tbuckley/cabot-search huggingface dataset:
Insights into the Management of Emerging Infections: Regulating Variant Creutzfeldt-Jakob Disease Transfusion Risk in the UK and the US
Authors: Maya L Ponte
Journal: PLoS Medicine (2006)

Variant Creutzfeldt-Jakob disease (vCJD) is a human prion disease caused by infection with the agent of bovine spongiform encephalopathy. After the recognition of vCJD in the UK in 1996, many nations implemented policies intended to reduce the hypothetical risk of transfusion transmission of vCJD. This was despite the fact that no cases of transfusion transmission had yet been identified. In December 2003, however, the first case of vCJD in a recipient of blood from a vCJD-infected donor was announced. The aim of this study is to ascertain and compare the factors that influenced the motivation for and the design of regulations to prevent transfusion transmission of vCJD in the UK and US prior to the recognition of this case.
British Paediatric and Adolescent Bone Group's position statement on vitamin D deficiency
Authors: P. Arundel, S. F. Ahmed, J. Allgrove, N. J. Bishop, C. P. Burren, B. Jacobs, M. Z. Mughal, A. C. Offiah, N. J. Shaw
Journal: BMJ (2012)

Because of the lack of well designed studies on vitamin D and health,1 the British Paediatric and Adolescent Bone Group has produced a position statement based on current expert opinion. This statement is supported by the British Society of Paediatric Radiology and child protection and nutrition committees of the Royal College of Paediatrics …
Combined Fourier Amplitude and Phase Imaging in Patients with Coronary Artery Disease
Authors: KARL E. ALCAN, WILLIAM ROBESON, MARTIN C. GRAHAM, CHRISTOPHER PALESTRO, FRANCIS H. OLIVER, RICHARD S. BENUA
Journal: Clinical Nuclear Medicine (1984)

ourier amplitude and phase image analysis were evaluated in 66 patients. Thirty patients served as a control group and 36 had coronary artery disease (CAD). Each patient in our control group had a rest and exercise radionuclide cineangiogram (RNCA) study (60 total). The amplitude and phase images for controls were uniform. No statistically significant difference in the histogram distribution of amplitude or phase occurred between rest and exercise. Twenty-five patients with CAD had a prior myocardial infarction (Ml). Fourier analysis, when compared to the left ventricular ejection fraction (LVEF) and visual cine wall motion analysis, improved the sensitivity of the rest RNCA study to detect CAD from 68% to 92%. Regional Fourier amplitude and phase image analysis demonstrated an 85% sensitivity in localizing regions of previous infarction. Thirteen of 25 patients with prior Ml and an additional 11 patients with recent onset of angina but no previous infarction, had exercise RNCA studies. When compared to cardiac catheterization data, regional Fourier amplitude and phase image analysis demonstrated sensitivities of 87% and 80%, respectively, in correctly identifying clinically significant major coronary artery involvement in these two subsets of patients. Fourier amplitude and phase image analysis were also able to distinguish normals from patients with previous Ml, and patients with CAD but no prior infarction. All comparisons were statistically significant. We conclude that the semiquantitative image analysis of Fourier amplitude and phase data increases the clinical utility of the RNCA study in patients with CAD.
Cyclic RGDyk-conjugated LMWH-taurocholate derivative as a targeting angiogenesis inhibitor
Authors: Asarasin Adulnirath, Seung Woo Chung, Jooho Park, Seung Rim Hwang, Ji-Young Kim, Victor C. Yang, Sang Yoon Kim, Hyun Tae Moon, Youngro Byun
Journal: Journal of Controlled Release (2012)
Extracellular Discontinuities in Cardiac Muscle
Authors: Madison S. Spach, J. Francis Heidlage, Paul C. Dolber, Roger C. Barr
Journal: Circulation Research (1998)

Abstract —It has become of fundamental importance to understand variations in the shape of the upstroke of the action potential in order to identify structural loading effects. One component of this goal is a detailed experimental analysis of the time course of the foot of the cardiac action potential (V m foot) during propagation in different directions in anisotropic cardiac muscle. To this end, we performed phase-plane analysis of transmembrane action potentials during anisotropic propagation in adult working myocardium. The results showed that during longitudinal propagation there was initial slowing of V m foot that resulted in deviations from a simple exponential; corollary changes occurred at numerous sites during transverse propagation. We hypothesized that the effect on V m foot observed in the experimental data was created by the microscopic structure, especially the capillaries. This hypothesis predicts that the phase-plane trajectory of V m foot will deviate from linearity in the presence of a high density of capillaries, and that a linear trajectory will occur in the absence of capillaries. Comparison of the results of Fast and Kléber ( Circ Res . 1993;73:914–925) in a monolayer of neonatal cardiac myocytes, which is devoid of capillaries, and our results in newborn ventricular muscle, which is rich in capillaries, showed drastic differences in V m foot as predicted. Because this comparison provided experimental support for the capillary hypothesis, we explored the underlying biophysical mechanisms due to interstitial electrical field effects, using a “2-domain” model of myocytes and capillaries separated by interstitial space. The model results show that a propagating interstitial electrical field induces an inward capacitive current in the inactive capillaries that causes a feedback effect on the active membrane (source) that slows the initial rise of its action potential. The results show unexpected mechanisms related to extracellular structural loading that may play a role in selected conduction disturbances, such as in a reperfused ischemic region surrounded by normal myocardium.
F-18 Fluorodeoxyglucose Uptake in a Benign Gastric Ulcer
Authors: Eugene Lin
Journal: Clinical Nuclear Medicine (2007)

A 78-year-old woman with lung cancer underwent an F-18 fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT). Focal FDG uptake was noted in the stomach which was associated with an area of thickening and ulceration on the CT scan. Endoscopy and biopsy demonstrated a benign gastric ulcer.
A Retrospective Analysis of Primary Tumour Histology and Survival in Breast Cancer Patients Developing Symptomatic Brain Metastases Treated with Whole Brain Radiotherapy (WBRT) at Mount Vernon Cancer Centre (MVCC).
Authors: R. Miller, M. Assoku, M. Assoku, D. Krell, P. Sasieni, P. Mulholland, P. Mulholland
Journal: Cancer Research (2009)

Abstract Background: The purpose of this study was to determine the influence of primary tumour histology on survival following WBRT for brain metastases in patients with breast cancer.Methods: From treatment records we identified 294 patients with brain metastases and a diagnosis of primary breast cancer who were treated with WBRT at MVCC from January 2000 until December 2008. We obtained information from case notes and original pathology reports regarding TNM staging and receptor status: Estrogen (ER), progesterone (PR) and human epidermal growth factor receptor-2 (HER-2). Dates of diagnosis and death were sourced from records at MVCC, the Thames Cancer Registry and GP practices.Results: We obtained receptor status, TNM staging and dates of death for 294 patients; 19 were excluded as date of death could not be verified. The dates of primary diagnosis for the study cohort ranged from 1983 to 2008. The median age at diagnosis was 52 (range 24-81, interquartile range 42-62).Analysis of age at primary diagnosis expressed as &amp;lt; 50 or ≥ 50 demonstrated improved survival in the younger age group (HR 0.64 95% CI 0.50-0.83). Time to brain relapse amongst patients receiving WBRT was not related to initial tumour size (p=0.8) but was related to the number of affected nodes (reduced by 9 months per node, p=0.038) and women with (non-brain) metastatic disease at diagnosis had WBRT on average 2.4 years earlier than those that did not (p=0.004). TNM staging did not affect post WBRT survival. After adjusting for age at diagnosis (&amp;lt;,≥50), post WBRT survival was not affected by age at treatment. Controlling for the influence of age at diagnosis, Cox regression analysis of survival post WBRT demonstrated improved survival for ER positive patients (HR 0.66 95% CI 0.49-0.90). Survival post WBRT was not significantly influenced by HER-2 (HR 0.81 95% CI 0.55-1.19) or PR (HR 0.91 95% C.I. 0.63-1.33) status. Patients who experience late brain relapse (&amp;gt; 4 years post diagnosis) have slightly better survival post WBRT (HR 0.77, p=0.054). ER positive patients in this study developed brain metastases on average 1.8 years later than ER negative patients (95% CI 0.9-2.8).Conclusions: In this cohort ER positive patients who relapse in the brain do so later and live longer following WBRT (figure 1). Our data suggests that HER-2 status has little effect on post WBRT survival. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 4110.
Abstract 1655: Genome-wide association study for age at onset in breast cancer: results from the Seoul Breast Cancer Study
Authors: Hyuna Sung, Ji-Yeob Choi, Minkyo Song, Sujee Jeon, Sue K. Park, Keun-Young Yoo, Dong-Young Noh, Sei-Hyun Ahn, Daehee Kang
Journal: Cancer Research (2012)

Abstract Introduction: While the incidence of breast cancer is relatively low in Korean women, the proportion of breast cancer that develops in younger age is much higher than in western countries. Family-based linkage study has focused on the identification of a region which is associated with the age at onset in familial breast cancer. However, genetic factors for onset age of breast cancer are still largely unknown. While genome-wide association studies (GWAS) have identified over 20 susceptibility loci for breast cancer, no previous study has examined the relationship between the common genetic variations and the age at onset in breast cancer. Methods: To identify genetic factors underlying onset age of breast cancer, we investigated the association between genetic variants and age at diagnosis in 2,155 breast cancer cases. Over 1.9 million SNPs either directly genotyped using Affymetrix 6.0 or imputed with HapMap 2.0 as a reference panel were evaluated after quality control. Tests of association were conducted with Plink v1.01 using the additive genetic model and Mach2qtl with allelic dosages in a linear regression model in which onset age was included as a dependent variable (continuous). The differences of mean age across genotype-groups were also compared using one-way analysis of variance. Results: The mean age at onset in breast cancer was 48.1 ± 9.31. The SNPs with p-value less than 1×10-5 obtained from linear regression were clustered into two regions: two SNPs (rs6684400 and rs6659875) are at 1q25.3 in intergenic region between ZNF648 and GLUL gene; the other two (rs669576 and rs667007) are at 11q25 in intronic region of NTM gene. Per-allele effect size was 1.4 ± 0.30 (p = 4.84E-06) for rs6684400 C allele and 3.1 ± 0.68 for rs669576 T allele (p = 7.11E-06). The mean age at onset for the rs6684400 G/G, C/G and C/C groups were found to be 47.2 ± 9.00, 48.1 ± 9.32 and 49.7 ± 9.59, respectively (p = 0.0001). As for the rs669576, the mean age at onset for G/G, G/T and T/T groups were 47.8 ± 9.15, 50.9 ± 10.38 and 54.3 ± 7.80, respectively (p &amp;lt; 0.0001) Conclusions: Our study suggests that the common genetic variants may be closely linked to age at onset in breast cancer. Further validation with a larger sample size is required to validate our result. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1655. doi:1538-7445.AM2012-1655
Steroids and Spontaneous Tendon Rupture
Authors: Philip Sylbert
Journal: JAMA (1964)

<h3>To the Editor:—</h3> I read with interest the report by Twining et al on spontaneous tendon rupture associated with lupus erythematosus (<i>JAMA</i><b>189:</b>377 [Aug 3] 1964). Although the authors make a good case for the hypothesis that the disease itself causes the phenomenon, earlier reports place more emphasis on the role of corticosteroids. Bilateral Achilles tendon rupture occurring spontaneously during the course of long-term therapy with various steroids has been reported on at least four occasions. Interestingly, two of the patients were also being treated for disseminated lupus erythematosus.<sup>1,2</sup>The other two were asthmatics,<sup>3,4</sup>although at the time of the Achilles ruptures a diagnosis of polyarteritis nodosa was being considered in one of these.<sup>4</sup> Since no episode of this type has apparently been reported during the course of nonsteroid-treated lupus, it may well be that both factors are essential for its occurrence. In this connection, the
Clay Ingestion and Hypokalemia
Authors: NANCY E. GARY
Journal: Annals of Internal Medicine (1982)

Letters and Corrections1 October 1982Clay Ingestion and HypokalemiaNANCY E. GARY, M.D., ROBERT P. EISINGER, M.D.NANCY E. GARY, M.D.Search for more papers by this author, ROBERT P. EISINGER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-97-4-622_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We read with interest the article on clay ingestion as a cause of hypokalemia by Gonzalez and colleagues (1). The data presented certainly suggest that clay acts to bind potassium in vitro. But in the absence of measured urinary electrolytes, a mineralocorticoid-like effect of the clay or other concurrently ingested agent cannot be excluded. Ammonium glycyrrhizate is an ingredient of natural licorice and some chewing tobaccos, and causes sodium retention, potassium loss, and suppression of the renin-angiotensin-aldosterone axis (2).Without knowledge of the patient's dietary intake or urinary excretion of sodium, the plasma renin value is difficult...References1. GONZALEZOWENSUNGAROWERKWENTZ JWPEP. Clay ingestion: a rare cause of hypokalemia. Ann Intern Med. 1982;97:65-6. LinkGoogle Scholar2. HARRINGTONKASSIRER JJ. Metabolic alkalosis. In: Acid/Base. Boston: Little, Brown and Co.; 1982:227-306. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University of Medicine and Dentistry of New Jersey-Rutgers Medical School Piscataway, NJ 08854 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByInvoluntary soil ingestion and geophagia: A source and sink of mineral nutrients and potentially harmful elements to consumers of earth materialsHypokalemic Myopathy in Pregnancy Caused by Clay IngestionPica Associated with Renal and Electrolyte Disorders 1 October 1982Volume 97, Issue 4Page: 622-622KeywordsBlood plasmaExcretionIngestionPotassiumSaltsSodium Issue Published: 1 October 1982 PDF DownloadLoading ...
Merry Christmas for Patients with Hemophilia B
Authors: Katherine P. Ponder
Journal: New England Journal of Medicine (2011)

Hemophilia B (also known as Christmas disease) is due to deficiency of coagulation factor IX (FIX). In this issue of the Journal, Nathwani et al. report the first unequivocal evidence of successful gene therapy for hemophilia B — a major advance in this field.1 This success for hemophilia may translate into gene therapy for other blood protein deficiencies.Hemophilia is due to deficiency in a coagulation factor and results in a bleeding disorder that often involves joints and muscles. The most common types are hemophilia A and B, which are due to deficiencies of factor VIII and FIX, respectively, and . . .
Abstract B59: Wild-type ALK and both ALK-R1275Q and ALK-F1174L activating mutations display a strong oncogenic activity in vivo in murine neural crest progenitor cells via cooperation with c-myc
Authors: Annick Mühlethaler-Mottet, Gisèle Montavon, Marjorie Flahaut, Nicolas Jauquier, Jean-Marc Joseph, Olivier Delattre, Lukas Sommer, Isabelle Janoueix-Lerosey, Nicole Gross
Journal: Cancer Research (2014)

Abstract Neuroblastoma (NB), a neural crest-derived embryonal tumor, is a heterogeneous childhood malignancy that often presents as an incurable disease. The anaplastic lymphoma receptor tyrosine kinase gene (ALK) was shown to be overexpressed, mutated or amplified in the majority of NB. The most common mutation, ALK-F1174L displayed an efficient transforming activity in vivo, and was shown in transgenic mouse models to drive NB formation and to cooperate with MYCN in the oncogenic process. In this project, we aimed at comparing the in vivo oncogenic potential of ALK-wt, with the two most frequent activating mutations ALK-F1174L (only present in sporadic NB), and ALK-R1275Q (present in familial and sporadic NB). Our strategy included the stable expression of ALK-wt and mutated variants into murine neural crest progenitor cells (JoMa1), which are the well-recognized NB progenitors. In vitro, only ALK-F1174L and ALK-R1275Q conferred an oncogenic potential to JoMa1 cells as measured by clonogenic assays. In contrast, in vivo experiments showed that JoMa1 cells expressing ALK-wt, as well as activating mutations ALK-R1275Q and ALK-F1174L rapidly produced highly aggressive tumors after subcutaneous or orthotopic (adrenal gland) implantations in nude mice. JoMa1-ALK-F1174L cells induced the fastest tumor growth as compared to JoMa1-ALK-R1275Q and JoMa1-ALK-wt cells, revealing the tremendous tumorigenic potential of ALK-F1174L cells. Interestingly, as a result from ALK activation, orthotopic tumors or their derived cell lines strongly upregulated c-myc expression. Moreover, specific ALK inhibition using TAE684, or c-myc inhibition with 10058-F4, completely abrogated the in vitro clonogenic capacity of tumor-derived cell lines. Such observations suggest that the tumorigenic potential of neural crest progenitor cells is strongly dependent on both ALK and c-myc activity. Our study demonstrates for the first time an oncogenic activity of ALK-R1275Q and ALK-wt when overexpressed in neural crest cells, and reveals the complex interactions between ALK and the myc oncogene family in neural crest cell-derived tumor formation. Citation Format: Annick Mühlethaler-Mottet, Gisèle Montavon, Marjorie Flahaut, Nicolas Jauquier, Jean-Marc Joseph, Olivier Delattre, Lukas Sommer, Isabelle Janoueix-Lerosey, Nicole Gross. Wild-type ALK and both ALK-R1275Q and ALK-F1174L activating mutations display a strong oncogenic activity in vivo in murine neural crest progenitor cells via cooperation with c-myc. [abstract]. In: Proceedings of the AACR Special Conference on Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; Nov 3-6, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;74(20 Suppl):Abstract nr B59.
Record Heat May Have Contributed to a Banner Year for West Nile Virus
Authors: Bridget M. Kuehn
Journal: JAMA (2012)

With nearly 4000 cases of West Nile virus reported to the US Centers for Disease Control and Prevention (CDC) as of early October, more than 5 times the number of cases reported in 2011, the 2012 West Nile virus season has been one of the worst since the virus emerged in the United States in 1999.
Diminished Lipoxin Biosynthesis in Severe Asthma
Authors: Bruce D. Levy, Caroline Bonnans, Eric S. Silverman, Lyle J. Palmer, Gautham Marigowda, Elliot Israel
Journal: American Journal of Respiratory and Critical Care Medicine (2005)

Rationale and Objectives: Severe asthma is characterized by increased airway inflammation that persists despite therapy with corticosteroids. It is not, however, merely an exaggeration of the eosinophilic inflammation that characterizes mild to moderate asthma; rather, severe asthma presents unique features. Although arachidonic acid metabolism is well appreciated to regulate airway inflammation and reactivity, alterations in the biosynthetic capacity for both pro- and antiinflammatory eicosanoids in severe asthma have not been determined.Methods: Patients with severe asthma were identified according to National Heart, Lung, and Blood Institute Severe Asthma Research Program criteria. Samples of whole blood from individuals with severe or moderate asthma were assayed for biosynthesis of lipoxygenase-derived eicosanoids.Measurements and Main Results: The counterregulatory mediator lipoxin A4 was detectable in low picogram amounts, using a novel fluorescence-based detection system. In activated whole blood, mean lipoxin A4 levels were decreased in severe compared with moderate asthma (0.4 [SD 0.4] ng/ml vs. 1.8 [SD 0.8] ng/ml, p = 0.001). In sharp contrast, mean levels of prophlogistic cysteinyl leukotrienes were increased in samples from severe compared with moderate asthma (112.5 [SD 53.7] pg/ml vs. 64.4 [SD 24.8] pg/ml, p = 0.03). Basal circulating levels of lipoxin A4 were also decreased in severe relative to moderate asthma. The marked imbalance in lipoxygenase-derived eicosanoid biosynthesis correlated with the degree of airflow obstruction.Conclusions: Mechanisms underlying airway responses in severe asthma include underproduction of lipoxins. This is the first report of a defect in lipoxin biosynthesis in severe asthma, and suggests an alternative therapeutic strategy that emphasizes natural counterregulatory pathways in the airways.
Maumee: My Walden Pond
Authors: Roger C. Bone
Journal: JAMA (1996)

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