tbuckley/cabot-search huggingface dataset:
Biomaterials: Nanowell‐Trapped Charged Ligand‐Bearing Nanoparticle Surfaces: A Novel Method of Enhancing Flow‐Resistant Cell Adhesion (Adv. Healthcare Mater. 7/2013)
Authors: Phat L. Tran, Jessica R. Gamboa, Katherine E. McCracken, Mark R. Riley, Marvin J. Slepian, Jeong‐Yeol Yoon
Journal: Advanced Healthcare Materials (2013)

Jeong-Yeol Yoon, Marvin J. Slepian, and co-workers describe on page 1019 a novel method utilizing nanofabrication techniques to create surfaces with enhanced endothelial adhesion and retention under flow. The system utilizes nano texture, charge, and ligands all combined together, uniquely assembled on the substrata surface, to create ensemble nanotextured surfaces. This new method may be of particular utility for enhancing flow-resistant endothelialization of cardiovascular devices.
Surgical Management of Acute Pancreatitis
Authors: John M. Howard
Journal: JAMA (1960)

A review of clinical experiences with 350 patients with acute pancreatitis and several hundred patients with other acute abdominal diseases revealed that the diagnosis of acute pancreatitis is primarily a bedside diagnosis. Laboratory aids are helpful here, yet unreliable. The mortality rate from acute pancreatitis has fallen to approximately eight per cent since the advent of better transfusion and antibacterial therapy. A recent development in the understanding of pancreatitis has been the realization that this term covers several diseases. Gallstone pancreatitis seldom leads to chronic pancreatitis and can be interrupted by definitive gallstone surgery. Alcoholic pancreatitis characteristically leads to chronic pancreatitis and responds poorly to biliary tract surgery.
Chlamydia psittaci-eradicating antibiotic therapy in patients with advanced-stage ocular adnexal MALT lymphoma
Authors: A.J.M. Ferreri, G.P. Dognini, M. Ponzoni, L. Pecciarini, M.G. Cangi, G. Santambrogio, A.G. Resti, C. De Conciliis, S. Magnino, E. Pasini, N. Vicari, R. Dolcetti, C. Doglioni
Journal: Annals of Oncology (2007)
Pediatric Gastrointestinal Endoscopy Textbook and Atlas
Authors: R. K Russell
Journal: Gut (2007)

<b>Background:</b> Mechanical circulatory support may be considered in patients with severe acute right ventricular (RV) failure due to massive pulmonary embolism (PE). <b>Method:</b> We report outcomes&nbsp;in consecutive patients referred to our ECMO service for acute PE complicated by cardiogenic shock and received a percutaneous right ventricular assist device (pRVAD)&nbsp; between December 2019 and December 2020. <b>Results:</b> Four patients (mean age 49±15 yrs) with&nbsp;persistent cardiogenic shock&nbsp;and severe RV failure from acute PE received Protek Duo Oxy-RVADs. Haemodynamic status and RV function improved with pRVAD support and all patients were decannulated after a mean duration of 8±2.9 days. There were no device-related complications. One patient died of hospital aquired pneumonia 15 days after decannulation. <b>Conclusion:</b> In this initial series of patients with PE related severe acute RV failure, pRVADs resulted in hemodynamic benefits with reversal of shock.
Use of Induced Pluripotent Stem Cells to Recapitulate Pulmonary Alveolar Proteinosis Pathogenesis
Authors: Takuji Suzuki, Christopher Mayhew, Anthony Sallese, Claudia Chalk, Brenna C. Carey, Punam Malik, Robert E. Wood, Bruce C. Trapnell
Journal: American Journal of Respiratory and Critical Care Medicine (2013)

In patients with pulmonary alveolar proteinosis (PAP) syndrome, disruption of granulocyte/macrophage colony-stimulating factor (GM-CSF) signaling is associated with pathogenic surfactant accumulation from impaired clearance in alveolar macrophages.The aim of this study was to overcome these barriers by using monocyte-derived induced pluripotent stem (iPS) cells to recapitulate disease-specific and normal macrophages.We created iPS cells from two children with hereditary PAP (hPAP) caused by recessive CSF2RA(R217X) mutations and three normal people, differentiated them into macrophages (hPAP-iPS-Mφs and NL-iPS-Mφs, respectively), and evaluated macrophage functions with and without gene-correction to restore GM-CSF signaling in hPAP-iPS-Mφs.Both hPAP and normal iPS cells had human embryonic stem cell-like morphology, expressed pluripotency markers, formed teratomas in vivo, had a normal karyotype, retained and expressed mutant or normal CSF2RA genes, respectively, and could be differentiated into macrophages with the typical morphology and phenotypic markers. Compared with normal, hPAP-iPS-Mφs had impaired GM-CSF receptor signaling and reduced GM-CSF-dependent gene expression, GM-CSF- but not M-CSF-dependent cell proliferation, surfactant clearance, and proinflammatory cytokine secretion. Restoration of GM-CSF receptor signaling corrected the surfactant clearance abnormality in hPAP-iPS-Mφs.We used patient-specific iPS cells to accurately reproduce the molecular and cellular defects of alveolar macrophages that drive the pathogenesis of PAP in more than 90% of patients. These results demonstrate the critical role of GM-CSF signaling in surfactant homeostasis and PAP pathogenesis in humans and have therapeutic implications for hPAP.
Dispensing Sample Drugs
Authors: Buff B. Burtis, Bernard G. Keller
Journal: Annals of Internal Medicine (1973)

Letters, Comments, and Corrections1 February 1973Dispensing Sample DrugsBUFF B. BURTIS, M.D., BERNARD G. KELLER JR.BUFF B. BURTIS, M.D.Search for more papers by this author, BERNARD G. KELLER JR.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-78-2-305_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Drug samples have become a needed tool in our teaching clinic but have presented problems. For their solution, we have developed a new clinic dispensary that is run by supervised pharmacy students and stocked entirely by drug samples donated for use by our interns and residents. This plan's benefits in education and safety, as well as in better service to the community's medically indigent persons, make it desirable for any large, teaching, outpatient department.Many samples have been given to our house staff by representatives of pharmaceutical companies. Our clinics have become the depository for most of... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDAzocines 1 February 1973Volume 78, Issue 2Page: 305-305KeywordsDrugsMedical educationOutpatientsSafety Issue Published: 1 February 1973 PDF downloadLoading ...
Central blockade of TLR4 improves cardiac function and attenuates myocardial inflammation in angiotensin II-induced hypertension
Authors: Rahul B. Dange, Deepmala Agarwal, Gustavo S. Masson, Jorge Vila, Brad Wilson, Anand Nair, Joseph Francis
Journal: Cardiovascular Research (2014)

Understanding the novel signalling pathways involved in the pathogenesis of hypertension is vital for the development of effective therapeutic strategies. Recent evidence suggests a role for Toll-like receptor (TLR) 4 in the development of cardiovascular diseases. Although brain has been implicated in the pathogenesis of hypertension, the role of brain TLR4 in hypertension is largely unexplored. Therefore, we investigated the role of brain TLR4 in angiotensin (Ang) II-induced hypertension and whether central TLR4 blockade has cardioprotective effects in hypertension.Hypertension was induced in male Sprague-Dawley rats by delivering AngII for 14 days. The rats were administered either specific TLR4 blocker, viral inhibitory peptide (VIPER), or control peptide, intracerebroventricularly. Blood pressure, and cardiac hypertrophy and function, was evaluated by radiotelemetry and echocardiography, respectively. Blood and paraventricular nucleus were collected for measurement of plasma norepinephrine (NE), tumour necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and TLR4 expression, respectively. Heart was analysed for TNF-α, IL-1β, inducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NFκB), and renin-angiotensin system (RAS) components. Hypertensive rats had dramatically increased TLR4 expression compared with normotensive rats. Central blockade of TLR4 delayed progression of hypertension and improved cardiac hypertrophy and function in hypertensive rats. TLR4 blockade significantly reduced myocardial TNF-α, IL-1β, iNOS levels, NFκB activity, and altered RAS components in hypertensive rats. These results were associated with reduced circulating NE levels in VIPER-treated hypertensive rats.These results provide mechanistic evidence that AngII-induced hypertensive effects are mediated, at least in part, by brain TLR4, and that brain TLR4 blockade attenuates AngII-induced hypertensive response, possibly via down-regulation of myocardial inflammatory molecules and sympathetic activity.
Establishment of a Simple and Practical Procedure Applicable to Therapeutic Angiogenesis
Authors: Shinichi Kanno, Nobuyuki Oda, Mayumi Abe, Sachiko Saito, Katsuyoshi Hori, Yasunobu Handa, Koichi Tabayashi, Yasufumi Sato
Journal: Circulation (1999)

Therapeutic angiogenesis is thought to be beneficial for serious ischemic diseases. This investigation was designed to establish a simple and practical procedure applicable to therapeutic angiogenesis.When cultured skeletal muscle cells were electrically stimulated at a voltage that did not cause their contraction, vascular endothelial growth factor (VEGF) mRNA was augmented at an optimal-frequency stimulation. This increase of VEGF mRNA was derived primarily from transcriptional activation. Electrical stimulation increased the secretion of VEGF protein into the medium. This conditioned medium then augmented the growth of endothelial cells. The effect of electrical stimulation was further confirmed in a rat model of hindlimb ischemia. The tibialis anterior muscle in the ischemic limb was electrically stimulated. The frequency of stimulation was 50 Hz and strength was 0.1 V, which was far below the threshold for muscle contraction. After a 5-day stimulation, there was a significant increase in blood flow within the muscle. Immunohistochemical analysis revealed that VEGF protein was synthesized and capillary density was significantly increased in the stimulated muscle. Rats tolerated this procedure very well, and there was no muscle contraction, muscle injury, or restriction in movement.We propose this procedure as a simple and practical method of therapeutic angiogenesis.
N-Terminal Pro-B-Type Natriuretic Peptide Is a Major Predictor of the Development of Atrial Fibrillation
Authors: Kristen K. Patton, Patrick T. Ellinor, Susan R. Heckbert, Robert H. Christenson, Christopher DeFilippi, John S. Gottdiener, Richard A. Kronmal
Journal: Circulation (2009)

Background— Atrial fibrillation (AF), the most common cardiac rhythm abnormality, is associated with significant morbidity, mortality, and healthcare expenditures. Elevated B-type natriuretic peptide levels have been associated with the risk of heart failure, AF, and mortality. Methods and Results— The relation between N-terminal pro-B-type natriuretic peptide (NT-proBNP) and AF was studied in 5445 Cardiovascular Health Study participants with the use of relative risk regression for predicting prevalent AF and Cox proportional hazards for predicting incident AF. NT-proBNP levels were strongly associated with prevalent AF, with an unadjusted prevalence ratio of 128 for the highest quintile (95% confidence interval, 17.9 to 913.3; P &lt;0.001) and adjusted prevalence ratio of 147 for the highest quintile (95% confidence interval, 20.4 to 1064.3; P &lt;0.001) compared with the lowest. After a median follow-up of 10 years (maximum of 16 years), there were 1126 cases of incident AF (a rate of 2.2 per 100 person-years). NT-proBNP was highly predictive of incident AF, with an unadjusted hazard ratio of 5.2 (95% confidence interval, 4.3 to 6.4; P &lt;0.001) for the development of AF for the highest quintile compared with the lowest; for the same contrast, NT-proBNP remained the strongest predictor of incident AF after adjustment for an extensive number of covariates, including age, sex, medication use, blood pressure, echocardiographic parameters, diabetes mellitus, and heart failure, with an adjusted hazard ratio of 4.0 (95% confidence interval, 3.2 to 5.0; P &lt;0.001). Conclusions— In a community-based population of older adults, NT-proBNP was a remarkable predictor of incident AF, independent of any other previously described risk factor.
Acute kidney injury in cirrhosis
Authors: Guadalupe Garcia-Tsao, Chirag R. Parikh, Antonella Viola
Journal: Hepatology (2008)

Abstract Acute renal failure (ARF), recently renamed acute kidney injury (AKI), is a relatively frequent problem, occurring in approximately 20% of hospitalized patients with cirrhosis. Although serum creatinine may underestimate the degree of renal dysfunction in cirrhosis, measures to diagnose and treat AKI should be made in patients in whom serum creatinine rises abruptly by 0.3 mg/dL or more (≥26.4 μmol/L) or increases by 150% or more (1.5-fold) from baseline. The most common causes of ARF (the term is used interchangeably with AKI) in cirrhosis are prerenal azotemia (volume-responsive prerenal AKI), acute tubular necrosis, and hepatorenal syndrome (HRS), a functional type of prerenal AKI exclusive of cirrhosis that does not respond to volume repletion. Because of the progressive vasodilatory state of cirrhosis that leads to relative hypovolemia and decreased renal blood flow, patients with decompensated cirrhosis are very susceptible to developing AKI with events associated with a decrease in effective arterial blood volume. HRS can occur spontaneously but is more frequently precipitated by events that worsen vasodilatation, such as spontaneous bacterial peritonitis. Conclusion: Specific therapies of AKI depend on the most likely cause and mechanism. Vasoconstrictors are useful bridging therapies in HRS. Ultimately, liver transplantation is indicated in otherwise reasonable candidates in whom AKI does not resolve with specific therapy. (Hepatology 2008;48:2064-2077.)
POSSIBLE APPLICATION OF PHENOLTETRACHLORPHTHALEIN TEST TO OBSTRUCTIVE JAUNDICE
Authors: REUBEN OTTENBERG
Journal: JAMA (1923)

The diagnosis of complete obstruction of the common bile duct is usually easy. If, however, we are asked on any given day whether complete obstruction is still present, we cannot give a certain answer, because the subsidence of the symptoms on which the diagnosis rests—acholic stools, jaundice, choluria, bilirubinemia —takes a number of days. There are certain situations in which the answering of this question may be of great practical value. For example, if a surgeon about to operate on a patient with protracted jaundice due to stone in the common bile duct could ascertain that the stone had just passed spontaneously, he would in most instances postpone operation to a time when the patient's general condition was more favorable. The question might, of course, be answered by the use of the duodenal tube. But in the absence of bile, it is very difficult to be certain that the tip
The antiviral protein viperin inhibits hepatitis C virus replication via interaction with nonstructural protein 5A
Authors: Karla J. Helbig, Nicholas S. Eyre, Evelyn Yip, Sumudu Narayana, Kui Li, Guillaume Fiches, Erin M. McCartney, Rohit K. Jangra, Stanley M. Lemon, Michael R. Beard
Journal: Hepatology (2011)

The interferon-stimulated gene, viperin, has been shown to have antiviral activity against hepatitis C virus (HCV) in the context of the HCV replicon, although the molecular mechanisms responsible are not well understood. Here, we demonstrate that viperin plays an integral part in the ability of interferon to limit the replication of cell-culture-derived HCV (JFH-1) that accurately reflects the complete viral life cycle. Using confocal microscopy and fluorescence resonance energy transfer (FRET) analysis, we demonstrate that viperin localizes and interacts with HCV nonstructural protein 5A (NS5A) at the lipid-droplet (LD) interface. In addition, viperin also associates with NS5A and the proviral cellular factor, human vesicle-associated membrane protein-associated protein subtype A (VAP-A), at the HCV replication complex. The ability of viperin to limit HCV replication was dependent on residues within the C-terminus, as well as an N-terminal amphipathic helix. Removal of the amphipathic helix-redirected viperin from the cytosolic face of the endoplasmic reticulum and the LD to a homogenous cytoplasmic distribution, coinciding with a loss of antiviral effect. C-terminal viperin mutants still localized to the LD interface and replication complexes, but did not interact with NS5A proteins, as determined by FRET analysis.In conclusion, we propose that viperin interacts with NS5A and the host factor, VAP-A, to limit HCV replication at the replication complex. This highlights the complexity of the host control of viral replication by interferon-stimulated gene expression.
Comparison of survival of amiodarone-treated patients with coronary artery disease and malignant ventricular arrhythmias with that of a control group with coronary artery disease
Authors: G. Neal Kay, David B. Pryor, Kerry L. Lee, Frank E. Harrell, Joyce C. Pressley, Marcel R. Gilbert, Lawrence D. German
Journal: Journal of the American College of Cardiology (1987)
Patrick Christopher Steptoe, MD
Authors: Audrey Lowe
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 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
Association of National Initiatives to Improve Cardiac Arrest Management With Rates of Bystander Intervention and Patient Survival After Out-of-Hospital Cardiac Arrest
Authors: Mads Wissenberg, Freddy K. Lippert, Fredrik Folke, Peter Weeke, Carolina Malta Hansen, Erika Frischknecht Christensen, Henning Jans, Poul Anders Hansen, Torsten Lang-Jensen, Jonas Bjerring Olesen, Jesper Lindhardsen, Emil L. Fosbol, Søren L. Nielsen, Gunnar H. Gislason, Lars Kober, Christian Torp-Pedersen
Journal: JAMA (2013)

Out-of-hospital cardiac arrest is a major health problem associated with poor outcomes. Early recognition and intervention are critical for patient survival. Bystander cardiopulmonary resuscitation (CPR) is one factor among many associated with improved survival.To examine temporal changes in bystander resuscitation attempts and survival during a 10-year period in which several national initiatives were taken to increase rates of bystander resuscitation and improve advanced care.Patients with out-of-hospital cardiac arrest for which resuscitation was attempted were identified between 2001 and 2010 in the nationwide Danish Cardiac Arrest Registry. Of 29,111 patients with cardiac arrest, we excluded those with presumed noncardiac cause of arrest (n = 7390) and those with cardiac arrests witnessed by emergency medical services personnel (n = 2253), leaving a study population of 19,468 patients.Temporal trends in bystander CPR, bystander defibrillation, 30-day survival, and 1-year survival.The median age of patients was 72 years; 67.4% were men. Bystander CPR increased significantly during the study period, from 21.1% (95% CI, 18.8%-23.4%) in 2001 to 44.9% (95% CI, 42.6%-47.1%) in 2010 (P < .001), whereas use of defibrillation by bystanders remained low (1.1% [95% CI, 0.6%-1.9%] in 2001 to 2.2% [95% CI, 1.5%-2.9%] in 2010; P = .003). More patients achieved survival on hospital arrival (7.9% [95% CI, 6.4%-9.5%] in 2001 to 21.8% [95% CI, 19.8%-23.8%] in 2010; P < .001). Also, 30-day survival improved (3.5% [95% CI, 2.5%-4.5%] in 2001 to 10.8% [95% CI, 9.4%-12.2%] in 2010; P < .001), as did 1-year survival (2.9% [95% CI, 2.0%-3.9%] in 2001 to 10.2% [95% CI, 8.9%-11.6%] in 2010; P < .001). Despite a decrease in the incidence of out-of-hospital cardiac arrests during the study period (40.4 to 34.4 per 100,000 persons in 2001 and 2010, respectively; P = .002), the number of survivors per 100,000 persons increased significantly (P < .001). For the entire study period, bystander CPR was positively associated with 30-day survival, regardless of witnessed status (30-day survival for nonwitnessed cardiac arrest, 4.3% [95% CI, 3.4%-5.2%] with bystander CPR and 1.0% [95% CI, 0.8%-1.3%] without; odds ratio, 4.38 [95% CI, 3.17-6.06]). For witnessed arrest the corresponding values were 19.4% (95% CI, 18.1%-20.7%) vs 6.1% (95% CI, 5.4%-6.7%); odds ratio, 3.74 (95% CI, 3.26-4.28).In Denmark between 2001 and 2010, an increase in survival following out-of-hospital cardiac arrest was significantly associated with a concomitant increase in bystander CPR. Because of the co-occurrence of other related initiatives, a causal relationship remains uncertain.
Letter by Lehmann Regarding Articles “Electrocardiographic Abnormalities That Predict Coronary Heart Disease Events and Mortality in Postmenopausal Women: The Women’s Health Initiative” and “Electrocardiographic Predictors of Incident Congestive Heart Failure and All-Cause Mortality in Postmenopausal Women: the Women’s Health Initiative”
Authors: Michael H. Lehmann
Journal: Circulation (2006)
Reprogramming of MLL-AF9 leukemia cells into pluripotent stem cells
Authors: Y Liu, H Cheng, S Gao, X Lu, F He, L Hu, D Hou, Z Zou, Y Li, H Zhang, J Xu, L Kang, Q Wang, W Yuan, S Gao, T Cheng
Journal: Leukemia (2013)

The 'Yamanaka factors' (Oct4, Sox2, Klf4 and c-Myc) are able to generate induced pluripotent stem (iPS) cells from different cell types. However, to what degree primary malignant cells can be reprogrammed into a pluripotent state has not been vigorously assessed. We established an acute myeloid leukemia (AML) model by overexpressing the human mixed-lineage leukemia-AF9 (MLL-AF9) fusion gene in mouse hematopoietic cells that carry Yamanaka factors under the control of doxycycline (Dox). On addition of Dox to the culture, the transplantable leukemia cells were efficiently converted into iPS cells that could form teratomas and produce chimeras. Interestingly, most chimeric mice spontaneously developed the same type of AML. Moreover, both iPS reprogramming and leukemia reinitiation paths could descend from the same leukemia-initiating cell. RNA-seq analysis showed reversible global gene expression patterns between these interchangeable leukemia and iPS cells on activation or reactivation of MLL-AF9, suggesting a sufficient epigenetic force in driving the leukemogenic process. This study represents an important step for further defining the potential interplay between oncogenic molecules and reprogramming factors during MLL leukemogenesis. More importantly, our reprogramming approach may be expanded to characterize a range of hematopoietic malignancies in order to develop new strategies for clinical diagnosis and treatment.