tbuckley/cabot-search huggingface dataset:
The Cooperative Prostate Cancer Tissue Resource
Authors: Jonathan Melamed, Milton W. Datta, Michael J. Becich, Jan M. Orenstein, Rajiv Dhir, Sylvia Silver, Marie Fidélia-Lambert, André Kadjacsy-Balla, Virgilia Macias, Ashokkumar Patel, Paul D. Walden, Maarten C. Bosland, Jules J. Berman
Journal: Clinical Cancer Research (2004)

Abstract Purpose: The Cooperative Prostate Cancer Tissue Resource (CPCTR) is a National Cancer Institute-supported tissue bank that provides large numbers of clinically annotated prostate cancer specimens to investigators. This communication describes the CPCTR to investigators interested in obtaining prostate cancer tissue samples. Experimental Design: The CPCTR, through its four participating institutions, has collected specimens and clinical data for prostate cancer cases diagnosed from 1989 onward. These specimens include paraffin blocks and frozen tissue from radical prostatectomy specimens and paraffin blocks from prostate needle biopsies. Standardized histopathological characterization and clinical data extraction are performed for all cases. Information on histopathology, demography (including ethnicity), laboratory data (prostate-specific antigen values), and clinical outcome related to prostate cancer are entered into the CPCTR database for all cases. Materials in the CPCTR are available in multiple tissue formats, including tissue microarray sections, paraffin-embedded tissue sections, serum, and frozen tissue specimens. These are available for research purposes following an application process that is described on the CPCTR web site (www.prostatetissues.org). Results: The CPCTR currently (as of October 2003) contains 5135 prostate cancer cases including 4723 radical prostatectomy cases. Frozen tissues, in some instances including patient serum samples, are available for 1226 cases. Biochemical recurrence data allow identification of cases with residual disease, cases with recurrence, and recurrence-free cases. Conclusions: The CPCTR offers large numbers of highly characterized prostate cancer tissue specimens, including tissue microarrays, with associated clinical data for biomarker studies. Interested investigators are encouraged to apply for use of this material (www.prostatetissues.org).
Serum immunoglobulins and lymphocyte transformation studies in coeliac disease.
Authors: T E Blecher, A Brzechwa-Ajdukiewicz, C F McCarthy, A E Read
Journal: Gut (1969)

Several reports have now appeared of an increased incidence of disorders of the lymphoreticular system in coeliac disease.These disorders have ranged from splenic atrophy (Engel, 1939) to more generalized lymphoreticular atrophy (McCarthy, Fraser, Evans, and Read, 1966), and an increased incidence of malignant reticulosis, particularly involving the gastrointestinal tract (Gough, Read, and Naish, 1962; Austad, Cornes, Gough, McCarthy, and Read, 1967; Harris, Cooke, Thompson, and Waterhouse, 1967).Furthermore an association with hypo- gammoglobulinaemia (Huizenga, Wollaeger, Green, and McKenzie, 1961) and more recently with specific deficiencies of the immunoglobulins IgA (Crabbe and Heremans, 1967) or IgM (Hobbs and Hepner, 1968) have been found in patients with this disease.Phytohaemagglutinin (PHA)-induced lym- phocyte transformation has been found to be defective in some malignant disorders of the lympho- reticular system such as Hodgkin's disease (Hersh and Oppenheim, 1965), giant follicular lymphoblastoma, and reticulosarcoma (Hirschhorn, Schreibman, Bach, and Siltzbach, 1964).In view of these findings, and the association already mentioned of disorders of this group with coeliac disease, we have studied the serum immuno- globulin levels in 30 patients with coeliac disease not on gluten-free diets, and in order to examine any relationship between the immunoglobulin pattern and PHA-induced transformation of circulating lymphocytes, we have also studied the latter para- meter in 10 of the patients selected at random.Trans- formation and DNA synthesis (on autoradiography) were assessed by two culture techniques using whole- leucocyte-rich plasma or washed leucocytes, respec- tively.On each occasion lymphocytes from two normal individuals were also cultured and reciprocal serum-exchange cultures between patients and controls were performed to determine whether any abnormalities which might occur in cultures of the patients' blood would be imposed on the control lymphocytes by the patients' sera, or conversely, on July 12, 2023 by guest.
Control of Oxalate Formation from L-Hydroxyproline in Liver Mitochondria
Authors: Tatsuya Takayama, Kimio Fujita, Kazuo Suzuki, Michiko Sakaguchi, Michio Fujie, Erina Nagai, Shinya Watanabe, Arata Ichiyama, Yoshihide Ogawa
Journal: Journal of the American Society of Nephrology (2003)

ABSTRACT. Serine:pyruvate/alanine:glyoxylate aminotransferase (SPT/AGT) is largely located in mitochondria in carnivores, whereas it is entirely found within peroxisomes in herbivores and humans. In rat liver, SPT/AGT is found in both of these organelles, and only the mitochondrial enzyme is markedly induced by glucagon. Although SPT/AGT is a bifunctional enzyme involved in the metabolism of both L-serine and glyoxylate, its contribution to L-serine metabolism is independent of mitochondrial or peroxisomal localization (Xue HH et al., J Biol Chem 274: 16028-16033, 1999). Therefore, the species-specific and food habit-dependent organelle distribution might be required for proper metabolism of glyoxylate at the subcellular site of its formation. Glyoxylate formation from glycolate and that from L-hydroxyproline have been shown to occur in peroxisomes and mitochondria, respectively. The present study found that urinary excretion of oxalate was markedly increased when a large dose of L-hydroxyproline or glycolate was administered to rats. Oxalate formation from L-hydroxyproline but not that from glycolate was significantly reduced when mitochondrial SPT/AGT had been induced by glucagon. The hydroxyproline content of collagen is 10 to 13%, and collagen accounts for about 30% of total animal protein; therefore, these results suggest that an important role of mitochondrial SPT/AGT in carnivores is to convert L-hydroxyproline-derived glyoxylate into glycine in situ, preventing undesirable overflow into the production of oxalate. E-mail: [email protected]
Effectiveness of a stress management program in smoking cessation. Randomized control trial
Authors: Maria Michou, Stamatoula Tsikrika, Christina Gratziou, George Chrousos, Christina Darviri
Journal: European Respiratory Journal (2013)

Although smoking habit remains a public health issue, current therapies for smoking cessation are not very effective. Stress can be a critical factor for inefficient results. A non-blind randomized control trial was designed to examine if a stress management program, as a complementary therapy, can increase smoking cessation rates. 49 individuals participated in the research (26 interventions and 23 controls). Participants received medication or/and medical counseling. In the intervention arm an 8 week stress management program was given, including: progressive muscle relaxation, guided imagery and autogenic training, with lifestyle instructions. Measurements included: a Daily Routine, Lifestyle and Health Questionnaire, Perceived Stress Scale (PSS), Health Locus of Control Scale (HLC), Depression Anxiety Stress Scale (DASS-21), Fagerstrom Test for Nicotine Dependence and Salivary Cortisol. Both groups resulted in a statistically significant reduction in daily cigarettes and nicotine dependence. The intervention’s group smoking rates were higher than the control’s group (77% and 43% respectively). Additionally, the interventions had a significant reduction in PSS score (p
Calmodulin Mutations Associated With Recurrent Cardiac Arrest in Infants
Authors: Lia Crotti, Christopher N. Johnson, Elisabeth Graf, Gaetano M. De Ferrari, Bettina F. Cuneo, Marc Ovadia, John Papagiannis, Michael D. Feldkamp, Subodh G. Rathi, Jennifer D. Kunic, Matteo Pedrazzini, Thomas Wieland, Peter Lichtner, Britt-Maria Beckmann, Travis Clark, Christian Shaffer, D. Woodrow Benson, Stefan Kääb, Thomas Meitinger, Tim M. Strom, Walter J. Chazin, Peter J. Schwartz, Alfred L. George
Journal: Circulation (2013)

Life-threatening disorders of heart rhythm may arise during infancy and can result in the sudden and tragic death of a child. We performed exome sequencing on 2 unrelated infants presenting with recurrent cardiac arrest to discover a genetic cause.We ascertained 2 unrelated infants (probands) with recurrent cardiac arrest and dramatically prolonged QTc interval who were both born to healthy parents. The 2 parent-child trios were investigated with the use of exome sequencing to search for de novo genetic variants. We then performed follow-up candidate gene screening on an independent cohort of 82 subjects with congenital long-QT syndrome without an identified genetic cause. Biochemical studies were performed to determine the functional consequences of mutations discovered in 2 genes encoding calmodulin. We discovered 3 heterozygous de novo mutations in either CALM1 or CALM2, 2 of the 3 human genes encoding calmodulin, in the 2 probands and in 2 additional subjects with recurrent cardiac arrest. All mutation carriers were infants who exhibited life-threatening ventricular arrhythmias combined variably with epilepsy and delayed neurodevelopment. Mutations altered residues in or adjacent to critical calcium binding loops in the calmodulin carboxyl-terminal domain. Recombinant mutant calmodulins exhibited several-fold reductions in calcium binding affinity.Human calmodulin mutations disrupt calcium ion binding to the protein and are associated with a life-threatening condition in early infancy. Defects in calmodulin function will disrupt important calcium signaling events in heart, affecting membrane ion channels, a plausible molecular mechanism for potentially deadly disturbances in heart rhythm during infancy.
DNA Double-Strand Breaks Form in Bystander Cells after Microbeam Irradiation of Three-dimensional Human Tissue Models
Authors: Olga A. Sedelnikova, Asako Nakamura, Olga Kovalchuk, Igor Koturbash, Stephen A. Mitchell, Stephen A. Marino, David J. Brenner, William M. Bonner
Journal: Cancer Research (2007)

Abstract The “radiation-induced bystander effect,” in which irradiated cells can induce genomic instability in unirradiated neighboring cells, has important implications for cancer radiotherapy and diagnostic radiology as well as for human health in general. Although the mechanisms of this effect remain to be elucidated, we reported previously that DNA double-strand breaks (DSBs), directly measured by γ-H2AX focus formation assay, are induced in bystander cultured cells. To overcome the deficiencies of cultured cell studies, we examined α-particle microbeam irradiation–induced bystander effects in human tissue models, which preserve the three-dimensional geometric arrangement and communication of cells present in tissues in vivo. In marked contrast to DNA DSB dynamics in irradiated cells, in which maximal DSB formation is seen 30 min after irradiation, the incidence of DSBs in bystander cells reached a maximum by 12 to 48 h after irradiation, gradually decreasing over the 7-day time course. At the maxima, 40% to 60% of bystander cells were affected, a 4- to 6-fold increase over controls. These increases in bystander DSB formation were followed by increased levels of apoptosis and micronucleus formation, by loss of nuclear DNA methylation, and by an increased fraction of senescent cells. These findings show the involvement of DNA DSBs in tissue bystander responses and support the notion that bystander DNA DSBs are precursors to widespread downstream effects in human tissues. Bystander cells exhibiting postirradiation signs of genomic instability may be more prone than unaffected cells to become cancerous. Thus, this study points to the importance of considering the indirect biological effects of radiation in cancer risk assessment. [Cancer Res 2007;67(9):4295–302]
Deficiency of natural anticoagulant proteins C, S, and antithrombin in portal vein thrombosis: a secondary phenomenon?
Authors: N C Fisher
Journal: Gut (2000)

Hereditary deficiencies of natural anticoagulant proteins are implicated in the pathogenesis of portal vein thrombosis (PVT). Secondary deficiencies of these proteins have also been reported in PVT, making interpretation of concentrations difficult.To characterise the coagulation profiles in adult patients with PVT and to investigate the possible mechanisms of natural anticoagulant protein deficiency.Twenty nine adult patients with portal hypertension caused by PVT, and normal biochemical liver function tests.Routine coagulation profiles and concentrations of proteins C, S, and antithrombin were measured; where indicated, corresponding concentrations in parents were also measured. Synchronous peripheral and hepatic or splenic vein concentrations were compared in seven patients undergoing interventional procedures, as were peripheral concentrations before and after shunt surgery in three patients.Deficiencies of one or more of the natural anticoagulant proteins occurred in 18 patients (62%), with six patients having combined deficiency of all three proteins. There were strong correlations between prothrombin and partial thromboplastin time ratios and concentrations of natural anticoagulant proteins. Family studies in nine cases of anticoagulant protein deficiency revealed possible hereditary deficiency in only three cases, and significantly lower concentrations of anticoagulant proteins in all PVT cases compared with parents. Levels of anticoagulant proteins tended to be lower in hepatic veins but higher in splenic veins compared with peripheral vein concentrations. Peripheral concentrations decreased after shunt surgery.Deficiency of natural anticoagulant proteins is common in PVT and is probably a secondary phenomenon in most cases, occurring as part of a global disturbance of coagulation variables. The mechanism for this remains unclear but may result from a combination of reduced hepatic blood flow and portosystemic shunting itself.
Physical activity and obesity in children
Authors: Andrew P Hills, Lars Bo Andersen, Nuala M Byrne
Journal: British Journal of Sports Medicine (2011)

Globally, obesity is affecting an increasing proportion of children. Physical activity plays an important role in the prevention of becoming overweight and obese in childhood and adolescence, and reducing the risk of obesity in adulthood. Puberty and the following adolescent period are acknowledged as particularly vulnerable times for the development of obesity due to sexual maturation and, in many individuals, a concomitant reduction in physical activity. In many Western settings, a large proportion of children and adolescents do not meet recommended physical activity guidelines and, typically, those who are more physically active have lower levels of body fat than those who are less active. Active behaviours have been displaced by more sedentary pursuits which have contributed to reductions in physical activity energy expenditure. Without appropriate activity engagement there is an increased likelihood that children will live less healthy lives than their parents. Owing to the high risk of overweight adolescents becoming obese adults, the engagement of children and adolescents in physical activity and sport is a fundamental goal of obesity prevention.
Early genetic events in T cell development analyzed by in situ hybridization.
Authors: D M Pardoll, B J Fowlkes, R I Lechler, R N Germain, R H Schwartz
Journal: The Journal of Experimental Medicine (1987)

In situ hybridization was used to investigate the expression of T cell receptor (TCR) alpha, beta, and gamma mRNAs in developing fetal and adult precursor thymocytes. gamma transcription was observed at the earliest time tested (day 12), followed by beta 12 h later, and TCR alpha on day 16. The early beta transcripts appeared to be from unrearranged or incompletely rearranged (D-J-C) beta loci. V beta region transcription was first detectable on day 14 and transcription of different V beta genes was induced at different times. These results delineate a schedule sequence of TCR gene activation, which begins within 1 d after entry of stem cells into the fetal thymus.
VESICAL SCHISTOSOMIASIS COMPLICATED BY CARCINOMA
Authors: N. H. Fairley
Journal: BMJ (1931)

MTHEBARITISORAL 983 that he knew of no case where a fit characterized by upward or downward movemcnt of the eyes was asso- ciated with disease of the cerebral hemispheres.There appears to be an innate co-ordinated upward mQvement of the eyes associated with the emotions, and related to a centre at a lower level.The eyes roll upward in sleep, and I have noted how in infancy, at an age when the vegetative centres are apt to take control, the eyes roll up in convulsions caused by gastro-intestinal irritation.Other Ocular Symptoms Other ocular symptoms noted among my patients are excessive blinking, fluttering of the eyelids, and difficulty in moving the eyes in a vertical direction when told to
Prognostic value of osteoprotegerin in heart failure after acute myocardial infarction
Authors: Thor Ueland, Rune Jemtland, Kristin Godang, John Kjekshus, Aina Hognestad, Torbjørn Omland, Iain B. Squire, Lars Gullestad, Jens Bollerslev, Kenneth Dickstein, Pål Aukrust
Journal: Journal of the American College of Cardiology (2004)
Short-Course Antiretroviral Therapy in Primary HIV Infection
Authors: S Fidler, K Porter, F Ewings, J Frater, G Ramjee, D Cooper, H Rees, M Fisher, M Schechter, P Kaleebu, G Tambussi, S Kinloch, J M Miro, A Kelleher, M McClure, S Kaye, M Gabriel, R Phillips, J Weber, A Babiker
Journal: New England Journal of Medicine (2013)

Short-course antiretroviral therapy (ART) in primary human immunodeficiency virus (HIV) infection may delay disease progression but has not been adequately evaluated.
Cardiorespiratory Fitness as a Quantitative Predictor of All-Cause Mortality and Cardiovascular Events in Healthy Men and Women
Authors: Satoru Kodama
Journal: JAMA (2009)

Epidemiological studies have indicated an inverse association between cardiorespiratory fitness (CRF) and coronary heart disease (CHD) or all-cause mortality in healthy participants.To define quantitative relationships between CRF and CHD events, cardiovascular disease (CVD) events, or all-cause mortality in healthy men and women.A systematic literature search was conducted for observational cohort studies using MEDLINE (1966 to December 31, 2008) and EMBASE (1980 to December 31, 2008). The Medical Subject Headings search terms used included exercise tolerance, exercise test, exercise/physiology, physical fitness, oxygen consumption, cardiovascular diseases, myocardial ischemia, mortality, mortalities, death, fatality, fatal, incidence, or morbidity. Studies reporting associations of baseline CRF with CHD events, CVD events, or all-cause mortality in healthy participants were included.Two authors independently extracted relevant data. CRF was estimated as maximal aerobic capacity (MAC) expressed in metabolic equivalent (MET) units. Participants were categorized as low CRF (< 7.9 METs), intermediate CRF (7.9-10.8 METs), or high CRF (> or = 10.9 METs). CHD and CVD were combined into 1 outcome (CHD/CVD). Risk ratios (RRs) for a 1-MET higher level of MAC and for participants with lower vs higher CRF were calculated with a random-effects model.Data were obtained from 33 eligible studies (all-cause mortality, 102 980 participants and 6910 cases; CHD/CVD, 84 323 participants and 4485 cases). Pooled RRs of all-cause mortality and CHD/CVD events per 1-MET higher level of MAC (corresponding to 1-km/h higher running/jogging speed) were 0.87 (95% confidence interval [CI], 0.84-0.90) and 0.85 (95% CI, 0.82-0.88), respectively. Compared with participants with high CRF, those with low CRF had an RR for all-cause mortality of 1.70 (95% CI, 1.51-1.92; P < .001) and for CHD/CVD events of 1.56 (95% CI, 1.39-1.75; P < .001), adjusting for heterogeneity of study design. Compared with participants with intermediate CRF, those with low CRF had an RR for all-cause mortality of 1.40 (95% CI, 1.32-1.48; P < .001) and for CHD/CVD events of 1.47 (95% CI, 1.35-1.61; P < .001), adjusting for heterogeneity of study design.Better CRF was associated with lower risk of all-cause mortality and CHD/CVD. Participants with a MAC of 7.9 METs or more had substantially lower rates of all-cause mortality and CHD/CVD events compared with those with a MAC of less 7.9 METs.
Calmodulin Inhibitor W-7 Unmasks a Novel Electrocardiographic Parameter That Predicts Initiation of Torsade de Pointes
Authors: T. David Gbadebo, Robert W. Trimble, Michelle S.C. Khoo, Joel Temple, Dan M. Roden, Mark E. Anderson
Journal: Circulation (2002)

Background — We have shown that the calmodulin inhibitor W-7 suppresses torsade de pointes (TdP) without shortening the QT interval, which is consistent with other findings that QT prolongation, per se, is insufficient to generate TdP. ECGs were analyzed from a well-characterized animal model of TdP to identify more reliable predictors of this life-threatening ventricular arrhythmia. Methods and Results — TdP was induced using methoxamine and clofilium in 12 of 14 rabbits pretreated with vehicle control, whereas pretreatment with W-7 (50 μmol/kg), an inhibitor of the intracellular Ca 2+ -binding protein calmodulin, significantly suppressed TdP induction (1 of 11 rabbits with TdP, P &lt;0.001). W-7 did not affect heart rate, increases in QT intervals, or dispersion compared with measurements in vehicle-treated control animals. However, a progressive and significant increase in the ratio of U-wave to T-wave amplitude (UTA) occurred before TdP onset in control animals, and this was prevented by W-7. Conclusions — Selective suppression of TdP inducibility by W-7, without shortening the duration of cardiac repolarization, allowed identification of the UTA ratio as a new electrocardiographic index for predicting TdP onset. These findings are consistent with the idea that prolonged repolarization is not the proximate cause of arrhythmia initiation, and they suggest that an increased UTA ratio reflects activation of intracellular Ca 2+ /calmodulin–dependent processes that are required for triggering TdP in this model.
Facile Fabrication of Egg White Macroporous Sponges for Tissue Regeneration
Authors: Sasan Jalili‐Firoozinezhad, Sareh Rajabi‐Zeleti, Parvaneh Mohammadi, Emanuele Gaudiello, Shahin Bonakdar, Mehran Solati‐Hashjin, Anna Marsano, Nasser Aghdami, Arnaud Scherberich, Hossein Baharvand, Ivan Martin
Journal: Advanced Healthcare Materials (2015)

The availability of 3D sponges combining proper biochemical, biophysical, and biomechanical properties with enhanced capacity of in vivo engraftment and vascularization is crucial in regenerative medicine. A simple process is developed to generate macroporous scaffolds with a well‐defined architecture of interconnected pores from chicken egg white (EW), a material with protein‐ and growth factor‐binding features which has not yet been employed in regenerative medicine. The physicomechanical properties and degradation rates of the scaffold are finely tuned by using varying concentrations of the cross‐linker, 1‐ethyl‐3‐(3‐dimethylaminopropyl) carbodiimide hydrochloride, without alteration of the biochemical traits. In vitro, EW scaffolds supported active metabolism, proliferation, and migration of human dermal fibroblasts, thereby generating uniform cellular constructs. In vivo, subcutaneous implantation in mice reveals negligible immune reaction and efficient cell and tissue ingrowth. Angiogenesis into EW scaffolds is enhanced as compared to standard collagen type I sponges used as reference material, likely due to significantly higher adsorption of the proangiogenic factor vascular endothelial growth factor. In summary, a material is presented derived by facile processing of a highly abundant natural product. Due to the efficient subcutaneous engraftment capacity, the sponges can find utilization for soft tissue regeneration.