tbuckley/cabot-search huggingface dataset:
Etiology of Cor Pulmonale
Authors: David Shander
Journal: JAMA (1990)

<h3>To the Editor. —</h3> The review article entitled "Chronic Cor Pulmonale: Etiology and Management"<sup>1</sup>is thorough in its discussion but incomplete in its scope. Certainly the subject of chronic cor pulmonale should include a discussion of at least three other common causes of this process: chronic left ventricular failure, mitral valve stenosis, and chronic mountain sickness. Although the mechanism of chronic cor pulmonale in these clinical states varies significantly, the pathophysiology is similar to that described for some of the other processes mentioned in the article. While the authors may have intentionally omitted these clinical syndromes, I think that a thorough discussion of the problem of chronic cor pulmonale demands their inclusion.
Regional entrainment of atrial fibrillation studied by high-resolution mapping in open-chest dogs.
Authors: C Kirchhof, F Chorro, G J Scheffer, J Brugada, K Konings, Z Zetelaki, M Allessie
Journal: Circulation (1993)

BACKGROUND It recently has been demonstrated that during atrial fibrillation, a short and variable excitable gap exists, allowing regional control of atrial fibrillation by local stimulation. In the present study, we visualized the process of excitation during regional entrainment of atrial fibrillation by rapid pacing. METHODS AND RESULTS In six open-chest dogs, the excitation of the left atrial free wall was mapped using a spoon-shaped mapping electrode (248 points). Episodes of atrial fibrillation were induced by burst pacing (50 Hz, 2 seconds). During atrial fibrillation, the electrograms showed rapid irregular activity with a median cycle length of 98 +/- 16 ms (mean +/- SD, n = 6). Rapid pacing in the center of the mapping electrode at intervals slightly shorter or longer than the median atrial fibrillation interval resulted in regional capture of atrial fibrillation. The window of entrainment was 16 +/- 5 ms. Mapping of atrial fibrillation showed that the left atrium was activated by fibrillatory wavelets coming from different directions. During entrainment, a relatively large area with a diameter of about 4 cm was activated by uniform wave fronts propagating away from the site of stimulation. The area of entrainment was limited by intra-atrial conduction block and by collision with fibrillation waves. Regional control of atrial fibrillation was lost by pacing either too slowly or too rapidly. In the first case, retrograde invasion of the area of entrainment by fibrillatory waves resulted in depolarization of the pacing site prior to the stimulus. Pacing too rapidly caused acceleration of atrial fibrillation by induction of local intra-atrial reentry circuits with a revolution time shorter than the pacing interval. CONCLUSIONS During atrial fibrillation, an area with a diameter of about 4 cm can be entrained by local pacing. The resulting reduction in fibrillating tissue mass was not sufficient to terminate atrial fibrillation. Extension of the area of entrainment was limited by intra-atrial conduction block, whereas entrainment at a too high rate resulted in acceleration of atrial fibrillation by induction of local microreentry.
Abstract 2730: Novel animal models of pancreatic cancer induced by smoking and chronic pancreatitis.
Authors: Shiping Xu, Paul J. Grippo, Oxana M. Khayrutdinova, Samuel W. French, Stephen J. Pandol, Anna S. Gukovskaya, Mouad Edderkaoui
Journal: Cancer Research (2013)

Abstract Background and Aims: Smoking and pancreatitis are two major risk factors for pancreatic cancer. We developed novel mouse models of pancreatic cancer induced by smoking and chronic pancreatitis. We used two pancreatic cancer mouse models induced by overexpression of Kras with two different degrees of disease complexity. Methods: Wild type (WT), EL-Kras and Pdx1-Cre;LSL-Kras transgenic mice were subjected to a major cigarette smoke compound nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) at doses close to those accumulated with smoking (100mg/kg) or exposed to tobacco smoke (80mg/m3) in tobacco smoke chambers for five days a week during 6 weeks. Standard model of chronic pancreatitis induced by cerulein injections (50μg/kg) for 3 weeks was applied to WT and Pdx1-Cre;LSL-Kras mice. Mice were then sacrificed and pancreatic tissue analyzed. Apoptosis was assessed by TUNEL. Autophagy was assessed by measuring autophagic markers LC3-II and p62. Pancreatic lesions, proliferation, fibrosis and inflammation were analyzed by immunohistochemistry. Epithelial to mesenchymal transition (EMT) and expression of stem cell markers were analyzed by Western. Results: NNK and exposure to tobacco smoke significantly increased the number and stage of pancreatic neoplastic (PanIN) lesions in Kras transgenic mice. Smoking stimulated fibrosis and stellate cells activation but had no significant effect on inflammation. EMT markers (decrease in E-Cadherin and increase in vimentin protein levels) were stimulated by NNK and tobacco smoke exposure in both WT and transgenic mice. NNK decreased apoptosis and LC3-II level in Kras mice. In addition, smoking stimulated expression of stem cell markers sox2 and CD133. Cerulein stimulated fibrosis, stellate cells activation, inflammation, and slightly stimulated EMT in WT and transgenic mice. Combination of smoking and cerulein had additive effect on stimulation of PanIN lesion formation, fibrosis, EMT and stem cell markers induction. Conclusion: The results indicate that both tobacco smoke and chronic cerulein pancreatitis promote pancreatic cancer progression in both EL-Kras and Pdx1-Cre;LSL-Kras mice models. Smoking acts through enhancing fibrosis and EMT; whereas pancreatitis stimulates mainly inflammation and fibrosis. Smoking and pancreatitis have additive effect on fibrosis, EMT and acquiring of stem cell characteristics. Citation Format: Shiping Xu, Paul J. Grippo, Oxana M. Khayrutdinova, Samuel W. French, Stephen J. Pandol, Anna S. Gukovskaya, Mouad Edderkaoui. Novel animal models of pancreatic cancer induced by smoking and chronic pancreatitis. [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 2730. doi:10.1158/1538-7445.AM2013-2730
SEROLOGICAL EVIDENCE OF IMMUNITY WITH COEXISTING SENSITIZATION IN A TYPE OF HUMAN ALLERGY (HAY FEVER)
Authors: Robert A. Cooke, James H. Barnard, Selian Hebald, Arthur Stull
Journal: The Journal of Experimental Medicine (1935)

Using ragweed hay fever as the representative of a certain type of allergy we have made studies to determine if possible the mechanism of the protection afforded by specific injections thus far established only by clinical observation. 1. Blood transfusions and serum injections from clinically immune, treated patients stopped the clinical reaction in untreated patients, thus indicating a transferable immunity. 2. The amount of skin sensitizing antibody in the serum was found to be practically unchanged by specific injections. 3. Injection of allergen-antibody mixtures into normal skin showed an immediate (1 hour) reaction when sites were made if serum of untreated cases (Serum A) was used but none or slight reaction if serum of treated cases (Serum P) was used. 4. When sites made with allergen-antibody mixtures were tested after 48 hours, reactions were absent with Serum A mixtures if enough allergen had been used, but were positive with mixtures of Serum P even though a much stronger allergen was contained in the mixture. 5. The primary inhibition of reactions with mixtures including Serum P was not due to antihistamine effect nor to binding of skin sensitizing antibody nor to binding or lysis of allergen. 6. The inhibiting antibody appears to be specific. 7. These serological studies supported by transfusion experiments have been interpreted by us as showing the development under treatment of a peculiar blocking or inhibiting type of immune antibody that prevented the action of allergen on the sensitizing antibody and hence showed in the type of human allergy under consideration (hay fever) the coexistence of sensitization and immunity.
Childhood bronchial asthma in a desert country
Authors: I.‐L. Strannegard, Ö. Strannegård
Journal: Allergy (1990)

A 3 year‐study of emergency room visits (total 50,300) to the paediatric clinic of the main teaching hospital in Kuwait revealed that the rates of bronchial asthmatic attacks increased significantly from 8.8 % of all visits during the 1st year to 14.9% during the 3rd year. The seasonal distribution of asthmatic attacks showed maximum rates during the winter and minimum values in the summer, giving a very close inverse correlation to temperature and direct correlation to relative humidity. A similar, excellent correlation was seen between asthmatic attacks and upper respiratory infections. Occurrence of atmospheric pollen, which characteristically shows a bi‐annual pattern i Kuwait, was not found to correlate with asthma attack rates. Neither was there any demonstrable effect of dust storms on the frequency of asthmatic attacks in the children. Independent of season, the boy to girl ratio among the asthma cases was remarkably constant, around 2:1.
MicroRNA-182 drives metastasis of primary sarcomas by targeting multiple genes
Authors: Mohit Sachdeva, Jeffrey K. Mito, Chang-Lung Lee, Minsi Zhang, Zhizhong Li, Rebecca D. Dodd, David Cason, Lixia Luo, Yan Ma, David Van Mater, Rebecca Gladdy, Dina C. Lev, Diana M. Cardona, David G. Kirsch
Journal: Journal of Clinical Investigation (2014)

Metastasis causes most cancer deaths, but is incompletely understood. MicroRNAs can regulate metastasis, but it is not known whether a single miRNA can regulate metastasis in primary cancer models in vivo. We compared the expression of miRNAs in metastatic and nonmetastatic primary mouse sarcomas and found that microRNA-182 (miR-182) was markedly overexpressed in some tumors that metastasized to the lungs. By utilizing genetically engineered mice with either deletion of or overexpression of miR-182 in primary sarcomas, we discovered that deletion of miR-182 substantially decreased, while overexpression of miR-182 considerably increased, the rate of lung metastasis after amputation of the tumor-bearing limb. Additionally, deletion of miR-182 decreased circulating tumor cells (CTCs), while overexpression of miR-182 increased CTCs, suggesting that miR-182 regulates intravasation of cancer cells into the circulation. We identified 4 miR-182 targets that inhibit either the migration of tumor cells or the degradation of the extracellular matrix. Notably, restoration of any of these targets in isolation did not alter the metastatic potential of sarcoma cells injected orthotopically, but the simultaneous restoration of all 4 targets together substantially decreased the number of metastases. These results demonstrate that a single miRNA can regulate metastasis of primary tumors in vivo by coordinated regulation of multiple genes.
Capsid-specific T-cell Responses to Natural Infections With Adeno-associated Viruses in Humans Differ From Those of Nonhuman Primates
Authors: Hua Li, Marcio O Lasaro, Bei Jia, Shih Wen Lin, Larissa H Haut, Katherine A High, Hildegund CJ Ertl
Journal: Molecular Therapy (2011)

Hepatic adeno-associated virus serotype 2 (AAV2)-mediated gene transfer failed to achieve sustained transgene product expression in human subjects. We formulated the hypothesis that rejection of AAV-transduced hepatocytes is caused by AAV capsid-specific CD8+ T cells that become reactivated upon gene transfer. Although this hypothesis was compatible with clinical data, which showed a rise in circulating AAV capsid-specific T cells following injection of AAV vectors, it did not explain that AAV vectors achieved long-term transgene expression in rhesus macaques, which are naturally infected with AAV serotypes closely related to those of humans. To address this apparent contradiction, we tested human and rhesus macaque samples for AAV capsid-specific T cells by intracellular cytokine staining combined with staining for T-cell subset and differentiation markers. This highly sensitive method, which could provide a tool to monitor adverse T-cell responses in gene transfer trials, showed that AAV capsid-specific CD8+ and CD4+ T cells can be detected in blood of naturally infected humans and rhesus macaques. They are present at higher frequencies in rhesus macaques. Furthermore, T cells from humans and rhesus macaques exhibit striking differences in their differentiation status and in their functions, which may explain the disparate duration of AAV-mediated gene transfer in these two species. Hepatic adeno-associated virus serotype 2 (AAV2)-mediated gene transfer failed to achieve sustained transgene product expression in human subjects. We formulated the hypothesis that rejection of AAV-transduced hepatocytes is caused by AAV capsid-specific CD8+ T cells that become reactivated upon gene transfer. Although this hypothesis was compatible with clinical data, which showed a rise in circulating AAV capsid-specific T cells following injection of AAV vectors, it did not explain that AAV vectors achieved long-term transgene expression in rhesus macaques, which are naturally infected with AAV serotypes closely related to those of humans. To address this apparent contradiction, we tested human and rhesus macaque samples for AAV capsid-specific T cells by intracellular cytokine staining combined with staining for T-cell subset and differentiation markers. This highly sensitive method, which could provide a tool to monitor adverse T-cell responses in gene transfer trials, showed that AAV capsid-specific CD8+ and CD4+ T cells can be detected in blood of naturally infected humans and rhesus macaques. They are present at higher frequencies in rhesus macaques. Furthermore, T cells from humans and rhesus macaques exhibit striking differences in their differentiation status and in their functions, which may explain the disparate duration of AAV-mediated gene transfer in these two species.
Mechanisms of fiber-induced genotoxicity.
Authors: M C Jaurand
Journal: Environmental Health Perspectives (1997)

The mechanisms of particle-induced genotoxicity have been investigated mainly with asbestos fibers. The results are summarized and discussed in this paper. DNA damage can be produced by oxidoreduction processes generated by fibers. The extent of damage yield depends on experimental conditions: if iron is present, either on fibers or in the medium, damage is increased. However, iron reactivity does not explain all the results obtained in cell-free systems, as breakage of plasmid DNA was not directly associated with the amount of iron released by the fibers. The proximity of DNA to the site of generation of reactive oxygen species (ROS) is important because these species have an extremely short half-life. Damage to cellular DNA can be produced by oxidoreduction processes that originate from cells during phagocytosis. Secondary molecules that are more stable than ROS are probably involved in DNA damage. Oxidoreduction reactions originating from cells can induce mutations. Genotoxicity is also demonstrated by chromosomal damage associated with impaired mitosis, as evidenced by chromosome missegregation, spindle changes, alteration of cell cycle progression, formation of aneuploid and polyploid cells, and nuclear disruption. In some of these processes, the particle state and fiber dimensions are considered important parameters in the generation of genotoxic effects.
GM-CSF in Hodgkin Disease
Authors: Geraldine P. Schechter
Journal: Annals of Internal Medicine (1992)

Letters15 June 1992GM-CSF in Hodgkin DiseaseGeraldine P. Schechter, MDGeraldine P. Schechter, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-116-12-1033 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors: I wish to call your attention to three errors in the otherwise excellent paper by Gulati and Bennett (1). Two are minor and involve the SI units for blood cell concentration values. The investigators, I am sure, meant 20 x 109/L (not 200 x 109/L) for the threshold for platelet transfusion and 80 g/L (not 80 g/dL) for the threshold for red cell transfusion (p. 178, column 2, paragraph 1).The third error is more substantive and concerns the drawing of Figure 2 (p. 179). The text states that the 32-month actuarial survivals of the granulocyte-macrophage colony-stimulating...Reference1. GulatiBennett SC. Granulocyte-macrophage colony-stimulating factor (GM-CSF) as adjunct therapy in relapsed Hodgkin disease. Ann Intern Med. 1992;116:177-82. LinkGoogle Scholar1. GulatiBennett SC. Granulocyte-macrophage colony-stimulating factor (GM-CSF) as adjunct therapy in relapsed Hodgkin disease. Ann Intern Med. 1992;116:177-82. LinkGoogle Scholar1. GulatiBennett SC. Granulocyte-macrophage colony-stimulating factor (GM-CSF) as adjunct therapy in relapsed Hodgkin disease. Ann Intern Med. 1992;116:177-82. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Geraldine P. Schechter, MDAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byGabexat 15 June 1992Volume 116, Issue 12_Part_1Page: 1033-1034KeywordsAttentionBlood cellsGranulocyte macrophage colony stimulating factorHodgkin lymphomaPlatelets ePublished: 1 December 2008 Issue Published: 15 June 1992 PDF downloadLoading ...
Nasal inhalation of the glucocorticoid budesonide from a spacer for the treatment of patients with pollen rhinitis and asthma
Authors: B. Pedersen, R. Dahl, N. Lindqvist, N. Mygind
Journal: Allergy (1990)

Glucorticoid sprays are increasingly used for the treatment of allergic rhinitis and asthma. This therapy is highly effective, and side effects are few and mild. It was the aim of the present study to evaluate a physiological nasal inhalation technique, which results in airway deposition of the steroid molecule similar to that of inhaled allergen particles. Thirty adults with grass pollen‐induced rhinitis and asthma inhaled the steroid molectile budesonide through the nose from a pressurized aerosol attached to a spacer device. Compared with inhalation of placebo, the treatment resulted in a significant reduction of nasal symptoms ( P =0.005), of bronchial symptoms ( P =0.005), bat not of eye symptoms. In addition, nasal peak inspiratory flow ( P =0.0003) and oral peak expiratory flow ( P =0.02) increased. There was no difference between budesonide and placebo with regard to local side effects, such as nose bleeding, hoarseness, and irritation in mouth and throat. It is concluded that nasal inhalation of a steroid from a spacer offers effective therapy of pollen rhinitis and asthma without significant local side effects. This therapeutic modality may have advantages over the ordinarily used nasal and bronchial spray treatment in patients with both rhinitis and asthma, especially when conventionel spray therapy is associated with local side effects.
1081-56 Evolution of percutaneous coronary intervention in acute myocardial infarction: Insights from a large single center database
Authors: Gunasekaran Sengottuvel, Thierry Lefèvre, Yves Louvard, Pierre Dumas, Mehran Monchi, Christophe Loubeyre, Oscar Tavolaro, Marie-Claude Morice
Journal: Journal of the American College of Cardiology (2004)
GPs accept patients' vote on fundholding
Authors: M. A Varnam, M. Barker
Journal: BMJ (1995)

Result ofHeaftests and chest radiography and interventions offered in 170 studentsfrom overseas Heaftest Chest radiography Outcome Grade No (%) Result No(%) Intervention No (%/) 0 8 (5) Abnormal 2 (1) Chemoprophylaxis 7 (4) 1 28 (17) Child (no radiography) 8 (5) Offered BCG 1 (1) 2 105 (62) Old tuberculosis 1(1) Followed up 11(7) 3 12 (7) Refused 10 (6) Discharged 151 :89) 4 8 (5) Normal 149 (88) Refused test 9 (5)
Personal responsibility, not rationing, is the way forward
Authors: S. Goldbeck-Wood
Journal: BMJ (1997)

Germany's president, Dr Roman Herzog, called for more personal responsibility on the part of patients and more care with scarce resources at the 100th annual congress of the German medical association last week.

Speaking at the conference's opening ceremony, Dr Herzog criticised the “free lunch” mentality of some patients, saying: “We are each responsible for our own health. A healthcare …
Increasing Prevalence of Metabolic Syndrome in Korea
Authors: Soo Lim, Hayley Shin, Jung Han Song, Soo Heon Kwak, Seon Mee Kang, Ji Won Yoon, Sung Hee Choi, Sung Il Cho, Kyong Soo Park, Hong Kyu Lee, Hak Chul Jang, Kwang Kon Koh
Journal: Diabetes Care (2011)

The number of people with metabolic syndrome is increasing worldwide, and changes in socioenvironmental factors contribute to this increase. Therefore, investigation of changes in metabolic syndrome and its components in South Korea, where rapid socioenvironmental changes have occurred in recent years, would be foundational in setting up an effective strategy for reducing this increasing trend.We compared the prevalence and pattern of metabolic syndrome among participants in the Korean National Health and Nutrition Examination Surveys for 1998, 2001, 2005, and 2007. In each survey, stratified, multistage, probability-sampling designs and weighting adjustments were conducted to represent the entire Korean population. The revised National Cholesterol Education Program criteria were used as the definition of metabolic syndrome. All biochemical parameters were measured in a central laboratory.A total of 6,907 (mean ± SE age 45.0 ± 0.2 years), 4,536 (45.5 ± 0.2), 5,373 (47.1 ± 0.2), and 2,890 (49.9 ± 0.3) Koreans over 20 years of age have participated in the studies in 1998, 2001, 2005, and 2007, respectively. The age-adjusted prevalence of metabolic syndrome increased significantly from 24.9% in 1998, 29.2% in 2001, and 30.4% in 2005 to 31.3% in 2007. Among the five components, the level of low HDL cholesterol increased the most, by 13.8% over the 10 years. Abdominal obesity and hypertriglyceridemia followed, with 8.7 and 4.9% increases, respectively.Because dyslipidemia and abdominal obesity were major factors in increasing the prevalence of metabolic syndrome in Koreans for the past 10 years, lifestyle interventions should be conducted at the national level to reduce the burden and consequences of metabolic syndrome.
Prurigo pigmentosa: role of ICAM-1 in the localization of the eruption
Authors: Y. TERAKl, T. SHIOHARA, M. NAGASHIMA, T. NISHIKAWA
Journal: British Journal of Dermatology (1991)

Journal Article Prurigo pigmentosa: role of ICAM‐1 in the localization of the eruption Get access Y. TERAKl, Y. TERAKl Department of Dermatology Keio University School of Medicine, Tokyo, Japan Search for other works by this author on: Oxford Academic Google Scholar T. SHIOHARA, T. SHIOHARA Department of Dermatology, Kyorin University School of Medicine, Tokyo, Japan Search for other works by this author on: Oxford Academic Google Scholar M. NAGASHIMA, M. NAGASHIMA Department of Dermatology, Kyorin University School of Medicine, Tokyo, Japan Search for other works by this author on: Oxford Academic Google Scholar T. NISHIKAWA T. NISHIKAWA Department of Dermatology Keio University School of Medicine, Tokyo, Japan Dr T. Nishikawa, Department of Dermatology. Keio University School of Medicine, 35 Shinanomachi, Shinjuku‐ku. Tokyo 160, Japan. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 125, Issue 4, 1 October 1991, Pages 360–363, https://doi.org/10.1111/j.1365-2133.1991.tb14172.x Published: 01 October 1991