tbuckley/cabot-search huggingface dataset:
Theory testing and the global array
Authors: Thomas A. Stoffregen, Benoît G. Bardy
Journal: Behavioral and Brain Sciences (2004)

The new commentaries raise important issues about the target article (Stoffregen &amp; Bardy 2001). The commentaries also highlight some assumptions, often implicit, that underlie traditional interpretations of perception. We argue that evaluation of the global array and its implications for perception requires both analytical research on specification in the global array and new empirical research on the use of information in the global array for the control of action.
The effect of carvedilol-loaded biodyvYsio stent on neointimal hyperplasia in a porcine coronary stent restenosis model
Authors: Weon Kim, Myung Ho Jeong, Gwang Soo Cha, Young Joon Hong, Jeong Gwan Cho, Jong Chun Park, Jung Chaee Kang
Journal: Journal of the American College of Cardiology (2003)
Best Treatment Strategies in High-Risk Multiple Myeloma: Navigating a Gray Area
Authors: Giada Bianchi, Paul G. Richardson, Kenneth C. Anderson
Journal: Journal of Clinical Oncology (2014)

Article Tools ONCOLOGY GRAND ROUNDS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2014.55.7900 Journal of Clinical Oncology - published online before print June 2, 2014 PMID: 24888801 Best Treatment Strategies in High-Risk Multiple Myeloma: Navigating a Gray Area Giada BianchixGiada BianchiSearch for articles by this author , Paul G. RichardsonxPaul G. RichardsonSearch for articles by this author , Kenneth C. AndersonxKenneth C. AndersonSearch for articles by this author Show More Dana-Farber Cancer Institute, Boston, MA https://doi.org/10.1200/JCO.2014.55.7900 First Page Full Text PDF Figures and Tables © 2014 by American Society of Clinical Oncology
A Retrospective Assessment of Occupational Exposure to Elemental Carbon in the U.S. Trucking Industry
Authors: Mary E. Davis, Jaime E. Hart, Francine Laden, Eric Garshick, Thomas J. Smith
Journal: Environmental Health Perspectives (2011)

Despite considerable epidemiologic evidence about the health effects of chronic exposure to vehicle exhaust, efforts at defining the extent of risk have been limited by the lack of historical exposure measurements suitable for use in epidemiologic studies and for risk assessment.We sought to reconstruct exposure to elemental carbon (EC), a marker of diesel and other vehicle exhaust exposure, in a large national cohort of U.S. trucking industry workers.We identified the predictors of measured exposures based on a statistical model and used this information to extrapolate exposures across the cohort nationally. These estimates were adjusted for changes in work-related conditions over time based on a previous exposure assessment of this industry, and for changes in background levels based on a trend analysis of historical air pollution data, to derive monthly estimates of EC exposure for each job and trucking terminal combination between 1971 and 2000.Occupational exposure to EC declined substantially over time, and we found significant variability in estimated exposures both within and across job groups, trucking terminals, and regions of the United States. Average estimated EC exposures during a typical work shift ranged from < 1 μg/m³ in the lowest exposed category in the 1990s to > 40 μg/m³ for workers in the highest exposed jobs in the 1970s.Our results provide a framework for understanding changes over time in exposure to EC in the U.S. trucking industry. Our assessment should minimize exposure misclassification by capturing variation among terminals and across U.S. regions, and changes over time.
Exercise and hypertension
Authors: S. J. Jacober
Journal: JAMA (1995)

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
Tissue Plasminogen Activator and Risk of Myocardial Infarction
Authors: Johanna G. van der Bom, Peter de Knijff, Frits Haverkate, Michiel L. Bots, Piet Meijer, Paulus T. V. M. de Jong, Albert Hofman, Cornelis Kluft, Diederick E. Grobbee
Journal: Circulation (1997)

Background Impaired fibrinolytic capacity, as assessed by euglobulin clot lysis time or plasma concentration of fibrinolytic parameters, has been associated with an increased risk of myocardial infarction (MI). We studied the association of a polymorphism in the gene for TPA and of plasma concentrations of TPA (antigen and activity) with the prevalence of MI. Methods and Results A case-control study was performed. Subjects with a history of MI (n=121) and controls (n=250) were drawn from the Rotterdam Study, a population-based cohort study of 7983 subjects ≥55 years old. We determined TPA antigen and activity in plasma and genotyped all subjects for the Alu repeat insertion/deletion polymorphism in intron h in the TPA gene. Homozygosity for the insertion was associated with twice as many cases of MI as was homozygosity for the deletion (odds ratio, 2.24; 95% CI, 1.11-4.50). TPA antigen was positively associated with the risk of MI; compared with that in the lowest quartile, the relative risks (odds ratio) in the second, third, and upper quartiles were 1.7 (CI, 0.9-3.3), 2.3 (1.2-4.4), and 2.0 (1.0-3.8), respectively. When adjusted for body mass index, HDL and total cholesterol, systolic and diastolic blood pressures, and current smoking, the risk associated with TPA antigen concentration was attenuated. Increased concentrations of TPA activity tended to be associated with an increased risk of MI. Conclusions This study provides evidence for an independent association of the insertion allele of the insertion/deletion polymorphism in the TPA gene with nonfatal MI. Increased TPA antigen is associated with an increased risk of MI; however, this association was not independent of cardiovascular disease risk factors.
The Human Homolog of Rat Jagged1Expressed by Marrow Stroma Inhibits Differentiation of 32D Cells through Interaction with Notch1
Authors: Linheng Li, Laurie A Milner, Yu Deng, Mineo Iwata, Amy Banta, Lynn Graf, Santica Marcovina, Cynthia Friedman, Barbara J Trask, Leroy Hood, Beverly Torok-Storb
Journal: Immunity (1998)
Optimizing tumor targeting of the lipophilic EGFR-binding radiotracer SKI 243 using a liposomal nanoparticle delivery system
Authors: Oula Penate Medina, Nagavarakishore Pillarsetty, Athanasios Glekas, Blesida Punzalan, Valerie Longo, Mithat Gönen, Pat Zanzonico, Peter Smith-Jones, Steven M. Larson
Journal: Journal of Controlled Release (2010)
How the left lung is perfused after ligating the left pulmonary artery in the pig at birth: clinical implications for the hypoperfused lung
Authors: S G HAWORTH, M DE LEVAL, F J MACARTNEY
Journal: Cardiovascular Research (1981)

The left pulmonary artery and ductus arteriosus were ligated in 14 pigs at birth. Animals were sacrificed at intervals from 2 to 24 weeks of age. In the right lung the pulmonary artery and in the left, either the distal pulmonary artery, bronchial arteries or both were injected. The fixed lung specimens were studied by arteriography, dissection and microscopic examination of serial and random sections of lung tissue. The bronchial arterial circulation to, and within the right lung appeared normal and was similar to that described in the human lung. In the left lung, the bronchial arterial circulation hypertrophied rapidly during the first 2 weeks, and large anastomoses between pulmonary and systemic circulations were found at the same sites as in the normal pig lung. The position and structural characteristics of the anastomosing arteries is described in the different types of broncho-pulmonary connection. In most animals aged 16 weeks or more, peripheral bronchial arteries immediately proximal to the anastomotic sites, developed intimal and medial proliferation. The left lung continued to grow although in all animals it was small. The axial pulmonary artery and its branches became smaller with age. These findings help explain how the lung is perfused and grows in children with congenital heart disease and an acquired collateral pulmonary arterial circulation.
Predictive Value of Programmed Ventricular Stimulation After Catheter Ablation of Post-Infarction Ventricular Tachycardia
Authors: Miki Yokokawa, Hyungjin Myra Kim, Kazim Baser, William Stevenson, Koichi Nagashima, Paolo Della Bella, Pasquale Vergara, Gerhard Hindricks, Arash Arya, Katja Zeppenfeld, Marta de Riva Silva, Emile G. Daoud, Sunil Kumar, Karl-Heinz Kuck, Ronald Tilz, Shibu Mathew, Hamid Ghanbari, Rakesh Latchamsetty, Fred Morady, Frank M. Bogun
Journal: Journal of the American College of Cardiology (2015)
Abstract P4-07-19: MicroRNA miR-24 enhances tumor angiogenesis and metastasis in breast cancer
Authors: Z Xu, X Wang, L Fang
Journal: Cancer Research (2013)

Abstract MicroRNAs (miRNA) are non-coding single-stranded RNA molecules, which are produced from endogenous transcripts of short stem-loop structures. Through binding to the 3’-untranslated region (3’UTR) of different target messenger RNAs (mRNAs), microRNAs can repress the translation of the target mRNAs. Recent studies have shown that miR-24 can inhibit apoptosis of cancer cells and cardiomyocytes, and can accelerate cell proliferation. Up-regulation of miR-24 has been observed in oral carcinoma and is one of the most abundant miRNAs in cervical cancer. However, the role of miR-24 in breast cancer cell angiogenesis and metastasis is not clear. We analyzed microRNA miR-24 levels in patients with breast carcinoma and found that miR-24 was higher in breast carcinoma samples than in breast benign tissues. We generated constructs expressing miR-24 and studied its functions using both in vitro and in vivo techniques. We found that the ectopic expression of miR-24 promoted breast cancer angiogenesis and metastasis. Cell migration assays indicated that expression of miR-24 promoted migration of MT-1 cells and 4T1 cells. We examined proliferation of MT-1 cells and 4T1 cells transfected with miR-24 or the control vector. The experiments showed that the miR-24 transfected cells had high rates of proliferation than the vector-transfected cells. In vivo experiments indicated that the expression of miR-24 enhanced tumor growth, metastasis to lung tissues, and decreased overall mouse survival. Tumor sections were also probed with anti-CD34 antibody to examine angiogenesis. We found that miR-24 expression increased tumor-associated vascularization. We further performed tumor metastatic assays. DNA was isolated from lung tissues and subjected to PCR to indicate metastasis of the cancer cells. Typical metastatic lesions in the lungs are shown. In the miR-24 expressing cells and tumors, expression of the phosphatases PTPN9 and PTPRF were repressed. We confirmed that miR-24 could directly target both PTPN9 and PTPRF. Consistent with this, we found that the levels of PTPN9 and PTPRF were lower in the patients with metastatic breast carcinoma. Ectopic expression of PTPN9 and PTPRF decreased cell migration, and tumor metastasis. Our study demonstrates that miR-24 is highly expressed in human breast carcinoma. This finding suggests a role of miR-24 in breast cancer development/progression. Our results suggest that miR-24 plays a key role in breast cancer angiogenesis and metastasis. miR-24 could potentially be a target for cancer intervention. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P4-07-19.
A Functional Polymorphism in the COMT Gene and Performance on a Test of Prefrontal Cognition
Authors: Anil K. Malhotra, Lisa J. Kestler, Chiara Mazzanti, John A. Bates, Terry Goldberg, David Goldman
Journal: American Journal of Psychiatry (2002)

OBJECTIVE: In the prefrontal cortex, the enzyme catechol O-methyltransferase (COMT) is critical in the metabolic degradation of dopamine, a neurotransmitter hypothesized to influence human cognitive function. The COMT gene contains a functional polymorphism, Val158Met, that exerts a fourfold effect on enzyme activity. The current study investigated whether prefrontal cognition varies with COMT genotype. METHOD: Val158Met was genotyped in 73 healthy volunteers. A task of prefrontal cognition, the Wisconsin Card Sorting Test, was also administered. RESULTS: Subjects with only the low-activity met allele made significantly fewer perseverative errors on the Wisconsin Card Sorting Test than did subjects with the val allele. CONCLUSIONS: These data are consistent with those of previous studies, suggesting that a functional genetic polymorphism may influence prefrontal cognition.
Rapidly evolving skin manifestations due to progressive thrombosis in a patient with paroxysmal nocturnal haemoglobinuria resolved with prompt initiation of eculizumab
Authors: E.F.M. Otters, G. Zarafonitis, E.J. Steenbergen, P.G.M. Valk, P. Muus
Journal: British Journal of Dermatology (2014)

Funding sources: none. Conflicts of interests: P.M. has sat on advisory boards for Alexion. Dear Editor, Paroxysmal nocturnal haemoglobinuria (PNH) is a rare acquired clonal disorder of the haematopoietic stem cell. PNH arises from mutations in the PIGA gene, which encodes glycosylphosphatidylinositol (GPI)‐anchored proteins. Consequently, these mutations result in a deficiency of GPI‐anchored proteins in cell membranes.1 This deficiency causes PNH red blood cells to be susceptible to complement‐induced intravascular haemolysis.2 However, PNH is also characterized by a high rate of thrombosis.3 4 Venous and arterial thrombosis can be the first symptom of PNH. PNH‐induced thrombosis often occurs at unusual sites and may progress in days to weeks.5 Moreover, thromboembolic complications and consequences are the leading cause of morbidity and death in PNH.4 The pathogenesis of thrombosis in PNH is complex and not completely elucidated at this time.3 The clinical picture of PNH is highly variable and depends on the PNH clone size, factors of complement activation and whether or not there is an underlying bone marrow disease. Complications of PNH occur spontaneously or can be triggered by bacterial or viral infections, for example by highly contagious parvovirus B19.6 7 Cutaneous manifestations of PNH comprise rapidly evolving purpura, haemorrhagic bullae and ulcerations presumably due to necrosis, secondary to intravascular clotting.8 9 10
Is social interaction based on guile or honesty?
Authors: Matthew L. Brooks, William B. Swann
Journal: Behavioral and Brain Sciences (2011)

Abstract Von Hippel &amp; Trivers suggest that people enhance their own self-views as a means of persuading others to adopt similarly inflated perceptions of them. We question the existence of a pervasive desire for self-enhancement, noting that the evidence the authors cite could reflect self-verification strivings or no motive whatsoever. An identity negotiation framework provides a more tenable approach to social interaction.
On Being a Patient
Authors: Frank Davidoff
Journal: Annals of Internal Medicine (1996)

Editorials15 January 1996On Being a PatientFrank Davidoff, MD, EditorFrank Davidoff, MD, EditorSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-124-2-199601150-00015 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Since it began in Annals 5 years ago, “On Being a Doctor” has attracted enthusiastic interest and attention. Many readers tell us it is the first thing they read when their copy arrives. Authors send an average of about three manuscripts a week to this department (some 7% of our total submissions), and 73 of the best pieces have been collected into a widely read book. Our authors tell about the sobering, satisfying, anguishing, exhilarating experiences of doctoring; their stories are always deeply felt. And increasingly, they tell the story from the other side of the desk, the other end ...References1. Laine C, Davidoff F. Patient-centered medicine. A professional evolution. JAMA. [In press]. Google Scholar2. Matthews DA, Suchman AL, Branch WT Jr. Making “connexions”: enhancing the therapeutic potential of patient-clinician relationships. Ann Intern Med. 1993; 118:973-7. Google Scholar3. Balint M. The Doctor, his Patient, and the Illness. New York: International Universities Press; 1964. Google Scholar4. Kleinman A. The Illness Narratives: Suffering, Healing and the Human Condition. New York: Basic Books; 1988. Google Scholar5. Charon R. Doctor-patient/reader-writer: learning to find the text. Soundings. 1989:72:137-52. Google Scholar6. Sontag S. Illness as Metaphor. New York: Farrar, Straus and Giroux; 1978. Google Scholar7. Pinner M, BF Miller. When Doctors are Patients. New York: WW Norton; 1952. Google Scholar8. Mandell H, Spiro H. When Doctors Get Sick. New York: Plenum Medical Book Co.; 1987. Google Scholar9. Last EC. For Corrie. Ann Intern Med. 1996; 124:271-2. Google Scholar Author, Article, and Disclosure InformationAuthors: Frank Davidoff, MD, Editor PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byIn Memoriam: Dr. Frank Davidoff: Leading Annals as It Entered the 21st CenturyChristine Laine, MD, MPH„Pamiętam, zdarzyło się to w sobotę rano, około 10”. Fachowe publikacje medyczne oparte na relacjach pacjentów i lekarzyNarcolepsy: Let the Patient's Voice Awaken Us!Chapitre 12. La médecine factuelle et les rapports de casLes rapports de cas, vestiges du passé ?Caring for Colleagues 15 January 1996Volume 124, Issue 2Page: 269-270KeywordsDecision makingDisabilitiesHand strengthHearingHeartPerception ePublished: 15 August 2000 Issue Published: 15 January 1996 Copyright & PermissionsCopyright © 1996 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Developmental Exposure to Polychlorinated Biphenyls Interferes with Experience-Dependent Dendritic Plasticity and Ryanodine Receptor Expression in Weanling Rats
Authors: Dongren Yang, Kyung Ho Kim, Andrew Phimister, Adam D. Bachstetter, Thomas R. Ward, Robert W. Stackman, Ronald F. Mervis, Amy B. Wisniewski, Sabra L. Klein, Prasada Rao S. Kodavanti, Kim A. Anderson, Gary Wayman, Isaac N. Pessah, Pamela J. Lein
Journal: Environmental Health Perspectives (2008)

BackgroundNeurodevelopmental disorders are associated with altered patterns of neuronal connectivity. A critical determinant of neuronal connectivity is the dendritic morphology of individual neurons, which is shaped by experience. The identification of environmental exposures that interfere with dendritic growth and plasticity may, therefore, provide insight into environmental risk factors for neurodevelopmental disorders.ObjectiveWe tested the hypothesis that polychlorinated biphenyls (PCBs) alter dendritic growth and/or plasticity by promoting the activity of ryanodine receptors (RyRs).Methods and ResultsThe Morris water maze was used to induce experience-dependent neural plasticity in weanling rats exposed to either vehicle or Aroclor 1254 (A1254) in the maternal diet throughout gestation and lactation. Developmental A1254 exposure promoted dendritic growth in cerebellar Purkinje cells and neocortical pyramidal neurons among untrained animals but attenuated or reversed experience-dependent dendritic growth among maze-trained littermates. These structural changes coincided with subtle deficits in spatial learning and memory, increased [3H]-ryanodine binding sites and RyR expression in the cerebellum of untrained animals, and inhibition of training-induced RyR upregulation. A congener with potent RyR activity, PCB95, but not a congener with negligible RyR activity, PCB66, promoted dendritic growth in primary cortical neuron cultures and this effect was blocked by pharmacologic antagonism of RyR activity.ConclusionsDevelopmental exposure to PCBs interferes with normal patterns of dendritic growth and plasticity, and these effects may be linked to changes in RyR expression and function. These findings identify PCBs as candidate environmental risk factors for neurodevelopmental disorders, especially in children with heritable deficits in calcium signaling.
Diagnosis of acute rejection in liver transplantation
Authors: K. Höckerstedt, I. Lautenschlager, J. Ahonen, B. Eklund, H. Isoniemi, C. Korsbäck, J. Mäkinen, H. Mäkisalo, R. Orko, E. Pettersson, M. Salaspuro, B. Scheinin, T.M. Scheinin, E. von Willebrand
Journal: Journal of Hepatology (1988)
BMA has made a poor health bill worse
Authors: S. P. Hambling
Journal: BMJ (2011)

Disappointingly, the BMA has not championed the benefits of bringing clinicians to the forefront of commissioning. Far too much time has been spent focusing on the weak points of the government’s proposals,1 so losing the parts that would clearly benefit health systems and patients.

Our commissioning agenda was always how to repatriate decisions from management and to drive forward collaboration and cooperation among the mosaic of service providers. The …
Suppression, attention, and effort: A proposed enhancement for a promising theory
Authors: David A. Schwartz, J. Eric Ivancich, Stephen Kaplan
Journal: Behavioral and Brain Sciences (1997)

Although Glenberg's theory benefits from the incorporation of a suppression concept, a more differentiated view of suppression would be even more effective. We propose such a concept (based on the attention framework first developed by William James in the late nineteenth century), showing how it accounts for phenomena that Glenberg describes and also for phenomena that he ignores.
Medical Devices: Significant vs Nonsignificant Risk
Authors: William H. Huffaker
Journal: JAMA (1995)

To the Editor.  —I read with interest the article by Dr Sherertz and Mr Streed.1However, I disagree with the authors' conclusion. I believe much of the problem is with the FDA and not with the manufacturers. The FDA makes it difficult for a manufacturer to make even small alterations in a product. Additional expensive studies can be required even though changes are minimal. Some companies have started restricting their products from being used for medical purposes because of fears of litigation.  The FDA's attitude is that a medical device should have no risk. While this may be a very noble goal, is it achievable? Should not physicians, in discussions with their patients, be the ones to decide on an appropriate level of risk? I would hope that in the future the FDA can take a more realistic approach toward risk and safety. When the government becomes too restrictive,