tbuckley/cabot-search huggingface dataset:
Effect of chrysin on airway inflammation induced by cigarette smoke in mice
Authors: Hao Wang, Diandian Li, Liuqun Jia, Lian Liu, Yanqiu Wu, Caishuang Pang, Yongchun Shen, Fuqiang Wen
Journal: European Respiratory Journal (2014)

Objective: Cigarette smoke(CS) is known to cause airway inflammation. The present study aimed to investigate the effects of chrysin on airway inflammation induced by CS in mice, and explore the possible mechanism.  Methods: Mice were exposed to CS for 6 days per week for 4 weeks, low-dose(5 mg/kg·d) or high-dose(10 mg/kg·d) chrysin was intraperitoneally injected prior to CS exposure. TNF-α, IL-1β and IL-8 levels in bronchoalveolar lavage fluid(BALF) were detected by ELISA. Myeloperoxidase(MPO) levels in lung homogenate were tested by chemical chromatometry. The expressions of phospho-Extracellular signal-Regulated Kinase(p-ERK) and phospho-38 Mitogen-Activated Protein Kinase(p-38MAPK) in lung homogenate were measured using Western Blot. Pathological changes were evaluated with H&E staining.  Results:The mean levels of TNF-α, IL-1β, IL-8 in BALF and MPO in lung homogenate of mice exposed to CS were significantly elevated respectively compared to controls(p  Conclusion: Chrysin suppresses airway inflammation induced by cigarette smoke in mice, the phosphorylation of ERK and 38MAPK may be involved in this process. These findings suggest that chrysin has anti-inflammation effect upon CS-induced inflammatory airway diseases.
Abstract 16932: Embryonic Stem Cell Derived Exosomes Revive Endogenous Repair Mechanisms in Failing Hearts
Authors: Mohsin Khan, Suresh K Verma, Alexander R Mackie, Prasanna Krishnamurthy, Erin Vaughan, Venkata N Garikipati, Veronica Ramirez, Erin Lambers, Tatiana Abramova, Aiko Ito, Sol Misener, Gangjian Qin, Walter J Koch, Raj Kishore
Journal: Circulation (2014)

Rationale:  Embryonic stem cells (ESCs) hold great promise for cardiac regeneration but are susceptible to ethical concerns, lack of autologous donors and teratoma formation. Recently, it has been observed that beneficial effects of stem cells are mediated by exosomes secreted under various physiological conditions. ESCs have the ability to produce exosomes however their effect in the context of the heart is unknown.   Objective:  Determine the effect of ESC derived exosomes in augmenting endogenous cardiac repair mechanisms in the heart following myocardial infarction.   Methods and Results:  Exosomes were isolated from mouse ESCs (mES Ex) or embryonic fibroblasts (MEFs) by ultracentrifugation and verified by Flotillin-1 immunoblot analysis. Induction of pluripotent markers, survival and in vitro tube formation was enhanced in target cells receiving ESC exosomes. Cardiac therapeutic potential of ESC exosomes was assessed in a mouse model for myocardial infarction. Enhanced neovascularization, reduced apoptosis and fibrosis was consistent with resurgence of cardiac proliferative response in hearts receiving mES Ex compared to MEF Ex and saline treated animals at 4 weeks post infarction. Importantly, enhanced cardiac progenitor cell (CPC) survival, proliferation and cardiac commitment in vitro concurrent with increased CPCs numbers in vivo 4 weeks after mES Ex transfer. miRNA Array of ESC and MEF exosomes revealed significant enrichment of miR290-295 cluster and particularly miR-294 in ESC exosomes. Beneficial effect of mES Ex was tied to delivery of ESC specific miR-294 to the heart and in particular CPCs thereby promoting CPC survival and proliferation as analyzed by FACS cell death and CyQuant assay respectively. Enhanced G1/S transition was observed in CPCs treated with miR-294 in conjunction with significant reduction of G1 phase. Enhanced mRNA levels of cyclins A2 and E1 were observed in CPCs as well as in neonatal rat cardiomyocytes.   Conclusion:  mES Ex provide a novel cell free system that utilizes the immense regenerative power of the ES cells while avoiding the risks associated with ESC research. Furthermore, ESC exosomes possess cardiac regeneration ability and modulate both cardiomyocyte and CPC based repair programs in the heart.
Abstract 13415: Monocyte/Macrophage-Specific Insulin-Like Growth Factor-1 Receptor Deficiency Promotes Lipid Accumulation and Inflammatory Responses in Macrophages, Leading to Increased Atherosclerosis
Authors: Yusuke Higashi, Shaw-yung Shai, Sergiy Sukhanov, Patrice Delafontaine
Journal: Circulation (2014)

Macrophage (Mf) uptake of modified lipids, pro-inflammatory signaling and conversion to foam cells is a hallmark of atheroma formation. Insulin-like growth factor-1 (IGF-1) is a pleiotropic growth factor and its receptor (IGF1R) is expressed in various cell types including Mf, yet the role of Mf IGF1R signaling in atherogenesis is unknown. We created Mf-specific IGF1R-deficient mice on Apoe-/- background (Mf-IGF1R-KO) and found these mice had increased plaque burden (aortic root plaque size, 57.0 ± 14.9 % increase) and enhanced inflammatory phenotype (anti-Mac3 staining, Mf-IGF1R-KO, 31.3 ± 2.8 % vs. IGF1R flox, 22.5 ± 4.2 %). To determine mechanisms we exposed peritoneal Mf from Mf-IGF1R-KO mice (IGF1R-KO cells) and IGF1R-flox mice (IGF1R-WT cells) to acetylated LDL (acLDL) and oxidized LDL (oxLDL) and assessed proinflammatory cytokine and chemokine expression levels, lipid uptake, and cholesterol efflux. IGF1R-KO cells expressed higher levels of IL1α, IL6, and TNFα compared to IGF1R-WT cells (IL1α; 338±19 pg/mg protein vs. 32±1 pg/mg protein, P<0.01, IL6; 1167±37 pg/mg protein vs. 30±2, P<0.01, TNFα; 240±72 pg/mg protein vs. Not Detectable), whereas oxLDL did not further enhance cytokine expression. NFkB activity was significantly higher in IGF1R-KO cells than IGF1R-WT cells as determined by a solid-phase DNA binding assay. AcLDL or oxLDL uptake was not altered by IGF1R deficiency; however cholesterol efflux to apolipoprotein A1 was significantly impaired (decreased by 57.9±9.4 %, P<0.01). OxLDL upregulation of ATP-binding cassette transporter A1 was suppressed by 40.8±5.9 % (P<0.05) in IGF1R-KO cells indicating that IGF1R-deficiency impaired lipid efflux thereby promoting macrophage foam cell formation. Moreover, there was a concomitant decrease in oxLDL-upregulation of diacylglycerol acyltransferase 1, consistent with dysregulation of lipid homeostasis. Thus Mf IGF-1R deficiency is markedly pro-inflammatory and disrupts Mf lipid trafficking by reducing cholesterol efflux, resulting in increased atherosclerotic plaque formation. These data suggest that IGF-1 regulation of Mf inflammatory responses and lipid metabolism may provide a novel therapeutic approach for the treatment of atherosclerotic vascular disease.
Abstract 2673: Myoblast Transplantation Improves Cardiac Function Whether the Cells are Implanted Early or Late After Coronary Ligation
Authors: Patrick Farahmand, Richard D Weisel, Philippe Menasche, Ren-Ke Li
Journal: Circulation (2007)

Background: The inability of skeletal myoblasts to transdifferentiate into cardiomyocytes supports the hypothesis that their beneficial effects on cardiac function after a myocardial infarction (MI) are mediated by paracrine effects. In order to explore the role of the timing of cell therapy on the resultant angiogenesis and matrix remodeling, we compared the effects of myoblast transplantation early or late after MI. Methods: MI was generated in Lewis rats by coronary artery ligation. Skeletal myoblasts (5X10 6 ) or control media were injected into the scar and border zone either 5 days (early; n=33) or 30 days (late; n=29) after ligation. Function was assessed by echocardiography before transplantation (Tx), and 14 and 30 days thereafter. Invasive hemodynamics were measured with a Millar catheter at 30 days after Tx, following which explanted hearts were processed to assess LV volumes (computerized planimetry), fibrillar collagen (confocal microscopy), and myoblast engraftment, angiogenesis and extra-cellular matrix characteristics (immunohistochemistry). Results: Load-independent indices of left ventricular (LV) function (Emax, preload recruitable stroke work) were significantly increased in myoblast recipients compared with controls regardless of whether cells were implanted early (p=0.003, p=0.03, respectively) or late (p=0.003, p=0.0007, respectively) after MI. Changes in fractional shortening (by echocardiography) followed a similar pattern. These changes were associated with a significant reduction in LV volume (p=0.04, p=0.01 for early and late Tx groups vs. controls, respectively), and an increase in angiogenesis (p=0.02) whether the myoblasts were injected early or late after MI. The length and width of collagen fibers both in the scar and remote myocardium were also significantly increased (p&lt;0.001) regardless of the timing of myoblast injection. Conclusions: The data suggest that myoblast transplantation improved cardiac function whether cells were injected early or late after MI. In each case, functional recovery was associated with enhanced angiogenesis, favourable effects on extracellular matrix remodeling, and improved LV geometry, supporting the paracrine hypothesis for myoblast transplantation.
SCREENING FOR TUBERCULOSIS IN A CIVILIAN POPULATION BY FLUOROGRAPHY
Authors: Bruce H. Douglas, Carl C. Birkelo
Journal: Annals of Internal Medicine (1941)

Article1 November 1941SCREENING FOR TUBERCULOSIS IN A CIVILIAN POPULATION BY FLUOROGRAPHYBRUCE H. DOUGLAS, M.D., F.A.C.P., CARL C. BIRKELO, M.D.BRUCE H. DOUGLAS, M.D., F.A.C.P.Search for more papers by this author, CARL C. BIRKELO, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-15-5-853 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe control of tuberculosis must be based on the same general principles that are applicable to the control of all communicable diseases. Since there is no effective means so far developed for immunizing the population against tuberculosis, the efforts to prevent its occurrence must rest largely on limiting the spread of the organism responsible for the cause of the disease. Since bovine tuberculosis has been so well controlled in this country the one remaining important source of tubercle bacilli is the persons who have tuberculosis. It therefore becomes of prime importance to detect as far as possible all the cases...References1. EDWARDS HR: Tuberculosis case finding, Am. Rev. Tuberc., 1940, xli, 1-159. Google Scholar2. POTTER HE: Carman Lecture, June 1938. Google Scholar3. POTTERDOUGLASBIRKELO HEBHCC: Miniature x-ray chest film, Radiology, 1940, xxxiv, 283. CrossrefGoogle Scholar4. BRIDGE E: Fluoroscopic roentgenography, Am. Rev. Tuberc., 1940, xlii, 155. Google Scholar5. DOUGLASBIRKELO BHCC: Miniature x-ray film of the chest, Am. Rev. Tuberc., 1941, xliii, 106-116. Google Scholar6. FELLOWSORDWAY HHWH: Fluoroscopy versus physical findings in the detection of pulmonary tuberculosis, Trans. Nat. Tuberc. Assoc., 1937, p. 51. Google Scholar7. DE ABREULINDBERG MDO: Process and apparatus for roentgen photography, Am. Jr. Roentgenol., 1939, xli, 662. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Detroit, Michigan*Read at the Boston meeting of the American College of Physicians, April 25, 1941. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThe problem of unsuspected tuberculosis in pregnancy 1 November 1941Volume 15, Issue 5Page: 853-857 ePublished: 1 December 2008 Issue Published: 1 November 1941 PDF downloadLoading ...
Antithrombotic activity of BM-573, a novel thromboxane modulator, in rat arterial thrombosis model, pig myocardial infarction model and its effect on bleeding time
Authors: Jean-Michel Dogné, Philippe Kolh, S. Rolin, Vincent Tchana-Sato, Julien Hanson, X. De Leval, Bernard Lambermont, Alexandre Ghuysen, M. Petein, Laurence de Leval, B. Masereel, Bernard Pirotte
Journal: Blood (2003)
The Epidemiology of Vitreoretinal Interface Abnormalities as Detected by Spectral-Domain Optical Coherence Tomography
Authors: Stacy M. Meuer, Chelsea E. Myers, Barbara E.K. Klein, Maria K. Swift, Yijun Huang, Sapna Gangaputra, Jeong W. Pak, Ronald P. Danis, Ronald Klein
Journal: Ophthalmology (2014)
Synoptical table of idiopathic interstital pneumonia (IIP) findings in computed tomography (CT) – A practical tool and systematic review
Authors: Markus Unnewehr, Bernhard Schaaf, Claus Peter Heußel
Journal: European Respiratory Journal (2014)

Reading CT of IIP often is a challenge for both pulmonologists and radiologists because the diseases are  their findings and combinations are complex and the differential diagnoses (DD) are vast.  The aim was to facilitate reading CT of IIP. We composed a synoptical table containing relevant CT findings of each IIP. Before, we conducted a systematic review about the typical findings of IIP in CT and compared it with our clinical experience.  The literature research did not reveal the existence of a synoptical table of the IIP findings. The table columns contain the relevant findings reticular, nodular, ground glass, consolidation, traction bronchiectases, special findings, as well as their distribution, and common DD. The table rows contain the IIP according to the current international classification. The quantitative and / or qualitative description (e. g. rare, always, perilymphatic) of each CT finding as found in the literature was transferred into the cells of a table. To further support quick orientation, a plain table layout was chosen.  The table is the first literature-based synoptical presentation of IIP findings as a practical tool for the daily work of reading CT.
Abstract 19798: Should Downsizing Still Be the Gold Standard for Treatment of Ischemic Mitral Regurgitation?
Authors: Boris Robic, Alexander Van De Bruaene, Thijs Cools, Jan Verwerft, Alaaddin Yilmaz, Urbain Mees, Marc Hendrikx
Journal: Circulation (2014)

Background: Mitral valve annuloplasty (MVA) or replacement (MVR) are common strategies in the treatment of functional ischemic mitral regurgitation (FIMR). However, the issue of functional stenosis during exercise in MVA patients was raised. This study aims to compare exercise hemodynamics of MVA and MVR patients. Methods: Thirty patients (23 MVA, 66.8±8.8 y at repair, and 7 MVR, 66.1±5.5y) underwent exercise echocardiography. Stroke volume, ejection fraction, cardiac index, mitral valve gradient, mitral valve area and pulmonary artery pressures were evaluated at rest and at peak exercise. Results: Both patient groups had comparable exercise capacity (65±16 vs 67±15 %predicted; P=0.760). In MVA patients, stroke volume (38±14 to 39±14 mL; P=0.707) and ejection fraction (51±15 to 55±14%; P=0.123) did not change, whereas cardiac index (2.9±1.1 to 4.2±1.2 L/min.m 2 ; P&lt;0.0001), mitral valve gradient (peak 11.8±4.6 to 21.3±7.6 mmHg; mean 5.2±2.2 to 11.3±4.9 mmHg; both P&lt;0.0001) and pulmonary artery pressure (33±10 to 51±16 mmHg; P&lt;0.0001) increased during exercise. In MVR patients, stroke volume (29±7 to 35±7 ml; P=0.006), ejection fraction (52±12 to 61±14%; P=0.009), cardiac index (2.0±0.4 to 3.1±0.9 L/min.m 2 ; P=0.006), mitral valve gradient (peak 9.8±3.8 to 22.0±7.5 mmHg; mean 4.8±1.8 to 12.3±4.3 mmHg; both P&lt;0.05) and pulmonary artery pressure (32±5 to 45±9 mmHg; P=0.006) all increased during exercise. Cardiac index at rest (P=0.040) and at peak exercise (P=0.038) was slightly higher in the MVA group, whereas pulmonary artery pressures at rest (P=0.750) and at peak exercise (P=0.293) were not statistically different. Total pulmonary resistance did not change during exercise (P=0.115 and P=0.546 for MVA and PVR respectively). In MVA, there was a relation between peak mitral valve gradient at rest and pulmonary artery pressure at rest (R=0.525, P=0.017) and at peak exercise (R=0.508; P=0.022). Conclusions: Surgical repair achieves leaflet coaptation at the expense of raised transmitral gradients. Even after successful MVA, patients had worse exercise hemodynamics and lack of mitral valve opening reserve. Therefore we should question downsizing as the gold standard for treatment of FIMR and look for a more patient tailored approach.
THE DIAGNOSIS OF ACUTE VIRAL HEPATITIS SIMULATING AN ABDOMINAL EMERGENCY: A CASE REPORT
Authors: E L ROLETT, M H SLEISENGER
Journal: Annals of Internal Medicine (1959)

Excerpt Although abdominal pain is common in the preicteric phase of acute viral hepatitis, it is rarely of sufficient intensity to simulate an acute surgical condition; occasionally, however, there is not only severe distress but also marked upper abdominal tenderness, direct and rebound. Because of the dangers in laparotomy in individuals with liver disease, awareness that hepatitis may simulate an abdominal disorder which requires surgery is important. Correct early diagnosis is imperative, and may be facilitated by measurement of serum glutamic oxaloacetic transaminase and the clinical effect of corticotropin (ACTH). Our recent experience with such a patient is reported. CASE REPORT
Tuberculosis and other Communicable Diseases.
Authors: J. Arthur Myers
Journal: Annals of Internal Medicine (1960)

When the countless advances by medical science during recent decades are appraised in the light of their total impact on human welfare, the most impressive and significant will be concerned with the field of infectious diseases. Many of these achievements are reviewed in this volume in contributions by leaders in their special subjects. The editor is a well-known specialist in public health and preventive medicine whose studies in tuberculosis are outstanding. The present volume fulfills the desire to center attention on the communicable nature of tuberculosis and comparable infectious diseases. This and the concept of early recognition and prompt isolation in prevention of such diseases should make the volume useful to the medical student and practitioner, as well as a textbook in nursing and public health courses. Much preventive work remains to be done even though diagnostic, therapeutic, prophylactic, and epidemiologic measures are well established. None of these diseases has
BODILY BUILD AND HEREDITY IN CORONARY THROMBOSIS
Authors: Grace A. Goldsmith, Fredrick A. Willius
Journal: Annals of Internal Medicine (1937)

Article1 February 1937BODILY BUILD AND HEREDITY IN CORONARY THROMBOSISGRACE A. GOLDSMITH, M.D., FREDRICK A. WILLIUS, M.D., F.A.C.P.GRACE A. GOLDSMITH, M.D.Search for more papers by this author, FREDRICK A. WILLIUS, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-10-8-1181 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe importance of habitus in its association with certain pathologic states has been the subject of considerable discussion in recent years. The coexistence of obesity and hypertension has often been emphasized. It has been our clinical impression that many individuals who have coronary thrombosis are overweight, but no adequate statistics are available regarding this question. The tendency for abnormal degrees of arteriosclerosis and their premature manifestation to occur with unusual regularity in certain families, and the proclivity of angina pectoris to be a familial disease have been recognized for many years.To investigate the importance of bodily build and heredity... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Rochester, Minnesota*Received for publication November 3, 1936.From the Division of Medicine, The Mayo Clinic, Rochester, Minnesota. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byLIST OF REFERENCESDie Coronarerkrankungen. Coronarinsuffizienz, Angina pectoris und HerzinfarktRelationship of body weight to acute myocardial infarctionTHE FAMILIAL OCCURRENCE OF HYPERTENSION AND CORONARY ARTERY DISEASE, WITH OBSERVATIONS CONCERNING OBESITY AND DIABETES*†CAROLINE BEDELL THOMAS, F.A.C.P., BERNICE HIRSCHHORN COHENBODY WEIGHT VERSUS WEIGHT STANDARDS IN CORONARY ARTERY DISEASE AND A HEALTHY GROUP*STANLEY M. GARN, MENARD M. GERTLER, SAMUEL A. LEVINE, F.A.C.P., PAUL D. WHITE, F.A.C.P.Heart disease in the SouthErbbiologie und Erbpathologie des KreislaufapparatesDie Klinik der CoronarerkrankungenInfarction of the heart 1 February 1937Volume 10, Issue 8Page: 1181-1186KeywordsAnginaHeredityHypertensionObesityOverweightThrombosis ePublished: 1 December 2008 Issue Published: 1 February 1937 PDF downloadLoading ...
Abstract 2731: PELP1 promotes DNA double-strand break repair via alternative-NHEJ: Implications in therapy resistance
Authors: Samaya R. Krishnan, Binoj C. Nair, Gangadhara R. Sareddy, Monica Mann, Ratna K. Vadlamudi
Journal: Cancer Research (2014)

Abstract Estrogen Receptor positive breast cancer is commonly treated with hormonal therapy; however, many patients acquire therapy resistance, a major clinical problem. Recent evidence suggests that the accumulation of chromosomal abnormalities via increased error-prone Alternative-Non-Homologous End Joining (A-NHEJ) DNA repair pathway could contribute to breast cancer therapy resistance. Proline, Glutamic acid, Leucine rich Protein-1 (PELP1), an oncogenic co-regulator for transcription factors, is commonly overexpressed in breast cancer, and its deregulation has been implicated in therapy resistance. Our recent studies identified PELP1 as a novel substrate of the DNA damage response (DDR) kinases. In this study, we discovered that PELP1 regulates the A-NHEJ pathway, and we developed a novel peptide drug that targets PELP1-A-NHEJ axis for the treatment of therapy resistance. Our results suggest that PELP1 is phosphorylated at Ser1033 by DDR kinases and phosphorylated PELP1 co-localizes with the gamma-H2AX foci. Using Homologous Recombination (HR) and NHEJ pathway specific reporter assays, we found that PELP1 knockdown decreases NHEJ, with no apparent effect on the HR pathway. Further, using A-NHEJ specific reporter cell line, we found that PELP1 knockdown decreased the frequency of A-NHEJ, while PELP1 overexpression increased the repair frequency. PELP1's ability to regulate A-NHEJ pathway was further confirmed by sequencing repaired plasmids and by quantitating the degree of end resection. More importantly, metaphase chromosome spreads revealed gross chromosomal abnormalities in PELP1 deregulated breast cancer cells. Mechanistic studies revealed that PELP1 interacts with Mre11, and modulates the degree of end resection at the DNA double strand breaks. Mapping studies identified the C-terminus of PELP1 as the binding site for Mre11. Using yeast based genetic screen composed of 10 million peptides, we identified a unique peptide, PIP3 that binds the C-terminus of PELP1. We developed a stapled peptide of PIP3 (sPIP3), which functioned as a potent cytotoxic agent for breast cancer cells with little activity on normal cells. Further, sPIP3 efficiently inhibited the A-NHEJ pathway and significantly, reduced survival and promoted apoptosis of therapy resistant model cells. Collectively, these findings suggest that PELP1 plays a critical role in the A-NHEJ pathway and sPIP3 represents a novel drug for the treatment of therapy resistant breast cancer. Citation Format: Samaya R. Krishnan, Binoj C. Nair, Gangadhara R. Sareddy, Monica Mann, Ratna K. Vadlamudi. PELP1 promotes DNA double-strand break repair via alternative-NHEJ: Implications in therapy resistance. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2731. doi:10.1158/1538-7445.AM2014-2731