tbuckley/cabot-search huggingface dataset:
Epidemiological trends of pre-malignant gastric lesions: a long-term nationwide study in the Netherlands
Authors: A C de Vries, G A Meijer, C W N Looman, M K Casparie, B E Hansen, N C T van Grieken, E J Kuipers
Journal: Gut (2007)

The pre-malignant gastric lesions atrophic gastritis (AG), intestinal metaplasia (IM) and dysplasia (DYS) have long been identified as principal risk factors for gastric cancer.To evaluate epidemiological time trends of pre-malignant gastric lesions in the Netherlands.Patients with a first diagnosis of AG, IM or DYS between 1991 and 2005 were identified in the Dutch nationwide histopathology registry. The number of new diagnoses per year were evaluated relative to the total number of patients with a first gastric biopsy. Time trends were evaluated with age-period-cohort models using logistic regression analysis.In total, 23 278 patients were newly diagnosed with AG, 65 937 patients with IM, and 8517 patients with DYS. The incidence of AG declined similarly in men and women with 8.2% per year [95% CI 7.9% to 8.6%], and DYS with 8.1% per year [95% CI 7.5% to 8.6%]. The proportional number of new IM cases declined with 2.9% per year [95% CI 2.7% to 3.1%] in men and 2.4% [95% CI 2.2% to 2.6%] in women. With age-period-cohort models a cohort phenomenon was demonstrated for all categories of pre-malignant gastric lesions in men and in women with IM and DYS. Period phenomena with a larger decline in number of diagnoses after 1996 were also demonstrated for AG and IM.The incidence of pre-malignant gastric lesions is declining. Period and cohort phenomena were demonstrated for diagnoses of AG and IM. These findings imply that a further decrease of at least 24% in the incidence of gastric cancer in the coming decade may be anticipated in Western countries without specific intervention.
Combined gene therapy with suicide gene and interleukin-12 is more efficient than therapy with one gene alone in a murine model of hepatocellular carcinoma
Authors: Marek Drozdzik, Cheng Qian, Xiaoming Xie, Dacheng Peng, Roberto Bilbao, Guillermo Mazzolini, Jesus Prieto
Journal: Journal of Hepatology (2000)
Principles of Appropriate Antibiotic Use for Treatment of Uncomplicated Acute Bronchitis: Background
Authors: Ralph Gonzales, John G. Bartlett, Richard E. Besser, Richelle J. Cooper, John M. Hickner, Jerome R. Hoffman, Merle A. Sande
Journal: Annals of Internal Medicine (2001)

The following principles of appropriate antibiotic use for adults with acute bronchitis apply to immunocompetent adults without complicating comorbid conditions, such as chronic lung or heart disease. 1. The evaluation of adults with an acute cough illness or a presumptive diagnosis of uncomplicated acute bronchitis should focus on ruling out serious illness, particularly pneumonia. In healthy, nonelderly adults, pneumonia is uncommon in the absence of vital sign abnormalities or asymmetrical lung sounds, and chest radiography is usually not indicated. In patients with cough lasting 3 weeks or longer, chest radiography may be warranted in the absence of other known causes. 2. Routine antibiotic treatment of uncomplicated acute bronchitis is not recommended, regardless of duration of cough. If pertussis infection is suspected (an unusual circumstance), a diagnostic test should be performed and antimicrobial therapy initiated. 3. Patient satisfaction with care for acute bronchitis depends most on physician–patient communication rather than on antibiotic treatment.
Telomere-Driven Karyotypic Complexity Concurs with p16INK4a Inactivation in <i>TP53</i>-Competent Immortal Endothelial Cells
Authors: Victoria W. Wen, Kaida Wu, Sheik Baksh, Rebecca A. Hinshelwood, Richard B. Lock, Susan J. Clark, Malcolm A.S. Moore, Karen L. MacKenzie
Journal: Cancer Research (2006)

Abstract Critically short telomeres promote chromosomal fusions, which in TP53-defective cells initiate the formation of cytogenetic aberrations that are typical of human cancer cells. Expression of the enzyme telomerase stabilizes normal and aberrant chromosomes by maintaining telomere length. However, previous investigations, including our own, have shown that overexpression of telomerase reverse transcriptase (hTERT) does not prevent net telomere shortening in human endothelial cells. In the present study, two mass cultures of hTERT-transduced bone marrow endothelial cells (BMhTERT) and 26 clones were employed to further investigate the immortalization process and consequences of telomere shortening. Eighty-five percent (22 of 26) of the clones and both mass cultures were immortalized. However, cytogenetic analyses revealed recurring cytogenetic aberrations in the mass cultures and 12 representative clones. Several of the recurring aberrations, including +5p, +11, −13, +19, and +20, and nonreciprocal translocations involving 17p and 2p were previously implicated in human carcinogenesis. One mass culture and a subset of clones (5 of 12) had complex karyotypes, characterized by cytogenetic heterogeneity and at least five chromosomal abnormalities. p16INK4a was silenced exclusively in the five clones and mass culture with complex karyotypes, whereas the p53/p21cip1 pathway was defective in only one clone. Telomere dysfunction was implicated in the evolution of complex karyotypes by the presence of anaphase bridges, telomere associations, and dicentric chromosomes. These results show that complex karyotypes can evolve in TP53-competent cells and provide evidence that p16INK4a functions as a gatekeeper to prevent telomere-driven cytogenetic evolution. These investigations provide new insight to the role of p16INK4a as a tumor suppressor. (Cancer Res 2006; 66(22): 10691-700)
Successful Skin Homografts After the Administration of High Dosage X Radiation and Homologous Bone Marrow
Authors: Joan Michel Main, Richmond T. Prehn
Journal: JNCI Journal of the National Cancer Institute (1955)

Journal Article Successful Skin Homografts After the Administration of High Dosage X Radiation and Homologous Bone Marrow Get access Joan Michel Main, Joan Michel Main National Cancer Institute,3Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar Richmond T. Prehn Richmond T. Prehn National Cancer Institute,3Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 15, Issue 4, February 1955, Pages 1023–1029, https://doi.org/10.1093/jnci/15.4.1023 Published: 01 February 1955 Article history Received: 25 October 1954 Published: 01 February 1955
Continuously proliferating allospecific T cells. I. Specificity of cooperation with allogeneic B cells in the humoral antibody response to sheep erythrocytes.
Authors: J D Waterfield, G Dennert, S L Swain, R W Dutton
Journal: The Journal of Experimental Medicine (1979)

Allospecific mouse T cells, positively selected in one-way mixed lymphocyte culture were maintained for 3 yr in tissue culture by sequential restimulation. Such proliferating T cells were tested for their ability to induce a positive allogeneic effect: activating B cells in an in vitro primary humoral response to sheep erythrocytes. It was found that such T lymphocytes could function as helper cells. Helper activity was shown to be specific in that the B cells activated had to share major histocompatibility complex (H-2) antigens with the strain used for selection of the cell line. Intra H-2 mapping showed that antigens coded in the IAk subregion played an important role in the induction of the positive allogeneic effect. Supernatant factors could substitute for the allogeneic T cells in activation of the in vitro humoral response. However, such supernates exhibited no strain specificity. Therefore, the specificity seen in the positive allogeneic effect is presumably a consequence of the alloantigenic recognition receptors intrinsic to the T cells, and not to any biologically restricting properties of the allogeneic effect factor itself.
Risk of Venous Thromboembolism With the Angiogenesis Inhibitor Bevacizumab in Cancer Patients
Authors: Shobha Rani Nalluri, David Chu, Roger Keresztes, Xiaolei Zhu, Shenhong Wu
Journal: JAMA (2008)

<h3>Context</h3>Venous thromboembolism is one of the leading causes of morbidity and mortality in patients with cancer. Concerns have arisen regarding the risk of venous thromboembolism with the novel antiangiogenic agent bevacizumab, a recombinant humanized monoclonal antibody to vascular endothelial growth factor that is widely used in cancer treatment. Currently, the role of bevacizumab in venous thromboembolism is controversial.<h3>Objective</h3>To assess the overall risk of venous thromboembolism associated with the use of bevacizumab, a systematic review and meta-analysis of published randomized controlled trials was performed.<h3>Data Sources</h3>The databases of PubMed and Web of Science were searched for articles published in the English language from January 1966 until January 2008 and abstracts presented at American Society of Clinical Oncology conferences held between January 2000 and January 2008 were searched to identify relevant clinical trials.<h3>Study Selection and Data Extraction</h3>Eligible studies included prospective randomized controlled trials in which standard antineoplastic therapy was used with and without bevacizumab and data on venous thromboembolism were available. Summary incidence rates, relative risks (RRs), and 95% confidence intervals (CIs) were calculated using random-effects or fixed-effects models based on the heterogeneity of included studies.<h3>Data Synthesis</h3>A total of 7956 patients with a variety of advanced solid tumors from 15 randomized controlled trials were identified and included for analysis. Among those patients receiving bevacizumab, the summary incidences of all-grade and high-grade venous thromboembolism were 11.9% (95% CI, 6.8%-19.9%) and 6.3% (95% CI, 4.8%-8.3%), respectively. Patients treated with bevacizumab had a significantly increased risk of venous thromboembolism with an RR of 1.33 (95% CI, 1.13-1.56; P &lt; .001) compared with controls. The risk was significantly increased for both all-grade and high-grade venous thromboembolism. In addition, the risk was similarly increased for bevacizumab at 2.5 mg/kg per week (low dose; RR, 1.31 [95% CI, 1.08-1.60]; P = .007) and 5 mg/kg per week (high dose; RR, 1.31 [95% CI, 1.02-1.68]; P = .04).<h3>Conclusion</h3>The use of bevacizumab was significantly associated with an increased risk of developing venous thromboembolism in cancer patients receiving this drug.
Persistent Activation of a Swelling-Activated Cation Current in Ventricular Myocytes From Dogs With Tachycardia-Induced Congestive Heart Failure
Authors: Henry F. Clemo, Bruce S. Stambler, Clive M. Baumgarten
Journal: Circulation Research (1998)

Abstract —The hypothesis that cellular hypertrophy in congestive heart failure (CHF) modulates mechanosensitive (ie, swelling- or stretch-activated) channels was tested. Digital video microscopy and amphotericin–perforated-patch voltage clamp were used to measure cell volume and ion currents in ventricular myocytes isolated from normal dogs and dogs with rapid ventricular pacing–induced CHF. In normal myocytes, osmotic swelling in 0.9× to 0.6× isosmotic solution (296 mOsm/L) was required to elicit an inwardly rectifying swelling-activated cation current ( I Cir,swell ) that reversed near –60 mV and was inhibited by 10 μmol/L Gd 3+ , a mechanosensitive channel blocker. Block of I Cir,swell by Gd 3+ simultaneously reduced the volume of normal cells in hyposmotic solutions by up to ≈10%, but Gd 3+ had no effect on volume in isosmotic solution. In contrast, I Cir,swell was persistently activated under isosmotic conditions in CHF myocytes, and Gd 3+ decreased cell volume by ≈8%. Osmotic shrinkage in 1.1× to 1.5× isosmotic solution inhibited both I Cir,swell and Gd 3+ -induced cell shrinkage in CHF cells, whereas osmotic swelling only slightly increased I Cir,swell . The K 0.5 and Hill coefficient for Gd 3+ block of I Cir,swell and Gd 3+ -induced cell shrinkage were estimated as ≈2.0 μmol/L and ≈1.9, respectively, for both normal and CHF cells. In both groups, the effects of Gd 3+ on current and volume were blocked by replacing bath Na + and K + and were linearly related with varying Gd 3+ concentration and the degree of cell swelling. CHF thus altered the set point for and caused persistent activation of I Cir,swell . This current may contribute to dysrhythmias, hypertrophy, and altered contractile function in CHF and may be a novel target for therapy.
Huygens versus Fermat: No clear winner
Authors: Paul J. H. Schoemaker
Journal: Behavioral and Brain Sciences (2003)

How should we assess the appeal of multiple scientific theories when they can all explain a particular empirical phenomenon of interest? We contrast Huygens' and Fermat's explanations of the law of refraction of light and find that neither dominates the other when considering multiple criteria for assessing the overall appeal of a scientific theory. The absence of teleology in Huygens' account is a strong plus compared to Fermat's. But Huygens' wave theory scores less well with respect to other desiderata for a scientific theory. In this case, there does not appear to be a clear winner, nor need there be one.
Myocardial sarcolemmal ATPase in dogs with induced mitral insufficiency
Authors: J. C. KHATTER, K. PRASAD
Journal: Cardiovascular Research (1976)

Journal Article Myocardial sarcolemmal ATPase in dogs with induced mitral insufficiency Get access J. C. KHATTER, J. C. KHATTER From the Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Sask S7N 0W0, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar K. PRASAD K. PRASAD From the Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Sask S7N 0W0, Canada Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 10, Issue 6, November 1976, Pages 637–641, https://doi.org/10.1093/cvr/10.6.637 Published: 01 November 1976
Co-polysomy of chromosome 1q and 19p predicts worse prognosis in 1p/19q codeleted oligodendroglial tumors: FISH analysis of 148 consecutive cases
Authors: X. Ren, H. Jiang, X. Cui, Y. Cui, J. Ma, Z. Jiang, D. Sui, S. Lin
Journal: Neuro-Oncology (2013)

This study aimed to evaluate the prognostic significance of co-polsomy of chromosome 1q and 19p in 1p/19q codeleted oligodendroglial tumors (ODGs). In a series of 148 ODGs with 1p/19q deletion, co-polysomy of 1q and 19p was detected by fluorescence in situ hybridization (FISH). Log-rank analysis and Cox regression methods were used to compare Kaplan–Meier plots and identify factors associated with worse prognosis. There were 104 (70.3%) low-grade ODGs and 44 (29.7%) high-grade ODGs. Co-polysomy was independently associated with shorter progression-free survival and overall survival in 1p/19q codeleted ODGs, irrespective of tumor grades. The odds ratio of without and with co-polysomy was 0.263 (95% confidence interval [CI], 0.089–0.771; P = .015) for progression-free survival and 0.213 (95% CI, 0.060–0.756; P = .017) for overall survival. Subgroup analysis confirmed this trend in both low-grade and high-grade ODGs, although the P value for high-grade ODGs was marginally significant. Co-polysomy of 1q and 19p could be used as a marker to independently predict worse prognoses and guide individual therapy in 1p/19q codeleted ODGs.
A case of agnogenic myeloid metaplasia evolving into acute myelogenous leukemia associated with the development of trisomy 11 in bone marrow cells
Authors: Chi V. Dang, Peter H. Stein, Daryl R. Gress, Gina A. Dallabetta, Walter L. Bender
Journal: American Journal of Hematology (1985)

Abstract An 83‐year‐old woman who had a 5‐year history of agnogenic myeloid metaplasia and a previous normal marrow cell karyotype presented with acute myelogenous leukemia (AML) associated with the development of trisomy 11 in 100% of cultured marrow cells. Isolated trisomy 11 in marrow cells has been reported previously in five cases of AML, suggesting that trisomy 11 is a nonrandom chromosomal aberration associated with AML.
Inhibition of Toll-Like Receptor-7 (TLR-7) or TLR-7 plus TLR-9 Attenuates Glomerulonephritis and Lung Injury in Experimental Lupus
Authors: Rahul D. Pawar, Allam Ramanjaneyulu, Onkar P. Kulkarni, Maciej Lech, Stephan Segerer, Hans-Joachim Anders
Journal: Journal of the American Society of Nephrology (2007)

Small nuclear RNA and associated lupus autoantigens activate B cells and dendritic cells via Toll-like receptor-7 (TLR-7); therefore, TLR-7 may represent a potential therapeutic target in lupus. MRL lpr mice were administered an injection of either saline or synthetic oligodeoxynucleotides with immunoregulatory sequences (IRS) that specifically block signaling via TLR-7 (IRS 661) or via TLR-7 and TLR-9 (IRS 954, which uses a active sequence from IRS 661 along with a TLR-9 inhibitory sequence) from weeks 11 to 24 of age. IRS 661 and IRS 954 both significantly reduced the weight of spleen and lymph nodes as well as serum levels of TNF as compared with saline-treated MRL lpr mice. Only IRS 661 but not IRS 954 significantly reduced serum levels of IL-12p40, anti-dsDNA IgG(2a), IgG(2b), and anti-Smith IgG. Both IRS localized to the kidney after intraperitoneal injection and significantly improved the activity index and chronicity index for lupus nephritis in MRL lpr mice. This was associated with significant reduction of renal glomerular and interstitial macrophage infiltrates and the number of interstitial T cells. Autoimmune lung injury was also attenuated with IRS 661 and IRS 954. These data demonstrate that TLR-7 antagonism, initiated after the onset of autoimmunity, can prevent autoimmune kidney and lung injury in MRL lpr mice. Concomitant blockade of TLR-9 with IRS 954 neutralized the effect of TLR-7 blockade on dsDNA IgG(2a), dsDNA IgG(2b), and Smith antigen autoantibodies but had neither additive nor opposing effects on autoimmune lung and kidney injury. Hence, TLR-7 is proposed as a novel and potential therapeutic target in systemic lupus erythematosus.
Autoregulatory Responses of Cat Mesenteric Arterioles Measured in Vivo
Authors: PAUL C. JOHNSON
Journal: Circulation Research (1968)

The purpose of these studies was to measure changes in the diameter of arterioles as large-artery pressure was varied. Changes in diameter were measured with a flying spot microscope in blood vessels of the mesentery of anesthetized cats. Arterial pressure was reduced in a single step and held at a constant level until the change in the diameter was complete. In experiments on 34 arterioles, 10 vessels showed a simple decrease in diameter as pressure was reduced; 24 showed a biphasic response. In the latter group the vessel narrowed for the first 5 to 15 seconds, but after this time an autoregulatory response occurred and the vessel dilated. In 12 of these vessels the diameter became larger in hypotension than it had been at normal arterial pressure. When pressure was suddenly restored, the vessel dilated further but returned to the control size as the autoregulatory response occurred. Analysis of the findings suggests that conditions of stability are satisfied in various portions of the pressure range.
Test-Firing Ammunition for Spliceosome Inhibition in Cancer
Authors: Scott M. Dehm
Journal: Clinical Cancer Research (2013)

E7107 is a derivative of the pladienolide family of natural product spliceosome inhibitors, which targets the U2 small nuclear ribonucleoprotein (snRNP) subunit SF3b. The results of a first-in-human trial with E7107 have been reported, representing an important translational step toward the goal of modulating RNA splicing for cancer therapy. Clin Cancer Res; 19(22); 6064-6. ©2013 AACR.
A general chemotherapy myelotoxicity score to predict febrile neutropenia in hematological malignancies
Authors: M. Moreau, J. Klastersky, A. Schwarzbold, F. Muanza, A. Georgala, M. Aoun, A. Loizidou, M. Barette, S. Costantini, M. Delmelle, L. Dubreucq, M. Vekemans, A. Ferrant, D. Bron, M. Paesmans
Journal: Annals of Oncology (2009)
Left ventricular function following attempted surgical repair of tetralogy of Fallot.
Authors: A P Rocchini, J F Keane, M D Freed, A R Castaneda, A S Nadas
Journal: Circulation (1978)

Left ventricular function was assessed by angiographic methods in 40 patients (ages 3-27), 1-12 years following repair of tetralogy of Fallot. Twenty of the 40 patients (group A) had a satisfactory repair with a pulmonary-systemic flow ratio (Qp/Qs) less then or equal to 1.5 and a right ventricular systolic pressure of less than or equal to 60% of the left ventricular value. The other 20 patients (group B) had a Qp/Qs greater than 1.5 and/or a right ventricular systolic pressure greater than 60% of the left ventricular value. Group A patients had a normal left ventricular end-diastolic volume (LVEDV), end-diastolic pressure (LVEDP), ejection fraction (LVEF), and mass (LVM), while the group B patients had significantly elevated LVEDV, LVEDP, LVM, and a significantly depressed LVEF. These findings indicate that patients with a satisfactory hemodynamic repair of tetralogy of Fallot have normal left ventricular function while patients with postoperative unsatisfactory hemodynamics have significantly impaired left ventricular function.
Expression of Mutated <i>IGHV3-23</i> Genes in Chronic Lymphocytic Leukemia Identifies a Disease Subset with Peculiar Clinical and Biological Features
Authors: Riccardo Bomben, Michele Dal-Bo, Dania Benedetti, Daniela Capello, Francesco Forconi, Daniela Marconi, Francesco Bertoni, Rossana Maffei, Luca Laurenti, Davide Rossi, Maria Ilaria Del Principe, Fabrizio Luciano, Elisa Sozzi, Ilaria Cattarossi, Antonella Zucchetto, Francesca Maria Rossi, Pietro Bulian, Emanuele Zucca, Milena S. Nicoloso, Massimo Degan, Roberto Marasca, Dimitar G. Efremov, Giovanni Del Poeta, Gianluca Gaidano, Valter Gattei
Journal: Clinical Cancer Research (2010)

B-cell chronic lymphocytic leukemia (CLL) is a clinically heterogeneous disease whose outcome can be foreseen by investigating the mutational status of immunoglobulin heavy chain variable (IGHV) genes. Moreover, a different prognosis was reported for CLL expressing specific IGHV genes in the context or not of stereotyped B-cell receptors. Here we investigated novel associations between usage of specific IGHV genes and clinical features in CLL.Among 1,426 CLL-specific IG-rearrangements, stereotyped B-cell receptor clusters never utilized the IGHV3-23 gene. Given this notion, this study was aimed at characterizing the IGHV3-23 gene in CLL, and identifying the properties of IGHV3-23-expressing CLL.IGHV3-23 was the second most frequently used (134 of 1,426) and usually mutated (M; 109 of 134) IGHV gene in our CLL series. In the vast majority of M IGHV3-23 sequences, the configuration of the 13 amino acids involved in superantigen recognition was consistent with superantigen binding. Clinically, M IGHV3-23 CLL had shorter time-to-treatment than other M non-IGHV3-23 CLL, and multivariate analyses selected IGHV3-23 gene usage, Rai staging, and chromosomal abnormalities as independent prognosticators for M CLL. Compared with M non-IGHV3-23 CLL, the gene expression profile of M IGHV3-23 CLL was deprived in genes, including the growth/tumor suppressor genes PDCD4, TIA1, and RASSF5, whose downregulation is under control of miR-15a and miR-16-1. Accordingly, relatively higher levels of miR-15a and miR-16-1 were found in M IGHV3-23 compared with M non-IGHV3-23 CLL.Altogether, expression of the IGHV3-23 gene characterizes a CLL subset with distinct clinical and biological features.