tbuckley/cabot-search huggingface dataset:
Analysis and functional classification of transcripts from the nematode Meloidogyne incognita
Authors: James P McCarter, Makedonka Dautova Mitreva, John Martin, Mike Dante, Todd Wylie, Uma Rao, Deana Pape, Yvette Bowers, Brenda Theising, Claire V Murphy, Andrew P Kloek, Brandi J Chiapelli, Sandra W Clifton, David Mck Bird, Robert H Waterston
Journal: Genome biology (2003)

Abstract Background Plant parasitic nematodes are major pathogens of most crops. Molecular characterization of these species as well as the development of new techniques for control can benefit from genomic approaches. As an entrée to characterizing plant parasitic nematode genomes, we analyzed 5,700 expressed sequence tags (ESTs) from second-stage larvae (L2) of the root-knot nematode Meloidogyne incognita . Results From these, 1,625 EST clusters were formed and classified by function using the Gene Ontology (GO) hierarchy and the Kyoto KEGG database. L2 larvae, which represent the infective stage of the life cycle before plant invasion, express a diverse array of ligand-binding proteins and abundant cytoskeletal proteins. L2 are structurally similar to Caenorhabditis elegans dauer larva and the presence of transcripts encoding glyoxylate pathway enzymes in the M. incognita clusters suggests that root-knot nematode larvae metabolize lipid stores while in search of a host. Homology to other species was observed in 79% of translated cluster sequences, with the C. elegans genome providing more information than any other source. In addition to identifying putative nematode-specific and Tylenchida -specific genes, sequencing revealed previously uncharacterized horizontal gene transfer candidates in Meloidogyne with high identity to rhizobacterial genes including homologs of nodL acetyltransferase and novel cellulases. Conclusions With sequencing from plant parasitic nematodes accelerating, the approaches to transcript characterization described here can be applied to more extensive datasets and also provide a foundation for more complex genome analyses.
Pneumothorax in adults with cystic fibrosis dependent on nasal intermittent positive pressure ventilation (NIPPV): a management dilemma
Authors: C S Haworth
Journal: Thorax (2000)

AbstractThe management of pneumothorax in three adult patients with cystic fibrosis dependent on nasal intermittent positive pressure ventilation is described.cystic fibrosisnasal intermittent positive pressure ventilation (NIPPV)pneumothorax
The Cambridge and King's College Hospital Experience of Liver Transplantation, 1968-1983
Authors: Keith Rolles, Roger Williams, James Neuberger, Roy Calne
Journal: Hepatology (1984)

The postoperative course of 138 transplants performed in 137 patients in the Cambridge and King’s College Hospital series between May 2, 1968 and April 1, 1983 is presented. During the last 15 years, criteria for selection of transplant candidates has been improved and types of disease categories, both suitable and unsuitable for liver transplantation, have been defined. The acceptance of the concept of brain death and the use of heart-beating donors in the United Kingdom since 1976 has greatly improved the quality of donor organs. Changes in surgical technique, particularly with regard to biliary tract drainage, have reduced morbidity and mortality from biliary tract complications since 1975. The use of partial cardiopulmonary bypass in selected cases and changes in immunosuppressive drug regimens have not significantly improved our overall results. Despite these changes based on our experience, the perioperative mortality in the Cambridge and King’s College Hospital series remains disturbingly high.
The Effect of Liraglutide, a Long-Acting Glucagon-Like Peptide 1 Derivative, on Glycemic Control, Body Composition, and 24-h Energy Expenditure in Patients With Type 2 Diabetes
Authors: Helle Harder, Lene Nielsen, Tu D.T. Thi, Arne Astrup
Journal: Diabetes Care (2004)

OBJECTIVE—Glucagon-like peptide (GLP)-1 is a gut hormone that exerts incretin effects and suppresses food intake in humans, but its therapeutic use is limited due to its short half-life. This was a randomized, double-blind, parallel-group, placebo-controlled trial investigating the effect of the long-acting GLP-1 derivative liraglutide (NN2211) on glycemic control, body weight, body composition, and 24-h energy expenditure in obese subjects with type 2 diabetes. RESEARCH DESIGN AND METHODS—Thirty-three patients (mean ± SD) aged 60.0 ± 9.5 years, with HbA1c 7.5 ± 1.2% and BMI 36.6 ± 4.1 kg/m2, were randomized to treatment with a single daily subcutaneous dose of 0.6 mg liraglutide (n = 21) or placebo (n = 12) for 8 weeks. In addition to weight and glycemic parameters, body composition was assessed by dual-energy X-ray absorptiometry (DEXA) scanning and 24-h energy expenditure in a respiratory chamber. RESULTS—After 8 weeks, liraglutide reduced fasting serum glucose (liraglutide, −1.90 mmol/l, and placebo, 0.27 mmol/l; P = 0.002) and HbA1c (liraglutide, −0.33%, and placebo, 0.47%; P = 0.028) compared with placebo. No change in body weight was detected (liraglutide, −0.7 kg, and placebo, −0.9 kg; P = 0.756). There was a nonsignificant trend toward a decrease in total fat mass (liraglutide, −0.98%, and placebo, −0.12%; P = 0.088) and toward an increase in lean body mass (liraglutide, 1.02%, and placebo, 0.23%; P = 0.118) in the liraglutide group compared with the placebo group. Twenty-four-hour energy expenditure was unaffected by the treatment (liraglutide, −12.6 kJ/h, and placebo, −13.7 kJ/h; P = 0.799). CONCLUSIONS—Eight weeks of 0.6-mg liraglutide treatment significantly improved glycemic control without increasing weight in subjects with type 2 diabetes compared with those on placebo. No influence on 24-h energy expenditure was detected.
Hypertension and microvascular remodelling
Authors: François Feihl, Lucas Liaudet, Bernard I. Levy, Bernard Waeber
Journal: Cardiovascular Research (2008)

In the present review, microvascular remodelling refers to alterations in the structure of resistance vessels contributing to elevated systemic vascular resistance in hypertension. We start with some historical aspects, underscoring the importance of Folkow’s contribution made half a century ago. We then move to some basic concepts on the biomechanics of blood vessels, and explicit the definitions proposed by Mulvany for specific forms of remodelling, especially inward eutrophic and inward hypertrophic. The available evidence for the existence of remodelled resistance vessels in hypertension comes next, with relatively more weight given to human, in comparison with animal data. Mechanisms are discussed. The impact of antihypertensive drug treatment on remodelling is described, again with emphasis on human data. Some details are given on the three studies to date which point to remodelling of subcutaneous resistance arteries as an independent predictor of cardiovascular risk in hypertensive patients. We terminate by considering the potential role of remodelling in the pathogenesis of end-organ damage and in the perpetuation of hypertension.
The Critical Importance of Urinary Concentrating Ability in the Generation of Urinary Carbon Dioxide Tension
Authors: Jose A. L. Arruda, Luiz Nascimento, Pradeep K. Mehta, Donald R. Rademacher, John T. Sehy, Christof Westenfelder, Neil A. Kurtzman
Journal: Journal of Clinical Investigation (1977)

Measurement of urine to blood (U-B) carbon dioxide tension (PCO2) gradient during alkalinization of the urine has been suggested to assess distal H+ secretion. A fact that has not been considered in previous studies dealing with urinary PCO2 is that dissolution of HCO3 in water results in elevation of PCO2 which is directly proportional to the HCO3 concentration. To investigate the interrelationship of urinary HCO3 and urinary acidification, we measured U-B PCO2 in (a) the presence of enhanced H+ secretion and decreased concentrating ability i.e., chronic renal failure (CRF), (b) animals with normal H+ secretion and decreased concentrating ability, Brattleboro (BB) rats, and (c) the presence of both impaired H+ secretion and concentrating ability (LiCl treatment and after release of unilateral ureteral obstruction). At moderately elevated plasma HCO3 levels (30-40 meq/liter), normal rats achieved a highly alkaline urine (urine pH > 7.8) and raised urine HCO3 concentration and U-B PCO2. At similar plasma HCO3 levels, BB rats had a much higher fractional water excretion and failed to raise urine pH, urine HCO3 concentration, and U-B PCO2 normally. At a very high plasma HCO3 (>50 meq/liter), BB rats raised urine pH, urine HCO3 concentration, and U-B PCO2 to the same levels seen in normals. CRF rats failed to raise urine pH, urine HCO3, and U-B PCO2 normally at moderately elevated plasma HCO3 levels; at very high plasma HCO3 levels, CRF rats achieved a highly alkaline urine but failed to raise U-B PCO2. Dogs and patients with CRF were also unable to raise urine pH, urine HCO3 concentration, and U-B PCO2 normally at moderately elevated plasma HCO3 levels. In rats, dogs, and man, U-B PCO2 was directly related to urine HCO3 concentration and inversely related to fractional water excretion. At moderately elevated plasma HCO3 levels, animals with a distal acidification defect failed to raise U-B PCO2; increasing the plasma HCO3 to very high levels resulted in a significant increase in urine HCO3 concentration and U-B PCO2. The observed urinary PCO2 was very close to the PCO2 which would be expected by simple dissolution of a comparable amount of HCO3 in water. These data demonstrate that, in highly alkaline urine, urinary PCO2 is largely determined by concentration of urinary HCO3 and cannot be used as solely indicating distal H+ secretion.
On linking comparative metacognition and theory of mind
Authors: Josep Call
Journal: Behavioral and Brain Sciences (2003)

Smith et al.'s article provides a convincing argument for devoting increased research attention to comparative metacognition. However, this increased attention should be complemented with establishing links with comparative theory of mind (ToM) research, which are currently missing. I present a task in which pairs of subjects are presented with incomplete information in an object-choice situation that could be used to establish that link.
Myosin isoenzymes in normal and hypertrophied human ventricular myocardium.
Authors: J J Mercadier, P Bouveret, L Gorza, S Schiaffino, W A Clark, R Zak, B Swynghedauw, K Schwartz
Journal: Circulation Research (1983)

We tested the hypothesis that hypertrophy of the human heart is associated with the redistribution of ventricular isomyosins. Human cardiac myosin was isolated from autopsy samples of left ventricular free wall of patients with cardiac hypertrophy and of fetal, young, and adult subjects without heart disease. The following parameters were studied: electrophoretic migration in denaturing and non-denaturing conditions; immunological cross-reactivities with three different types of antibodies; and early phosphate burst size and steady state ATPase activities stimulated by K+-EDTA, Ca++, Mg++, and actin. The antibodies were chosen for their ability to recognize selectively the rat V1 and V3 cardiac isomyosins. The first type was a monoclonal antibody, CCM-52, prepared against embryonic chick cardiac myosin, the second was an anti-beef atrial myosin, and the third was an anti-rat V1 myosin. CCM-52 reacted with a greater affinity with rat V3 than with rat V1, and was a probe of mammalian V3. Anti-beef atrial myosin and anti-rat V1 myosin both recognized specifically beef atrial and rat V1 myosins, and were thus considered as probes of mammalian V1. Under non-denaturing conditions, human myosins migrated as rat V3 isomyosin; under denaturing conditions, no difference was observed in any of the electrophoretic parameters between all samples tested, except for the fetal hearts which contained a fetal type of light chain. The immunological studies indicated that human myosins were composed mostly of a V3 type (HV3), but contained also some V1 isomyosin. A technique was developed to quantify the amount of human VI isomyosin which was found to range from almost 0 to 15% of total myosin, and to vary from one heart to the other, regardless of the origin of the heart. Enzymatic studies showed no significant difference between normal, hypertrophied, and fetal hearts in any of the activities tested. However, there was a significant correlation between Ca++-stimulated ATPase activities and HV1 amount (at 0.05 M KCl, n = 18, r2 equal 0.49, P less than 0.01; at 0.5 M KCl, n = 18, r 2 = 0.5, P less than 0.01). These data demonstrate the heterogeneity of human ventricular myosin, which appears to be composed, as in other mammalian species, of V1 and V3 isoforms of different ATPase activities (V1 greater than V3). However it seems that V1 to V3 shifts do not appear to be of physiological significance in the adaptation of human heart to chronic mechanical overloads.
Infrequent Tumor Initiative of the Children's Oncology Group: Initial Lessons Learned and Their Impact on Future Plans
Authors: Alberto S. Pappo, Mark Krailo, Zhengjia Chen, Carlos Rodriguez-Galindo, Gregory Reaman
Journal: Journal of Clinical Oncology (2010)

The merger of the Pediatric Oncology Group, Children's Cancer Group, the Intergroup Rhabdomyosarcoma Study Group, and the National Wilms Tumor Study Group in 2000 offered the newly formed Children's Oncology Group (COG), an opportunity to study rare cancers that had not been the subject of organized evaluation within the context of a cooperative group. In 2002, the COG formed the rare tumor committee which is comprised of four subcommittees. This article details the experience of the infrequent tumor subcommittee for the period of 2002 to 2007. During the initial implementation of this strategy, we have observed low rates of registration within the COG registry and low levels of participation in open banking, biology, and first-line therapeutic studies. This initial experience has allowed us to develop alternative strategies to increase registration rates and clinical trial enrollments. It is hoped that these new plans will allow us to increase our ability to better understand the biology and improve the treatment outcome of young patients with infrequent cancers. Furthermore, our initial experience has demonstrated to us the potential power of expanded cooperation and collaboration at a global level.
Health belief model predicts adherence to CPAP before experience with CPAP
Authors: S. Olsen, S. Smith, T. Oei, J. Douglas
Journal: European Respiratory Journal (2008)

Adherence to continuous positive airway pressure (CPAP) therapy for obstructive sleep apnoea (OSA) is often poor. Biomedical indices explain little of the variance in CPAP use. The present study tested a health belief model of adherence in order to determine the contribution of psychological constructs as compared to biomedical indices in the prediction of CPAP adherence. Consecutive patients (n = 77) newly diagnosed with OSA and naïve to CPAP treatment (had never tried CPAP before) completed questionnaires at baseline (prior to CPAP treatment). The questionnaires assessed: outcome expectancy with treatment, self-efficacy, functional outcomes of sleepiness, and perceived risk of negative health outcomes. Physiological data were obtained from a standard clinical diagnostic sleep study. CPAP adherence was assessed at 4-month follow-up. Health belief model constructs alone explained 21.8% of the variance in CPAP adherence, whereas health belief model constructs and biomedical indices together explained 31.8% of the variance in CPAP adherence. The greatest proportion of CPAP adherence was explained by higher outcome expectancies with treatment, greater functional limitations as a result of sleepiness and lower risk perception. The results suggest that patients have developed beliefs and expectations about obstructive sleep apnoea and continuous positive airway pressure even before they try continuous positive airway pressure treatment. These beliefs and expectations predict the patients' adherence to effective therapy.
Pulmonary Air Crescent Sign
Authors: Kai-Ling Lee, Hung-Hua Liang, Chi-Li Chung, Shi-Hsin Hsiao, Chung-Hung Shih
Journal: JAMA Surgery (2013)

A 62-year-old man was admitted to our hospital with a concern of productive cough, profuse hemoptysis, and intermittent breathlessness for about 5 months. He had a 50-year history of cigarette smoking and had stopped smoking 5 months prior to being seen.
Molecular Stratification of Diagnostically Challenging High-Grade Gliomas Composed of Small Cells
Authors: Andrey Korshunov, Regina Sycheva, Andrey Golanov
Journal: Clinical Cancer Research (2004)

Abstract Purpose: There is considerable morphologic overlap between various entities of high-grade gliomas, and, therefore, a further planning of their optimal treatment is a controversial issue. The aim of this study was molecular stratification of morphologically ambiguous high-grade gliomas composed from small cells. Fluorescence in situ hybridization (FISH) with commercially available probes was used for this purpose. Experimental Design: We analyzed a set of 114 high-grade small-cell gliomas that were difficult to interpret diagnostically because of their distinct cytological origin. FISH assay with locus probes for EGFR, p16, PTEN, and 1p and 19q was done. Results: Morphologically uniform high-grade gliomas composed of small cells varied greatly in terms of molecular features and clinical outcome. Four clinically relevant subsets of patients whose tumors showed distinctly different molecular profiles were identified as follows: (a) 13 patients whose tumors exhibited no discernable molecular alterations (5-year survival rate, 83%); (b) 20 patients whose tumors harbored either 1p/19q codeletion or isolated deletion of 19q unaccompanied by other molecular abnormalities (5-year survival rate, 59%); (c) 35 patients whose tumors showed p16 and/or PTEN deletions unaccompanied by EGFR amplification (5-year survival rate, 8%); and (d) 46 patients whose tumors harbored EGFR amplification (5-year survival rate, 0). Conclusions: The FISH method provides clinically useful information in the molecular analysis of morphologically ambiguous malignant small-cell gliomas that could potentially enhance the quality of patient care.
Clinical peculiarities of mycoplasmosis and chlamydiosis in asthma
Authors: Alevtina Sharavii, Svetlana Smirnova, Sergey Tereshchenko
Journal: European Respiratory Journal (2013)

Aim: To study clinical peculiarities of mycoplasmosis and chlamydiosis in bronchial asthma (BA).  Materials and Methods: We examined 239 subjects in the ages of 17 to 78 years: BA patients (n=187) and control group (healthy, n=52). After the results of laboratory tests we have marked those contaminated with chlamydia (102), mycoplasma (92), without contamination (47) in BA. We have carried out questionnaire survey, clinical examination, determined Chlamydophila pneumoniae et psittaci, Chlamydia trachomatis, mycoplasma pneumoniae, mycoplasma hominis antigens and antibodies to them. We have implemented immune enzyme analysis of blood serum, antigens by the technique of direct immune fluorescence of smears from oropharynx mucosa.  Results: We have marked the following characteristics of mycoplasmosis, chlamydiosis clinical picture in BA: temperature increase in the evening up to 37.9 C (59%); obtrusive cough with purulent sputum (80.8%); mixed dyspnea (73.1%); combination of symptoms (low-grade fever, cough, dyspnea). Broncho-obstructive syndrome was accompanied by respiration function (RF) disturbance of mixed character. We have found atopic BA contaminated with mycoplasma in 42.3% subjects, pseudo atopic BA – in 57.5%, mixed BA – in 57.7%; with chlamydia these indices were 33.3%, 44.1%, 45.7%, respectively. Low-grade fever, cough and mixed dyspnea had been revealed more often in BA with mysoplasma, chlamydia contamination as compared to without contamination group.  Conclusion: We have determined clinical peculiarities of mycoplasmosis and chlamydiosis in bronchial asthma: low-grade fever, obtrusive cough with purulent sputum, dyspnea, RF disturbances of mixed character.
The t(8;22) in chronic myeloid leukemia fuses BCR to FGFR1: transforming activity and specific inhibition of FGFR1 fusion proteins
Authors: Asuman Demiroglu, E. Joanna Steer, Carol Heath, Kerry Taylor, Mark Bentley, Steven L. Allen, Prasad Koduru, Judith P. Brody, Geoffrey Hawson, Robyn Rodwell, Mary-Lou Doody, Fernando Carnicero, Andreas Reiter, John M. Goldman, Junia V. Melo, Nicholas C. P. Cross
Journal: Blood (2001)
Phosphoglycerate dehydrogenase diverts glycolytic flux and contributes to oncogenesis
Authors: Jason W Locasale, Alexandra R Grassian, Tamar Melman, Costas A Lyssiotis, Katherine R Mattaini, Adam J Bass, Gregory Heffron, Christian M Metallo, Taru Muranen, Hadar Sharfi, Atsuo T Sasaki, Dimitrios Anastasiou, Edouard Mullarky, Natalie I Vokes, Mika Sasaki, Rameen Beroukhim, Gregory Stephanopoulos, Azra H Ligon, Matthew Meyerson, Andrea L Richardson, Lynda Chin, Gerhard Wagner, John M Asara, Joan S Brugge, Lewis C Cantley, Matthew G Vander Heiden
Journal: Nature Genetics (2011)
Epigenetic Events Highlight the Challenge of Validating Prognostic Biomarkers During the Clinical and Biologic Evolution of Prostate Cancer
Authors: Phillip G. Febbo
Journal: Journal of Clinical Oncology (2009)

The association of molecular events with prostate cancer behavior presents dual opportunities for increased molecular insight and improved care.The promise of molecular oncology relies on the belief that optimal clinical care will result from a comprehensive understanding of the molecular pathogenesis of cancer and the specific genetic events present within an individual's tumor.In this issue of Journal of Clinical Oncology, Richiardi et al 1 have associated methylation of APC with poor prognosis in two independent cohorts of prostate cancer patients.The strong association between epigenetic silencing of APC and poor prognosis additionally supports a role for WNT/␤-catenin signaling in aggressive prostate cancer and introduces a novel prognostic biomarker with which clinicians may be able to better anticipate prostate cancer behavior.Epigenetic silencing of targeted genes is one of the earliest molecular alterations commonly found in prostate neoplasia.Methylation of the CpG-enriched promoter region of GSTP1 has been recognized for more than a decade as a frequent, early event with potential as a diagnostic biomarker.More comprehensive screens of promoter methylation patterns demonstrate consistent changes associated with the development and progression of prostate cancer 2,3 and, in the first publication from the Cancer Genome Atlas Project supported by the National Human Genome Research Institute of the National Institutes of Health, epigenetic silencing was complementary to genetic loss in activating critical signaling pathways. 4Thus, epigenetic control of gene expression is fundamental to cancer biology; as a result, assays for epigenetic alterations have the potential to become accurate diagnostic, prognostic, and predictive biomarkers.Richiardi et al 1 report on a retrospective analysis of promoter methylation of three genes, GSTP1, RUNX3, and APC, in two cohorts of patients with prostate cancer from Turin, Italy.Men were diagnosed with prostate cancer after biopsy of the prostate, transurethral resection of the prostate, or radical prostatectomy, and each had available paraffin-embedded tumor tissue and long-term follow-up.The first cohort was comprised of specimens collected in the 1980s, before widespread use of prostate-specific antigen (PSA) screening (n ϭ 216; 1982 to 1988), and the second cohort included specimens collected in the 1990s (n ϭ 243; 1993 to 1996) after the adoption of PSA screening.Promoter methylation of the APC gene was associated with increased risk of prostate cancer-specific mortality in both cohorts (1980s hazard ratio [HR], 1.42; 95% CI, 0.98 to 2.07; 1990s cohort HR, 1.57; 95% CI, 0.95 to 2.62; combined HR, 1.49; 95% CI, 1.11 to 2.00).Promoter 3088