tbuckley/cabot-search huggingface dataset:
The First Aphorism of Hippocrates
Authors: George Dock
Journal: Annals of Internal Medicine (1932)

Article1 July 1932The First Aphorism of HippocratesGEORGE DOCK, M.D., Sc.D., F.A.C.P.GEORGE DOCK, M.D., Sc.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-6-1-129 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptWe all claim descent, as physicians, from the philosophers and physicians of the great period of Greek civilization, the fifth century, B.C., and yet in the rapid increase of current literature we may easily forget what that means. Of course, we can easily revive our knowledge in any of a number of excellent works on Medical History, old or new; or, we can reread any chapter or number of chapters in the Hippocratic Writings. In the following I have chosen one book, namely, the Aphorisms, and traced it down through the centuries, at long intervals, to be sure, seeing how... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Pasadena, Calif.*Presented at the San Francisco Meeting of the American College of Physicians, April 4, 1932. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 July 1932Volume 6, Issue 1Page: 129-142KeywordsLibraries ePublished: 1 December 2008 Issue Published: 1 July 1932 PDF downloadLoading ...
Abstract 13937: Efficacy of Early Induction of Therapeutic Hypothermia for Patients with Return of Spontaneous Circulation after Out-of-Hospital Cardiac Arrest (J-PULSE-Hypo Study)
Authors: Masakazu Matsuzaki, Ken Nagao, Taketomo Soga, Asuka Kasai, Hiroshi Nonogi, Naohiro Yonemoto, Hiroyuki Yokoyama, J-PULSE-Hypo investigators
Journal: Circulation (2010)
Ownership and Use of Tissue Specimens for Research—Reply
Authors: Rina Hakimian, David Korn
Journal: JAMA (2005)

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
Relationship Between Levels of Advanced Glycation End Products and Their Soluble Receptor and Adverse Outcomes in Adults With Type 2 Diabetes
Authors: Merlin C. Thomas, Mark Woodward, Bruce Neal, Qiang Li, Raelene Pickering, Michel Marre, Bryan Williams, Vlado Perkovic, Mark E. Cooper, Sophia Zoungas, John Chalmers, Graham S. Hillis
Journal: Diabetes Care (2015)

This study explored whether activation of the receptor for advanced glycation end products (RAGE) is implicated in the development of diabetes complications.A case-cohort study was performed in 3,763 participants with prevalent diabetes in the Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) trial. The hazard ratios (HRs) for death, major cardiovascular events, and new or worsening nephropathy were derived using Cox regression models, and the ability of sRAGE and AGE levels to reclassify the risk of nephropathy was assessed.After adjustment for a range of possible confounders and other risk factors, sRAGE levels were associated with all-cause mortality (HR 1.11 for a 1-SD increase of log sRAGE [95% CI 1.00-1.22]; P = 0.045) and new or worsening nephropathy (HR 1.20 for a 1-SD increase of log sRAGE [95% CI 1.02-1.41]; P = 0.032). Circulating AGE levels were also independently associated with new or worsening nephropathy (HR 1.21 for a 1-SD increase [95% CI 1.08-1.36]; P = 0.001). Both markers also significantly improved the accuracy with which the 5-year risk of new or worsening nephropathy could be predicted (net reclassification index in continuous model, 0.25 for sRAGE and 0.24 for AGE levels).In adults with type 2 diabetes, increased levels of sRAGE are independently associated with new or worsening kidney disease and mortality over the next 5 years. Higher levels of AGE are also associated with an increased risk of adverse renal outcomes. The AGE/RAGE axis may be of importance in the prevention and management of diabetes complications.
Adhesion Molecules
Authors: Paul S. Frenette, Denisa D. Wagner
Journal: New England Journal of Medicine (1996)

A diverse system of adhesion molecules and adhesion receptors participates in orchestrating vital biologic phenomena, such as embryogenesis, cell growth and differentiation, and wound repair. Over the past decade there has been immense progress in our understanding of adhesion molecules and their complex interactions. We review the main classes of adhesion receptors and give examples of diseases in which they have been found to be involved.Among the many types of adhesion receptors on the cell surface, four major families stand out (Figure 1). The integrins are membrane glycoproteins with two subunits, designated α and β. An important feature of . . .
Ongoing spread of colistin-resistant Klebsiella pneumoniae in different wards of an acute general hospital, Italy, June to December 2011
Authors: C Mammina, C Bonura, F Di Bernardo, A Aleo, T Fasciana, C Sodano, M A Saporito, M S Verde, R Tetamo, D M Palma
Journal: Eurosurveillance (2012)

Binary file ES_Abstracts_Final_ECDC.txt matches
Abstract 17036: Flk1 Mediated Activation of ER71 and Specification of Cardiovascular Lineages
Authors: Tara L Rasmussen, Alicia Wallis, Xiaozhong Shi, Junghun Kweon, Naoko Koyano-Nakagawa, Daniel J Garry
Journal: Circulation (2011)

We have previously demonstrated that Ets Related Protein 71 (ER71) is essential for primitive hematopoiesis and development of the endothelial/endocardial lineages. Lack of ER71 results in early (E8.0-E9.0) embryonic lethality. We generated an ER71-EYFP transgenic reporter mouse model using FACS and transcriptome analysis and determined that hematopoieitic and endothelial/endocardial molecular programs are restricted to the FACS sorted ER71-EYFP+ population. Using immunohistochemical techniques, we observed coexpression of EYFP (representing ER71 expression) and Flk1 between E7.0 and E9.5. However, Flk1 expression appears to precede ER71 expression in the primitive streak. Based on our observation that ER71 mutants phenocopy Flk1 null embryos at E8.0, we undertook a genetic analysis to determine whether Flk1 was upstream of ER71. We analyzed Flk1 expression in the ER71 mutant background by utilizing the Flk1-LacZ allele, FACS analysis, and qPCR. While Flk1-LacZ shows an aberrant spatial expression pattern, the frequency of cells expressing Flk1 is unchanged at E7.75 and is decreased modestly (two-fold) at E8.0. This demonstrates that Flk1 is not completely dependent on ER71 expression. In contrast, crossing the ER71-EYFP transgenic reporter allele into the Flk1 null background revealed that ER71 expression at E7.75 and E8.0 is dependent on Flk1. Furthermore, we have identified an evolutionarily conserved NFAT binding site in the essential ER71 promoter. NFAT is a family of transcription factors known to mediate a VEGF signalling cascade that involves the Flk1 receptor and Calcineurin. We have used ChIP and EMSA to verify that NFAT directly binds the ER71 promoter. Using transcriptional assays, we further demonstrate that ER71 is regulated by NFAT and Calcineurin. Collectively, these studies support the hypothesis that a Flk1-ER71 network specifies and coordinates the endothelial/endocardial lineages during cardiovascular development.
Unusual intracytoplasmic inclusions in acute myeloblastic leukemia
Authors: David J. Wolf, Mark A. Fialk, Janet Mouradian, Eugene L. Gottfried, Mark W. Pasmantier
Journal: American Journal of Hematology (1980)

Abstract Unusual intracytoplasmic inclusions within early granulocyte precursor cells from a patient with acute myeloblasts leukemia (AML) are described. Based upon their staining characteristics and electron‐ and light‐microscopic appearance, the inclusions are distinctly different from any previously described. The inclusions display a variety of shapes, including rectangles, squares, circles, ovals, and irregular, globular forms. Most of the inclusions are refractile and crystal‐like. The possible composition of these inclusions is discussed. They are compared with inclusions previously described within leukemic and granulocytic cells.
697. Correction of Lysosomal Storage within the Brain of Adult MPS VII Mice Following Intrahepatic Administration of a Recombinant Adeno-Associated Virus Vector
Authors: Kristin Backstrom, Chuansong Wang, Chiou-Miin Wang, Thomas J. Sferra
Journal: Molecular Therapy (2004)

Mucopolysaccharidosis type VII (MPS VII; Sly disease) is a lysosomal storage disease (LSD) caused by a deficiency of the acid hydrolase β-glucuronidase. Deficiency of this enzyme results in the lysosomal accumulation of glycosaminoglycans in most organs, including the brain. In the mouse model of this disorder, widespread correction of the central nervous system manifestations has not been observed with peripherally administered therapies in adult animals. The objective of this study was to evaluate the effect of peripheral administration of an rAAV vector on lysosomal storage within the brain of adult MPS VII mice.
Abstract 20158: Long-Term Device-Related Adverse Events After Implantable Cardioverter-Defibrillator Therapy
Authors: Isuru Ranasinghe, Craig Parzynski, James V Freeman, Rachel P Dreyer, Joseph S Ross, Joseph G Akar, Harlan M Krumholz, Jeptha P Curtis
Journal: Circulation (2014)

Background: Long-term implantable cardioverter-defibrillator (ICD) adverse events are poorly documented. In the NCDR ICD Registry™, a nationally representative cohort, we calculated the rate of long-term post-discharge device related adverse events. Methods: We included first-time ICD implants from 2006-2010 that could be matched with Medicare fee-for-service claims data to identify outcomes. We excluded patients if they had a previous ICD or pacemaker, CABG during their procedure, or were not discharged alive. The primary outcome was device reoperation (involving the generator, leads, pocket, or a combination) for device malfunction, infection, other complications (wound disruption, cardiac perforation, etc.), or reoperation for battery end-of-life and/or device upgrade. Analysis was performed using unadjusted cumulative incidence functions taking into consideration the competing risk of death. Results: We identified 185,263 ICD implants of which 114,649 (19.7% single-chamber, 41.3% dual-chamber, 38.8% CRT-D) could be matched to Medicare data (mean age 74.8±6.2 years, 72.5% male).Of these, 83.5% were for primary prevention of sudden cardiac death. The median follow up was 2.7 yrs (max follow-up 6 yrs). At least 1 reoperation occurred in 15.5% of patients by 6 yrs and more than 80% of these reoperations occurred after the early (&gt;90 days) post-implantation period (Figure). Reoperation rates for specific complications (per 1000 patient yrs) were device malfunction (14.3), infection (5.1), other device related complications (18.4) and reoperation for generator battery end-of-life and/or device upgrade (12.9). The crude reoperation rate (for any cause) was similar among device types (P=0.19). Conclusion: Patients continue to have adverse outcomes in the years post ICD implantation, predominately from device malfunction. Our next steps are to identify patient, device, and provider factors associated with these long-term adverse events.
DNA-PK and ATR are responsible for the G2 checkpoint activation by the nucleoside analog CNDAC
Authors: Xiaojun Liu, Akira Matsuda, William Plunkett
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4902 

The nucleoside analog CNDAC (2’- C -cyano-2’-deoxy-1-β-D-arabino-pentofuranosyl-cytosine) has a novel mechanism of action of causing a single strand break subsequent to its incorporation into DNA, which associates with activation of the G2 checkpoint. The Chk1-Cdc25C-Cdk1/Cyclin B pathway is activated in instituting this G2 arrest (Cancer Res. 2005, 65:6874-81). In order to define the role of upstream DNA damage checkpoint sensors, particularly the major PI 3-kinase family proteins, we used genetically defined cell lines and PI 3-kinase inhibitors to determine the biological response to CNDAC at minimal concentrations causing cell cycle arrest. Exposure of fibroblasts, ATM mutant, vector control and repleted lines, to CNDAC for 24 hr increased the G2 population equally; also phospho-Ser345 of Chk1 increased in both mutant and repleted lines, suggesting ATM is not required to activate the G2 checkpoint in response to CNDAC. However, clonogenic assays showed the CNDAC concentration needed to kill 90% of the ATM mutant cells was 20-fold less than that for the repleted cells, indicating ATM is essential for cell survival after DNA damage by CNDAC. In contrast to the AT lines, there was no sensitization of clonogenicity in DNA-PK mutant glioblastoma cells (M059-J) compared to the wild type (M059-K). Both M059-K and -J cells arrested in G2 upon CNDAC treatment. However, significantly more M059-J cells progressed through G2 following CNDAC treatment and were trapped in mitosis by nocodazole compared to the wild type. M059-K cells incubated with CNDAC and nocodazole had a mitotic index of <3%, whereas the mitotic index of M059-J cells (10.8%, p<0.01) was about half of that in cells treated with nocodazole alone. Thus, it appears that DNA-PK is partially responsible for G2 checkpoint activation by CNDAC. Two PI 3-kinase inhibitors, caffeine and wortmannin, were used to suppress CNDAC-induced G2 checkpoint. Caffeine (3 mM) was capable of abolishing CNDAC-induced G2 arrest in human AML ML-1, ATM mutant and colon cancer HCT116 cells. Considering that ATM is not involved, it appears that ATR might be important for this G2 checkpoint activation. Wortmannin completely abolished CNDAC-induced G2 arrest in ML-1 and ATM mutant cells at a lower concentration (10 μM). As ATM was not detectable in ML-1 cells, even under the condition of IR, these results indicated that DNA-PK is essential for the G2 checkpoint activation by CNDAC in these lines. In HCT116 cells, CNDAC-induced G2 arrest was reduced from 48% to 33% by 10 μM wortmannin, and was further abolished to a level less than untreated cells (17%) by 100 μM wortmannin, indicating participation of ATR in this G2 checkpoint pathway. Together, our data demonstrated both DNA-PK and ATR are responsible for CNDAC-induced activation of the G2 checkpoint.
189. Sendai Virus Mediated Angiopoietin-1 Gene Therapy for Cardiovascular Diseases
Authors: Yoshinori Ito, Jinghua Huang, Takeshi Uzuka, Yukiko Honma, Hironari Dehari, Masayoshi Kobune, Kiminori Nakamura, Makoto Inoue, Mamoru Hasegawa, Hirofumi Hamada
Journal: Molecular Therapy (2004)

Background: Sendai virus (SeV) is negative-stranded RNA virus, which is classified as a type I parainfluenza virus belonging to the family of Paramyxoviridae. SeV has been known as rodent respiratory virus, however it is considered to be non-pathogen for humans. Recently, efficient gene transduction into various types of cells and tissue has been reported. Angiopoietin-1 (Ang1) is a critical angiogenic factor for vascular maturation and enhances vascular endothelial growth factor (VEGF)-induced angiogenesis in a complementary manner. Previously we reported Ang1 gene therapy clearly promoted myocardial angiogenesis and prevented remodeling in a rat AMI model. In the present study, we created recombinant Sendai virus vector (SeVV) encoding human Ang1 and evaluated therapeutic effect in the cardiovascular diseases. We also evaluated the angiogenic effect of mesenchymal stem cells (MSCs) transplantation with SeVV-mediated Ang1 gene modification.
Abstract 15346: Human Peripheral blood-derived Sphere as a Niche for Adult Stem-Progenitor Cell Self-Renewal
Authors: Jin Hur, Jonghanne Park, Sang Eun Lee, Chang-Hwan Yoon, Jae Hee Jang, Ji Min Yang, Tae-Kyu Lee, Han-Mo Yang, Ju-Young Kim, Eun Ju Lee, Hyun-Jai Cho, Hyun-Jae Kang, Byung-Hee Oh, Young-Bae Park, Hyo-Soo Kim
Journal: Circulation (2010)

Background: Human peripheral blood is a promising source of autologous stem-progenitor cells such as endothelial progenitor cells or hematopoietic stem cells However, the rarity of stem cell popula...
Pediatric Sleep Medicine Comes of Age
Authors: Lynne Lamberg
Journal: JAMA (2005)

AMELIA ISLAND,FLA—A fussy baby fails to grow normally. A 7-year-old who has autism goes to sleep at 9 PM but awakens for thedayat2 AM.A9-year-oldcannotsit still inclassandseldomcompletes homework.A17-year-oldhonorstudent attendsbandpractice, staysuplate to finishhomework, anddrives through a red lightonthewaytoschool thenextmorning, clipping a delivery van. One in 4 children and adolescents has a problem with sleep that warrants a physician’s attention, specialists in pediatric sleep medicine say. Yet such problems often go unrecognized. Children who sleep too little or sleep poorly are more apt to be inattentive and hyperactive—tired and wired—than overtly drowsy. At a recent meeting here sponsored by Brown Medical School, Providence, RI, pediatric sleep specialists discussed ways to boost practitioner and public awareness of such symptoms and sought to define priorities for basic and clinical research, patient care, and public policy for their young field. The 130 attendees included pediatricians, pulmonologists, psychiatrists, and neurologists, as well as psychologists, social workers, and nurses.
Differential sensitivity of subsets of monocyte-derived macrophages to apoptosis; its impact on lung inflammation
Authors: Nisha Kurian, Danen Cunoosamy
Journal: European Respiratory Journal (2014)

Macrophages represent the largest population of innate immune cells present in the lung. Their chronic activation is thought to contribute to pathophysiological changes associated with COPD. The role of differentially polarised macrophage phenotypes in chronic lung inflammation is poorly understood.The ability to generate in-vitro polarize cells therefore allows us to examine how these various subsets modulate inflammatory changes1. Furthermore, the imbalance in the regulation of apoptosis of these cells may be one contributing factor to disease. The aim of this study is to characterize differences in apoptosis pathways of GMCSF (M1-like) or MCSF (M2-like) polarized monocyte-derived macrophages (MDM), as a surrogate to tissue-derived alveolar macrophages. Isolated human monocytes were allowed to differentiate into macrophages for 6 days in either MCSF or GMCSF supplemented XVivo10 media. The ability of staurosporine to induce apoptosis in differentially polarised MDM were then characterised by quantifying the extent of caspase 3/7 activation. Treatment with staurosporine time and dose-dependently enhanced caspase3/7 activation in M1-like and M2-like MDM. M1-like MDM were less sensitive to apoptosis in comparison to M2-like MDM. These findings suggest differences in the apoptotic signaling pathways associated with these two macrophage subsets could be a contributing factor to disease progression. Future work will be aimed at further characterizing these differences.

1. Rey-Giraud,F et al., 2012 PLoS ONE 7(8): e42656. doi:10.1371/journal.pone.0042656.
Abstract 11847: Genotype-Guided Vitamin K Antagonist Dosing Algorithms Improve Time in Therapeutic Range: A Systematic Review and Meta-Analysis
Authors: Emilie P Belley-Côté, Hasib Hanif, Frederick D’Aragon, John Eikelboom, Jeffrey L Anderson, Mark Borgman, Daniel E Jonas, Stephen Kimmel, Anke H Maitland-van der Zee, Munir Pirmohamed, Richard Whitlock
Journal: Circulation (2014)

Introduction:  Variability in vitamin K antagonist (VKA) dosing is partially explained by CYP2C9 and VKORC1 polymorphisms. Genotype-guided VKA dosing may improve quality of anticoagulation and outcomes. We performed a meta-analysis to determine whether genotype-guided VKA dosing algorithms decrease a composite of death, thromboembolic events and major bleeding and improve time in therapeutic range (TTR).   Methods:  We searched MEDLINE, EMBASE, CENTRAL, trial registries and conference proceedings for randomized trials comparing genotype-guided and non genotype-guided VKA dosing algorithms in adults initiating anticoagulation. Data was extracted in duplicate and pooled using a random effects model.   Results:  We included 12 studies involving 3217 patients. Nine studies reported at least one of the components of the composite outcome (2483 patients, 94 events). Pooled data indicate that the relative risk for the composite outcome was similar in both groups (0.82; 95%CI 0.55,1.22) with no evidence of heterogeneity (×2=5.76, p=0.57, I2=0%). The genotype-guided group had higher TTR (mean difference 4.31; 95% CI 0.35,8.26; heterogeneity ×2=43.31, p   Conclusions:  Genotype-guided compared with non genotype-guided VKA dosing algorithms did not decrease a composite of death, thromboembolism and major bleeding but resulted in improved TTR. The improvement in TTR appeared to be isolated in the subgroup of studies using a fixed VKA dosing algorithm in the non genotype-guided group.
Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice
Authors: Jean-Philippe Pradere, Johannes Kluwe, Samuele De Minicis, Jing-Jing Jiao, Geum-Youn Gwak, Dianne H. Dapito, Myoung-Kuk Jang, Nina D. Guenther, Ingmar Mederacke, Richard Friedman, Ana-Cristina Dragomir, Costica Aloman, Robert F. Schwabe
Journal: Hepatology (2013)

Although it is well established that hepatic macrophages play a crucial role in the development of liver fibrosis, the underlying mechanisms remain largely elusive. Moreover, it is not known whether other mononuclear phagocytes such as dendritic cells (DCs) contribute to hepatic stellate cell (HSC) activation and liver fibrosis. We show for the first time that hepatic macrophages enhance myofibroblast survival in a nuclear factor kappa B (NF-κB)-dependent manner and thereby promote liver fibrosis. Microarray and pathway analysis revealed no induction of HSC activation pathways by hepatic macrophages but a profound activation of the NF-κB pathway in HSCs. Conversely, depletion of mononuclear phagocytes during fibrogenesis in vivo resulted in suppressed NF-κB activation in HSCs. Macrophage-induced activation of NF-κB in HSCs in vitro and in vivo was mediated by interleukin (IL)-1 and tumor necrosis factor (TNF). Notably, IL-1 and TNF did not promote HSC activation but promoted survival of activated HSCs in vitro and in vivo and thereby increased liver fibrosis, as demonstrated by neutralization in coculture experiments and genetic ablation of IL-1 and TNF receptor in vivo. Coculture and in vivo ablation experiments revealed only a minor contribution to NF-κB activation in HSCs by DCs, and no contribution of DCs to liver fibrosis development, respectively.Promotion of NF-κB-dependent myofibroblast survival by macrophages but not DCs provides a novel link between inflammation and fibrosis.