tbuckley/cabot-search huggingface dataset:
Acupuncture for Horses
Authors: John J. Satory
Journal: JAMA (1972)

<h3>To the Editor.—</h3> It is interesting to read the recent various articles and letters of comment on acupuncture. Many have felt the effectiveness is due to a hypnotic state. However, on a recent visit to an acupuncture clinic in Taiwan, I saw 10 to 15 patients being treated for various ailments and I also thought that, possibly, these people might be hypnotized until I visited a Chinese (mainland) medical supply house in Hong Kong to get an acupuncture model, only to find out that a model of a horse is also available with its meridian lines and points. One could hardly attribute effects in horses to hypnotism.
OMEGA, a Randomized, Placebo-Controlled Trial to Test the Effect of Highly Purified Omega-3 Fatty Acids on Top of Modern Guideline-Adjusted Therapy After Myocardial Infarction
Authors: Bernhard Rauch, Rudolf Schiele, Steffen Schneider, Frank Diller, Norbert Victor, Helmut Gohlke, Martin Gottwik, Gerhard Steinbeck, Ulrike Del Castillo, Rudolf Sack, Heinrich Worth, Hugo Katus, Wilhelm Spitzer, Georg Sabin, Jochen Senges
Journal: Circulation (2010)

Background— There is no randomized, double-blind trial testing the prognostic effect of highly purified omega-3 fatty acids in addition to current guideline-adjusted treatment of acute myocardial infarction. Methods and Results— OMEGA is a randomized, placebo-controlled, double-blind, multicenter trial testing the effects of omega-3-acid ethyl esters-90 (1 g/d for 1 year) on the rate of sudden cardiac death in survivors of acute myocardial infarction, if given in addition to current guideline-adjusted treatment. Secondary end points were total mortality and nonfatal clinical events. Patients (n=3851; female, 25.6%; mean age, 64.0 years) were randomized in 104 German centers 3 to 14 days after acute myocardial infarction from October 2003 until June 2007. Acute coronary angiography was performed in 93.8% and acute percutaneous coronary intervention in 77.8% of all patients. During a follow-up of 365 days, the event rates were (omega and control groups) as follows: sudden cardiac death, 1.5% and 1.5% ( P =0.84); total mortality, 4.6% and 3.7% ( P =0.18); major adverse cerebrovascular and cardiovascular events, 10.4% and 8.8% ( P =0.1); and revascularization in survivors, 27.6% and 29.1% ( P =0.34). Conclusions— Guideline-adjusted treatment of acute myocardial infarction results in a low rate of sudden cardiac death and other clinical events within 1 year of follow-up, which could not be shown to be further reduced by the application of omega-3 fatty acids. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00251134.
Radiation and Thyroid Cancer
Authors: Carl R. Makarewicz
Journal: JAMA (1984)

Radiation-induced damage is a complex network of interlinked signaling pathways, which may result in apoptosis, cell cycle arrest, DNA repair, and cancer.The development of thyroid cancer in response to radiation, from nuclear catastrophes to chemotherapy, has long been an object of study.A basic overview of the ionizing and non-ionizing radiation effects of the sensitivity of the thyroid gland on radiation and cancer development has been provided.In this review, we focus our attention on experiments in cell cultures exposed to ionizing radiation, ultraviolet light, and proton beams.Studies on the involvement of specific genes, proteins, and lipids are also reported.This review also describes how lipids are regulated in response to the radiation-induced damage and how they are involved in thyroid cancer etiology, invasion, and migration and how they can be used as both diagnostic markers and drug targets.
Glucose metabolism in lean patients with mild type 2 diabetes mellitus: Evidence for insulin-sensitive and insulin-resistant variants
Authors: Daniel A. Garc[iacute]a-Est[eacute]vez, David Ara[uacute]jo-Vilar, [Aacute]ngeles Saavedra-Gonz[aacute]lez, Gloria Fiestras-Janeiro, Jos[eacute] Cabezas-Cerrato
Journal: Metabolism (2002)
Incidentally Evaluating the Status of Renal Function in Technetium-99m DISIDA Hepatobiliary Imaging
Authors: WEI-JEN SHIH, FRANK H. DeLAND, JOHN J. COUPAL, PEGGY A. DOMSTAD
Journal: Clinical Nuclear Medicine (1986)

During hepatobiliary imaging studies, approximately 9% of Tc-99m DISIDA normally is excreted via the kidney. In routine 2, 5, 10, 15, 30, 45, and 60-minute images, the kidneys and urinary bladder are best visualized at 5-10 minutes and after 10-15 minutes, respectively. Nonvisualization of the kidney and/or urinary bladder may indicate renal dysfunction. To evaluate this hypothesis, Tc-99m DISIDA hepatobiliary images of 63 patients were correlated with concurrent serum BUN and creatinine levels (measured within 24 hours of the hepatobiliary study). Serum creatinine and BUN values were normal in patients with renal visualization. In patients without renal visualization, 17 of 19 had abnormal BUN and creatinine levels. The values of BUN and creatinine were significantly elevated (P < 0.001) in patients without renal visualization when compared with those showing renal visualization. One patient had visualization of a single kidney due to a nephrectomy; in another, persistent visualization was due to hydronephrosis. Nonvisualization of the kidneys and/or urinary bladder suggests abnormal renal function, and asymmetric renal activity raises the possibility of renal disease.
Symptoms and the early diagnosis of lung cancer
Authors: S S Birring
Journal: Thorax (2005)

<h3>Abstract</h3> K-mer-based methods are widely used in bioinformatics, but there are many gaps in our understanding of their statistical properties. Here, we consider the simple model where a sequence S (e.g. a genome or a read) undergoes a simple mutation process whereby each nucleotide is mutated independently with some probability r, under the assumption that there are no spurious k-mer matches. How does this process affect the k-mers of S? We derive the expectation and variance of the number of mutated k-mers and of the number of islands (a maximal interval of mutated k-mers) and oceans (a maximal interval of non-mutated k-mers). We then derive hypothesis tests and confidence intervals for r given an observed number of mutated k-mers, or, alternatively, given the Jaccard similarity (with or without minhash). We demonstrate the usefulness of our results using a few select applications: obtaining a confidence interval to supplement the Mash distance point estimate, filtering out reads during alignment by Minimap2, and rating long read alignments to a de Bruijn graph by Jabba.
The General Medical Council and the future of revalidation:Profession needs to debate regulator's role
Authors: Olusola O A Oni
Journal: BMJ (2005)

The General Medical Council and the future of revalidation GMC member respondsEditor-Esmail and Kmietowicz give an inaccurate account of the General Medical Council's policy development on revalidation, ignoring an iterative process with interested parties since 1998 in an attempt to introduce the most fundamental change to medical regulation since its foundation in 1858. 1 2 The GMC clearly has had regard to the legitimate interests of three principal groups-government and the NHS, patients and the public, and the various tribes that make up the UK medical profession.Despite suggestions to the contrary, an initial exploratory meeting on revalidation convened by Sir Donald Irvine in June 1998 was held in the context of a high profile professional conduct case, but well before the Bristol inquiry report and absolutely nothing to do with Rodney Ledward or, indeed, Harold Shipman.It was recognised then that some doctors were not keeping fully up to date nor were they indulging in reflective practice.Irvine correctly proposed that there was a need to make registration with the GMC more meaningful to the public than a mere recognition that doctors had reached a certain standard of professional knowledge in their early 20s.Both articles promote the idea that the doctors' regulator should be filling the vacuum within the NHS created by its failing to fulfil its public responsibility to monitor doctors' clinical standards.Clinical governance is now, slowly, being developed and eventually will extend from systems and teams to individuals-but is it reasonable, as both authors postulate, that such monitoring should become the financial and moral responsibility of the GMC sitting in London and Manchester rather than local managers at the coalface?Although revalidation is a continuing process, it becomes summative only every five years.The NHS and its local systems must not be allowed to abrogate their responsibility for the safety of patients on a day to day basis.Nor should they demand that the GMC and its prime function of assuring fitness to practise and the meaning of the medical register be inappropriately promoted as the first line of defence for the maintenance of clinical quality and safety.
Hippocrates of Ostia
Authors: William H. Strange
Journal: JAMA (1968)

<h3>To the Editor:—</h3> The article by Richards on Hippocrates (<b>204</b>:1049, 1968) contains an error, it would appear to me, as immense as the ancient Persian Empire was immense. Dr. Richards states: On the other side, "Similarly, I will not give to a woman a pessary for abortion," is a statement not only out of line with Hippocratic as well as all other surgical practice, but is not part of any ancient moral code, except the Pythagorean. One recalls, for example, how both feticide and infanticide were practices recommended in Plato's ideal republic. Abortions were condemned by the laws of the ancient Persian Empire, and violators were dealt with as willful murderers.<sup>1,2</sup>Similarly, as shown in the<i>Didache</i>, abortions were opposed by the very earliest Christian communities.<sup>3</sup>"I will not abort a woman," is a statement indeed in line with ancient moral codes besides the Pythagorean, and it
Treatment to Prevent Hepatitis B Virus Reactivation in Patients With Lymphoma Receiving Chemotherapy
Authors: Jihoon Baang
Journal: JAMA (2015)

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Smear tests: deja vu
Authors: J. Nottingham
Journal: BMJ (2001)

EDITOR—I refer to Goodman's review on cancer screening and misunderstanding by the media.1 In an editorial on the rising risk of litigation in Pap smear interpretation, DeMay gives the following analogy: You are a firefighter. You arrive at a burning house and hear screaming. There are 10 people inside. You run …
Phosphoinositide 3-Kinase γ Protects Against Catecholamine-Induced Ventricular Arrhythmia Through Protein Kinase A–Mediated Regulation of Distinct Phosphodiesterases
Authors: Alessandra Ghigo, Alessia Perino, Hind Mehel, Alexandra Zahradníková, Fulvio Morello, Jérôme Leroy, Viacheslav O. Nikolaev, Federico Damilano, James Cimino, Elisa De Luca, Wito Richter, Ruth Westenbroek, William A. Catterall, Jin Zhang, Chen Yan, Marco Conti, Ana Maria Gomez, Grégoire Vandecasteele, Emilio Hirsch, Rodolphe Fischmeister
Journal: Circulation (2012)

Phosphoinositide 3-kinase γ (PI3Kγ) signaling engaged by β-adrenergic receptors is pivotal in the regulation of myocardial contractility and remodeling. However, the role of PI3Kγ in catecholamine-induced arrhythmia is currently unknown.Mice lacking PI3Kγ (PI3Kγ(-/-)) showed runs of premature ventricular contractions on adrenergic stimulation that could be rescued by a selective β(2)-adrenergic receptor blocker and developed sustained ventricular tachycardia after transverse aortic constriction. Consistently, fluorescence resonance energy transfer probes revealed abnormal cAMP accumulation after β(2)-adrenergic receptor activation in PI3Kγ(-/-) cardiomyocytes that depended on the loss of the scaffold but not of the catalytic activity of PI3Kγ. Downstream from β-adrenergic receptors, PI3Kγ was found to participate in multiprotein complexes linking protein kinase A to the activation of phosphodiesterase (PDE) 3A, PDE4A, and PDE4B but not of PDE4D. These PI3Kγ-regulated PDEs lowered cAMP and limited protein kinase A-mediated phosphorylation of L-type calcium channel (Ca(v)1.2) and phospholamban. In PI3Kγ(-/-) cardiomyocytes, Ca(v)1.2 and phospholamban were hyperphosphorylated, leading to increased Ca(2+) spark occurrence and amplitude on adrenergic stimulation. Furthermore, PI3Kγ(-/-) cardiomyocytes showed spontaneous Ca(2+) release events and developed arrhythmic calcium transients.PI3Kγ coordinates the coincident signaling of the major cardiac PDE3 and PDE4 isoforms, thus orchestrating a feedback loop that prevents calcium-dependent ventricular arrhythmia.
Genome-wide association analysis of metabolic traits in a birth cohort from a founder population
Authors: Chiara Sabatti, Susan K Service, Anna-Liisa Hartikainen, Anneli Pouta, Samuli Ripatti, Jae Brodsky, Chris G Jones, Noah A Zaitlen, Teppo Varilo, Marika Kaakinen, Ulla Sovio, Aimo Ruokonen, Jaana Laitinen, Eveliina Jakkula, Lachlan Coin, Clive Hoggart, Andrew Collins, Hannu Turunen, Stacey Gabriel, Paul Elliot, Mark I McCarthy, Mark J Daly, Marjo-Riitta Järvelin, Nelson B Freimer, Leena Peltonen
Journal: Nature Genetics (2008)
An unusual case of transient papular mucinosis associated with carpal tunnel syndrome
Authors: C.J.M. STEPHENS, J.S. ROSS, R. CHARLES-HOLMES, P.H. MCKEE, M.M. BLACK
Journal: British Journal of Dermatology (1993)

A 67‐year‐old man presented with discrete mucinous papules on the scalp and fingers, and bilateral carpal tunnel syndrome. Both features remitted spontaneously within several months. The acral distribution, and histopathological features, were in keeping with the recently described acral persistent papular mucinosis. Involvement of the scalp, however, has not previously been described, and transient mucin deposition is unusual. The history of bilateral carpal tunnel compression raises the possibility of extracutaneous involvement, not previously reported in this group of patients.
The Relationship between Prenatal PCB Exposure and Intelligence (IQ) in 9-Year-Old Children
Authors: Paul W. Stewart, Edward Lonky, Jacqueline Reihman, James Pagano, Brooks B. Gump, Thomas Darvill
Journal: Environmental Health Perspectives (2008)

Several epidemiologic studies have demonstrated relationships between prenatal exposure to polychlorinated biphenyls (PCBs) and modest cognitive impairments in infancy and early childhood. However, few studies have followed cohorts of exposed children long enough to examine the possible impact of prenatal PCB exposure on psychometric intelligence in later childhood. Of the few studies that have done so, one in the Great Lakes region of the United States reported impaired IQ in children prenatally exposed to PCBs, whereas another found no association.This study was designed to determine whether environmental exposure to PCBs predicts lower IQ in school-age children in the Great Lakes region of the northeastern United States.We measured prenatal exposure to PCBs and IQ at 9 years of age in 156 subjects from Oswego, New York. We also measured > 50 potential predictors of intelligence in children, including repeated measures of the home environment [Home Observation for Measurement of the Environment (HOME)], socioeconomic status (SES), parental IQ, alcohol/cigarette use, neonatal risk factors, and nutrition.For each 1-ng/g (wet weight) increase in PCBs in placental tissue, Full Scale IQ dropped by three points (p = 0.02), and Verbal IQ dropped by four points (p = 0.003). The median PCB level was 1.50 ng/g, with a lower quartile of 1.00 ng/g and an upper quartile of 2.06 ng/g. Moreover, this association was significant after controlling for many potential confounders, including prenatal exposure to methylmercury, dichlorodiphenyldichloroethylene, hexachlorobenzene, and lead.These results, in combination with similar results obtained from a similar study in the Great Lakes conducted 10 years earlier, indicate that prenatal PCB exposure in the Great Lakes region is associated with lower IQ in children.
Misleading exercise electrocardiograms
Authors: D. Ashton, B. Davies
Journal: BMJ (1987)

less about a seriQus primary care information service than general practitioners who have taken up the VAMP and Meditel options, butpresumably no great multinational company has offered to pay for it.If one did he would face the same dilemma, inevitable in a society that has abdicated social decision to the stock market.
Consultants and their future
Authors: A B Shrank
Journal: BMJ (1982)

<h3>Abstract</h3> Based on the transcriptome analysis of 555 sarcomas, we identified a group of tightly clustered leiomyosarcomas (LMS) due to their gene expression homogeneity. We named them “hLMS” and the other LMS “oLMS”. We derived a transcriptional signature able to identify each group and used it to classify patients from two independent cohorts. In all cohorts, hLMS were preferentially carried by women, located in the internal trunk, highly differentiated, and similarly altered at the genomic level. Based on integrative bioinformatic analysis, we show that hLMS originate from vascular smooth muscle cells presenting both contractile and synthetic characteristics, while oLMS could derive from fibroblasts. We found strong <i>MYOCD</i> expression to be an hLMS-specific driver and show that the MYOCD/SRF axis is essential only for hLMS survival. Identification of hLMS could become standard clinical practice, leading to the development of specific effective treatments with MYOCD/SRF inhibitors. <h3>Statement of significance</h3> Leiomyosarcomas (LMS) are currently treated as a single entity. However, we have now identified a transcriptionally, genomically and clinically homogeneous subgroup of LMS. Their oncogenesis is driven by the acquisition of high differentiation through <i>MYOCD</i> over-expression. This confers them sensitivity to MYOCD/SRF inhibitors, which could thus become a potential therapeutic target.
Relation between extent of coronary artery disease and blood viscosity.
Authors: G D Lowe, M M Drummond, A R Lorimer, I Hutton, C D Forbes, C R Prentice, J C Barbenel
Journal: BMJ (1980)

Blood viscosity (shear rate 100/s) and its major determinants (packed cell volume, plasma fibrinogen concentration, and plasma viscosity) were measured before coronary angiography in 50 men aged 30-55 and related to the extent of coronary artery disease. Twenty-six men had extensive disease (stenosis of two or three major coronary vessels), and 24 had either stenosis of one vessel or no stenosis. The 26 men with extensive disease had significantly higher mean blood viscosity than those with mild or no disease and 25 healthy controls (p less than 0.001). The increased viscosity was due partly to a higher packed cell volume and partly to a higher fibrinogen concentration; plasma viscosity was not significantly increased. These differences could not be explained by smoking history. These results suggest an association between increased blood viscosity and extensive coronary artery disease in men, which merits further investigation.
Abstract 5288: PHLPP controls cell polarity by negatively regulating the activity of atypical PKC in colon cancer cells
Authors: Xiaopeng Xiong, Xin li, Tianyan Gao
Journal: Cancer Research (2014)

Abstract The proper establishment of epithelial polarity allows cells to sense and to respond signals that arise from the microenvironment in a spatiotemporally controlled manner. Increasing evidence has suggested that disruption of polarity promotes the malignant progression of cancer cells. However, the molecular mechanism underlying polarity regulation in the initiation and progression of colon cancer remains largely unknown. PHLPP belongs to a novel family of Ser/Thr protein phosphatases that consists of PHLPP1 and PHLPP2 isoforms. Previously, we have identified conventional PKC isoforms as substrates of PHLPP. Here, we demonstrated that PHLPP controls phosphorylation levels of atypical PKC (aPKC) isoforms, including PKCζ and PKCι, as well. Overexpression of either PHLPP isoform resulted in a decrease in aPKC phosphorylation at both the activation loop (Thr403/410) and the turn motif (Thr555/560) sites in colon cancer cells; conversely, knockdown of PHLPP increased aPKC phosphorylation. In addition, in vitro dephosphorylation experiments revealed that both aPKC isoforms are direct substrates of PHLPP. Since aPKC has been widely implicated in the regulation of cell polarity in intestinal epithelial cells, we determined the function of PHLPP in establishing cell polarity using a 3-D Matrigel culture model. Whereas control Caco2 cells form well polarized cysts in 2 weeks, PHLPP depletion alters the acinar structure by inducing the formation of multiple lumens. Interestingly, knockdown of PKCζ, but not PKCι, results in similar disruption of the polarized lumen structure in Caco2 cells, suggesting that PHLPP may regulate cell polarity through dephosphorylating PKCζ. Taken together, our results identify both aPKC isoforms as novel substrates of PHLPP and downregulation of PHLPP may promote tumorigenesis in colon cancer by disrupting cell polarity. Citation Format: Xiaopeng Xiong, Xin li, Tianyan Gao. PHLPP controls cell polarity by negatively regulating the activity of atypical PKC in colon cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 5288. doi:10.1158/1538-7445.AM2014-5288
Functional genomics of the CDKN2A/B locus in cardiovascular and metabolic disease: what have we learned from GWASs?
Authors: Sarah Anissa Hannou, Kristiaan Wouters, Réjane Paumelle, Bart Staels
Journal: Trends in Endocrinology and Metabolism (2015)

Genome-wide association studies (GWASs) provide an unprecedented opportunity to examine, on a large scale, the association of common genetic variants with complex diseases like type 2 diabetes (T2D) and cardiovascular disease (CVD), thus allowing the identification of new potential disease loci. Using this approach, numerous studies have associated SNPs on chromosome 9p21.3 situated near the cyclin-dependent kinase inhibitor 2A/B (CDKN2A/B) locus with the risk for coronary artery disease (CAD) and T2D. However, identifying the function of the nearby gene products (CDKN2A/B and ANRIL) in the pathophysiology of these conditions requires functional genomic studies. We review the current knowledge, from studies using human and mouse models, describing the function of CDKN2A/B gene products, which may mechanistically link the 9p21.3 risk locus with CVD and diabetes.