tbuckley/cabot-search huggingface dataset:
Informed Consent and Abortion
Authors: Bruce Ferguson
Journal: JAMA (1990)

<h3>To the Editor.—</h3> In response to a recent article,<sup>1</sup>several letters to the editor<sup>2</sup>commented on the issue of informed consent in pregnancy and legislatively mandated disclosure of information prior to induced abortion. As a physician who has provided abortion services for 20 years, my practice has been to inform the patient of her alternatives according to the standards of the American College of Obstetricians and Gynecologists: "In the event of an unwanted pregnancy, the physician should counsel the patient about her options: 1) continuing the pregnancy to term and keeping the infant, 2) continuing the pregnancy to term and offering the infant for legal adoption, or 3) aborting the pregnancy."<sup>3</sup>Other ethicists confirm the importance of such informed consent for<i>all</i>pregnant patients, whether planning to continue the pregnancy or not.<sup>4</sup>Informed consent and decision counseling for patients seeking abortions is also a national standard,
A model of asynchronous left ventricular relaxation predicting the bi-exponential pressure decay
Authors: R. W BROWER, S. MEIJ, P. W SERRUYS
Journal: Cardiovascular Research (1983)

A new model for the pressure relaxation of the left ventricle is proposed. The model presumes that the myocardium relaxes asynchronously, but that when regions begin to relax, after a delay, the local wall stress decays as a mono-exponential process. This formulation results in an apparently bi-exponential process (two time constants) which has been previously reported. It is shown that the ratio of the two time constants (T2/T1) can be interpreted as the fraction of the myocardium which relaxes synchronously. Data are presented illustrating the Model during transient coronary occlusion in patients undergoing percutaneous transluminal coronary angioplasty.
Mechanisms of Hepatocyte Growth Factor–Mediated Vascular Smooth Muscle Cell Migration
Authors: Harry Ma, Tina M. Calderon, Tamar Kessel, Anthony W. Ashton, Joan W. Berman
Journal: Circulation Research (2003)

The migration of vascular smooth muscle cells (SMCs) from the media into the neointima and their subsequent proliferation is important in the pathogenesis of atherosclerosis. This process is regulated by multiple factors, including growth factors, and involves changes in the interaction of SMCs with the extracellular matrix and in intracellular signaling cascades that regulate cell movement. We demonstrated previously that hepatocyte growth factor (HGF) is expressed in human atherosclerotic plaques. Although HGF has been shown to promote SMC migration, the mechanisms involved in this process have not been characterized fully. In this study, inhibitory antibodies were used to determine which integrins mediated HGF-induced SMC migration. Inhibition of beta1 or beta3 integrin resulted in a significant decrease in migration. Subsequent experiments were performed to characterize additional biochemical mechanisms involved in HGF-mediated migration. HGF induced the redistribution of focal adhesions, the activation of focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2) and their increased association with beta1 and beta3 integrins, and the production of pro-matrix metalloproteinase-2. Migration levels were significantly reduced by cotreatment of SMCs with the extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor, UO126, the p38 inhibitor, SB203580, or the phosphatidylinositol-3 kinase inhibitor, LY294002. In HGF-treated SMCs, focal adhesion redistribution and FAK and Pyk2 activation were decreased by ERK1/2 inhibition. Neither SB203580 nor LY294002 inhibited HGF-induced ERK1/2 activation. Thus, ERK1/2 signaling may play an important role in HGF-mediated SMC migration by contributing to focal adhesion redistribution and FAK and Pyk2 activation.
Comparative genomic analysis of fungal genomes reveals intron-rich ancestors
Authors: Jason E Stajich, Fred S Dietrich, Scott W Roy
Journal: Genome biology (2007)

Eukaryotic protein-coding genes are interrupted by spliceosomal introns, which are removed from transcripts before protein translation. Many facets of spliceosomal intron evolution, including age, mechanisms of origins, the role of natural selection, and the causes of the vast differences in intron number between eukaryotic species, remain debated. Genome sequencing and comparative analysis has made possible whole genome analysis of intron evolution to address these questions. We analyzed intron positions in 1,161 sets of orthologous genes across 25 eukaryotic species. We find strong support for an intron-rich fungus-animal ancestor, with more than four introns per kilobase, comparable to the highest known modern intron densities. Indeed, the fungus-animal ancestor is estimated to have had more introns than any of the extant fungi in this study. Thus, subsequent fungal evolution has been characterized by widespread and recurrent intron loss occurring in all fungal clades. These results reconcile three previously proposed methods for estimation of ancestral intron number, which previously gave very different estimates of ancestral intron number for eight eukaryotic species, as well as a fourth more recent method. We do not find a clear inverse correspondence between rates of intron loss and gain, contrary to the predictions of selection-based proposals for interspecific differences in intron number. Our results underscore the high intron density of eukaryotic ancestors and the widespread importance of intron loss through eukaryotic evolution.
Evidence for risk of bias in cluster randomised trials: review of recent trials published in three general medical journals
Authors: S. Puffer
Journal: BMJ (2003)

<h3>Abstract</h3> <b>Objective</b> To examine the prevalence of a risk of bias associated with the design and conduct of cluster randomised controlled trials among a sample of recently published studies. <b>Design</b> Retrospective review of cluster randomised trials published in the <i>BMJ, Lancet</i>, and <i>New England Journal of Medicine</i> from January 1997 to October 2002. <b>Main outcome measures</b> Prevalence of secure randomisation of clusters, identification of participants before randomisation (to avoid foreknowledge of allocation), differential recruitment between treatment arms, differential application of inclusion and exclusion criteria, and differential attrition. <b>Results</b> Of the 36 trials identified, 24 were published in the <i>BMJ</i>,11 in the <i>Lancet</i>, and a single trial in the <i>New England Journal of Medicine</i>. At the cluster level, 15 (42%) trials provided evidence for secure allocation and 25 (69%) used stratified allocation. Few trials showed evidence of imbalance at the cluster level. However, some evidence of susceptibility to risk of bias at the individual level existed in 14 (39%) studies. <b>Conclusions</b> Some recently published cluster randomised trials may not have taken adequate precautions to guard against threats to the internal validity of their design.
Computed Tomography in the Emergency Department Setting
Authors: Lawrence R. Goodman
Journal: JAMA Internal Medicine (2013)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Airway response to salbutamol: effect of regular salbutamol inhalations in normal, atopic, and asthmatic subjects.
Authors: J E Harvey, A E Tattersfield
Journal: Thorax (1982)

This study was designed to determine whether resistance to the airway effects of the beta-agonist, salbutamol, would develop in three groups of subjects while taking large doses of inhaled salbutamol. Six normal non-atopic, six atopic non-asthmatic, and eight atopic asthmatic subjects were studied by an identical technique. The development of resistance was assessed from salbutamol dose-response studies in which the airway response was measured as specific airway conductance (sGaw). Further evidence was sought in the atopic and asthmatic subjects by measuring the airway response to a standard histamine inhalation challenge and the protective effect of 100 micrograms salbutamol on this challenge, and by six-hourly peak flow recordings. Subjects were assessed before and during four weeks in which they took inhaled salbutamol regularly in doses increasing to 500 microgram quid in week 4. Normal subjects showed a progressive reduction in the bronchodilator (sGaw) response to salbutamol during the four weeks, indicating the progressive development of resistance. The atopic subjects, both asthmatic and non-asthmatic, showed no reduction in the response to salbutamol during the four weeks, nor any change in the response to histamine challenge or in regular peak flow readings. These results demonstrate that asthmatic patients do not develop bronchial beta-adrenoceptor resistance easily and suggests that they and atopic non-asthmatic subjects are less susceptible to its development than normal subjects.
Comparison of myocardial deformation and velocity dyssynchrony for identification of responders to cardiac resynchronization therapy
Authors: Donato Mele, Tiziano Toselli, Fabio Capasso, Giuseppe Stabile, Marcello Piacenti, Massimo Piepoli, Sara Giatti, Catherine Klersy, Luciano Sallusti, Roberto Ferrari
Journal: European Journal of Heart Failure (2009)
MYC Drives <i>Pten/Trp53</i>-Deficient Proliferation and Metastasis due to IL6 Secretion and AKT Suppression via PHLPP2
Authors: Dawid G. Nowak, Hyejin Cho, Tali Herzka, Kaitlin Watrud, Daniel V. DeMarco, Victoria M.Y. Wang, Serif Senturk, Christof Fellmann, David Ding, Tumas Beinortas, David Kleinman, Muhan Chen, Raffaella Sordella, John E. Wilkinson, Mireia Castillo-Martin, Carlos Cordon-Cardo, Brian D. Robinson, Lloyd C. Trotman
Journal: Cancer Discovery (2015)

We have recently recapitulated metastasis of human PTEN/TP53-mutant prostate cancer in the mouse using the RapidCaP system. Surprisingly, we found that this metastasis is driven by MYC, and not AKT, activation. Here, we show that cell-cell communication by IL6 drives the AKT-MYC switch through activation of the AKT-suppressing phosphatase PHLPP2, when PTEN and p53 are lost together, but not separately. IL6 then communicates a downstream program of STAT3-mediated MYC activation, which drives cell proliferation. Similarly, in tissues, peak proliferation in Pten/Trp53-mutant primary and metastatic prostate cancer does not correlate with activated AKT, but with STAT3/MYC activation instead. Mechanistically, MYC strongly activates the AKT phosphatase PHLPP2 in primary cells and prostate cancer metastasis. We show genetically that Phlpp2 is essential for dictating the proliferation of MYC-mediated AKT suppression. Collectively, our data reveal competition between two proto-oncogenes, MYC and AKT, which ensnarls the Phlpp2 gene to facilitate MYC-driven prostate cancer metastasis after loss of Pten and Trp53.Our data identify IL6 detection as a potential causal biomarker for MYC-driven metastasis after loss of PTEN and p53. Second, our finding that MYC then must supersede AKT to drive cell proliferation points to MYC inhibition as a critical part of PI3K pathway therapy in lethal prostate cancer.
Towards a universal model of reading
Authors: Ram Frost
Journal: Behavioral and Brain Sciences (2012)

Abstract In the last decade, reading research has seen a paradigmatic shift. A new wave of computational models of orthographic processing that offer various forms of noisy position or context-sensitive coding have revolutionized the field of visual word recognition. The influx of such models stems mainly from consistent findings, coming mostly from European languages, regarding an apparent insensitivity of skilled readers to letter order. Underlying the current revolution is the theoretical assumption that the insensitivity of readers to letter order reflects the special way in which the human brain encodes the position of letters in printed words. The present article discusses the theoretical shortcomings and misconceptions of this approach to visual word recognition. A systematic review of data obtained from a variety of languages demonstrates that letter-order insensitivity is neither a general property of the cognitive system nor a property of the brain in encoding letters. Rather, it is a variant and idiosyncratic characteristic of some languages, mostly European, reflecting a strategy of optimizing encoding resources, given the specific structure of words. Since the main goal of reading research is to develop theories that describe the fundamental and invariant phenomena of reading across orthographies, an alternative approach to model visual word recognition is offered. The dimensions of a possible universal model of reading, which outlines the common cognitive operations involved in orthographic processing in all writing systems, are discussed.
Over-expression of calpastatin inhibits calpain activation and attenuates myocardial dysfunction during endotoxaemia
Authors: X. Li, Y. Li, L. Shan, E Shen, R. Chen, T. Peng
Journal: Cardiovascular Research (2009)

AimsLipopolysaccharide (LPS) induces cardiomyocyte caspase-3 activation and proinflammatory factors, in particular tumour necrosis factor-alpha (TNF-α) production, both of which contribute to myocardial dysfunction during sepsis. The present study was to investigate the roles of calpain/calpastatin system in cardiomyocyte caspase-3 activation, TNF-α expression, and myocardial dysfunction during LPS stimulation.
How Much VEGF Do You Need?
Authors: Peter W. Mathieson
Journal: Journal of the American Society of Nephrology (2006)

Vascular endothelial growth factor (VEGF) is a protein that all renal scientists and clinicians need to know about. There are recent comprehensive reviews of the complex biology of VEGF and its receptors ([1][1]) and of its role in the kidney ([2][2]). In summary, VEGF is a potent mediator of
BCL11A deletions result in fetal hemoglobin persistence and neurodevelopmental alterations
Authors: Anindita Basak, Miroslava Hancarova, Jacob C. Ulirsch, Tugce B. Balci, Marie Trkova, Michal Pelisek, Marketa Vlckova, Katerina Muzikova, Jaroslav Cermak, Jan Trka, David A. Dyment, Stuart H. Orkin, Mark J. Daly, Zdenek Sedlacek, Vijay G. Sankaran
Journal: Journal of Clinical Investigation (2015)

A transition from fetal hemoglobin (HbF) to adult hemoglobin (HbA) normally occurs within a few months after birth. Increased production of HbF after this period of infancy ameliorates clinical symptoms of the major disorders of adult β-hemoglobin: β-thalassemia and sickle cell disease. The transcription factor BCL11A silences HbF and has been an attractive therapeutic target for increasing HbF levels; however, it is not clear to what extent BCL11A inhibits HbF production or mediates other developmental functions in humans. Here, we identified and characterized 3 patients with rare microdeletions of 2p15-p16.1 who presented with an autism spectrum disorder and developmental delay. Moreover, these patients all exhibited substantial persistence of HbF but otherwise retained apparently normal hematologic and immunologic function. Of the genes within 2p15-p16.1, only BCL11A was commonly deleted in all of the patients. Evaluation of gene expression data sets from developing and adult human brains revealed that BCL11A expression patterns are similar to other genes associated with neurodevelopmental disorders. Additionally, common SNPs within the second intron of BCL11A are strongly associated with schizophrenia. Together, the study of these rare patients and orthogonal genetic data demonstrates that BCL11A plays a central role in silencing HbF in humans and implicates BCL11A as an important factor for neurodevelopment.
Aromatase Inhibitor–Associated Arthralgias
Authors: Rowan T. Chlebowski
Journal: Journal of Clinical Oncology (2009)

1. Spea SL, Hannan CM, Willey SC, et al: Nipple-sparing mastectomy. Plast Reconst Surg 123:1665-1673, 2009 2. Brachtel EF, Rusby JE, Michaelson JS, et al: Occult nipple involvement in breast cancer: Clinicopathologic findings in 316 consecutive mastectomy specimens. J Clin Oncol 27:4949-4955, 2009 3. Early Breast Cancer Trialists’ Collaborative Group: Effect of radiotherapy and of differences in the extent of surgery for early breast cancer on local recurrence and 15-year survival: An overview of the randomized trials. Lancet 266:2087-2106, 2005 4. Opatt D, Morrow M, Hawley S, et al: Conflicts in decision-making for breast cancer surgery. Ann Surg Oncol 14:2463-2469, 2007 5. Collins ED, Moore CP, Clay KF, et al: Can women with early-stage breast cancer make an informed decision for mastectomy? J Clin Oncol 27:519-525, 2009
Transgenic Nude Mouse with Ubiquitous Green Fluorescent Protein Expression as a Host for Human Tumors
Authors: Meng Yang, Jose Reynoso, Ping Jiang, Lingna Li, Abdool R. Moossa, Robert M. Hoffman
Journal: Cancer Research (2004)

Abstract We report here the development of the transgenic green fluorescent protein (GFP) nude mouse with ubiquitous GFP expression. The GFP nude mouse was obtained by crossing nontransgenic nude mice with the transgenic C57/B6 mouse in which the β-actin promoter drives GFP expression in essentially all tissues. In crosses between nu/nu GFP male mice and nu/+ GFP female mice, the embryos fluoresced green. Approximately 50% of the offspring of these mice were GFP nude mice. Newborn mice and adult mice fluoresced very bright green and could be detected with a simple blue–light-emitting diode flashlight with a central peak of 470 nm and a bypass emission filter. In the adult mice, the organs all brightly expressed GFP, including the heart, lungs, spleen, pancreas, esophagus, stomach, and duodenum. The following systems were dissected out and shown to have brilliant GFP fluorescence: the entire digestive system from tongue to anus; the male and female reproductive systems; brain and spinal cord; and the circulatory system, including the heart and major arteries and veins. The skinned skeleton highly expressed GFP. Pancreatic islets showed GFP fluorescence. The spleen cells were also GFP positive. Red fluorescent protein (RFP)–expressing human cancer cell lines, including PC-3-RFP prostate cancer, HCT-116-RFP colon cancer, MDA-MB-435-RFP breast cancer, and HT1080-RFP fibrosarcoma were transplanted to the transgenic GFP nude mice. All of these human tumors grew extensively in the transgenic GFP nude mouse. Dual-color fluorescence imaging enabled visualization of human tumor–host interaction by whole-body imaging and at the cellular level in fresh and frozen tissues. The GFP mouse model should greatly expand our knowledge of human tumor–host interaction.
In Vivo Sensitivity and Resistance of Chronic Myelogenous Leukemia Cells to a-Interferon: Correlation with Receptor Binding and Induction of 2, 5-Oligoadenylate Synthetase
Authors: Michael G. Rosenblum, Beth L. Maxwell, Moshe Talpaz, Peter J. Kelleher, Kenneth B. McCredie, Jordan U. Gutterman
Journal: Cancer Research (1986)

Fourteen patients with chronic myelogenous leukemia were treated with partially pure leukocyte interferon (HuIFN alpha). The binding of recombinant leukocyte clone A IFN and the induction of 2',5'-oligoadenylate synthetase (2,5A) in peripheral blood cells were studied to determine whether they correlate with clinical response to IFN therapy. The mean pretherapy binding of radiolabeled recombinant leukocyte clone A IFN to peripheral blood cells was 0.053 +/- 0.02 (SE) fmol (53 +/- 20 amol)/10(6) cells and 0.049 +/- 0.015 fmol/10(6) cells in sensitive and resistant patients, respectively. Twenty-four h after the first HuIFN alpha dose, the binding of recombinant leukocyte clone A IFN decreased 3- to 8-fold in both sensitive and resistant patients. The activity of 2,5A synthetase was induced approximately 100-fold in sensitive patients from a pretherapy mean of 3 +/- 2 nmol/mg to a maximum of 317 +/- 184 nmol/mg during therapy. In contrast, 2,5A synthetase was induced from a pretherapy mean of 0.9 +/- 0.9 nmol/mg to only 6.7 +/- 4.9 nmol/mg in resistant patients. In two patients originally sensitive to HuIFN alpha who developed resistance to therapy, receptors were present in both sensitive and resistant disease stages and appeared to down regulate with therapy regardless of response. In these two patients, 2,5A synthetase was significantly induced with therapy in the sensitive stage but not in the resistant stage. This study shows that lack of clinical response to interferon therapy may coincide with failure to induce 2,5A synthetase activity. This suggests that resistance to alpha-interferon therapy may be mediated by events beyond receptor binding resulting in a failure to induce enzymes responsible for mediation of interferon antiproliferative effects.
Derivation of Human Induced Pluripotent Stem Cells for Cardiovascular Disease Modeling
Authors: Kamileh Narsinh, Kazim H. Narsinh, Joseph C. Wu
Journal: Circulation Research (2011)

The successful derivation of human induced pluripotent stem cells (hiPSCs) by dedifferentiation of somatic cells offers significant potential to overcome obstacles in the field of cardiovascular disease. hiPSC derivatives offer incredible potential for new disease models and regenerative medicine therapies. However, many questions remain regarding the optimal starting materials and methods to enable safe, efficient derivation of hiPSCs suitable for clinical applications. Initial reprogramming experiments were carried out using lentiviral or retroviral gene delivery methods. More recently, various nonviral methods that avoid permanent and random transgene insertion have emerged as alternatives. These include transient DNA transfection using plasmids or minicircles, protein transduction, or RNA transfection. In addition, several small molecules have been found to significantly augment hiPSC derivation efficiency, allowing the use of a fewer number of genes during pluripotency induction. We review these various methods for the derivation of hiPSCs, focusing on their ultimate clinical applicability, with an emphasis on their potential for use as cardiovascular therapies and disease-modeling platforms.