tbuckley/cabot-search huggingface dataset:
Normal Coronary Flow Reserve After Arterial Switch Operation for Transposition of the Great Arteries
Authors: Gylfi Oskarsson, Erkki Pesonen, Peter Munkhammar, Staffan Sandström, Peeter Jögi
Journal: Circulation (2002)

Recent studies performed with positron emission tomography have suggested that coronary flow reserve (CFR) is moderately to severely reduced after the arterial switch operation (ASO). These findings are of great concern but have not been confirmed by other methods.Eleven symptom-free children were studied between 4 and 11 (median 6.0) years after the ASO. Flow velocity in the left anterior descending (LAD) and right coronary arteries (RCA) was measured with a 0.014-inch Doppler FloWire (Cardiometrics) before and after intracoronary injection of adenosine (0.5 microg/kg) and nitroglycerin (5 microg/kg). CFR was defined as the ratio of hyperemic to basal average peak velocity (APV). The median (range) CFR in the LAD was 3.7 (3.0 to 4.8) and 3.4 (2.9 to 4.8) in the RCA. The increase in APV after intracoronary injection of nitroglycerin was 300% (240% to 420%) in the LAD and 260% (190% to 460%) in the RCA. APV at rest was 15.0 (14.0 to 21.0) cm/s in the LAD and 16.0 (9.6 to 30.0) cm/s in the RCA. A linear relation was found between right ventricular systolic pressure and resting APV in the RCA (r=0.77, P=0.0056), and between resting APV and CFR (r=-0.61, P<0.05) in the RCA.The CFR and coronary vasoreactivity to nitroglycerin in children treated for transposition of the great arteries with the ASO was within normal limits. Increased right ventricular pressure and myocardial hypertrophy can cause increased resting coronary flow velocity in the RCA and affect CFR negatively.
567 RELATIONSHIP BETWEEN HBV CCCDNA AND HBsAg LEVELS IS ASSOCIATED WITH HBeAg STATUSES OF CHRONIC HEPATITIS B PATIENTS
Authors: L. Lu, D.-W. Ye, Y.-D. Wang, A.Y.K. Kwok, A. Wong, Y.-H. Yueng, H.-Y. Zhang, S. Bowden, R. Batrla-Utermann, S. Locarnini, G.K.K. Lau
Journal: Journal of Hepatology (2009)
Abstract 2557: Genetic variants in microRNA genes and breast cancer risk.
Authors: Alicia C. Beeghly-Fadiel, Hyuna Sung, Ben Zhang, Ji-Yeob Choi, Ryan J. Delahanty, Jirong Long, Yu-Tang Gao, Wei Lu, Qiuyin Cai, Xiao Ou Shu, Daehee King, Wei Zheng
Journal: Cancer Research (2013)

Abstract microRNA (miRNA) are small noncoding molecules that function as regulators of the genome. Genetic variants in miRNA binding sites and miRNA genes have begun to be evaluated in relation to disease risk; however, no studies have yet comprehensively evaluated miRNA variants in relation to breast cancer risk. Using a two stage study design, and genome-wide association study (GWAS) data, we evaluated genetic variants within 1,425 miRNA genes (±5kb). In Stage 1, a total of 2,213 common genetic variants were evaluated among 2,876 breast cancer cases and 2,285 controls using data from the Shanghai Breast Cancer Genetics Study. Nominally significant associations (P value ≤0.05) were found for 108 variants in 96 genetic loci (r²≥0.6). In Stage 2, 94 variants in 84 loci were evaluated among 2,225 cases and 2,052 controls from the Seoul Breast Cancer Study; nine variants in eight loci had nominally significant associations. In analyses of the two study stages combined, 14 loci had highly significant associations (P value ≤0.01) and 19 additional loci had significant associations (P value ≤0.05) with breast cancer risk, all with consistent directions of association between the two study stages. These 36 variants in 33 loci have been mapped to 16 miRNA genes, many in the promoter regions. Based on our findings, genetic variants in miRNA genes are likely to contribute to breast cancer susceptibility. Citation Format: Alicia C. Beeghly-Fadiel, Hyuna Sung, Ben Zhang, Ji-Yeob Choi, Ryan J. Delahanty, Jirong Long, Yu-Tang Gao, Wei Lu, Qiuyin Cai, Xiao Ou Shu, Daehee King, Wei Zheng. Genetic variants in microRNA genes and breast cancer risk. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2557. doi:10.1158/1538-7445.AM2013-2557
Abstract 154: Genome-wide profiling of histone and DNA methylation in prostate cells during EMT and malignant transformation
Authors: Xi-Song Ke, Yi Qu, Wen-Cheng Li, Cheng Yang, Varda Rotter, Anne Margrete Oyan, Karl-Henning Kalland
Journal: Cancer Research (2010)

Abstract The loss of epithelial characteristics and the acquisition of a migratory phenotype, referred to as epithelial to mesenchymal transition (EMT), is a crucial event in tumor metastasis. Epigenetic modifications have been shown to be very critical in gene regulation during carcinogenesis, yet the role in EMT remains to be clarified. We report here a genome-wide analysis of histone methylation (H3K4me3 and H3K27me3), DNA methylation (DNAMe) and gene expression profiles in epithelial cells (EP156T) and their progeny mesenchymal cells (EPT1) and transformed cells (EPT2) in a cell culture model of stepwise prostate carcinogenesis. We found that H3K4me3 and H3K27me3 are very clear marks of active or repressed genes, while DNA methylation is only slightly associated with gene repression in all three cell lines. However, DNA methylation is a strong silencing mark when H3K4me3/DNAMe bivalently marked genes were excluded. Analysis of the transcription activities of genes with bivalent marks showed that H3K4me3/K27me3 is a repressive mark while H3K4me3/DNAMe is an active mark of gene expression. In individual genes, the transcription activities of genes with bivalent marks most likely correspond to the stronger mark. Furthermore, quantitative changes of H3K4me3 or H3K27me3 during EMT were correlated positively and negatively to activated and repressed transcription, respectively. Finally, a set of critical genes during EMT, including epithelial cell junction genes and the EMT inducers, FGFRs, were identified to show consistent changes concerning epigenetic modification and gene expression. All these findings provide the first blueprint of genome-wide epigenetic modification during EMT in prostate cells. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 154.
Inhibition of Adaptive Immunity by IL9 Can Be Disrupted to Achieve Rapid T-cell Sensitization and Rejection of Progressive Tumor Challenges
Authors: Dominique B. Hoelzinger, Ana Lucia Dominguez, Peter A. Cohen, Sandra J. Gendler
Journal: Cancer Research (2014)

The tolerogenic cytokine IL9 promotes T regulatory cell function and allergic airway inflammation, but it has not been extensively studied in cancer. In this report, we used IL9-deficient mice to investigate the effects of IL9 in multiple models of breast and colon cancer development. Eliminating endogenous IL9 enabled sensitization of host T cells to tumors, leading to their early rejection without the requirement of vaccines or immunomodulatory therapies. Notably, IL9-deficient mice acquired immunologic memory, which actively protected from residual disease and tumor rechallenge, an effect linked to activation of CD8(+) T cells. Depletion of either CD8(+) or CD4(+) T cells abolished the benefits of IL9 loss to tumor control. Adoptive transfer experiments showed that T cells from tumor-rejecting IL9-deficient mice retained their effector competency in wild-type animals. Moreover, neutralizing IL9 antibody phenocopied the effects of IL9 gene deletion by slowing tumor progression in wild-type animals. Our results show the ability of IL9 to function as an inhibitor of adaptive immunity that prevents the formation of immunologic memory to a growing tumor, highlighting the potential for IL9 neutralization as a unique tool for cancer immunotherapy.
Evidence That Low Titer IgE Antibodies to Milk and Wheat in Adults and Children with Eosinophilic Esophagitis May Be Directed Against a Minor Component of the Extract
Authors: Anubha Tripathi, Lisa J. Workman, Alicia Clark, Princess U. Ogbogu, Barrett Barnes, Scott P. Commins, Thomas Platts-Mills, Robert G. Hamilton, Elizabeth Erwin
Journal: Journal of Allergy and Clinical Immunology (2013)
Jaundice during Arsenotherapy
Authors: B. Green
Journal: BMJ (1945)

failure may also have aggravated the general condition and increased the size of the liver from acute passive congestion.No doubt the var-ious effusions and petechial haemorrhages were direct consequences of hepatic failure.In view of the extensive necrosis it is perhaps surprising that jaundice was completely absent.Either the liver destruc- tion was too rapid or this was really an example of extreme fatty degeneration of the organ following an acute infection -bronchopneumonia in this instance, as was stated in the his- tory.The latter explanation, however, was not supported by the histological findings, but certainly the possibility of a ful- minating virus hepatitis cannot be completely excluded.Lastly. of drugs sulohathiazole alone was given, to a total of 8 g. two weeks before death.Fatal cases of hepatitis are known to have followed sulphonamide therapy, and symptoms have niot always declared themselves until after the final with- drawal of the drug.Of all possible causes, this does seem the most feasible; but, unfortunately, the available evidence is inconclusive.
A single nucleotide polymorphism of Toll-like receptor 4 identifies the risk of developing graft failure after liver transplantation
Authors: Navdeep Dhillon, Liron Walsh, Bernd Krüger, Stephen C. Ward, James H. Godbold, Mohamed Radwan, Thomas Schiano, Barbara T. Murphy, Bernd Schröppel
Journal: Journal of Hepatology (2010)
Treatment of Primary Dysmenorrhea
Authors: Cetin K. Aydar
Journal: JAMA (1965)

PRIMARY (essential) dysmenorrhea has been described as pelvic pain with other accompanying disturbances, which occur just before or during menstruation without demonstrable pelvic or systemic disorder. Although primary dysmenorrhea is only a symptom, rather than a disease, it is one of the most common gynecologic complaints in women during the reproductive years. The pelvic pain is of a sharp, cramping, intermittent character, referred to the midline and the lower abdomen. At times it extends to the vagina, lower back, and thighs. Accompanying symptoms of primary dysmenorrhea may consist of nausea, vomiting, headache, backache, nervousness, irritability, joint pains, etc. The etiology of primary dysmenorrhea is not known; discussions of the many different theories are not within the scope of this study. However, it is most likely due to tetanic uterine contractions during the latter part of the luteal phase, as shown by Wilson and Kurzrok.<sup>1</sup>Primary dysmenorrhea only occurs in
Femoral head osteonecrosis in primary hypertrophic osteoarthropathy.
Authors: I Jajic
Journal: Annals of the Rheumatic Diseases (1993)

<b>Background:</b> Little is known about the effect of fibromyalgia on absence due to sickness in working populations. <b>Objective:</b> To examine the risk of absence due to sickness among employees with fibromyalgia. <b>Methods:</b> A prospective cohort study with 1-year follow-up of recorded and certified absence due to sickness after a survey of chronic diseases among 34 100 Finnish public sector employees (27 360 women and 6740 men) aged 17–65 years at baseline in 2000–2. <b>Results:</b> 20 224 days of absence due to sickness for the 644 employees with fibromyalgia and 454 816 days for others were documented. Of those with fibromyalgia, 67% had co-occurring chronic conditions such as osteoarthritis, rheumatoid arthritis, depression or other psychiatric disorders. Compared with employees with none of these chronic conditions, the hazard ratio (HR) adjusted for age, sex and occupational status was 1.85-fold (95% confidence interval (CI) 1.53 to 2.18) for people with fibromyalgia alone and 2.63-fold (95% CI 2.34 to 2.96) for employees with fibromyalgia with coexisting conditions. The excess rate of absence due to sickness was 61 episodes/100 person-years among people with fibromyalgia alone. Among employees with musculoskeletal and psychiatric disorders, secondary fibromyalgia was associated with a 1.4–1.5-fold increase in risk of absence. <b>Conclusion:</b> Fibromyalgia is associated with a substantially increased risk of medically certified absence due to sickness that is not accounted for by coexisting osteoarthritis, rheumatoid arthritis or psychiatric disorders.
The health impacts of exposure to indoor air pollution from solid fuels in developing countries: knowledge, gaps, and data needs.
Authors: Majid Ezzati, Daniel M Kammen
Journal: Environmental Health Perspectives (2002)

Globally, almost 3 billion people rely on biomass (wood, charcoal, crop residues, and dung) and coal as their primary source of domestic energy. Exposure to indoor air pollution (IAP) from the combustion of solid fuels is an important cause of morbidity and mortality in developing countries. In this paper, we review the current knowledge on the relationship between IAP exposure and disease and on interventions for reducing exposure and disease. We take an environmental health perspective and consider the details of both exposure and health effects that are needed for successful intervention strategies. We also identify knowledge gaps and detailed research questions that are essential in successful design and dissemination of preventive measures and policies. In addition to specific research recommendations, we conclude that given the interaction of housing, household energy, and day-to-day household activities in determining exposure to indoor smoke, research and development of effective interventions can benefit tremendously from integration of methods and analysis tools from a range of disciplines in the physical, social, and health sciences.
Induction of Prostaglandin E2 Pathway Promotes Gastric Hamartoma Development with Suppression of Bone Morphogenetic Protein Signaling
Authors: Hiroko Oshima, Hiraku Itadani, Hidehito Kotani, Makoto Mark Taketo, Masanobu Oshima
Journal: Cancer Research (2009)

Abstract Mutations in bone morphogenetic protein (BMP) receptor 1A (BMPR1A) are responsible for a subset of cases of juvenile polyposis (JP) syndrome that develops hamartomatous tumors in the gastrointestinal tract. Mouse genetic studies have shown that suppression of BMP signaling in the intestines causes JP-type hamartoma development. Here, we generated K19-Nog transgenic mice expressing noggin, a BMP antagonist, in gastric epithelium. However, inhibition of BMP signaling did not cause gastric phenotypes. We thus crossed K19-Nog with K19-C2mE mice that expressed Ptgs2 and Ptges in the stomach to generate compound transgenic mice. Expression of Ptgs2 and Ptges results in prostaglandin E2 (PGE2) biosynthesis, and both enzymes are induced in most human gastrointestinal tumors. Importantly, K19-Nog/C2mE compound mice developed gastric hamartomas that were morphologically similar to those found in JP with mucin-containing dilated cysts and inflammatory infiltration. Notably, treatment of K19-Nog/C2mE mice with a cyclooxygenase-2 inhibitor, celecoxib, significantly reduced tumor size with suppression of angiogenesis, suggesting that induction of the PGE2 pathway together with inhibition of BMP signaling is required for gastric hamartoma development. Moreover, microarray analyses revealed that canonical Wnt signaling target genes were not induced in K19-Nog/C2mE hamartomas, indicating that BMP inhibition and PGE2 induction lead to gastric hamartoma development independent of the Wnt/β-catenin pathway. These results, taken together, suggest that the PGE2 pathway is an effective preventive target against BMP-suppressed gastric hamartomas, as well as for Wnt/β-catenin–activated adenocarcinomas. [Cancer Res 2009;69(7):2729–33]
Increasing concentrations of prothrombin complex concentrate induce disseminated intravascular coagulation in a pig model of coagulopathy with blunt liver injury
Authors: Oliver Grottke, Till Braunschweig, Henri M. H. Spronk, Stephanie Esch, Annette D. Rieg, Rene van Oerle, Hugo ten Cate, Christina Fitzner, Rene Tolba, Rolf Rossaint
Journal: Blood (2011)
The Cost of Doing Business
Authors: Bonnie Salomon
Journal: Annals of Internal Medicine (2000)

Ad Libitum4 July 2000The Cost of Doing BusinessBonnie Salomon, MDBonnie Salomon, MDDeerfield, IL 60015Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-133-1-200007040-00006 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail What's his insurance?The psychiatrist on the cell phone demands.Don't know, the hassled ER doc answers.Oh, she knows.She knows no form letter, shined shoe companyWould ever look at thisHomeless, hobbling schizophrenic, eyes wild,Head on fire with delusions.The three Sports Illustrateds ... Author, Article, and Disclosure InformationAffiliations: Deerfield, IL 60015Corresponding Author: Bonnie Salomon, MD, 53 Crestview Drive, Deerfield, IL 60015. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 4 July 2000Volume 133, Issue 1Page: 34KeywordsAddictsEmergency departmentHearingHeartInterleukinsSports ePublished: 15 August 2000 Issue Published: 4 July 2000 Copyright & PermissionsCopyright © 2000 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Pleural effusion of a second neoplasm in a patient with B‐CLL: Two immunological compartments
Authors: D. Atanackovic, S. Brettner, S. Hegewisch‐Becker
Journal: American Journal of Hematology (2003)

Abstract We report the case of a patient with a chronic lymphocytic leukemia (CLL) who later developed a metastasized large‐cell neuroendocrine carcinoma of the lung that was complicated by a malignant pleural effusion. In contrast to the peripheral blood where the malignant B‐CLL cells represented &gt;99% of all lymphocytes, lymphocytes infiltrating the malignant effusion were mainly T cells. Nearly all of these T cells were CD4 + . This stood in sharp contrast to the peripheral blood where the CD4 + /CD8 + ratio remained balanced. A detailed analysis of the CD4 + T cells within the malignant effusion revealed that these cells uniformly expressed a CCR7 + CD62L + “non‐effector” phenotype. When the monoclonal B cells within the malignant effusion were analyzed, we found that these cells, in contrast to the B‐CLL cells in the peripheral blood, were negative for CD23 and expressed much higher levels of the adhesion molecules L‐selectin (CD62L) and CD11a. A deficient expression of these adhesion molecules might have led to a “trapping” of the majority of B‐CLL cells in the peripheral blood. This phenomenon might have contributed to the development of two highly different immunological compartments in this patient with CLL and pleural effusion of a solid tumor. Am. J. Hematol. 73:184–189, 2003. © 2003 Wiley‐Liss, Inc.
Pulmonary Vascular Congestion in Acute Myocardial Infarction: Hemodynamic and Radiologic Correlations
Authors: THOMAS J. MCHUGH
Journal: Annals of Internal Medicine (1972)

Simultaneous chest X ray, pulmonary capillary wedge pressure, and pulmonary artery oxygen saturation measurements were obtained in 30 patients with acute myocardial infarction. The severity of radiologic abnormalities generally correlated well with pulmonary capillary wedge pressure. Serious misinterpretation of left ventricular failure by X-ray criteria, although uncommon, occurred in the presence of "preclinical" failure, hypoxemia, or posttherapeutic phase-lags. Individual radiologic criteria of left ventricular failure appeared in a predictable sequence. Redistribution of flow appeared early, followed by loss of the sharp marginal contour of the pulmonary vessels, development of perihilar haze, and, finally, periacinar rosette formation. Thus, radiologic criteria of the degree of pulmonary vascular congestion, when related to pulmonary capillary wedge measurements, provide a basis for consistent and rational therapy of left ventricular failure secondary to acute myocardial infarction.
Exercise testing soon after myocardial infarction.
Authors: W Markiewicz, N Houston, R F DeBusk
Journal: Circulation (1977)

Forty-six men under age 70, without clinical congestive heart failure or unstable angina pectoris, performed treadmill tests 3, 5, 7, 9 and 11 weeks after myocardial infarction. Patients were more frequently able to perform moderate exertion (2 mph, 14% grade) at 7 and 11 weeks than at 3 weeks following infarction. Ischemic ST-segment depression, usually unaccompained by angina pectoris, occurred in 45% of patients and was associated with a significantly increased incidence of subsequent coronary events. The presence of exercise-induced ventricular ectopic activity provided little independent prognostic information. No serious complications occurred in 210 tests. Exercise testing soon after myocardial infarction provides objective information concerning the capacity to resume physical activity, including return to work. Two tests, at 3-5 weeks and at 7-11 weeks, appear to provide most of the information contined in five tests performed during this time.
Outcomes of the Botswana national HIV/AIDS treatment programme from 2002 to 2010: a longitudinal analysis
Authors: Mansour Farahani, Anusha Vable, Refeletswe Lebelonyane, Khumo Seipone, Marina Anderson, Ava Avalos, Tim Chadborn, Hailu Tilahun, Danae Roumis, Themba Moeti, Godfrey Musuka, Lesego Busang, Tendani Gaolathe, Kolaatamo C S Malefho, Richard Marlink
Journal: The Lancet Global Health (2013)
Does the substitution of cisplatin in a standard four drug regimen improve survival in small cell carcinoma of the lung? A comparison of two chemotherapy regimens.
Authors: A P Smith, G Anderson, G Chappell, D R Bowen
Journal: Thorax (1991)

Ninety five patients with small cell carcinoma of the lung were randomly assigned to one of two chemotherapy regimens (VACE or CVACE), each consisting of six cycles at three week intervals. The VACE regimen consisted of six cycles of vincristine 1.2 mg/m2, doxorubicin 40 mg/m2, and cyclophosphamide 700 mg/m2 on day 1 plus etoposide 110 mg/m2 daily for three days. The CVACE regimen was identical to the VACE regimen for cycles 3 and 4; cycles 1, 2, 4, and 6 consisted of etoposide 110 mg/m2 for three days plus cisplatin 100 mg/m2 with mannitol diuresis on the second day. Forty eight patients received VACE and 47 CVACE. Side effects resulted in withdrawal of four patients receiving VACE and six receiving CVACE. Three deaths were attributed to VACE and one to CVACE. Median survival did not differ between the two treatments overall, though there was a small increase in median survival in partial responders receiving CVACE. It is concluded that replacing four of the six cycles of VACE (vincristine, doxorubicin, cyclophosphamide, and etoposide) with etoposide and cisplatin conferred no overall advantage.
Diffuse intimal thickening of coronary arteries in patients with coronary spastic angina
Authors: Yuji Miyao, Kiyotaka Kugiyama, Hiroaki Kawano, Takeshi Motoyama, Hisao Ogawa, Michihiro Yoshimura, Tomohiro Sakamoto, Hirofumi Yasue
Journal: Journal of the American College of Cardiology (2000)