tbuckley/cabot-search huggingface dataset:
Quantification of absolute luminal diameter by computer-analyzed digital subtraction angiography: an assessment in human coronary arteries.
Authors: M C Rosenberg, L W Klein, J B Agarwal, G Stets, G A Hermann, R H Helfant
Journal: Circulation (1988)

Determination of absolute lumen diameters has been shown to be useful in predicting the functional importance of a coronary stenosis. In this study, both single-plane and orthogonal biplane digital subtraction angiograms were obtained in human cadaver coronary arteries. A single absolute diameter was calculated at the site of greatest narrowing in 20 segments by two automated computerized algorithms. Minimum and maximum diameters at the site of the stenosis were measured from pathologic sections prepared after pressure fixation. Method 1, which determines the edges by means of the first derivative of the videodensity curve, derived absolute diameters that fell between the pathologic minimum and maximum in 10 of 20 segments. Method 2, which determines the edges by an average of the first and second derivatives of the videodensity change, derived absolute diameters that fell between the pathologic minimum and maximum diameters in 15 of 20 segments. Method 1 correlated well with the maximum pathologic diameter (r = .76) and less well with the minrmum pathologic diameter (r = .67). Method 2 correlated very well with the maximum pathologic diameter (r = .79) and also correlated well with the minimum pathologic diameter (r = .74). As would be expected, the computerized algorithms tended to overestimate the minimum pathologic diameter and to underestimate the maximum pathologic diameter. In six segments, two orthogonal views were analyzed; no further accuracy was discernible over single-plane determinations. Thus quantitative coronary angiography by digital subtraction angiography is sufficiently accurate to be of use in the measurement of the severity of a coronary stenosis.
Distribution of the HindIII restriction fragment length polymorphism among patients with systemic lupus erythematosus with different concentrations of CR1.
Authors: H Satoh, E Yokota, K Tokiyama, T Kawaguchi, Y Niho
Journal: Annals of the Rheumatic Diseases (1991)

Sixty six patients with systemic lupus erythematosus (SLE) were genotyped using a HindIII restriction fragment length polymorphism identified by CR1.1 cDNA, then were followed up for an average of 50 months to evaluate the stability of their CR1 activities. The gene frequencies for the two alleles which correlate with the numeric expression of CR1 on the erythrocytes were not significantly different between 66 patients with SLE and 52 normal controls. A discrepancy between homozygosity for a high allele and a negative CR1 activity was found in many patients. These patients, however, had significantly lower concentrations of serum complement than did patients with a positive CR1, and some were in an active state of the disease. Furthermore, there were several patients in whom the CR1 activities changed from negative to positive together with an increase in serum complement. Our results suggest that the decreased expression of CR1 on erythrocytes in patients with SLE is not inherited, rather it is a consequence of the disease processes.
Investigation of the theory and mechanism of the origin of the second heart sound.
Authors: H N Sabbah, P D Stein
Journal: Circulation Research (1976)

To investigate further the origin of the second heart sound we studied human subjects, dogs, and a model in vitro of the cardiovascular system. Intra-arterial sound, pressure, and, where possible, flow and high speed cine (2,000 frames/sec) were utilized. The closure sound of the semilunar valves was of higher amplitude in be ventricles than in their respective arterial cavities. The direction of inscription of the main components of intra-arterial sound were opposite in direction to the components of intraventricular sound. Notches, representative of pressure increments, were noted on the ventricular pressure tracings and were coincident with the components of sound. The amplitude of the closure sound varied with diastolic pressure, but remained unchanged with augmentation of forward and retrograde aortic flow. Cines showed second sound to begin after complete valvular closure, and average leaflet closure rate was constant regardless of pressure. Hence, the semilunar valves, when closed, act as an elastic membrane and, when set into motion, generate compression and expansion of the blood, producing transient pressure changes indicative of sound. The magnitude of the initial stretch is related to the differential pressure between the arterial and ventricular chambers. Sound transients which follow the major components of the second sound appear to be caused by the continuing stretch and recoil of the leaflets. Clinically unexplained findings such as the reduced or absent second sound in calcific aortic stenosis and its paradoxical presence in congenital aortic stenosis may be explained by those observations.
Erythromycin Inhibits Rhinovirus Infection in Cultured Human Tracheal Epithelial Cells
Authors: Tomoko Suzuki, Mutsuo Yamaya, Kiyohisa Sekizawa, Masayoshi Hosoda, Norihiro Yamada, Satoshi Ishizuka, Akiko Yoshino, Hiroyasu Yasuda, Hidenori Takahashi, Hidekazu Nishimura, Hidetada Sasaki
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

To examine the effects of erythromycin on rhinovirus (RV) infection in airway epithelium, primary cultures of human tracheal epithelial cells were infected with the RV major subgroup, RV14, and the minor subgroup, RV2. Infection was confirmed by increases in viral RNA of the infected cells and viral titers of the supernatants. RV14 upregulated the expression of the mRNA and protein of intercellular adhesion molecule-1 (ICAM-1), the major RV receptor, and it increased the cytokine production. Erythromycin reduced the supernatant RV14 titers, RV14 RNA, the susceptibility to RV14 infection, and the production of ICAM-1 and cytokines. Erythromycin also reduced the supernatant RV2 titers, RV2 RNA, the susceptibility to RV2 infection, and cytokine production, although the inhibitory effects of erythromycin on the expression of the low-density lipoprotein receptor, the minor RV receptor, were small. Erythromycin reduced the nuclear factor-kappaB activation by RV14 and decreased the number of acidic endosomes in the epithelial cells. These results suggest that erythromycin inhibits infection by the major RV subgroup by reducing ICAM-1 and infection by both RV subgroups by blocking the RV RNA entry into the endosomes. Erythromycin may also modulate airway inflammation by reducing the production of proinflammatory cytokines and ICAM-1 induced by RV infection.
Brg-1 mediates the constitutive and fenretinide-induced expression of SPARC in mammary carcinoma cells via its interaction with transcription factor Sp1
Authors: Yong Zhong Xu, Mitra Heravi, Thusanth Thuraisingam, Sergio Di Marco, Thierry Muanza, Danuta Radzioch
Journal: Molecular Cancer (2010)

Abstract Background Secreted protein, acidic and rich in cysteine (SPARC) is a matricellular protein that mediates cell-matrix interactions. It has been shown, depending on the type of cancer, to possess either pro- or anti-tumorigenic properties. The transcriptional regulation of the SPARC gene expression has not been fully elucidated and the effects of anti-cancer drugs on this process have not been explored. Results In the present study, we demonstrated that chromatin remodeling factor Brg-1 is recruited to the proximal SPARC promoter region (-130/-56) through an interaction with transcription factor Sp1. We identified Brg-1 as a critical regulator for the constitutive expression levels of SPARC mRNA and protein in mammary carcinoma cell lines and for SPARC secretion into culture media. Furthermore, we found that Brg-1 cooperates with Sp1 to enhance SPARC promoter activity. Interestingly, fenretinide [N-4(hydroxyphenyl) retinamide, 4-HPR], a synthetic retinoid with anti-cancer properties, was found to up-regulate the transcription, expression and secretion of SPARC via induction of the Brg-1 in a dose-dependent manner. Finally, our results demonstrated that fenretinide-induced expression of SPARC contributes significantly to a decreased invasion of mammary carcinoma cells. Conclusions Overall, our results reveal a novel cooperative role of Brg-1 and Sp1 in mediating the constitutive and fenretinide-induced expression of SPARC, and provide new insights for the understanding of the anti-cancer effects of fenretinide.
ACC/AHA Clinical Performance Measures for Adults With Chronic Heart Failure
Authors: Robert O. Bonow, Susan Bennett, Donald E. Casey, Theodore G. Ganiats, Mark A. Hlatky, Marvin A. Konstam, Costas T. Lambrew, Sharon-Lise T. Normand, Ileana L. Pina, Martha J. Radford, Andrew L. Smith, Lynne Warner Stevenson, Robert O. Bonow, Susan J. Bennett, Gregory Burke, Kim A. Eagle, Harlan M. Krumholz, Costas T. Lambrew, Jane Linderbaum, Frederick A. Masoudi, Sharon-Lise T. Normand, James L. Ritchie, John S. Rumsfeld, John A. Spertus
Journal: Circulation (2005)
Review: In high-risk patients, fatty acid supplementation does not prevent coronary events
Authors: Brian Budenholzer
Journal: Annals of Internal Medicine (2014)

Source Citation Chowdhury R, Warnakula S, Kunutsor S, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk: A systematic review and meta-analysis. Ann Intern Med. 2014;160:398-406. 24723079
Exome sequencing reveals MCM8 mutation underlies ovarian failure and chromosomal instability
Authors: Saleh AlAsiri, Sulman Basit, Michelle A. Wood-Trageser, Svetlana A. Yatsenko, Elizabeth P. Jeffries, Urvashi Surti, Deborah M. Ketterer, Sibtain Afzal, Khushnooda Ramzan, Muhammad Faiyaz-Ul Haque, Huaiyang Jiang, Michael A. Trakselis, Aleksandar Rajkovic
Journal: Journal of Clinical Investigation (2014)

Premature ovarian failure (POF) is a genetically and phenotypically heterogeneous disorder that includes individuals with manifestations ranging from primary amenorrhea to loss of menstrual function prior to age 40. POF presents as hypergonadotropic hypogonadism and can be part of a syndrome or occur in isolation. Here, we studied 3 sisters with primary amenorrhea, hypothyroidism, and hypergonadotropic hypogonadism. The sisters were born to parents who are first cousins. SNP analysis and whole-exome sequencing revealed the presence of a pathogenic variant of the minichromosome maintenance 8 gene (MCM8, c.446C>G; p.P149R) located within a region of homozygosity that was present in the affected daughters but not in their unaffected sisters. Because MCM8 participates in homologous recombination and dsDNA break repair, we tested fibroblasts from the affected sisters for hypersensitivity to chromosomal breaks. Compared with fibroblasts from unaffected daughters, chromosomal break repair was deficient in fibroblasts from the affected individuals, likely due to inhibited recruitment of MCM8 p.P149R to sites of DNA damage. Our study identifies an autosomal recessive disorder caused by an MCM8 mutation that manifests with endocrine dysfunction and genomic instability.
Comparative Gene Evolution in Haemosporidian (Apicomplexa) Parasites of Birds and Mammals
Authors: D. C. Outlaw, R. E. Ricklefs
Journal: Molecular Biology and Evolution (2009)

Haemosporidian parasites of birds and mammals reproduce asexually inside nucleated and nonnucleated host erythrocytes, respectively. Because of these different parasite environments and because bird parasites are paraphyletic, we evaluated whether patterns of parasite molecular evolution differ between host groups. We compared two mitochondrial (mt) genes and one apicoplast gene across mammal Plasmodium, bird Plasmodium, and bird Parahaemoproteus. Using a molecular phylogenetic approach, we show that the parasite mt cytochrome b (cyt b), mt cytochrome oxidase I (COI), and the apicoplast caseinolytic protease C (ClpC) exhibit similar levels of sequence divergence, yet each gene tree presents a strikingly different pattern of internal versus terminal branch lengths. In cyt b, the ratio of nonsynonymous (NS)-to-synonymous substitutions (dN/dS) is markedly elevated along the internal branch linking mammalian and avian parasites despite the sister relationship between mammal and bird Plasmodium. This is not the case for either COI or ClpC. When NS substitutions are excluded from the parasite cyt b alignment, the resulting phylogenetic tree resembles that of COI (both with and without NS substitutions). The high dN/dS ratio in the cyt b branch separating avian and mammalian parasites and a mammal-parasite codon bias suggest that adaptive evolution has distinguished mammal and bird parasites.
Musculo-skeletal complications of jogging.
Authors: B. Corrigan
Journal: British Journal of Sports Medicine (1980)

To jog is to move or run at a leisurely pace, but is not without injury risk.The large increase in the number of people engaged in this activity is world wide, thirty million in the USA alone, and this has brought problems, not least commercial exploitation.Although most participants find the activity enjoyable and relaxing, some felt that it is an activity that promotes fitness by first making one crippled.Certain causative factors in production of injury can be recognised.
Dupuytren's contracture is associated with sprouting of substance P positive nerve fibres and infiltration by mast cells
Authors: T E O Schubert
Journal: Annals of the Rheumatic Diseases (2006)

Background: Extramedullary (EM) organ impairment in patients with multiple myeloma (MM) is a rare event, occurring mostly during disease relapse after high-dose chemotherapy with autologous or allogeneic stem cell transplantation. This manifestation is commonly associated with an unfavourable outcome. Previous studies suggested a correlation between the clinical course of patients with MM and EM and the cytogenetic findings, e.g. deletion of TP53 on 17p13. Materials and Methods: We investigated patients with these rare plasma cell organ infiltrations (n=17) as well as bone lesions or soft tissue lesions, known to be a common clinical feature of MM (n=14), using a newly established method of fluorescence in situ hybridization in combination with cytoplasmic immunoglobulin staining (cIg-FISH) on paraffin-embedded sections and a specific probe for TP53 on 17p13. Results and Conclusion: The incidence of del(17)(p13) was similar in both groups but overall it was higher when compared to published data obtained from bone marrow samples and material originating from osteolyses. Further investigations on a larger patient cohort are needed in order to confirm these findings.
A Chorionic Gonadotropin–Sensitive Mutation in the Follicle-Stimulating Hormone Receptor as a Cause of Familial Gestational Spontaneous Ovarian Hyperstimulation Syndrome
Authors: Claudine Vasseur, Patrice Rodien, Isabelle Beau, Agnès Desroches, Capucine Gérard, Loïc de Poncheville, Stéphanie Chaplot, Frédérique Savagner, Anne Croué, Elisabeth Mathieu, Najiba Lahlou, Philippe Descamps, Micheline Misrahi
Journal: New England Journal of Medicine (2003)

This Brief Report describes recurrent gestational spontaneous ovarian hyperstimulation syndrome in a family with a heterozygous mutation in the transmembrane domain of the receptor for follicle-sti...
Effect of Oxaliplatin, Fluorouracil, and Leucovorin With or Without Cetuximab on Survival Among Patients With Resected Stage III Colon Cancer
Authors: Steven R Alberts, Daniel J Sargent, Suresh G. Nair Md, Michelle R Mahoney, Margaret Mooney, Stephen N Thibodeau, Thomas C Smyrk, Frank A Sinicrope, Emily Chan, Sharlene Gill, Morton S Kahlenberg, Anthony F Shields, James T Quesenberry, Thomas A Webb, Gist H Farr, Barbara A Pockaj, Axel Grothey, Richard M Goldberg
Journal: JAMA (2012)

<h3>Context</h3>Leucovorin, fluorouracil, and oxaliplatin (FOLFOX) is the standard adjuvant therapy for resected stage III colon cancer. Adding cetuximab to FOLFOX benefits patients with metastatic wild-type KRAS but not mutated KRAS colon cancer.<h3>Objective</h3>To assess the potential benefit of cetuximab added to the modified sixth version of the FOLFOX regimen (mFOLFOX6) in patients with resected stage III wild-type KRAS colon cancer.<h3>Design, Setting, and Participants</h3>A randomized trial of 2686 patients aged 18 years or older at multiple institutions across North America enrolled following resection and informed consent between February 10, 2004, and November 25, 2009. The primary randomized comparison was 12 biweekly cycles of mFOLFOX6 with and without cetuximab. KRAS mutation status was centrally determined. The trial was halted after a planned interim analysis of 48% of predicted events (246/515) occurring in 1863 (of 2070 planned) patients with tumors having wild-type KRAS. A total of 717 patients with mutated KRAS and 106 with indeterminate KRAS were accrued. The 2070 patients with wild-type KRAS provided 90% power to detect a hazard ratio (HR) of 1.33 (2-sided α = .05), with planned interim efficacy analyses after 25%, 50%, and 75% of expected relapses.<h3>Main Outcome Measures</h3>Disease-free survival in patients with wild-type KRAS mutations. Secondary end points included overall survival and toxicity.<h3>Results</h3>Median (range) follow-up was 28 (0-68) months. The trial demonstrated no benefit when adding cetuximab. Three-year disease-free survival for mFOLFOX6 alone was 74.6% vs 71.5% with the addition of cetuximab (HR, 1.21; 95% CI, 0.98-1.49; P = .08) in patients with wild-type KRAS, and 67.1% vs 65.0% (HR, 1.12; 95% CI, 0.86-1.46; P = .38) in patients with mutated KRAS, with no significant benefit in any subgroups assessed. Among all patients, grade 3 or higher adverse events (72.5% vs 52.3%; odds ratio [OR], 2.4; 95% CI, 2.1-2.8; P &lt; .001) and failure to complete 12 cycles (33% vs 23%; OR, 1.6; 95% CI, 1.4-1.9; P &lt; .001) were significantly higher with cetuximab. Increased toxicity and greater detrimental differences in all outcomes were observed in patients aged 70 years or older.<h3>Conclusion</h3>Among patients with stage III resected colon cancer, the use of cetuximab with adjuvant mFOLFOX6 compared with mFOLFOX6 alone did not result in improved disease-free survival.<h3>Trial Registration</h3>clinicaltrials.gov Identifier: NCT00079274
The epidemiology of 1345 shoulder dislocations and subluxations in French Rugby Union players: a five-season prospective study from 2008 to 2013
Authors: Yoann Bohu, Shahnaz Klouche, Nicolas Lefevre, Jean-Claude Peyrin, Bernard Dusfour, Jean-Philippe Hager, Aurélie Ribaut, Serge Herman
Journal: British Journal of Sports Medicine (2014)

An understanding of the epidemiology of shoulder dislocation/subluxation in rugby union players could help develop targeted prevention programmes and treatment. We performed a multiyear epidemiological survey of shoulder dislocation/subluxation in a large cohort of rugby players.A descriptive epidemiological study was performed prospectively for five playing seasons (2008-2013) in all players licensed in the French Rugby Union. Rugby players were categorised into five groups by age. The player and the team physician reported the injury to the club insurance company if it occurred during training or a match. The goals of the study were to define the rate, type and causes of shoulder dislocation/subluxation.88,044 injuries were reported, including 1345 (1.5%) episodes of dislocation/subluxation in 1317 men and 28 women, mean age 22.5±5.9 years. About 10/10,000 men and 5/10,000 women reported an episode of shoulder dislocation/subluxation per season, including 83/10,000 senior professionals, 17/10,000 senior amateurs, 21/10,000 juniors, 12/10,000 cadets and <1/10,000 rugby school players. Shoulder dislocation/subluxation was significantly more frequent in senior and junior players (p<0.001). Injuries mainly occurred during a match (66%) in the middle of the season (44%). The most frequent playing position was forwards (56%) and the main mechanism was tackling (69%). When reported, the history of recurrence was found in 66% of injured players, fractures in 22% and acromioclavicular injury in 6.7%. Nerve injury was associated with shoulder dislocation in 6% of cases.Senior professionals and junior male forward rugby players with a history of shoulder dislocation/subluxation should receive special attention from sports medicine professionals and orthopaedic surgeons.
The identification of tuberculosis biomarkers in human urine samples
Authors: Brandy L. Young, Zandile Mlamla, Putuma P. Gqamana, Salome Smit, Teri Roberts, Jonathan Peter, Grant Theron, Ureshnie Govender, Keertan Dheda, Jonathan Blackburn
Journal: European Respiratory Journal (2014)

We aimed to determine whether shotgun proteomic approaches could be used to identify tuberculosis (TB)-specific biomarkers in the urine of well-characterised patients with active TB versus no TB. Patients with suspected TB (n=63) were classified as: definite TB ( Mycobacterium tuberculosis positive culture, n=21); presumed latent-TB infection (LTBI) ( M. tuberculosis negative culture, no radiological features of active TB, a positive QuantiFERON-TB Gold In-Tube (QFT-IT) test and a positive T-SPOT.TB test, n=24); and presumed non-TB/non-LTBI ( M. tuberculosis negative culture, no radiological features of active TB, a negative QFT-IT test and a negative T-SPOT.TB test, n=18). Urine proteins, in the range of 3–50 kDa, were collected, separated by a one-dimensional SDS-PAGE gel and digested using trypsin, after which high-performance liquid chromatography-tandem mass spectrometry was used to identify the urinary proteome. 10 mycobacterial proteins were observed exclusively in the urine of definite TB patients, while six mycobacterial proteins were found exclusively in the urine of presumed LTBI patients. In addition, a gene ontology enrichment analysis identified a panel of 20 human proteins that were significant discriminators (p&lt;0.05) for TB disease compared to no TB disease. Furthermore, seven common human proteins were differentially over- or under-expressed in the TB versus the non-TB group. These biomarkers hold promise for the development of new point-of-care diagnostics for TB.