tbuckley/cabot-search huggingface dataset:
Cost-Effectiveness of Eplerenone Compared With Placebo in Patients With Myocardial Infarction Complicated by Left Ventricular Dysfunction and Heart Failure
Authors: William S. Weintraub, Zefeng Zhang, Elizabeth M. Mahoney, Paul Kolm, John A. Spertus, Jaime Caro, Jack Ishak, Robert Goldberg, Joseph Tooley, Richard Willke, Bertram Pitt
Journal: Circulation (2005)

Background— In the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS), aldosterone blockade with eplerenone decreased mortality in patients with left ventricular systolic dysfunction and heart failure after acute myocardial infarction. The present study was performed to evaluate the cost-effectiveness of eplerenone compared with placebo in these patients. Methods and Results— A total of 6632 patients with left ventricular systolic dysfunction and heart failure after acute myocardial infarction were randomized to eplerenone or placebo and followed up for a mean of 16 months. The coprimary end points were all-cause mortality and the composite of cardiovascular mortality/cardiovascular hospitalization. The evaluation of resource use included hospitalizations, outpatient services, and medications. Eplerenone was priced at the average wholesale price, $3.60 per day. Survival beyond the trial period was estimated from data from the Framingham Heart Study, the Saskatchewan Health database, and the Worcester Heart Attack Registry. The incremental cost-effectiveness of eplerenone in cost per life-year and quality-adjusted life-year gained compared with placebo was estimated. The number of life-years gained with eplerenone was 0.1014 based on Framingham (95% CI, 0.0306 to 0.1740), 0.0636 with Saskatchewan (95% CI, 0.0229 to 0.1038), and 0.1337 with Worcester (95% CI, 0.0438 to 0.2252) data. Cost was $1391 higher over the trial period in the eplerenone arm (95% CI, 656 to 2165) because of drug cost. The incremental cost-effectiveness ratio was $13 718 per life-year gained with Framingham (96.7% under $50 000 per life-year gained), $21 876 with Saskatchewan, and $10 402 with Worcester. Conclusions— Eplerenone compared with placebo in the treatment of heart failure after acute myocardial infarction is effective in reducing mortality and is cost-effective in increasing years of life by commonly used criteria.
Safety education of pedestrians for injury prevention: a systematic review of randomised controlled trials
Authors: O. Duperrex
Journal: BMJ (2002)

<h3>Abstract</h3> <b>Objectives:</b> To quantify the effectiveness of safety education of pedestrians. <b>Design:</b> Systematic review of randomised controlled trials of safety education programmes for pedestrians of all ages. <b>Main outcome measures:</b> Effect of safety education on pedestrians9 injuries, behaviour, attitude, and knowledge and on pedestrian-motor vehicle collisions. Quality of trials: methods of randomisation; and numbers lost to follow up <b>Results:</b> We identified 15 randomised controlled trials of safety education programmes for pedestrians. Fourteen trials targeted children, and one targeted institutionalised adults. None assessed the effect of safety education on the occurrence of pedestrian injury, but six trials assessed its effect on behaviour. The effect of pedestrian education on behaviour varied considerably across studies and outcomes. <b>Conclusions:</b> Pedestrian safety education can change observed road crossing behaviour, but whether this reduces the risk of pedestrian injury in road traffic crashes is unknown. There is a lack of good evidence of effectiveness of safety education for adult pedestrians, specially elderly people. None of the trials was conducted in low or middle income countries. <h3>What is already known on this topic</h3> Road traffic crashes are a leading cause of death and disablement, and pedestrians are particularly vulnerable road users Several organisations strongly recommend road safety education As resources are limited, a key question concerns the relative effectiveness of different prevention strategies, including road safety education of pedestrians <h3>What this study adds</h3> This systematic review showed safety education for pedestrians could improve children9s knowledge and change their observed road crossing behaviour However, effects on pedestrian injury were unknown There is a lack of good evidence of effectiveness of safety education for adult pedestrians, especially elderly people, and in low and middle income countries
Differential Requirement for LAT and SLP-76 in GPVI versus T Cell Receptor Signaling
Authors: Barbi A. Judd, Peggy S. Myung, Achim Obergfell, Erin E. Myers, Alec M. Cheng, Stephen P. Watson, Warren S. Pear, David Allman, Sanford J. Shattil, Gary A. Koretzky
Journal: The Journal of Experimental Medicine (2002)

Mice deficient in the adaptor Src homology 2 domain-containing leukocyte phosphoprotein of 76 kD (SLP-76) exhibit a bleeding disorder and lack T cells. Linker for activation of T cells (LAT)-deficient mice exhibit a similar T cell phenotype, but show no signs of hemorrhage. Both SLP-76 and LAT are important for optimal platelet activation downstream of the collagen receptor, GPVI. In addition, SLP-76 is involved in signaling mediated by integrin αIIbβ3. Because SLP-76 and LAT function coordinately in T cell signal transduction, yet their roles appear to differ in hemostasis, we investigated in detail the functional consequences of SLP-76 and LAT deficiencies in platelets. Previously we have shown that LAT−/− platelets exhibit defective responses to the GPVI-specific agonist, collagen-related peptide (CRP). Consistent with this, we find that surface expression of P-selectin in response to high concentrations of GPVI ligands is reduced in both LAT- and SLP-76–deficient platelets. However, platelets from LAT−/− mice, but not SLP-76−/− mice, aggregate normally in response to high concentrations of collagen and convulxin. Additionally, unlike SLP-76, LAT is not tyrosine phosphorylated after fibrinogen binding to integrin αIIbβ3, and collagen-stimulated platelets deficient in LAT spread normally on fibrinogen-coated surfaces. Together, these findings indicate that while LAT and SLP-76 are equally required for signaling via the T cell antigen receptor (TCR) and pre-TCR, platelet activation downstream of GPVI and αIIbβ3 shows a much greater dependency on SLP-76 than LAT.
Pulmonary Vein Stenosis After Catheter Ablation of Atrial Arrhythmias
Authors: Niranjan Seshadri, Gian M. Novaro, Lourdes Prieto, Richard D. White, Andrea Natale, Richard A. Grimm, William J. Stewart
Journal: Circulation (2002)

A 78-year-old woman presented with a 2-month history of worsening dyspnea, orthopnea, and cough with hemoptysis.Her past medical history was significant for hypertension and severe mitral regurgitation for which she had undergone mitral valve repair 3 years previously.In addition, she had recurrent atrial tachycardia requiring 2 radiofrequency ablations, which included ablation of several left-sided pathways.The last ablation was performed 3 months before her presentation.A transesophageal echocardiogram was performed and showed turbulent Doppler flow and increased systolic and diastolic velocities in the right lower (Figure 1) and left upper pulmonary veins.A contrast-enhanced, retrospectively gated helical CT scan showed 60% to 70% stenoses of the right lower (Figure 2, left panel) and left upper pulmonary veins.A ventilation-perfusion scan revealed a large perfusion defect in the right lower lobe.The patient subsequently underwent a successful balloon dilation of the right lower and left upper pulmonary veins (Figure 3).Pulmonary artery pressures before dilation were 85/30 mm Hg, and dropped to 55/ 20 mm Hg immediately after dilation.A transesophageal echocardiogram performed after the procedure showed normal flows in the previously stenotic pulmonary veins.A CT scan completed several days after the procedure showed a reduction in the degree of stenosis in both right lower (Figure 2, right panel) and left upper pulmonary veins.The patient's acute symptoms were markedly improved, although her condition subsequently deteriorated secondary to multiple other medical problems.
Community acquired pneumonia: aetiology and prognostic index evaluation.
Authors: N C Karalus, R T Cursons, R A Leng, C B Mahood, R P Rothwell, B Hancock, S Cepulis, M Wawatai, L Coleman
Journal: Thorax (1991)

A 10 month prospective study of all adults admitted to Waikato Hospital with community acquired pneumonia was performed to assess aetiology, mortality, hospital stay, and the value of a prognostic index based on that obtained from a British Thoracic Society study. The 92 patients in the survey had a mean age of 56 (range 13-97) years. A microbiological diagnosis was established in 72%; Streptococcus pneumoniae (33%), Mycoplasma pneumoniae (18%), and influenza A virus (8%) were the most common microorganisms. Other causative organisms were Legionella pneumophila (4 cases), Staphylococcus aureus (3), Klebsiella pneumoniae (2), Haemophilus influenzae (2), Nocardia brasiliensis (1), and Acinetobacter calcoaceticus (1). Chlamydia sp, influenza B virus and adenovirus were each found in one case; all were cultured on nasopharygeal aspirates. Aspiration was considered to be the underlying cause in five patients, two with epilepsy and one with pseudobulbar palsy. Five of the six deaths that occurred were in patients over 75 years of age and the other was 69. In four of the six the established causative organisms were Chlamydia sp (1), K pneumoniae (1), and S aureus (2). Patients had a 16 fold increased risk of death if they had two or more of the following on admission: a respiratory rate of 30/minute or more, diastolic blood pressure of 60 mm Hg or less, and either confusion or a plasma urea concentration greater than 7.0 mmol/l.
Risk and predictors of infection leading to hospitalisation in a large primary-care-derived cohort of patients with inflammatory polyarthritis
Authors: J. Franklin, M. Lunt, D. Bunn, D. Symmons, A. Silman
Journal: Annals of the Rheumatic Diseases (2006)

The increased mortality observed in patients with rheumatoid arthritis is partly due to an increased occurrence of serious infections. A retrospective study from the Mayo Clinic found that infection risk is increased in rheumatoid arthritis. In particular, serious infection was associated with severe disease and use of corticosteroids. Robust estimates are required from prospective studies of incident cases.
Polyoma Virus and L Cell Relationship. II. A Curable Carrier System not Dependent on Interferon2
Authors: J. Donald Hare, Herbert R. Morgan
Journal: JNCI Journal of the National Cancer Institute (1964)

The persistent infection of strain L cells with polyoma virus can be characterized as follows: 1) A high proportion of cells may carry complete, infectious virus in their cytoplasm without obvious cytopathology and may enter and complete mitosis; 2) a low percentage of cells (<1–3%) enter a cytolytic cycle; 3) the infection can be cured by the cultivation of infected cells for a prolonged period in specific antiserum; 4) interferon is not responsible for the protection of exposed cells from the cytolytic effect of polyoma virus; and 5) a state of autologous interference may provide some protection for potentially susceptible cells.
Phase I/II Trial of Cetuximab and Erlotinib in Patients with Lung Adenocarcinoma and Acquired Resistance to Erlotinib
Authors: Yelena Y. Janjigian, Christopher G. Azzoli, Lee M. Krug, Leanne K. Pereira, Naiyer A. Rizvi, M Catherine Pietanza, Mark G. Kris, Michelle S. Ginsberg, William Pao, Vincent A. Miller, Gregory J. Riely
Journal: Clinical Cancer Research (2011)

In patients with epidermal growth factor receptor (EGFR) mutant lung adenocarcinoma, treatment with erlotinib or gefitinib is associated with a 75% radiographic response rate and progression-free survival of approximately 12 months. The most common mechanism of acquired resistance to erlotinib is development of a secondary mutation in EGFR, suggesting that these tumors continue to depend on EGFR signaling. We hypothesized that combined EGFR blockade would overcome acquired resistance to erlotinib in patients with lung adenocarcinoma. To evaluate the toxicity and efficacy of cetuximab and erlotinib in patients with acquired resistance to erlotinib, we conducted this phase I/II clinical trial.Patients with lung adenocarcinoma and clinically defined acquired resistance to erlotinib were treated with erlotinib 100 mg daily, along with cetuximab every 2 weeks in three escalating dose cohorts (250 mg/m(2), 375 mg/m(2), and 500 mg/m(2)). The recommended phase II dose was then evaluated in a two-stage trial, with a primary end point of objective response rate.A total of 19 patients were enrolled. The most common toxicities for the combination of cetuximab and erlotinib were rash, fatigue, and hypomagnesemia. The recommended phase II dose identified was cetuximab 500 mg/m(2) every 2 weeks and erlotinib 100 mg daily. At this dose and schedule, no radiographic responses were seen (0 of 13, 0%, 95% CI, 0-25).Combined EGFR inhibition, with cetuximab 500 mg/m(2) every 2 weeks and erlotinib 100 mg daily, had no significant activity in patients with acquired resistance to erlotinib.
DENSITY DISTRIBUTION ANALYSIS OF ANTIGEN-SENSITIVE CELLS IN THE RAT
Authors: J. Stephen Haskill
Journal: The Journal of Experimental Medicine (1969)

Analysis of the cell populations capable of initiating a response to sheep and horse erythrocyte antigens has been carried out by means of equilibrium density gradient centrifugation. The results indicate that there are at least six distinguishable AS cell populations for sheep erythrocytes, but only three for horse erythrocytes in the spleen of the Lewis rat. Evidence is presented for the existence of metabolic, physiological, and immunological differences among these populations. It is suggested that at least one population of AS cells responds only to the specific antigen and at least one other population is sensitive to stimulation by a broad range of antigens. It is assumed that the difference between these two AS cells results from a process of differentiation of AS cells primed into DNA synthesis by antigen stimulation.
C1-Esterase Inhibitor Protects Against Neointima Formation After Arterial Injury in Atherosclerosis-Prone Mice
Authors: Erdenechimeg Shagdarsuren, Kiril Bidzhekov, Yassin Djalali-Talab, Elisa A. Liehn, Mihail Hristov, Robert A. Matthijsen, Wim A. Buurman, Alma Zernecke, Christian Weber
Journal: Circulation (2007)

Background— Although activation of the complement system has been implicated in the progression of human atherosclerosis, its function during arterial remodeling after injury has not been investigated. Here, we examined the contribution of the complement cascade to neointima formation in apolipoprotein E–deficient mice using a C1-esterase inhibitor (C1-inhibitor). Methods and Results— Apolipoprotein E–deficient mice fed an atherogenic diet were subjected to wire-induced endothelial denudation of the carotid artery and treated with C1-inhibitor (Berinert; 15 IU IV) or vehicle perioperatively and subsequently every 2 days. The effectiveness of C1-inhibitor treatment was confirmed by measurement of plasma C1-inhibitor activity. A significant reduction in serum triglyceride levels was observed in C1-inhibitor–treated mice, whereas cholesterol levels did not differ. After 3 weeks, neointimal area was significantly reduced in C1-inhibitor–treated mice versus controls, whereas medial area was unaltered. This was associated with a significant decrease in neointimal and medial macrophage and CD3 + T-cell content. Expression of C3 mRNA was significantly reduced in plaques of C1-inhibitor–treated mice 10 days after injury, as assessed by reverse-transcription polymerase chain reaction. The peak in serum C3 levels after injury was markedly downregulated by C1-inhibitor, as evidenced by ELISA. Immunohistochemistry revealed strong expression of C3 and C3c, which colocalized to plaque macrophages and was reduced in C1-inhibitor–treated mice. C1-inhibitor impaired monocyte arrest on activated endothelium and platelets under flow conditions in vitro and leukocyte recruitment to carotid arteries 1 day after injury in vivo. Conclusions— C1-inhibitor limits neointimal plaque formation and inflammation. This may involve blockade of complement activation, inhibition of leukocyte recruitment, and reduced triglyceride levels, thus providing a multimodal approach to treat arterial disease.
Shank-interacting protein–like 1 promotes tumorigenesis via PTEN inhibition in human tumor cells
Authors: Lizhi He, Alistair Ingram, Adrian P. Rybak, Damu Tang
Journal: Journal of Clinical Investigation (2010)

Inactivation of phosphatase and tensin homolog (PTEN) is a critical step during tumorigenesis, and PTEN inactivation by genetic and epigenetic means has been well studied. There is also evidence suggesting that PTEN negative regulators (PTEN-NRs) have a role in PTEN inactivation during tumorigenesis, but their identity has remained elusive. Here we have identified shank-interacting protein-like 1 (SIPL1) as a PTEN-NR in human tumor cell lines and human primary cervical cancer cells. Ectopic SIPL1 expression protected human U87 glioma cells from PTEN-mediated growth inhibition and promoted the formation of HeLa cell-derived xenograft tumors in immunocompromised mice. Conversely, siRNA-mediated knockdown of SIPL1 expression inhibited the growth of both HeLa cells and DU145 human prostate carcinoma cells in vitro and in vivo in a xenograft tumor model. These inhibitions were reversed by concomitant knockdown of PTEN, demonstrating that SIPL1 affects tumorigenesis via inhibition of PTEN function. Mechanistically, SIPL1 was found to interact with PTEN through its ubiquitin-like domain (UBL), inhibiting the phosphatidylinositol 3,4,5-trisphosphate (PIP3) phosphatase activity of PTEN. Furthermore, SIPL1 expression correlated with loss of PTEN function in PTEN-positive human primary cervical cancer tissue. Taken together, these observations indicate that SIPL1 is a PTEN-NR and that it facilitates tumorigenesis, at least in part, through its PTEN inhibitory function.
Uric Acid. The Chemistry, Physiology and Pathology of Uric Acid and the Physiologically Important Purin Bodies, with a discussion of the Metabolism in Gout.
Authors: Francis H. McCrudden
Journal: JAMA (1906)

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
Inhibition of Development of Murine Melanoma Lung Metastases by Systemic Administration of Recombinant Platelet Factor 4
Authors: D. L. Kolber, T. L. Knisely, T. E. Maione
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Inhibition of Development of Murine Melanoma Lung Metastases by Systemic Administration of Recombinant Platelet Factor 4 Get access Donna L. Kolber, Donna L. Kolber Repligen CorporationCambridge, Mass Search for other works by this author on: Oxford Academic PubMed Google Scholar Terrence L. Knisely, Terrence L. Knisely Repligen CorporationCambridge, Mass Search for other works by this author on: Oxford Academic PubMed Google Scholar Theodore E. Maione Theodore E. Maione Repligen CorporationCambridge, Mass Correspondence to. Theodore E. Maione, Ph.D., Repligen Corporation, One Kendall Square, Bldg. 700, Cambridge, MA 02139. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 4, 15 February 1995, Pages 304–309, https://doi.org/10.1093/jnci/87.4.304 Published: 15 February 1995 Article history Received: 13 July 1994 Revision received: 08 November 1994 Accepted: 17 November 1994 Published: 15 February 1995
Relationship Between Baseline Glycemic Control and Cognitive Function in Individuals With Type 2 Diabetes and Other Cardiovascular Risk Factors: The Action to Control Cardiovascular Risk in Diabetes-Memory in Diabetes (ACCORD-MIND) Trial
Authors: Angela M. Abbatecola, Giuseppe Paolisso
Journal: Diabetes Care (2009)

In their recent article, Cukierman-Yaffe et al. (1) performed a cross-sectional study comparing the relationship of A1C and fasting plasma glucose (FPG) levels with performance on four cognitive tests of subjects from the Memory in Diabetes (MIND) substudy of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial. These authors showed that a chronic marker of hyperglycemia, A1C, was associated with significantly lower cognitive performance, whereas FPG did not have any effect. These findings extend those from previous reports regarding the progressive relationship between the degree of chronic hyperglycemia and cognitive dysfunction. However, over the last few years, postprandial hyperglycemia (PPG) has also been known to trigger cellular mechanisms leading …
Intracranial bleeding due to vitamin K deficiency: advantages of using a pediatric intensive care registry
Authors: Désirée Y. Visser, Nicolaas J. Jansen, Marloes M. Ijland, Tom J. de Koning, Peter M. van Hasselt
Journal: Intensive Care Medicine (2011)

To determine the incidence of late intracranial vitamin K deficiency bleeding (VKDB) in The Netherlands using the Dutch Pediatric Intensive Care Evaluation (PICE) registry.The PICE registry was used to identify all infants who were admitted to a Dutch pediatric intensive care unit (PICU) with intracranial bleeding between 1 January 2004 and 31 December 2007. Cases of confirmed late intracranial VKDB were used to calculate the incidence for each year. To estimate the completeness of ascertainment of the PICE registry, data from 2005 were compared with general surveillance data from that year.In the 4-year study period, 16/64 (25%) of the infants admitted with intracranial bleeding had late intracranial VKDB, resulting in an overall incidence of 2.1/100,000 live births (95% confidence interval 1.2-3.5). The single-year incidence varied markedly between 0.5 and 3.3 per 100,000 live births. All five ascertained cases in 2005 were identified using the PICE registry, while general surveillance identified only three.The PICE registry allows ongoing monitoring of the incidence of late intracranial VKDB and appears to be associated with a higher rate of completeness than general surveillance. We propose the use of pediatric intensive care registries to assess the efficacy of national vitamin K prophylactic regimens.