tbuckley/cabot-search huggingface dataset:
Korean Hemorrhagic Fever
Authors: Ho Wang Lee
Journal: JAMA (1988)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
A virus-induced molecular mimicry model of multiple sclerosis
Authors: Julie K. Olson, J. Ludovic Croxford, Miriam. A. Calenoff, Mauro C. Dal Canto, Stephen D. Miller
Journal: Journal of Clinical Investigation (2001)

Molecular mimicry is the process by which virus infection activates T cells that are cross-reactive with self antigens. Infection of SJL/J mice with the neurotropic picornavirus Theiler's murine encephalomyelitis virus (TMEV) leads to a progressive CD4(+) T cell-mediated demyelinating disease similar to multiple sclerosis. To study the potential of virus-induced molecular mimicry to initiate autoimmune demyelination, a nonpathogenic TMEV variant was engineered to encode a 30-mer peptide encompassing the immunodominant encephalitogenic myelin proteolipid protein (PLP139-151) epitope. Infection with the PLP139-151-encoding TMEV led within 10-14 days to a rapid-onset paralytic demyelinating disease characterized by PLP139-151-specific CD4(+) Th1 responses; insertion of a non-self ovalbumin sequence led to restoration of the normal late-onset disease. Early-onset disease was also observed in mice infected with a TMEV encoding PLP139-151 with an amino acid substitution at the secondary T cell receptor (TCR) contact residue (H147A), but not in mice infected with TMEV encoding a PLP139-151 substitution at the primary TCR contact (W144A). Most significantly, mice infected with TMEV encoding a Haemophilus influenzae mimic peptide, sharing only 6 of 13 amino acids with PLP139-151, displayed rapid-onset disease and developed cross-reactive PLP139-151-specific CD4(+) Th1 responses. To our knowledge, this is the first study showing that a naturally infectious virus encoding a myelin epitope mimic can directly initiate organ-specific T cell-mediated autoimmunity.
A tissue selective rapamycin analog inhibits MDA-MB-231 breast cancer cell-induced osteolytic bone metastases in nude mice
Authors: Chester Metcalf, Brendan Boyce, Yan Lu, Lianping Xing, Dong Zou, Mathew Thomas, Victor Rivera, Lori Berk, Narayana Narasimhan, Joseph Snodgrass, Noel Reid, Frank Wang, Scott Wardwell, Manfred Weigele, Camille Bedrosian, John Iuliucci, Tomi Sawyer, Tim Clackson
Journal: Cancer Research (2006)

4857   Bone metastases, frequent consequences of common malignancies such as breast, lung, and prostate cancer, involve complex molecular processes and are extremely difficult to treat. In the bone microenvironment, metastatic cancer cells produce osteoclast activating factors (e.g., PTHrP) that stimulate bone resorption. Bone-derived growth factors (e.g., TGF-β and IGF1) are subsequently released, promoting cancer-cell proliferation and the amplification of a cycle that produces net osteolytic (bone destructive) consequences. AP24170 is a rapamycin analog with a synthetically linked bone-targeted (BT) moiety. The bone-targeting functionality is designed to accumulate BT rapalogs such as AP24170 on bone, enhancing the anti-tumor and anti-osteolytic effects of mTOR inhibition at bone, and minimizing effects outside bone, compared to non-targeted rapamycin analogs. In this study, we tested this concept by examining the effects of AP24170 and rapamycin in an intracardiac MDA-MB-231 tumor cell injection model of bone osteolytic metastasis in nude mice. Three days post intracardiac cell inoculation, AP24170 and rapamycin were administered intravenously (biw and qw) to mice using equimolar doses (14 and 10 mg/kg, respectively) for a period of 3 weeks. Both AP24170 treated groups had a lower percentage of limb bones with cortical osteolytic lesions (24-21%) and fewer osteolytic lesions per mouse (1 met, av) than the comparable rapamycin treated groups (44-52% and 2-3 mets/mouse, av) as assessed by whole animal radiography. The vehicle treated mice developed osteolytic lesions in 85% of the bones examined and averaged 5 osteolytic limb lesions per mouse. The difference in potency between AP24170 and rapamycin was the opposite of that observed in prior  in vitro  cell assays, consistent with effective bone-targeting  in vivo . In a separate study, we examined systemic mTOR inhibitory effects by administering equimolar doses of each compound to mice, harvesting abdominal muscle 24 hr later, and assessing mTOR activity by measuring levels of phosphorylated S6 (pS6) by western blot. Rapamycin treatment elicited a clear dose-responsive reduction in pS6 levels, as expected, but AP24170 caused no apparent reduction of pS6, suggesting that the inhibitory effects of AP24170 are selective for bone. The tissue (bone) selective nature of AP24170 and the potent  in vivo  effects observed in this and other models of bone cancer make this class of compounds promising candidates for the treatment of both bone metastases and primary bone cancer.
Does antiretroviral therapy reduce HIV-associated tuberculosis incidence to background rates? A national observational cohort study from England, Wales, and Northern Ireland
Authors: Rishi K Gupta, Brian Rice, Alison E Brown, H Lucy Thomas, Dominik Zenner, Laura Anderson, Debora Pedrazzoli, Anton Pozniak, Ibrahim Abubakar, Valerie Delpech, Marc Lipman
Journal: The Lancet HIV (2015)
Managing Manic Depressive Disorders, by Ed Ved Varma
Authors: D. Ames
Journal: BMJ (1997)

Ed Ved Varma: Jessica Kingsley, £16.95, pp 188 ISBN 1 85302 347 7

Manic depressive (bipolar affective) disorders are serious mental illnesses that have a remitting and relapsing course. Unipolar depressions are the commonest disorders seen by psychiatrists, and bipolar disorder is the commonest diagnosis after schizophrenia among “new long stay” patients in British psychiatric facilities. Since the 1960s lithium prophylaxis has revolutionised the treatment of bipolar disorders, but the long term management of conditions that, in the acute phase, impair insight requires far more …
Ecological effects on the oro- and nasopharyngeal microflora in children after treatment of acute otitis media with cefuroxime axetil or amoxycillin-clavulanate as suspensions
Authors: B. Lund, C. Edlund, B. Rynnel-Dagöö, Y. Lundgren, J. Sterner, C.E. Nord
Journal: Clinical Microbiology and Infection (2001)
Abstract P367: Trends in Mortality and Recurrent Coronary Heart Disease Events Following an Acute Myocardial Infarction Among Medicare Beneficiaries, 2001 - 2009
Authors: Todd M Brown, Luqin Deng, David J Becker, Vera Bittner, Emily B Levitan, Robert S Rosenson, Monika M Safford, Paul Muntner
Journal: Circulation (2014)

Background: Few contemporary studies examine trends in recurrent coronary heart disease (CHD) events and mortality following acute myocardial infarction (AMI). Therefore, we examined rates of mortality, recurrent AMI, and recurrent CHD events in the year following AMI overall and by race and sex in the national 5% random sample of Medicare beneficiaries. Methods: Beneficiaries were included if they were enrolled in traditional Medicare fee-for-service coverage (Parts A and B), were not enrolled in a Medicare Advantage plan, and experienced an index AMI (ICD9 410.xx except 410.x2) between January 1, 2001 and December 31, 2009. We used Poisson regression to calculate and examine linear changes in age-adjusted rates for all-cause mortality, recurrent AMI, and recurrent CHD events (defined as a hospitalization for AMI in the primary discharge diagnosis position, percutaneous coronary intervention, or coronary artery bypass graft surgery) during the 365 days following hospital discharge for the index AMI. To provide adequate sample size to investigate trends in outcomes by race-sex groups, we pooled calendar years into 3 time periods (2001-2003, 2004-2006, and 2007-2009). Results: Overall, 48,688 beneficiaries were included; 46% were men, 90% were white, and 7% were black. Changes in pooled 3 year rates for mortality, recurrent AMI, and recurrent CHD in the first year following an index AMI are shown in the table. Overall, we observed a -3.8% change in pooled 3 year age-adjusted rates for mortality, a -15.0% change in pooled 3 year age-adjusted rates for recurrent AMI, and a -11.1% change in pooled 3 year age-adjusted rates for recurrent CHD events. However, mortality following AMI decreased only in white men, and reductions in recurrent AMI or CHD occurred only for white men and women and black men but not black women. Conclusions: Despite the overall favorable trends in lower mortality and recurrent AMI and CHD events following an index AMI, more efforts in reducing disparities in CHD by race and sex are needed.
441. Conditional Replication Competent Adenovirus Ad-mTERT-Δ19 Driven by Human Telomerase Promoter Replicates and Elicits Cytopathic Effect Specifically in Cancer Cells
Authors: Alexandra Bernshausen, Gabriel Glockzin, Klaus Mantwill, Hans-Dieter Royer, Karsten Juerchott, Bernd Gaensbacher, Per Sonne Holm
Journal: Molecular Therapy (2004)
THE CONTINUOUS METHOD OF TREATMENT OF EARLY SYPHILIS
Authors: Joseph Earle Moore
Journal: Annals of Internal Medicine (1936)

Article1 July 1936THE CONTINUOUS METHOD OF TREATMENT OF EARLY SYPHILISJOSEPH EARLE MOORE, M.D.JOSEPH EARLE MOORE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-10-1-30 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIf early syphilis is properly treated, late syphilis will almost, even if not quite, disappear. That early syphilis is not being properly treated is obvious from the fact that late syphilis is not disappearing. On the contrary, in every urban American community syphilis heads the list of reportable communicable diseases, and of the cases reported, more than half are late cases.1The proper treatment of early syphilis is of importance from three standpoints: that of the individual patient; that of the public health; and that of the public expense. The individual patient requires proper treatment in order to accomplish "cure"...Bibliography1. USILTON LJ: Trend of syphilis and gonorrhea in United States based on treated cases, Ven. Dis. Inform., 1935, xvi, 147-164. Google Scholar2. MOORE JE: The modern treatment of syphilis, 1933, C. C. Thomas, Springfield, Ill. Google Scholar3. STOKESCOLE JHHN: Cutaneous and mucosal relapse in early syphilis and its differentiation from reinfection, Ven. Dis. Inform., 1931, xii, 55-66. Ibid., and others: Coöperative clinical studies in the treatment of syphilis; early syphilis, Ven. Dis. Inform., 1932, xiii, 135, 165, 207, 253. Ibid.: Standard treatment procedures in early syphilis; a resumé of modern principles, Ven. Dis. Inform., 1934, xv, 149. Ibid., and others: What treatment in early syphilis accomplishes, Ven. Dis. Inform., 1934, xv, 341-363. Google Scholar4. THOMPSONBRUMFIELDCALDWELL WCWAL: The cost of syphilis in a representative American city, Am. Jr. Syph., Gon. and Ven. Dis. (To be published.) Google Scholar5. MOOREKEIDEL JEA: The treatment of early syphilis; a plan of treatment for routine use, Bull. Johns Hopkins Hosp., 1926, xxxix, 1-15. Google Scholar6. MOOREKEMP JEJE: The treatment of early syphilis; clinical results in 402 patients, Bull. Johns Hopkins Hosp., 1926, xxxix, 16-35. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Baltimore, Maryland*Presented at the Detroit meeting of the American College of Physicians, March 3, 1936.From the Syphilis Division of the Medical Clinic, the Johns Hopkins Hospital. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 July 1936Volume 10, Issue 1Page: 30-42KeywordsHospitalsPatientsPrevention, policy, and public healthSyphilis ePublished: 1 December 2008 Issue Published: 1 July 1936 PDF downloadLoading ...
Comparison of Treatment Strategies in Early Rheumatoid Arthritis
Authors: Yvonne P.M. Goekoop-Ruiterman, Jeska K. de Vries-Bouwstra, Cornelia F. Allaart, Derkjen van Zeben, Pit J.S.M. Kerstens, J. Mieke W. Hazes, Aelko H. Zwinderman, André J. Peeters, Johanna M. de Jonge-Bok, Constant Mallée, Wim M. de Beus, Peter B.J. de Sonnaville, Jacques A.P.M. Ewals, Ferdinand C. Breedveld, Ben A.C. Dijkmans
Journal: Annals of Internal Medicine (2007)

First-year results of the BeSt study showed that starting therapy for rheumatoid arthritis with several combinations of drugs produced more rapid clinical improvement and less progression of joint ...
Abstract 13548: Determination of Indication for Carotid Artery Stenting using Signal Intensity Ratio Evaluated by Magnetic Resonance Imaging-Comparative Study with Carotid Artery Stenting and Carotid Endarterectomy-
Authors: Kiyofumi Yamada, Masanori Kawasaki, Shinichi Yoshimura, Yukiko Enomoto, Takahiko Asano, Shinya Minatoguchi, Toru Iwama
Journal: Circulation (2010)

Background:  Carotid tissue components are associated with an incidence of embolic complications after carotid artery stenting (CAS) or carotid endarterectomy (CEA). The aim of study was to elucidate the relationship between tissue components and the incidence of new embolic lesions after CAS and CEA.   Methods:  We performed CAS in 56 patients and CEA in 25 patients with carotid stenosis. We also performed quantitative analyses of plaque characteristics in carotid arteries using T1 weighted black-blood magnetic resonance imaging (BB-MRI) before CAS and CEA. Signal intensity ratio (SIR) was defined as the ratio of signal intensity evaluated by BB-MRI in carotid plaques to that of sternocleidomastoid muscle. According to the criteria we and other investigators previously reported, the SIR was defined as “high”, when the SIR was ≥1.25. New ipsilateral silent ischemic lesions (NISIL) were evaluated by diffusion-weighted imaging of MRI comparing before and after CAS and CEA.   Results:  Forty-three plaques were classified as high SIR plaques. There were two minor strokes (2.5%) in high SIR group treated with CAS, whereas there was no stroke in high SIR group treated with CEA. In the high SIR group, the incidence of NISIL was higher in CAS group than CEA group (CAS vs CEA: 61% vs 13%, p=0.007), whereas there were no significant differences in the incidence of NISIL in the plaques with SIR    Conclusions:  Embolic complications occur more frequently after CAS than after CEA when SIR of carotid plaques ≥1.25. CEA should be selected when the SIR of carotid plaques is ≥1.25. Noninvasive quantitative tissue characterization in carotid plaques using BB-MRI is useful to determine the indication of CAS.
Abstract 11027: The Paracrine Factors Released From Mesenchymal Stem Cells Rejuvenate Cardiomyocytes Through Transfer of miRs and Regulation of Pten/ Akt Signaling Pathway
Authors: Bin Yu, Jingcai Wang, Min Gong, Yigang Wang, Millard Ronald W, Muhammad Ashraf, Meifeng Xu
Journal: Circulation (2014)

Our previous studies indicate that mesenchymal stem cells (MSC) overexpressing GATA-4 (MSCGATA-4) reduce infarction size and improve cardiac function in the myocardial ischemia via protecting cardiomyocytes (CM). In this study, we hypothesized that the paracrine factors of MSC rejuvenate CM through exosoemes (EXO) release resulting transferring bioactive factors and regulating the related signaling pathways. 1) We investigated the role of EXO on long-term culture-induced senescence. Primary neonatal CM were cultured in DMEM with 10% FBS for 3 days. The medium was replaced with serum free medium containing either EXO or 1% BSA. After 3 weeks, most CM displayed a senescent phenotype and a decreased beating frequency. While administration of EXO reduced significantly the percentage of SA β-gal positive CM and well restored the beating frequency of CM, particular EXOGATA-4 group showed a better Effect (Fig. A & B); 2) Two proliferation markers, Ki67 and Brdu, were examined in CM cultured for 7 days. EXO treat...
CALCIFICATION OF LEFT VENTRICULAR INFARCTION RECOGNIZED DURING LIFE
Authors: Milton C. Borman
Journal: Annals of Internal Medicine (1943)

Case Reports1 May 1943CALCIFICATION OF LEFT VENTRICULAR INFARCTION RECOGNIZED DURING LIFEMILTON C. BORMAN, M.D., F.A.C.P.MILTON C. BORMAN, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-18-5-857 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptCalcified myocardial infarcts have been rarely found during life, and still more rarely proved at necropsy. Calcification in the heart was diagnosed during life by roentgen-ray in 1911 by F. M. Groedel.1The first case thus recognized and proved by necropsy was that of Thomas Scholz2in 1924. Cohen and Levine3in 1937 reported the second case, which was also studied with the electrocardiograph. Parkinson4in 1938 added a third case proved at necropsy. Ours, the fourth case, was first discovered by roentgen-ray, and was studied with heart tracings and the kymograph. White5has stated that in rare cases actual...Bibliography1. GROEDEL FM: Reste Mitteilung ueber die Differenzierung einzelner Herzhoehlen im Roentgenbilde und den Nachweis von Kalkschatten i. d. Herzsilhouette intra vitam, Fortschr. a. d. Geb. d. Röntgenstrahlen, 1911, xvi, 337. Google Scholar2. SCHOLZ T: Calcification of the heart: its roentgenologic demonstration, Arch. Int. Med., 1924, xxxiv, 32-59. CrossrefGoogle Scholar3. COHENLEVINE JNHS: Calcification of myocardium with bone formation: report of a case, Arch. Int. Med., 1937, lx, 486-494. CrossrefGoogle Scholar4. PARKINSONBEDFORDTHOMSON JDEWA: Cardiac aneurysm, Quart. Jr. Med. N. S., 1938, vii, 455-478. Google Scholar5. WHITE PD: Heart disease, 1931, The Macmillan Company, New York. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Milwaukee, Wisconsin*Received for publication October 21, 1940.From the Medical Service, Sacred Heart Sanitarium, Milwaukee, Wisconsin. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCalcification of healed myocardial infarctsNumber of generations per year of the cabbage webworm, Hellula undalis FABRICIUSPostinfarction ventricular aneurysm 1 May 1943Volume 18, Issue 5Page: 857-865KeywordsElectrocardiographyHeartInfarctionMedical servicesMyocardial infarction Issue Published: 1 May 1943 PDF downloadLoading ...
Abstract 715: Vivo-Morpholino antisense oligomers decrease tumor growth in mice by altering mVEGF mRNA splicing to knock down mVEGF expression
Authors: Shan Jiang
Journal: Cancer Research (2014)

Abstract Vivo-Morpholino antisense oligomers can knock down gene expression by altering splicing of the pre-mRNA and generating a translational frameshift. VEGF overexpression is crucial for tumor growth and anti-VEGF therapies are promising in the treatment of certain cancers. Decreasing VEGF gene expression by exon deletion using Vivo-Morpholinos could suppress tumor growth. We examine the efficiency of mVEGF exon 2 deletion and tumor growth inhibition in mice injected with a Vivo-Morpholino oligomer (VMO-e2i2), which is designed to specifically delete the mVEGF exon 2 and cause downstream frameshifting in mVEGF protein. Mice bearing s.c. Lewis lung carcinoma tumors are I.V. injected with the VMO-e2i2 oligomers at 15mg/kg twice weekly for 2 weeks. VEGF exon 2 deletions are detected by RT-PCR in various tissues tested: approximately 100% exon 2 deletion in kidney, 80% in liver, 70% in skeletal muscles and 40% in s.c. tumors. The tumor volumes decrease by 6 fold over 16 days in mice injected with the VMO-e2i2 oligomers. Exon deletions are detected in various tissues including liver, small intestine, colon, skeletal and cardiac muscles, lung, stomach and kidney. The exon deletion mediated by Vivo-Morpholinos is target specific, dose-dependent and is detectable for more than 15 weeks after a single IV injection in mice. No significant toxicity is observed in mice injected with the effective dosage. Vivo-Morpholinos therefore represent a useful tool for cancer target identification and validation in rodent models and a possible therapeutic treatment. Citation Format: Shan Jiang. Vivo-Morpholino antisense oligomers decrease tumor growth in mice by altering mVEGF mRNA splicing to knock down mVEGF expression. [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 715. doi:10.1158/1538-7445.AM2014-715
Inducible caspase-9 suicide gene controls adverse effects from alloreplete T cells after haploidentical stem cell transplantation
Authors: Xiaoou Zhou, Gianpietro Dotti, Robert A. Krance, Caridad A. Martinez, Swati Naik, Rammurti T. Kamble, April G. Durett, Olga Dakhova, Barbara Savoldo, Antonio Di Stasi, David M. Spencer, Yu-Feng Lin, Hao Liu, Bambi J. Grilley, Adrian P. Gee, Cliona M. Rooney, Helen E. Heslop, Malcolm K. Brenner
Journal: Blood (2015)
Effect of Hormones on Mammary-Tumor Development From Transplanted Hyperplastic Alveolar Nodules in Hypophysectomized-Ovariectomized-Adrenalectomized C3H/Crgl Mice&lt;xref ref-type="fn" rid="FN1"&gt;2&lt;/xref&gt;
Authors: Satyabrata Nandi, Howard A. Bern
Journal: JNCI Journal of the National Cancer Institute (1961)

Hyperplastic alveolar nodules were transplanted into the mammary-gland-free fat pads of young C3H/Crgl female mice. The host animals were then hypophysectomized-ovariectomized-adrenalectomized and treated with various combinations of estradiol-17β, corticoids, and somatotropin. A combination of deoxycorticosterone + corticosterone + somatotropin permitted the development of tumors from the transplanted nodules. Both adrenal steroids were necessary, with somatotropin, to permit tumorigenesis. Large amounts of Cortisol resulted in lactogenesis in the nodules and inhibited neoplastic development. Estrogen, while not necessary for tumor formation, enhanced the tumorigenic action of corticoids + somatotropin.