tbuckley/cabot-search huggingface dataset:
Cystic Fibrosis Pulmonary Guidelines
Authors: Patrick A. Flume, Peter J. Mogayzel, Karen A. Robinson, Randall L. Rosenblatt, Lynne Quittell, Bruce C. Marshall
Journal: American Journal of Respiratory and Critical Care Medicine (2010)

Section:ChooseTop of pageAbstract <<METHODSRESULTSPNEUMOTHORAXCONCLUSIONReferencesCITING ARTICLES
The Heart and Electrocardiogram of an Alligator
Authors: L. MINOR BLACKFORD
Journal: Circulation (1956)

The phylogenetic evolution of the cardiovascular system of animals and man has been a subject of continued interest. The reported study of the cardiovascular system and electrocardiogram of the alligator bears on this subject. The author has cogently remarked that this journal, which has reported similar studies in the beluga whale, should be the vehicle of his report.—Ed.
Decrease in serum ALT and increase in serum HCV RNA during pregnancy in women with chronic hepatitis C
Authors: Anne Gervais, Yannick Bacq, Jacques Bernuau, Michèle Martinot, Anne Auperin, Nathalie Boyer, Afef Kilani, Serge Erlinger, Dominique Valla, Patrick Marcellin
Journal: Journal of Hepatology (2000)
mirMark: a site-level and UTR-level classifier for miRNA target prediction
Authors: Mark Menor, Travers Ching, Xun Zhu, David Garmire, Lana X Garmire
Journal: Genome biology (2014)

MiRNAs play important roles in many diseases including cancers. However computational prediction of miRNA target genes is challenging and the accuracies of existing methods remain poor. We report mirMark, a new machine learning-based method of miRNA target prediction at the site and UTR levels. This method uses experimentally verified miRNA targets from miRecords and mirTarBase as training sets and considers over 700 features. By combining Correlation-based Feature Selection with a variety of statistical or machine learning methods for the site- and UTR-level classifiers, mirMark significantly improves the overall predictive performance compared to existing publicly available methods. MirMark is available from https://github.com/lanagarmire/MirMark.
Inferring the Evolutionary History of Gene Clusters from Phylogenetic and Gene Order Data
Authors: M. Lajoie, D. Bertrand, N. El-Mabrouk
Journal: Molecular Biology and Evolution (2009)

Gene duplication is frequent within gene clusters and plays a fundamental role in evolution by providing a source of new genetic material upon which natural selection can act. Although classical phylogenetic inference methods provide some insight into the evolutionary history of a gene cluster, they are not sufficient alone to differentiate single- from multiple gene duplication events and to answer other questions regarding the nature and size of evolutionary events. In this paper, we present an algorithm allowing to infer a set of optimal evolutionary histories for a gene cluster in a single species, according to a general cost model involving variable length duplications (in tandem or inverted), deletions, and inversions. We applied our algorithm to the human olfactory receptor and protocadherin gene clusters, showing that the duplication size distribution differs significantly between the two gene families. The algorithm is available through a web interface at http://www-lbit.iro.umontreal.ca/DILTAG/.
A Contemporary Update on Pathology Reporting for Prostate Cancer: Biopsy and Radical Prostatectomy Specimens
Authors: Samson W. Fine, Mahul B. Amin, Daniel M. Berney, Anders Bjartell, Lars Egevad, Jonathan I. Epstein, Peter A. Humphrey, Christina Magi-Galluzzi, Rodolfo Montironi, Christian Stief
Journal: European Urology (2012)
Release of phospholipid fatty acid from human erythrocytes
Authors: Stephen B. Shohet
Journal: Journal of Clinical Investigation (1970)

To study the catabolism of erythrocyte phospholipids, human erythrocytes were labeled with radioactive fatty acid (FA). Labeling was performed by the two separate routes which together are thought to be responsible for the majority of phosphatide renewal in the red cell: (a) passive equilibration of erythrocytes with preformed acid-labeled red cell phosphatidylcholine (PC) and (b) active, "acylase"-dependent, incorporation of free fatty acid in the presence of ATP coenzyme A and magnesium. (As measured here "acylase" = the over-all effect of fatty acid thioesterification and the action of acyl-CoA: acylglycerophosphoryl acyltransferase.) The labeled cells were then reincubated in serum and the loss of radioactivity from cells into serum was examined. The phosphatide fatty acid introduced by these two routes was incorporated into two distinct cellular phosphatide pools with little mixing. The fatty acid in passively introduced phosphatidyl choline was released primarily as the intact phosphatide, whereas actively incorporated PC fatty acid was released primarily as free FA. As expected for an exchange process, the passively introduced PC was released at the same rate as it was introduced. However, the actively incorporated FA was released from the cell at a slower rate than its incorporation into PC. This latter phenomenon was explained by the observation of transfer of PC fatty acid to phosphatidyl ethanolamine and "neutral lipid" before its release to serum. This transfer process was inhibited by previous heating of the reincubation serum. The differences in the character of the released label, in the rate of release of the label, and in the influence of the reincubation serum all indicate separate pathways for the renewal of phosphatide introduced into red cells by these two routes.
Efficacy Results of a Trial of a Herpes Simplex Vaccine
Authors: Robert B. Belshe, Peter A. Leone, David I. Bernstein, Anna Wald, Myron J. Levin, Jack T. Stapleton, Iris Gorfinkel, Rhoda L. Ashley Morrow, Marian G. Ewell, Abbie Stokes-Riner, Gary Dubin, Thomas C. Heineman, Joann M. Schulte, Carolyn D. Deal
Journal: New England Journal of Medicine (2012)

Two previous studies of a herpes simplex virus type 2 (HSV-2) subunit vaccine containing glycoprotein D in HSV-discordant couples revealed 73% and 74% efficacy against genital disease in women who were negative for both HSV type 1 (HSV-1) and HSV-2 antibodies. Efficacy was not observed in men or HSV-1 seropositive women.
Residual Lifetime Risk for Developing Hypertension in Middle-aged Women and Men
Authors: Ramachandran S. Vasan, Alexa Beiser, Sudha Seshadri, Martin G. Larson, William B. Kannel, Ralph B. D'Agostino, Daniel Levy
Journal: JAMA (2002)

ContextThe long-term risk for developing hypertension is best described by the lifetime risk statistic. The lifetime risk for hypertension and trends in this risk over time are unknown.ObjectivesTo estimate the residual lifetime risk for hypertension in older US adults and to evaluate temporal trends in this risk.Design, Setting, and ParticipantsCommunity-based prospective cohort study of 1298 participants from the Framingham Heart Study who were aged 55 to 65 years and free of hypertension at baseline (1976-1998).Main Outcome MeasuresResidual lifetime risk (lifetime cumulative incidence not adjusted for competing causes of mortality) for hypertension, defined as blood pressure of 140/90 mm Hg or greater or use of antihypertensive medications.ResultsThe residual lifetime risks for developing hypertension and stage 1 high blood pressure or higher (≥140/90 mm Hg regardless of treatment) were 90% in both 55- and 65-year-old participants. The lifetime probability of receiving antihypertensive medication was 60%. The risk for hypertension remained unchanged for women, but it was approximately 60% higher for men in the contemporary 1976-1998 period compared with an earlier 1952-1975 period. In contrast, the residual lifetime risk for stage 2 high blood pressure or higher (≥160/100 mm Hg regardless of treatment) was considerably lower in both sexes in the recent period (35%-57% in 1952-1975 vs 35%-44% in 1976-1998), likely due to a marked increase in treatment of individuals with substantially elevated blood pressure.ConclusionThe residual lifetime risk for hypertension for middle-aged and elderly individuals is 90%, indicating a huge public health burden. Although the decline in lifetime risk for stage 2 high blood pressure or higher represents a major achievement, efforts should be directed at the primary prevention of hypertension.
Control of Breast Cancer Growth and Initiation by the Stem Cell–Associated Transcription Factor TCF3
Authors: Michal Slyper, Amit Shahar, Anat Bar-Ziv, Roy Z. Granit, Tamar Hamburger, Bella Maly, Tamar Peretz, Ittai Ben-Porath
Journal: Cancer Research (2012)

Regulatory factors controlling stem cell identity and self-renewal are often active in aggressive cancers and are thought to promote their growth and progression. TCF3 (also known as TCF7L1) is a member of the TCF/LEF transcription factor family that is central in regulating epidermal and embryonic stem cell identity. We found that TCF3 is highly expressed in poorly differentiated human breast cancers, preferentially of the basal-like subtype. This suggested that TCF3 is involved in the regulation of breast cancer cell differentiation state and tumorigenicity. Silencing of TCF3 dramatically decreased the ability of breast cancer cells to initiate tumor formation, and led to decreased tumor growth rates. In culture, TCF3 promotes the sphere formation capacity of breast cancer cells and their self-renewal. We found that in contrast to ES cells, where it represses Wnt-pathway target genes, TCF3 promotes the expression of a subset of Wnt-responsive genes in breast cancer cells while repressing another distinct target subset. In the normal mouse mammary gland, Tcf3 is highly expressed in terminal end buds, structures that lead duct development. Primary mammary cells are dependent on Tcf3 for mammosphere formation, and its overexpression in the developing gland disrupts ductal growth. Our results identify TCF3 as a central regulator of tumor growth and initiation, and a novel link between stem cells and cancer.
Dysregulation of ubiquitin homeostasis and β-catenin signaling promote spinal muscular atrophy
Authors: Thomas M. Wishart, Chantal A. Mutsaers, Markus Riessland, Michell M. Reimer, Gillian Hunter, Marie L. Hannam, Samantha L. Eaton, Heidi R. Fuller, Sarah L. Roche, Eilidh Somers, Robert Morse, Philip J. Young, Douglas J. Lamont, Matthias Hammerschmidt, Anagha Joshi, Peter Hohenstein, Glenn E. Morris, Simon H. Parson, Paul A. Skehel, Thomas Becker, Iain M. Robinson, Catherina G. Becker, Brunhilde Wirth, Thomas H. Gillingwater
Journal: Journal of Clinical Investigation (2014)

The autosomal recessive neurodegenerative disease spinal muscular atrophy (SMA) results from low levels of survival motor neuron (SMN) protein; however, it is unclear how reduced SMN promotes SMA development. Here, we determined that ubiquitin-dependent pathways regulate neuromuscular pathology in SMA. Using mouse models of SMA, we observed widespread perturbations in ubiquitin homeostasis, including reduced levels of ubiquitin-like modifier activating enzyme 1 (UBA1). SMN physically interacted with UBA1 in neurons, and disruption of Uba1 mRNA splicing was observed in the spinal cords of SMA mice exhibiting disease symptoms. Pharmacological or genetic suppression of UBA1 was sufficient to recapitulate an SMA-like neuromuscular pathology in zebrafish, suggesting that UBA1 directly contributes to disease pathogenesis. Dysregulation of UBA1 and subsequent ubiquitination pathways led to β-catenin accumulation, and pharmacological inhibition of β-catenin robustly ameliorated neuromuscular pathology in zebrafish, Drosophila, and mouse models of SMA. UBA1-associated disruption of β-catenin was restricted to the neuromuscular system in SMA mice; therefore, pharmacological inhibition of β-catenin in these animals failed to prevent systemic pathology in peripheral tissues and organs, indicating fundamental molecular differences between neuromuscular and systemic SMA pathology. Our data indicate that SMA-associated reduction of UBA1 contributes to neuromuscular pathogenesis through disruption of ubiquitin homeostasis and subsequent β-catenin signaling, highlighting ubiquitin homeostasis and β-catenin as potential therapeutic targets for SMA.
Human Pancreatic Cancer Tumors Are Nutrient Poor and Tumor Cells Actively Scavenge Extracellular Protein
Authors: Jurre J. Kamphorst, Michel Nofal, Cosimo Commisso, Sean R. Hackett, Wenyun Lu, Elda Grabocka, Matthew G. Vander Heiden, George Miller, Jeffrey A. Drebin, Dafna Bar-Sagi, Craig B. Thompson, Joshua D. Rabinowitz
Journal: Cancer Research (2015)

Glucose and amino acids are key nutrients supporting cell growth. Amino acids are imported as monomers, but an alternative route induced by oncogenic KRAS involves uptake of extracellular proteins via macropinocytosis and subsequent lysosomal degradation of these proteins as a source of amino acids. In this study, we examined the metabolism of pancreatic ductal adenocarcinoma (PDAC), a poorly vascularized lethal KRAS-driven malignancy. Metabolomic comparisons of human PDAC and benign adjacent tissue revealed that tumor tissue was low in glucose, upper glycolytic intermediates, creatine phosphate, and the amino acids glutamine and serine, two major metabolic substrates. Surprisingly, PDAC accumulated essential amino acids. Such accumulation could arise from extracellular proteins being degraded through macropinocytosis in quantities necessary to meet glutamine requirements, which in turn produces excess of most other amino acids. Consistent with this hypothesis, active macropinocytosis is observed in primary human PDAC specimens. Moreover, in the presence of physiologic albumin, we found that cultured murine PDAC cells grow indefinitely in media lacking single essential amino acids and replicate once in the absence of free amino acids. Growth under these conditions was characterized by simultaneous glutamine depletion and essential amino acid accumulation. Overall, our findings argue that the scavenging of extracellular proteins is an important mode of nutrient uptake in PDAC.
An unusual case of facial nerve palsy following soccer related minor head injury
Authors: E F Leitch, J R Hanson
Journal: British Journal of Sports Medicine (2006)

A 16 year old amateur soccer player sustained a minor head injury while contesting a ball in the air. He was unconscious for two minutes and remained “dizzy” for about an hour. After two days he developed a profound left lower motor neurone facial nerve palsy. He was found to have a complex fracture of the left petrous temporal bone, with fluid in the left middle ear and left mastoid. Treatment was conservative with oral steroids and oral co-amoxiclav and a left myringotomy to decompress his middle ear. The spectrum of aetiology, presentation, and prognosis for facial nerve injuries is discussed.
Balloon Catheter Therapy and Cardiac Valvular Disease
Authors: A Cribier, B Letac
Journal: Annual Review of Medicine (1989)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Stimulatory Effect of Topical Application of Caffeine on UVB-Induced Apoptosis in the Epidermis of p53 and Bax Knockout Mice
Authors: Yao-Ping Lu, You-Rong Lou, Qing-Yun Peng, Jian-Guo Xie, Allan H. Conney
Journal: Cancer Research (2004)

Abstract Shaved male or female p53(−/−) C57BL/6J mice and their wild-type littermates were irradiated once with UVB (60 mJ/cm2). The UVB-induced increase in apoptotic sunburn cells in p53(−/−) mice at 6–10 h after exposure to UVB was only 10–30% of that observed after treatment of p53(+/+) mice with UVB. Topical applications of caffeine immediately after UVB irradiation in female p53(+/+) or p53(−/−) mice enhanced the UVB-induced increase in apoptotic sunburn cells 6 h later by 127% and 563%, respectively. In another study, shaved female Bax(−/−) C57BL/6J mice and their wild-type littermates were irradiated once with UVB (60 mJ/cm2). The UVB-induced increase in apoptotic sunburn cells in Bax(−/−) mice at 6 h after exposure to UVB was only 14% of that observed after treatment of Bax(+/+) mice with UVB. Topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(−/−) mice with UVB enhanced the UVB-induced increases in apoptotic sunburn cells at 6 h by 214% and 467%, respectively, and topical application of caffeine immediately after irradiation of Bax(+/+) or Bax(−/−) mice with UVB enhanced the UVB-induced increase in caspase 3 (active form) positive cells at 6 h by 253% and 750%, respectively. The results indicate that UVB-induced increases in apoptosis in the epidermis of wild-type mice are predominantly (but not entirely) by p53- and Bax-dependent pathways and that topical application of caffeine can enhance UVB-induced increases in apoptosis by p53- and Bax-independent pathways.
Cognitive behavioural therapy as an adjunct to pharmacotherapy for primary care based patients with treatment resistant depression: results of the CoBalT randomised controlled trial
Authors: Nicola Wiles, Laura Thomas, Anna Abel, Nicola Ridgway, Nicholas Turner, John Campbell, Anne Garland, Sandra Hollinghurst, Bill Jerrom, David Kessler, Willem Kuyken, Jill Morrison, Katrina Turner, Chris Williams, Tim Peters, Glyn Lewis
Journal: The Lancet (2012)
Low-Density Lipoprotein in Hypercholesterolemic Human Plasma Induces Vascular Endothelial Cell Apoptosis by Inhibiting Fibroblast Growth Factor 2 Transcription
Authors: Chu-Huang Chen, Tao Jiang, Jun-Hai Yang, Wei Jiang, Jonathan Lu, Gopal K. Marathe, Henry J. Pownall, Christie M. Ballantyne, Thomas M. McIntyre, Philip D. Henry, Chao-Yuh Yang
Journal: Circulation (2003)

Background— Apoptosis of vascular endothelial cells (ECs) can be induced in vitro by experimentally modified LDL. Description of proapoptotic circulating lipoproteins may significantly enhance understanding of atherothrombosis pathophysiology. Methods and Results— Fast protein liquid chromatography of LDL samples from 7 asymptomatic, hypercholesterolemic patients yielded subfractions L 1 –L 5 in increasing electronegativity. L 4 and L 5 were not detectable or collectible in normolipidemic samples. In bovine aortic EC cultures, L 5 induced marked apoptosis and L 4 had a mild effect, whereas hypercholesterolemic or normolipidemic L 1 –L 3 had negligible effects. Compared with copper-oxidized LDL, L 5 was only mildly oxidized, although its propensity to form conjugated dienes in response to copper exceeded that of other subfractions. L 5 -induced apoptosis was associated with suppressed fibroblast growth factor 2 (FGF-2) transcription, as assessed by nuclear run-on analysis. Degrading platelet-activating factor (PAF)-like lipids in L 5 by a recombinant PAF acetylhydrolase prevented both FGF-2 downregulation and apoptosis. Furthermore, the ability of L 5 lipid extract to induce calcium influx into neutrophils was lost after pretreatment of the extract with PAF acetylhydrolase. FGF-2 supplementation, PAF receptor (PAFR) blockade with WEB-2086, and inactivation of PAFR-coupled G i protein with pertussis toxin all effectively attenuated L 5 -induced apoptosis. Conclusions— Our findings indicate that a highly electronegative, mildly oxidized LDL subfraction present in human hypercholesterolemic but not normolipidemic plasma can induce apoptosis in cultured ECs. The evidence that a freshly isolated LDL species modulates transcription of FGF-2 may provide a physiological insight into the mechanism of vascular EC apoptosis in hypercholesterolemia.
Incidence of "never events" among weekend admissions versus weekday admissions to US hospitals: national analysis
Authors: F. J. Attenello, T. Wen, S. Y. Cen, A. Ng, M. Kim-Tenser, N. Sanossian, A. P. Amar, W. J. Mack
Journal: BMJ (2015)

<b>Objective</b> To evaluate the association between weekend admission to hospital and 11 hospital acquired conditions recently considered by the Centers for Medicare and Medicaid as "never events" for which resulting healthcare costs are not reimbursed. <b>Design</b> National analysis. <b>Setting</b> US Nationwide Inpatient Sample discharge database. <b>Participants</b> 351 million patients discharged from US hospitals, 2002-10. <b>Main outcome measures</b> Univariate rates and multivariable likelihood of hospital acquired conditions among patients admitted on weekdays versus weekends, as well as the impacts of these events on prolonged length of stay and total inpatient charges. <b>Results</b> From 2002 to 2010, 351 170 803 patients were admitted to hospital, with 19% admitted on a weekend. Hospital acquired conditions occurred at an overall frequency of 4.1% (5.7% among weekend admissions versus 3.7% among weekday admissions). Adjusting for patient and hospital cofactors the probability of having one or more hospital acquired conditions was more than 20% higher in weekend admissions compared with weekday admissions (odds ratio 1.25, 95% confidence interval 1.24 to 1.26, P&lt;0.01). Hospital acquired conditions have a negative impact on both hospital charges and length of stay. At least one hospital acquired condition was associated with an 83% (1.83, 1.77 to 1.90, P&lt;0.01) likelihood of increased charges and 38% likelihood of prolonged length of stay (1.38, 1.36 to 1.41, P&lt;0.01). <b>Conclusion</b> Weekend admission to hospital is associated with an increased likelihood of hospital acquired condition, cost, and length of stay. Future protocols and staffing regulations must be tailored to the requirements of this high risk subgroup.
Predictive value of soluble haemoglobin scavenger receptor CD163 serum levels for survival in verified tuberculosis patients
Authors: T.B. Knudsen, P. Gustafson, G. Kronborg, T.B. Kristiansen, S.K. Moestrup, J.O. Nielsen, V. Gomes, P. Aaby, I. Lisse, H.J. Møller, J. Eugen-Olsen
Journal: Clinical Microbiology and Infection (2005)
"Whistleblowing": a health issue.
Authors: K J Lennane
Journal: BMJ (1993)

OBJECTIVE--To examine the response of organizations to "whistleblowing" and the effects on individual whistleblowers. DESIGN--Questionnaire survey of whistleblowers who contacted Whistleblowers Australia after its publicity campaign. SETTING--Australia. SUBJECTS--25 men and 10 women from various occupations who had exposed corruption or danger to the public, or both, from a few months to over 20 years before. RESULTS--All subjects in this non-random sample had suffered adverse consequences. For 29 victimization had started immediately after their first, internal, complaint. Only 17 approached the media. Victimization at work was extensive: dismissal (eight subjects), demotion (10), and resignation or early retirement because of ill health related to victimization (10) were common. Only 10 had a full time job. Long term relationships broke up in seven cases, and 60 of the 77 children of 30 subjects were adversely affected. Twenty nine subjects had a mean of 5.3 stress related symptoms initially, with a mean of 3.6 still present. Fifteen were prescribed long term treatment with drugs which they had not been prescribed before. Seventeen had considered suicide. Income had been reduced by three quarters or more for 14 subjects. Total financial loss was estimated in hundreds of thousands of Australian dollars in 17. Whistleblowers received little or no help from statutory authorities and only a modest amount from workmates. In most cases the corruption and malpractice continued unchanged. CONCLUSION--Although whistleblowing is important in protecting society, the typical organisational response causes severe and longlasting health, financial, and personal problems for whistleblowers and their families.