT and the 5-HTR2A agonist, DOI, increased melanogenesis in the three cell lines. These increased events were suppressed by 5-HTR2A antagonists or gene silencing of the HTR2A gene.5-HTR2A is involved in melanogenesis. These findings highlight the role of 5-HT and suggest new ways of controlling melanogenesis.
Arteriolar Oxygen Saturation, Cerebral Blood Flow, and Retinal Vessel Diameters
Authors: Frank Jan de Jong, Meike W. Vernooij, M. Kamran Ikram, M. Arfan Ikram, Albert Hofman, Gabriel P. Krestin, Aad van der Lugt, Paulus T.V.M. de Jong, Monique M.B. Breteler
Journal: Ophthalmology (2007)
DYSPHAGIA AND MITRAL VALVE DEFORMITY
Authors: A GOOTNICK
Journal: Annals of Internal Medicine (1949)

Case Reports1 March 1949DYSPHAGIA AND MITRAL VALVE DEFORMITYABRAHAM GOOTNICK, M.D.ABRAHAM GOOTNICK, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-30-3-662 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptDifficulty in swallowing is an unusual complication of cardiovascular disease. It occurs, in approximate order of frequency, in cases of aortic aneurysm, pericarditis with effusion, congenital anomaly of the aortic arch and dilatation of the left auricle. Left auricular enlargement as a cause of dysphagia is particularly rare. Bloomfield, in surveying the literature back to 1927, found only two such cases (cases 1 and 4 of Rösler) with a possible additional report in an untranslated Czechoslovakian journal.1Two other cases not included in Bloomfield's paper were described by Nichols and Ostrum in 1932.2Subsequent to Bloomfield's report, Newton and Levine...Bibliography1. BLOOMFIELD AL: Dysphagia with disorders of the heart and great vessels, Am. Jr. Med. Sci., 1940, cc, 289-299. CrossrefGoogle Scholar2. NICHOLSOSTRUM CFHW: Unusual dilatation of the left auricle, Am. Heart Jr., 1932, viii, 205-216. CrossrefGoogle Scholar3. NEWTONLEVINE FCSA: Decompression of chest for dysphagia due to marked cardiac enlargement, Jr. Thorac. Surg., 1942, xii, 151-157. CrossrefGoogle Scholar4. TINNEYSCHMIDTSMITH WSHWHL: The result of pressure from a dilated left auricle, Proc. Staff Meet. Mayo Clin., 1943, xviii, 476-480. Google Scholar5. STRAUS GD: Dysphagia: Review of clinical, roentgen ray, and esophagoscopic aspects of 150 cases, Wisconsin Med. Jr., 1943, xlii, 293-296. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Memphis, Tennessee*Received for publication May 14, 1947.From the Cardiovascular Section, Medical Service, Kennedy Veterans Administration Hospital.Published with permission of the Medical Director, Veterans' Administration, who assumes no responsibility for the opinions expressed or the conclusions drawn by the author. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1949Volume 30, Issue 3Page: 662-668KeywordsAneurysmsCardiovascular diseasesCongenital disordersDysphagiaMedical servicesSwallowing ePublished: 1 December 2008 Issue Published: 1 March 1949 PDF downloadLoading ...
Cervical stem cells: Isolation, characterization, and potential role in human papillomavirus (HPV)-induced cervical carcinogenesis
Authors: Astrid C. Baege, Patricia Day, Jonathan Vogel, Richard Schlegel, Carl C. Baker
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

3985 

Cervical cancer is still the second most common cancer in women worldwide. High risk HPV persistence is a necessary state for the emergence of cervical cancer, but the crucial factors determining persistent HPV infection are still largely unknown. It has been proposed that viral persistence only occurs upon targeted infection of specific cervical cells, potentially with stem cell properties. As specific markers have yet to be identified, cervical stem cells remain poorly characterized. Using fluorescence activated cell sorting, we successfully isolated a distinct minor subpopulation of putative cervical stem cells with undetectable transferrin receptor and very high integrin α6 cell surface expression. These cells possess many phenotypic characteristics and functional properties expected for epithelial stem cells, such as small cell size with a high nuclear:cytoplasmatic ratio, marker expression of undifferentiated epithelial cells (K14+, K1-), quiescence (as determined by cell cycle analysis and Ki-67 expression) and increased colony formation efficiency in vitro. All other cervical epithelial cell types differed significantly in phenotype and biological behavior. Transit amplifying cells expressed a 2-fold higher telomerase activity than putative stem cells, which can most likely be explained by their transiently higher proliferation index. Most importantly, we demonstrate that virtually all of these putative stem cells have a 10-fold higher binding capacity for papillomavirus-like particles than any other cervical epithelial subpopulation, suggesting that HPVs might indeed preferentially bind and infect these cells in vivo. Interestingly, our data indicate that this increased binding capacity is not a consequence of a higher number of cell surface heparan sulfate binding sites. Our results represent an important step towards identification of cervical epithelial stem cells and provide the basis for further investigations to determine if persistent infection and progression to pre-malignant and malignant cervical lesions requires initial infection of these cells.
Chromosomes in Primary and Transplanted Leukemias of AKR Mice
Authors: Resa Wakonig, H. F. Stich
Journal: JNCI Journal of the National Cancer Institute (1960)

Chromosome analyses were performed on leukemias of strain AKR mice, mostly on spleen but also on thymus, lymph nodes, and lymphosareomas. Spontaneous primary leukemias in a comparable stage of development showed a varying proportion of cells with aneuploid chromosome numbers, with a usual range from 39 to 42, but also there were cells with 43 and 44 chromosomes in 4 animals. Most of the 17 mice with primary leukemias, and 10 with leukemias and tumors resulting from transplantations, had a modal chromosome number of 40 (diploid). In 5 animals with primary leukemias the mode was 41, and 1 had 2 modes, 42 and 43. More than 80 percent diploid cells were found in 7 mice with primary leukemias and in 6 with leukemias or tumors resulting from transplantations. The chromosome morphology of the diploid cells was generally normal, though in 2 animals with predominantly diploid leukemias, several cells (8 and 18%) had a small marker chromosome. The predominance of diploidy was maintained during continued transplantation. This demonstrates that neoplastic cells can have a diploid chromosome complement without detectable abnormalities.
Abstract P368: N-Terminal Pro Brain Natriuretic Peptide and Microsize Myocardial Infarctions in the REasons for Geographic And Racial Differences in Stroke (REGARDS) Study
Authors: Raegan W Durant, Yulia A Khodneva, Emily B Levitan, Todd M Brown, Stephen Glasser, George Howard, Monika M Safford
Journal: Circulation (2014)

Background: N-terminal pro brain natriuretic peptide (NT-proBNP) has been associated with myocardial infarctions (MI), but less is known about the relationship between NT-proBNP and very small non ST-elevation MIs now routinely detectable with modern troponin assays. Since these “microsize MIs” confer high long-term coronary heart disease (CHD) risks, we examined the association of NT-proBNP with incident acute CHD events, total MIs, and two MI subtypes: microsize and typical MIs. Methods: REGARDS is a national cohort of 30,237 US community-dwelling black and white adults aged ≥45 recruited from 2003 to 2007. Expert-adjudicated outcomes included incident typical MIs (definite/probable MI with peak troponin ≥0.5 μg/L), incident microsize MIs (definite/probable MI with peak troponin &lt;0.5 μg/L), and total incident acute CHD (nonfatal MIs or CHD deaths). Low-level troponin elevations with the peak at least twice the upper limit of normal which did not have a rising and/or falling pattern or which had a non-ischemic cause were not considered MIs. We assembled a case-cohort study comprised of 1) a stratified random sample of participants free of CHD at baseline and not on dialysis (n=849); and 2) all incident acute CHD cases through 12/31/2010. NT-proBNP was measured in case-cohort participants at baseline and was dichotomized on the sample’s median value (73.3 pg/mL). Adjusted weighted Cox proportional hazards regression models examined associations of NT-proBNP and CHD endpoints, controlling for sociodemographics and CHD risk factors. Results: Over a median of 5.9 years follow-up, 139 microsize MIs, 315 typical MIs, and 146 non-MI CHD deaths occurred. NT-proBNP was associated with all CHD outcomes examined (Table). Conclusions: Above-median NT-proBNP was independently and strongly associated with all CHD endpoints with a suggestion of greater risks of incident microsize MI. A better understanding of the pathophysiologic differences between typical and microsize MIs is needed.
Topley and Wilson's Principles of Bacteriology and Immunity.
Authors: Henry P. Treffers
Journal: Annals of Internal Medicine (1946)

Topley &amp; Wilson has been regarded highly as a textbook ever since the first edition. Its good reputation has increased with the second edition, and there is little doubt that the present greatly enlarged third edition will add to the already large number of students who have learned to depend on Topley &amp; Wilson as the reliable counselor in matters bacteriologic and immunologic. Despite the double handicap of Professor Topley's death in January 1944 and the war, with the limitation of accessibility to foreign sources as only one of its many hardships, the new edition has been brought up to date and expanded. Two new chapters, on chemotherapy and on the bacteriology of air, have been added; one on soil microbiology has been left out. Separate chapters have been formed for the Shigella, the Salmonella and the psittacosis-lymphogranuloma group. In other respects the structure and treatment remain unchanged, which is
586. Gene Transfer of IP10, IP10+CD154 or IP10+IL12 cDNA Induces an Anti-Leukemic Immunity in a Murine Model of Acute Leukemia
Authors: Aurore Saudemont, Bruno Quesnel
Journal: Molecular Therapy (2004)

We have reported that vaccination of mice with leukemic cells transduced with CD154 and IL12 led to a significant protection and generation of cytotoxicity T lymphocytes (CTL) against leukemia cells. But, we obtained 30% of protection in therapeutic protocol with persistence of residual disease. So, it is necessary to improve this immune response. It's why we decided to compare the efficacy of IP10, IP10+CD154, IP10+IL12 gene transfer mediated antileukemic immunity in our aggressive murine model of acute leukemia, and to investigate how T and NK cells were affected by gene transfer and presence of residual disease.
Bortezomib produces high hematological response rates with prolonged renal survival in monoclonal immunoglobulin deposition disease
Authors: Camille Cohen, Bruno Royer, Vincent Javaugue, Raphael Szalat, Khalil El Karoui, Alexis Caulier, Bertrand Knebelmann, Arnaud Jaccard, Sylvie Chevret, Guy Touchard, Jean-Paul Fermand, Bertrand Arnulf, Frank Bridoux
Journal: Kidney International (2015)
Abstract 15578: The Combination of an Ostium Secundlum Type Atrial Septal Defect with a Pulmonary Arterial Thromboembolism Caused an Enlarged Pulmonary Artery, Pulmonary Hypertension and Recurrent Paradoxical Cerebral Embolism due to Deep Vein Thrombosis
Authors: Nobusada Funabashi, Hiroyuki Takaoka, Koya Ozawa, Nobuhiro Tanabe, Koichiro Tatsumi, Yoshio Kobayashi
Journal: Circulation (2014)

A 65 year old female was referred to our hospital with dyspnea on effort. When she was 42 years old, she was diagnosed by transthoracic echocardiology (TTE) with an ostium secundlum type atrial septal defect (ASD) with a pre-existing right to left shunt through the ASD. When she was 60 years old, she was diagnosed with a brain abscess due to a paradoxical cerebral embolism and admitted to our brain surgery ward a total of three times. The diagnosis was confirmed and treatment with Clopidogrel sulfate was started. Six months ago, she felt dyspnea on effort and gradually worsened. She was referred to our department for further examination. Chest X ray revealed cardiac enlargement with a cardiothoracic ratio of 61%. Serum d dimer and brain natriuretic peptide were elevated to 3.3μg/ml and 492pg/mL, respectively. TTE showed an enlarged PA, right atria (RA) and right ventricle (RV) with a thickened RV wall. A bidirectional shunt through a large ASD could also be observed. PA systolic pressure was estimated, by the pressure gradient from tricuspid valve regurgitation, at 94mmHg. CT revealed an enlarged, calcified PA with a mural thrombus, enlarged and thickened RV wall and a right to left shunt through the ASD. The LV was compressed by the RV, suggesting RV pressure load. Because a mural thrombus was observed in the PA, CT acquisitions of the lower extremities were added 3 minutes after contrast injection. An enlarged popliteal vein with a deep venous thrombus (DVT) was observed. Tadalafil was prescribed for pulmonary hypertension to improve oxygen concentration. Heparin followed by warfarin was administered for the DVT and mural thrombus in the PA. At follow up, CT showed no change to the mural thrombus in the PA, therefore home oxygen therapy was started. From experience of this case, and in subjects with Eisenmenger ASD, if severe PA dilation and PA hypertension and paradoxical cerebral embolism are detected, one should also suspect PA thromboembolism due to DVT.