tbuckley/cabot-search huggingface dataset:
561. Recombinant Adenovirus Carrying Spike Gene Induces Effective Humoral and Cellular Immunity Against SARS-CoV in Rats
Authors: Ranyi Liu, Lizhe Wu, Bijun Huang, Jialin Huang, Wenlin Huang
Journal: Molecular Therapy (2004)

Severe acute respiratory syndrome (SARS) is life threatening contagious disease caused by a novel coronavirus, named SARS-associated coronavirus (SARS-CoV). Now there still aren't specific effective medicine and remedy to prevent or cure SARS. The patients suffering SARS are always administered heteropathy or conservative therapeutics. In order to prevent SARS, it may be necessary to develop vaccines against SARS-CoV. Inactivated SARS-CoV by irradiating is the most facile and convenient vaccine, but inactivated vaccine presumably possess a potential risk which results in the infection of the vaccinated, e.g. inactivated measles virus vaccine. Therefore, it could be a promising strategy to develop DNA vaccine. S protein is responsible for recognizing and binding its receptor of host cells, and directing the fusion between viral and cell membranes. We constructed recombinant adenoviruses carrying S1 fragment (Ad-S1) or S1 and S2 fragment(Ad-S12) of spike gene of SARS-CoV strain BJ01. We have investigated the ability of these recombinant adenoviruses to induce SARS-CoV virus-specific immunity in Wistar rats. Rats were immunized subcutaneously or through airway with the two recombinant adenoviruses respectively at day 0, 7 and 21. Preliminary results showed that all of vaccinated animals generated the antibodies and T-cell responses against SARS-CoV spike protein, and showed strong neutralizing antibody responses to SARS-CoV infection in vitro. These results indicate that adenoviral-based vaccine carrying spike gene fragment is able to induce strong SARS-CoV-specific immune responses in rats, and promising for development of a protective vaccine against the infection of SARS-CoV.
Veno-arterial Difference in 1-Antitrypsin Levels
Authors: A. J. Woolcock, W. Green, A. Crockett
Journal: BMJ (1972)

α<sub>1</sub>-Antitrypsin levels, determined by radial immunodiffusion, were found to be higher in the venous than in the arterial blood of patients with pulmonary infections and in patients with obstructive airflow diseases. Large differences occurred in patients with both abnormalities. No difference was found in patients with other kinds of lung disease or in patients without lung disease. The veno-arterial difference probably occurs as blood passes through the lungs and probably results from alteration of the immunological properties of the α<sub>1</sub>-antitrypsin, perhaps by attachment to proteases, rather than absorption into the lung tissue. Further studies are needed to define the diseases in which this antienzyme plays an active part and to determine the mechanisms causing the difference.
Reply from Authors re: Manfred P. Wirth, Johannes Huber. What Really Matters Is Rarely Measured: Outcome of Routine Care and Patient-reported Outcomes. Eur Urol 2013;64:58–9
Authors: Khurshid A. Guru, James O. Peabody, Kamran Ahmed, Adam Kibel, Alon Weizer, Matthew Hayn, Raza Johar, Piyush Agarwal, M. Balbay, Ashok Hemal, Fred Muhletaler, Kenneth Nepple, John Pattaras, Joan Redorta, Koon-Ho Rha, Lee Richstone, Matthias Saar, Francis Schanne, Douglas Scherr, Stefan Siemer, Michael Stoekle, Timothy Wilson, Michael Woods, Bertrum Yuh, Peter Wiklund
Journal: European Urology (2013)
Abstract 11737: Heart Failure Patients Who Have Knowledge About Their Disease but Don’t Perform Self-Care Have Worse Clinical Outcomes
Authors: Naoko Kato, Koichiro Kinugawa, Tiny Jaarsma
Journal: Circulation (2014)

Introduction: Both knowledge and self-care are related to outcomes of heart failure (HF) patients. Some HF patients do not perform self-care even if they have knowledge about the disease and might be in need for special interventions. We aimed at describing characteristics of those patients and assessing their clinical outcomes. Methods: A total of 163 HF outpatients were enrolled (age 64, 70% male, NYHA I or II, 95%) and followed for 2 years. HF self-care risk score was calculated by counting the number of poor adherence to five self-care behaviors (medication, a low-sodium diet, exercise, daily weighing, and help-seeking behavior) (range, 0-6). Knowledge was assessed with a Japanese HF knowledge scale (range, 0-15). Subsequently, we classified patients into 4 groups (A-D) as shown in figure. We analyzed patient’s characteristics in group C (poor self-care but good knowledge) by ANOVA and Chi-square test. To assess clinical outcomes we used Kaplan-Meier method and Cox regression analysis. Results: The mean HF self-care risk score was 3.1±1.6 and the mean knowledge score was 10.9±2.9. In total, 45 patients (28%) were classified into Group C [76% male, mean B-type natriuretic peptide (BNP) levels, 164 pg/mL]. Compared with other groups, patients in Group C were likely to be younger (61±13 vs. 65±11 years, p=0.059). Their self-care scores did not correlate with their knowledge scores (p=0.99). During a 2-year follow-up period, 29 patients (18%) had HF hospitalization and/or cardiac death, with a significant higher rate in Group C (30%, Fig, p=0.04). After adjustment for age, BNP, and medical therapy, patients in Group C had 2.8 times higher risk of poor outcomes than other groups (hazard ratio=2.80, p=0.01). Conclusions: One-third of patients have HF knowledge but they do not perform self-care, and they have worse outcomes compared with other groups. Further study is necessary to examine those patients in more detail and to provide support for them to put knowledge into action.
Abstract 3994: Identifying molecular networks linked to colorectal liver metastasis progression during liver regeneration by RNA-seq
Authors: Eve Simoneau, Jarred Chicoine, Ayat Salman, Robert Sladek, Anthoula Lazaris, Ramila Amre, Peter Metrakos
Journal: Cancer Research (2014)

Abstract The only potential cure for colorectal liver metastasis (CRCLM) is hepatic resection; portal vein embolization (PVE) is used as an adjunct to stimulate liver regeneration and increase the number of resectable patients. PVE has been shown to enhance CRCLM progression in most patients. The objective of this study is to determine the molecular networks involved in CRCLM progression during liver regeneration, by transcriptome analysis (RNA-Seq). CRCLM RNA was procured prospectively from patients prior to and after PVE. 14 patients with PVE underwent tumor volumetric analysis (blinded from the transcriptome analysis) to determine stable vs. progressive disease. A subgroup of 9 patients had tumor progression (median 45.3% (95%CI 10.6-192.5%) increase in tumor volume) while the remaining patients exhibited stable disease and continuous chemotherapy response (median 26.0%(95%CI -53.1-1.2%) decrease in tumor volume) (p=0.0121), which was consistent with our published series of 123 patients. RNA extracted from tumor tissue (pre and post PVE) in a subset (n=6) of patients (median RNA Integrity number (RIN) scores 7.1 (6.2 - 9.0)) was used to prepare Illumina rRNA-depleted TruSeq stranded cDNA libraries for HiSeq 100bp paired-end sequencing. An average of 150 million reads and 91.8% genomic alignment was achieved per sample. The analysis revealed that several genes known to act as tumor suppressors in CRC (e.g. NR1H4 and HRG) are consistently down regulated post-PVE in the progressive group. Several canonical pathways (including acute phase response, LXR/RXR signaling) showed statistical enrichment for transcripts that were differentially expressed in patients with disease progression. This work aims to establish a comprehensive view of the transcriptional changes associated with CRCLM progression during liver regeneration, to identify the molecular mechanisms that drive metastatic progression in this unique context. Highlighting such mechanisms is a critical first step towards developing targeted therapeutic strategies that may mitigate the unwanted effects of liver regeneration on tumor growth. Citation Format: Eve Simoneau, Jarred Chicoine, Ayat Salman, Robert Sladek, Anthoula Lazaris, Ramila Amre, Peter Metrakos. Identifying molecular networks linked to colorectal liver metastasis progression during liver regeneration by RNA-seq. [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 3994. doi:10.1158/1538-7445.AM2014-3994
Studies of Sequential and Combination Antimetabolite Therapy in Acute Leukemia: 6-Mercaptopurine and Methotrexate
Authors: Emil Frei, Emil J. Freireich, Edmund Gehan, Donald Pinkel, James F. Holland, Oleg Selawry, Farid Haurani, Charles L. Spurr, Donald M. Hayes, G. Watson James, Harvey Rothberg, D. Bruce Sodee, R. Wayne Rundles, Leslie R. Schroeder, Barth Hoogstraten, Irving J. Wolman, D. G. Traggis, Talbert Cooper, B. R. Gendel, Franklin Ebaugh, Robert Taylor
Journal: Blood (1961)
Experience-dependent changes in cerebral activation during human REM sleep
Authors: Pierre Maquet, Steven Laureys, Philippe Peigneux, Sonia Fuchs, Christophe Petiau, Christophe Phillips, Joel Aerts, Guy Del Fiore, Christian Degueldre, Thierry Meulemans, André Luxen, Georges Franck, Martial Van Der Linden, Carlyle Smith, Axel Cleeremans
Journal: Nature Neuroscience (2000)
The Qualitative Analysis of Medicinal Preparations.
Authors: Henry Corbin Fuller
Journal: JAMA (1913)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Preliminary Results of Resection of Sympathetic Ganglia and Trunks in Seventeen Cases of Chronic "Infectious" Arthritis
Authors: Leonard G. Rowntree, Alfred W. Adson, Philip S. Hench
Journal: Annals of Internal Medicine (1930)

Article1 November 1930Preliminary Results of Resection of Sympathetic Ganglia and Trunks in Seventeen Cases of Chronic "Infectious" ArthritisLEONARD G. ROWNTREE, M.D., ALFRED W. ADSON, M.D., PHILIP S. HENCH, M.D.LEONARD G. ROWNTREE, M.D.Search for more papers by this author, ALFRED W. ADSON, M.D.Search for more papers by this author, PHILIP S. HENCH, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-4-5-447 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptResection of lumbar sympathetic ganglia and trunks for the relief of so called chronic infectious arthritis (rheumatoid arthritis, arthritis deformans) of the lower extremities was first employed in June, 1926. The operation was performed by Adson at the request of Rowntree. The rationale for the procedure, and the immediate results of the operation on the first patient, and the subsequent course of the disease have been presented by Rowntree and Adson. The degree of relief experienced in the lower extremities, particularly in the feet, caused the first patient to request earnestly a somewhat similar procedure to relieve the pain and... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Division of Medicine and Section on Neurologic Surgery The Mayo Clinic Rochester, Minnesota*Read before the American College of Physicians, Minneapolis, Minnesota, February 12, 1930. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTHE TREATMENT OF RHEUMATOID ARTHRITIS WITH HEXAMETHONIUM CHLORIDE: A PRELIMINARY REPORT*WARREN D. PLATT JR., M.D., IRVING H. STEINBERG, M.D.Therapeutische Versuche mit Eingriffen am Sympathicus bei verschiedenartigen ErkrankungenXVI. The Treatment of Rheumatism 1 November 1930Volume 4, Issue 5Page: 447-454KeywordsArthritisGangliaRheumatoid arthritis ePublished: 1 December 2008 Issue Published: 1 November 1930 PDF downloadLoading ...
Abstract P281: A Novel Mutation in Adiponectin Receptor 1 Contributes to Cardiac Hypertrophy and Cardiometabolic Dysregulation
Authors: Soojeong Kang, Perundurai S. Dhandapany, Sreejith Kunnoth, Uthiralingam Muthusami, Kumarasamy Thangaraj, Roger Hajjar, Andiappan Rathinavel, Djamel Lebeche
Journal: Circulation (2014)

Adiponectin, an adipocyte-derived cytokine, is known to influence cardiac remodeling and to suppress pathological cardiac growth and diabetes-induced disorders. Disruption of adiponectin or its receptor AdipoR1 has significant effects on cardiomyocyte hypertrophy and myocardial metabolism signal transduction. We recently identified a novel mutation in the AdipoR1 gene among 126 hypertrophic cardiomyopathy patients, including two family members with diabetes. Our screening identified a G&gt;A transition at 146th position that replaced the amino acid valine (GUG) into methionine (AUG) (V146M). The consequences of this mutation on cardiac function and metabolism are not known. Here, using adenoviral gene delivery system, we found that Ad.V146M increased cell size, protein synthesis, induced expression of hypertrophic gene markers and increased serine phosphorylation of insulin receptor substrate 1 (IRS1) compared to control Ad.βGal or wild type AdipoR1 (Ad.AR1) in cultured cardiomyocytes. We also discovered that p38 and mTOR were activated by AdipoR1 mutant, but not wild-type. Pharmacological inhibition of p38 (SB203580) and mTOR (rapamycin) reversed the Ad.V146M-induced hypertrophic responses. Adiponectin is also known to promote the uptake and oxidation of fatty acid and glucose through AR1 in cultured myocytes. Recent studies suggest that p38 acts as an essential mediator in regulating adiponectin-induced glucose uptake and fatty acid oxidation in C2C12 myocytes, and the serine phosphorylation of IRS1 at S636/639 is known to be mediated by mTOR pathway. AdipoR1 mutant significantly deceased glucose uptake, facilitated palmitate uptake and repressed insulin responses. Interestingly, inhibition of p38 and mTOR pathways significantly attenuated the effects of Ad.V146M on the expression of genes involved in lipid oxidation (peroxisome proliferator-activated receptor α, PPARα; carnitine palmitoyltransferase 1, CPT1) or glucose utilization (phosphofructokinase, muscle, PFK-M), respectively. Intriguingly, these findings were confirmed in vivo in cardiac-specific transgenic mice overexpressing AdipoR1 mutant. Taken together, these results suggest that a mutation in the AdipoR1 may contribute to the development of cardiomyopathy via alterations in mTOR/p38 pathways and cardiac metabolism.
Heart Strain and Its Consequences
Authors: Morris H. Kahn, Samuel Kahn
Journal: Annals of Internal Medicine (1928)

Article1 April 1928Heart Strain and Its ConsequencesMORRIS H. KAHN, M.A., M.D., SAMUEL KAHN, B.S., M.D.MORRIS H. KAHN, M.A., M.D.Search for more papers by this author, SAMUEL KAHN, B.S., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-1-10-790 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe subject of mechanical strain of the heart and great vessels has been considered in its clinical aspects in the medical literature since the middle of the nineteenth century. Following the pioneer work of Peacock, da Costa, Traube, Seitz, and Allbutt and Roy, the condition became recognized as a clinical entity. To Allbutt the greatest credit is, perhaps, due for describing a large number of cases, clearly demonstrating the operation of overwork and stress in the production of cardiac diseases—factors that had previously been overlooked or neglected by pathologists. The opportunities afforded in modern industry for the study of this... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York*From the Department of Cardiovascular Diseases, Beth Israel Hospital and the State Department of Labor—New York City. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1928Volume 1, Issue 10Page: 790-811KeywordsCardiovascular diseasesHeartHeart diseasesPathologists ePublished: 1 December 2008 Issue Published: 1 April 1928 PDF downloadLoading ...
Abstract P4-05-13: PTEN deletion is linked to adverse phenotype and poor prognosis in breast cancer
Authors: Eike Burandt, Martina Kluth, Valerie Kopperschmidt, Anja Mittenzwei, Annette Lebeau, Volkmar Müller, Isabell Witzel, Fritz Jänicke, Stefan Geist, Peter Paluchowski, Christian Wilke, Uwe Heilenkötter, Rainer Krech, Albert von d Assen, Ronald Simon, Patrick Lebok
Journal: Cancer Research (2015)

Abstract Deletions of chromosome 10q23, including the PTEN (phosphatase and tensin homolog) locus, are known to occur in breast cancer, but systematic analyses of its clinical relevance are lacking. We thus analyzed a tissue microarray (TMA) with 2,197 breast cancers by fluorescence in-situ hybridization (FISH) using a PTEN-specific probe, and found deletions in 19% of no special type, 9% of lobular, 46% of medullary and 4% of tubular cancers. 98.7% of deletions were heterozygous and 1.3% were homozygous. PTEN deletion was significantly linked to advanced tumor stage (p=0.0054), high tumor grade (p&amp;lt;0.0001), high tumor cell proliferation (Ki67 Labeling Index; p&amp;lt;0.0001), and shortened overall survival (p=0.0090). PTEN deletions were inversely associated with features of luminal type breast cancers (ER/PR positivity, CCND1 amplification). PTEN deletions were strongly linked to amplification of genes involved in the PTEN/AKT pathway such as MYC (p=0.0430) and HER2 (p=0.0065). Remarkably the combined analysis of MYC, HER2, and PTEN aberrations suggested that aberrations of multiple PTEN/AKT pathway genes have a strong additive effect on breast cancer prognosis. Cancers with two or three of these aberrations behaved significantly worse than cancers with none or one of these changes (p&amp;lt;0,0001). The particularly poor prognosis of patients with HER2 amplification and PTEN deletions challenges the concept of PTEN deletions interfering with trastuzumab therapy. In conclusion, PTEN deletion occurs in a relevant fraction of breast cancers, and is linked to aggressive tumors. Reduced PTEN function cooperates with MYC and HER2 activation in conferring aggressive phenotype to cancer cells. Citation Format: Eike Burandt, Martina Kluth, Valerie Kopperschmidt, Anja Mittenzwei, Annette Lebeau, Volkmar Müller, Isabell Witzel, Fritz Jänicke, Stefan Geist, Peter Paluchowski, Christian Wilke, Uwe Heilenkötter, Rainer Krech, Albert von d Assen, Ronald Simon, Patrick Lebok. PTEN deletion is linked to adverse phenotype and poor prognosis in breast cancer [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P4-05-13.
Abstract 2703: Effect of route and dosing regimen on efficacy of SH7139 in mouse Burkitt's lymphoma xenografts
Authors: Rodney Balhorn, Gary Mirick, Gerald L. DeNardo, Laurel Beckett, Judy Li, Saphon Hok, Monique Balhorn
Journal: Cancer Research (2014)

Abstract SH7139, our most advanced small molecule therapeutic for non-Hodgkin's lymphoma, was designed to bind to a unique site on HLA-DR10, a cell surface receptor found on B-cell lymphocytes and over-expressed on B-cell derived malignancies. Studies conducted with lymphoma and other cell lines have shown that SH7139 binds selectively and is highly cytotoxic only to tumor cells expressing HLA-DR10. A previous study also showed SH7139 to be highly effective in treating human Burkitt's lymphoma (Raji) in a mouse xenograft model. We have used this same mouse model to compare the efficacy of SH7139 delivered by different routes and using different treatment regimens. The results show that the greatest survival times were achieved with mice given SH7139 by i.p. injection on days 0, 7 and 14. Doses delivered i.p. on days 0, 2 and 4 and orally on days 0,7,14,21,28 and 35 were slightly less effective, and a single dose delivered i.p. on day 0 and three doses delivered orally on days 0, 7, and 14 were the least effective. The concentration of SH7139 that achieved these effects in vivo, which was determined by measuring xenograft uptake of 111-In-labeled SH7139, was found to be in the sub-nanomolar range. In addition to identifying the best route and dosing regimen for future studies and confirming the drug works in vivo at concentrations similar to those found to be effective in cells cultured in vitro, these studies also show the drug can be effective when administered orally. Citation Format: Rodney Balhorn, Gary Mirick, Gerald L. DeNardo, Laurel Beckett, Judy Li, Saphon Hok, Monique Balhorn. Effect of route and dosing regimen on efficacy of SH7139 in mouse Burkitt's lymphoma xenografts. [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 2703. doi:10.1158/1538-7445.AM2014-2703
Inhibition of Human Umbilical Vein Endothelial Cell Proliferation by the CXC Chemokine, Platelet Factor 4 (PF4), Is Associated With Impaired Downregulation of p21Cip1/WAF1
Authors: Grazia Gentilini, Nancy E. Kirschbaum, James A. Augustine, Richard H. Aster, Gian Paolo Visentin
Journal: Blood (1999)