tbuckley/cabot-search huggingface dataset:
Aspirin Prophylaxis for Migraine
Authors: D. J. Dalessio
Journal: JAMA (1990)

Migraine is not a disease in the usual sense of the term. It may be considered a condition or syndrome, perhaps an entity, and thus must have a pathophysiologic basis, about which there are many theories and few facts. Furthermore, the diagnosis of migraine may be difficult at times, and not all physicians will agree on the use of the term in specific patients.  To codify migraine in its multiple types and forms, two recent classifications of headache have been proposed. 1,2 The more comprehensive of these is a product of the International Headache Society, under the chairmanship of Jes Olesen, MD. This monumental work took 3 years, involved a steering committee and 12 subcommittees, and, published in its long form, is 96 pages including the index (the pocket abridged edition covers 16 pages). From this it may be inferred that use of the term migraine covers a lot of
A New Arenavirus in a Cluster of Fatal Transplant-Associated Diseases
Authors: Gustavo Palacios, Julian Druce, Lei Du, Thomas Tran, Chris Birch, Thomas Briese, Sean Conlan, Phenix-Lan Quan, Jeffrey Hui, John Marshall, Jan Fredrik Simons, Michael Egholm, Christopher D. Paddock, Wun-Ju Shieh, Cynthia S. Goldsmith, Sherif R. Zaki, Mike Catton, W. Ian Lipkin
Journal: New England Journal of Medicine (2008)

Three patients who received visceral-organ transplants from a single donor on the same day died of a febrile illness 4 to 6 weeks after transplantation. Culture, polymerase-chain-reaction (PCR) and serologic assays, and oligonucleotide microarray analysis for a wide range of infectious agents were not informative.We evaluated RNA obtained from the liver and kidney transplant recipients. Unbiased high-throughput sequencing was used to identify microbial sequences not found by means of other methods. The specificity of sequences for a new candidate pathogen was confirmed by means of culture and by means of PCR, immunohistochemical, and serologic analyses.High-throughput sequencing yielded 103,632 sequences, of which 14 represented an Old World arenavirus. Additional sequence analysis showed that this new arenavirus was related to lymphocytic choriomeningitis viruses. Specific PCR assays based on a unique sequence confirmed the presence of the virus in the kidneys, liver, blood, and cerebrospinal fluid of the recipients. Immunohistochemical analysis revealed arenavirus antigen in the liver and kidney transplants in the recipients. IgM and IgG antiviral antibodies were detected in the serum of the donor. Seroconversion was evident in serum specimens obtained from one recipient at two time points.Unbiased high-throughput sequencing is a powerful tool for the discovery of pathogens. The use of this method during an outbreak of disease facilitated the identification of a new arenavirus transmitted through solid-organ transplantation.
Impact of Patient-Prosthesis Mismatch and Aortic Valve Design on Coronary Flow Reserve After Aortic Valve Replacement
Authors: Farhad Bakhtiary, Mirko Schiemann, Omer Dzemali, Selami Dogan, Volker Schächinger, Hans Ackermann, Anton Moritz, Peter Kleine
Journal: Journal of the American College of Cardiology (2007)
Chronic Budd-Chiari syndrome due to obstruction of the intrahepatic portion of the inferior vena cava
Authors: D. V. Datta, S. Saha, S. A. K. Singh, B. B. Gupta, B. K. Aikat, K. S. Chugh, P. N. Chhuttani
Journal: Gut (1972)

Clinical features of obstruction of the intrahepatic portion of the inferior vena cava were observed in five out of the 11 patients with the Budd-Chiari syndrome seen during the last four years. These patients apparently formed a distinct group from the remaining six and resembled in clinical course, biochemical features, haemodynamic findings, and radiological investigations the patients described as cases of membranous obliteration of the intrahepatic portion of the inferior vena cava. The present study reports five such patients diagnosed with the help of venous catheterization, percutaneous hepatography, and haemodynamic studies. The value of distinguishing these patients from those with obstruction due to hepatic vein occlusion is highlighted because of the difference in the prognosis and treatment.
Calcitonin Gene-Related Peptide Mediates Acetylcholine-Induced Endothelium-Independent Vasodilation in Mesenteric Resistance Blood Vessels of the Rat
Authors: Makoto Takenaga, Hiromu Kawasaki, Akihiko Wada, Tanenao Eto
Journal: Circulation Research (1995)

Abstract The role of calcitonin gene-related peptide (CGRP)–containing vasodilator nerves in acetylcholine chloride (ACh)–induced vasodilation was studied in the perfused mesenteric vascular bed isolated from the rat. Bolus infusions of ACh at smaller doses (0.1 and 1 nmol) produced rapid and short-lived vasodilation. However, larger doses (10 and 100 nmol) of ACh caused a rapid and subsequent long-lasting vasodilator response in which the duration of vasodilation was prolonged in a concentration-dependent manner. Pretreatment with capsaicin (1 μmol/L for 20 minutes) significantly shortened the duration of vasodilator response to ACh but did not affect the initial rapid phase of ACh-induced vasodilation. Chemical removal of the vascular endothelium by perfusion with sodium deoxycholate (1.75 to 1.80 mg/mL) for 30 seconds and subsequent treatment with N ω -nitro- l -arginine (100 μmol/L) to inhibit nitric oxide synthesis abolished the initial rapid vasodilator action of ACh at any given concentration. However, in the same preparation, increasing concentrations (from 1 to 1000 nmol) of ACh produced only the long-lasting vasodilator responses in a concentration-dependent manner. This long-lasting vasodilator response to ACh infusion was abolished by capsaicin pretreatment (1 μmol/L), human CGRP[8-37] (CGRP receptor antagonist, 1 μmol/L), and atropine (muscarinic ACh receptor antagonist, 1, 10, and 100 nmol/L) but not by hexamethonium (nicotinic ACh receptor antagonist, 1 and 10 μmol/L). In the preparations without endothelium, the bolus infusion of ACh (300 nmol for 30 seconds) evoked a long-lasting vasodilation and release of CGRP-like immunoreactivities into the perfusate. These results suggest that the ACh-induced vasorelaxation consists of two elements: an initial transient endothelium-dependent component and a secondary long-lasting endothelium-independent component. Moreover, ACh activates muscarinic receptors located on CGRP-containing neurons to release CGRP, which then acts at CGRP receptors on vascular smooth muscles to cause the endothelium-independent vasodilation.
Biochemical and Morphological Alterations of Baboon Hepatic Mitochondria After Chronic Ethanol Consumption
Authors: Masao Arai, Maria A. Leo, Masayuki Nakano, Ellen R. Gordon, Charles S. Lieber
Journal: Hepatology (1984)

Baboons fed ethanol (50% of total calories) chronically develop ultrastructural alterations of hepatic mitochondria. To determine whether mitochondrial functions are also altered, mitochondria were isolated from nine baboons fed ethanol chronically and their pair-fed controls. At the fatty liver stage, ADP-stimulated respiration was depressed in ethanol-fed baboons by 59.4% with glutamate, 43.2% with acetaldehyde, 45.1% with succinate and 51.1% with ascorbate as substrates. A similar decrease was noted in the ADP/O ratio (14 to 28%) and respiratory control ratio (20 to 44%) with all substrates. Similar alterations of mitochondrial functions were observed in baboons with more advanced stages of liver disease, namely fibrosis. These changes after ethanol treatment were associated with decreases in the enzyme activities of mitochondrial respiratory chain: glutamate, NADH and succinate dehydrogenase (42, 24 and 28%, respectively), glutamate-, NADH-or succinate-cytochrome c reductase (42, 27 and 32%, respectively) and cytochrome oxidase (59.6%). The content of all cytochromes was also decreased in ethanol-fed baboons, especially aa 3 (57%). Moreover, [ 14 C] leucine incorporation into mitochondrial membranes was depressed by 21% after ethanol treatment. On the other hand, glutamate dehydrogenase activities of serum and cytosol in ethanol-fed baboons were significantly higher than those in pair-fed controls. Morphologically, mitochondria of ethanol-fed baboons were larger than those of pair-fed controls. However, the mitochondrial protein content per mitochondrial DNA was unchanged. From these results, we conclude that, morphologically and functionally, hepatic mitochondria in baboons are altered by chronic ethanol consumption; it is noteworthy that these changes are fully developed already at the fatty liver stage, and that morphological alteration appears to reflect the damage of mitochondrial membranes rather than an adaptive hypertrophy.
Failed Mitral Valvotomy
Authors: J. K. Ross
Journal: Thorax (1959)

When valvotomy for mitral stenosis brings no relief to the patient, or when after temporary relief the patient's disability reverts to its pre-operative level or worse, the operation must be regarded as a failure.Obviously, all patients needing a second valvotomy must be classed as failures.For the purpose of the present investigation are also included as surgical failures patients who have died over six months after operation, during the follow-up period (late deaths), and all who have developed embolism subsequent to but not directly attributable to the operation (late embolism).These surgical failures cannot usually be explained simply in terms of a single cause, for often they are due to a variety of adverse factors operating in combination.Nevertheless, analysis of a sufficiently large number of consecutive surgical failures, as already defined, may identify the major causes and permit their contribution to the bad result to be assessed. MATERIALThe records of every patient who has undergone mitral valvotomy at the Middlesex Hospital from the first operation in February, 1951, until December 31, 1956, have been examined, providing a minimum follow-up period of two years.The operations have been performed by Mr. T. Holmes Sellors and Mr. J. R. Belcher, and a smaller number by Mr. J. W. Jackson.The total number of cases investigated is 263, of which 61 fall in the failed category, but, of the 16 late deaths, three were due to incidental causes (one myocardial infarction, one peritonitis, and one carcinoma of the bronchus), and are therefore excluded for the purposes of analysis (Fig. 1).Thus there are 58 failures (22% of total valvotomies) available for consideration, and wherever applicable the 155 successful cases are used as a control series.
Dynamic instability of the Major Urinary Protein gene family revealed by genomic and phenotypic comparisons between C57 and 129 strain mice
Authors: Jonathan M Mudge, Stuart D Armstrong, Karen McLaren, Robert J Beynon, Jane L Hurst, Christine Nicholson, Duncan H Robertson, Laurens G Wilming, Jennifer L Harrow
Journal: Genome biology (2008)

Abstract Background The major urinary proteins (MUPs) of Mus musculus domesticus are deposited in urine in large quantities, where they bind and release pheromones and also provide an individual 'recognition signal' via their phenotypic polymorphism. Whilst important information about MUP functionality has been gained in recent years, the gene cluster is poorly studied in terms of structure, genic polymorphism and evolution. Results We combine targeted sequencing, manual genome annotation and phylogenetic analysis to compare the Mup clusters of C57BL/6J and 129 strains of mice. We describe organizational heterogeneity within both clusters: a central array of cassettes containing Mup genes highly similar at the protein level, flanked by regions containing Mup genes displaying significantly elevated divergence. Observed genomic rearrangements in all regions have likely been mediated by endogenous retroviral elements. Mup loci with coding sequences that differ between the strains are identified - including a gene/pseudogene pair - suggesting that these inbred lineages exhibit variation that exists in wild populations. We have characterized the distinct MUP profiles in the urine of both strains by mass spectrometry. The total MUP phenotype data is reconciled with our genomic sequence data, matching all proteins identified in urine to annotated genes. Conclusion Our observations indicate that the MUP phenotypic polymorphism observed in wild populations results from a combination of Mup gene turnover coupled with currently unidentified mechanisms regulating gene expression patterns. We propose that the structural heterogeneity described within the cluster reflects functional divergence within the Mup gene family.
[680] MUTATIONS OF ABCB4 GENE IN CHILDREN WITH PROGRESSIVE FAMILIAL INTRAHEPATIC CHOLESTASIS: A MULTICENTER ITALIAN STUDY
Authors: C. Colombo, P. Vajro, R. Iorio, E. Castellano, M.G. Marazzi, S. Martelossi, L. Costantino, D. De Giorgio, G. Maggiore
Journal: Journal of Hepatology (2007)
Non–Risk-Adapted Surveillance in Clinical Stage I Nonseminomatous Germ Cell Tumors: The Princess Margaret Hospital’s Experience
Authors: Jeremy F. Sturgeon, Malcolm J. Moore, David M. Kakiashvili, Ignacio Duran, Lynn C. Anson-Cartwright, Dominik R. Berthold, Padraig R. Warde, Mary K. Gospodarowicz, Ruth E. Alison, Justin Liu, Clement Ma, Greg R. Pond, Michael A. Jewett
Journal: European Urology (2010)
Quaking, an RNA-Binding Protein, Is a Critical Regulator of Vascular Smooth Muscle Cell Phenotype
Authors: Eric P. van der Veer, Ruben G. de Bruin, Adriaan O. Kraaijeveld, Margreet R. de Vries, Ilze Bot, Tonio Pera, Filip M. Segers, Stella Trompet, Janine M. van Gils, Marko K. Roeten, Cora M. Beckers, Peter J. van Santbrink, Anique Janssen, Coen van Solingen, Jim Swildens, Hetty C. de Boer, Erna A. Peters, Roel Bijkerk, Mat Rousch, Merijn Doop, Johan Kuiper, Martin Jan Schalij, Allard C. van der Wal, Stéphane Richard, Theo J.C. van Berkel, J. Geoffrey Pickering, Pieter S. Hiemstra, Marie Jose Goumans, Ton J. Rabelink, Antoine A.F. de Vries, Paul H.A. Quax, J. Wouter Jukema, Erik A.L. Biessen, Anton Jan van Zonneveld
Journal: Circulation Research (2013)

RNA-binding proteins are critical post-transcriptional regulators of RNA and can influence pre-mRNA splicing, RNA localization, and stability. The RNA-binding protein Quaking (QKI) is essential for embryonic blood vessel development. However, the role of QKI in the adult vasculature, and in particular in vascular smooth muscle cells (VSMCs), is currently unknown.We sought to determine the role of QKI in regulating adult VSMC function and plasticity.We identified that QKI is highly expressed by neointimal VSMCs of human coronary restenotic lesions, but not in healthy vessels. In a mouse model of vascular injury, we observed reduced neointima hyperplasia in Quaking viable mice, which have decreased QKI expression. Concordantly, abrogation of QKI attenuated fibroproliferative properties of VSMCs, while potently inducing contractile apparatus protein expression, rendering noncontractile VSMCs with the capacity to contract. We identified that QKI localizes to the spliceosome, where it interacts with the myocardin pre-mRNA and regulates the splicing of alternative exon 2a. This post-transcriptional event impacts the Myocd_v3/Myocd_v1 mRNA balance and can be modulated by mutating the quaking response element in exon 2a of myocardin. Furthermore, we identified that arterial damage triggers myocardin alternative splicing and is tightly coupled with changes in the expression levels of distinct QKI isoforms.We propose that QKI is a central regulator of VSMC phenotypic plasticity and that intervention in QKI activity can ameliorate pathogenic, fibroproliferative responses to vascular injury.
Airport screening for Ebola
Authors: D. Mabey, S. Flasche, W. J. Edmunds
Journal: BMJ (2014)

Will it make a difference?

On 9 October the UK government announced that “enhanced screening” for Ebola virus disease will be implemented at Heathrow and Gatwick airports and Eurostar terminals. Details of how this will be done are not yet available, but the objectives presumably are to identify people arriving from Sierra Leone, Guinea, or Liberia who may have been exposed to Ebola, assess whether they have symptoms consistent with Ebola, test those who do, and isolate anyone with positive results.

Several practical difficulties will need to be overcome to achieve these objectives. As most direct flights to the UK from Sierra Leone, Guinea, and Liberia have been discontinued because of the epidemic, passengers will be arriving from various European cities, and itineraries will need to be carefully checked to identify passengers arriving from those countries. Those who are identified will be asked to complete a questionnaire stating whether they have been in contact with sick people or have attended funerals in west Africa, and whether they have symptoms such as fever, headache, diarrhoea, or vomiting. People who answer “yes” to any of these questions will presumably …
Measuring Patient Survival on Hemodialysis
Authors: Steven M. Brunelli
Journal: Journal of the American Society of Nephrology (2009)

Considering the progression of ESRD—left untreated and in the context of maintenance hemodialysis—there can be little doubt that the delivered dose of hemodialysis impacts patient survival. What remains at issue is how best to operationally define hemodialysis dose, a necessary precondition to defining the dose that represents “enough” dialysis. Presently, hemodialysis dose is most often measured in terms of Kt/V urea,1 a mathematical ratio that seeks to balance urea removal (rate of removal, K , times treatment time, t ) with metabolic needs (represented loosely by the volume of distribution, V ).2 Curiously, data on the association between Kt/V urea and mortality are mixed, with some studies showing a potent and statistically significant relationship,3,4 and others finding none.5,6 In this issue of JASN , Argyropoulos et al. 7 examine data from a nationally representative cohort of incident hemodialysis patients to further examine the association between Kt/V urea and mortality and to explore incongruity between biologic mechanism and statistical modeling assumptions as one potential explanation for inconsistent findings among prior studies.

The authors analyzed data from 491 participants in the Choices for Health Outcomes in Caring for ESRD (CHOICE) study for whom …
Increased von Willebrand factor in the endocardium as a local predisposing factor for thrombogenesis in overloaded human atrial appendage
Authors: Mitsumasa Fukuchi, Jun Watanabe, Koji Kumagai, Yukio Katori, Shigeo Baba, Koji Fukuda, Takuya Yagi, Atsushi Iguchi, Hitoshi Yokoyama, Masahito Miura, Yutaka Kagaya, Shigekazu Sato, Koichi Tabayashi, Kunio Shirato
Journal: Journal of the American College of Cardiology (2001)
The prognostic significance of specific arterial lesions in acute renal allograft rejection.
Authors: V Nickeleit, E C Vamvakas, M Pascual, B J Poletti, R B Colvin
Journal: Journal of the American Society of Nephrology (1998)

Diagnosis of allograft dysfunction relies on the assessment of arterial lesions. This study was designed to evaluate the prognostic significance of common specific vascular lesions in acute allograft rejection. Renal allograft biopsies (n = 111) with acute cellular rejection were scored for endarteritis, mononuclear cell adherence to endothelial cells, endothelial activation, fibrinoid necrosis, foam cells, and intimal fibrosis. These vascular lesions and other classic histologic features were correlated with outcome. Rejection with endarteritis (found in 54% of biopsies) was less responsive to steroid treatment than rejection without endarteritis, as judged by recovery of creatinine in 3 wk (P = 0.03). Larger numbers of sampled arteries improved the predictive accuracy. Sticking of mononuclear cells to endothelial cells also correlated with steroid resistance (P < 0.05). Rejection with or without endarteritis responded to OKT3/antithymocyte globulin treatment equally well (61% versus 65%, respectively). Rejection with fibrinoid arterial necrosis (4% of biopsies) did not respond to either steroids or antibodies (0%). One-year graft failure was 21% without endarteritis, 28% with endarteritis, and 100% with fibrinoid necrosis. Activated endothelial cells and interstitial hemorrhage were associated with endarteritis and graft failure (all P < 0.05). None of the other scored features had any statistically significant correlation with outcome. Thus, specific arterial lesions (endarteritis, fibrinoid necrosis, activated endothelial cells, mononuclear cell margination) and interstitial hemorrhage, but not the extent of the interstitial infiltrate or tubulitis, are correlated with response to antirejection therapy and/or 1-yr clinical outcome. Grading systems for therapeutic trials and clinical management should emphasize scoring of specific vascular lesions.
Updates from the Fourth International Congress ‘Psoriasis: from Gene to Clinic’, The Royal College of Physicians, London, U.K., 1-3 December 2005
Authors: R.D.R. Camp
Journal: British Journal of Dermatology (2006)

The fourth 'Psoriasis: From Gene to Clinic' meeting was held in December 2005, its international status confirmed by the presence of almost 300 delegates from Europe, North America, Asia and Australasia. The meeting was co-organized by Jonathan Barker (St John's Institute of Dermatology, London) and Chris Griffiths (University of Manchester), who once again deserve congratulations for the success of their initiative. As its title suggests, the meeting was targeted at both clinical and basic scientists with a special interest in psoriasis, but in preparing this report the writer has selected presentations that caught his attention and that he felt able to review in a manner that might be of interest to the general readership of this Journal.
Short-Term Effects of the 2008 Cold Spell on Mortality in Three Subtropical Cities in Guangdong Province, China
Authors: Huiyan Xie, Zhibin Yao, Yonghui Zhang, Yanjun Xu, Xiaojun Xu, Tao Liu, Hualiang Lin, Xiangqian Lao, Shannon Rutherford, Cordia Chu, Cunrui Huang, Scott Baum, Wenjun Ma
Journal: Environmental Health Perspectives (2012)

Background: Few studies have been conducted to investigate the impact of extreme cold events on mortality in subtropical regions.Objective: In the present study we aimed to investigate the effects of the 2008 cold spell on mortality and the possibility of mortality displacement in three subtropical cities in China.Methods: Daily mortality, air pollution, and weather data were collected from 2006 to 2009 in Guangzhou, Nanxiong (no air pollutants), and Taishan. We used a polynomial distributed lag model (DLM) to analyze the relationship between the 2008 cold spell and mortality. To observe the mortality displacement of the cold spell, we estimated the cumulative effects at lag0, lag0–6, lag0–13, lag0–20, and lag0–27 separately.Results: During the 2008 cold spell, the cumulative risk of nonaccidental mortality increased significantly in Guangzhou [relative risk (RR) = 1.60; 95% CI: 1.19, 2.14] and Taishan (RR = 1.60; 95% CI: 1.06, 2.40) when lagged up to 4 weeks after the cold spell ended. Estimated effects at lag0–27 were more pronounced for males than for females, for respiratory mortality than for cardiovascular mortality, and for the elderly (≥ 75 years of age) than for those 0–64 years of age. Most of the cumulative RRs increased with longer lag times in Guangzhou and Taishan. However, in Nanxiong, the trend with cumulative RRs was less consistent, and we observed no statistically significant associations at lag0–27.Conclusion: We found associations between the 2008 cold spell and increased mortality in the three subtropical cities of China. The lag effect structure of the cold spell varied with location and the type of mortality, and evidence of short-term mortality displacement was inconsistent. These findings suggest that extreme cold is an important public health problem in subtropical regions.