tbuckley/cabot-search huggingface dataset:
Long-term proton pump inhibitor administration, H pylori and gastric cancer: lessons from the gerbil
Authors: J. G. Fox, E. J. Kuipers
Journal: Gut (2011)

The association between chronic active gastritis and pre-neoplastic conditions as well as invasive cancer of the stomach was established several decades ago. The risk of progression depended on the severity and distribution of gastritis, with cancer, in particular, occurring in subjects with pan-gastritis. Subsequently, Helicobacter pylori was recognised as the primary cause of chronic active gastritis, and it was demonstrated that the pattern of gastritis corresponded with the colonisation pattern of H pylori . We and others then showed both in animals and in humans that this pattern of colonisation and associated gastritis primarily depended on the level of acid output.1 2 Although this hypothesis was widely accepted, it led to intense debate when dealing with the safety of long-term treatment with profound acid suppressors. An elegant, long-awaited study from Japan published in this issue of Gut ( see page 624 ) provides compelling evidence that the pattern of H pylori colonisation depends on acid output and that this influences the long-term progression to neoplasia.3

The current study was based on experiments in gerbils, one of the well-established animal models for the study gastric disease induced by Helicobacter spp.4 Gerbils, used sparingly for biomedical research, were first reported as a model for experimental H pylori infection in 1991.5 Interestingly, the gerbil has been shown …
Two cases of EGFR mutation-positive lung adenocarcinoma that transformed into squamous cell carcinoma: successful treatment of one case with rociletinib
Authors: K. Haratani, H. Hayashi, S. Watanabe, H. Kaneda, T. Yoshida, M. Takeda, T. Shimizu, K. Nakagawa
Journal: Annals of Oncology (2015)
Neoadjuvant chemotherapy with infusional 5-fluorouracil, adriamycin and cyclophosphamide (iFAC) in locally advanced breast cancer: an early response predicts good prognosis
Authors: Y.W. Moon, S.Y. Rha, H.C. Jeung, W.I. Yang, C.O. Suh, H.C. Chung
Journal: Annals of Oncology (2005)

The aim of this study was to evaluate the efficacy and safety of neoadjuvant chemotherapy with infusional 5-fluorouracil (5-FU), adriamycin and cyclophosphamide (iFAC) in locally advanced breast cancer (LABC).Eighty-two LABC patients were treated with neoadjuvant iFAC chemotherapy including infusional 5-FU (1000 mg/m2, continuous intravenous infusion, days 1-3), adriamycin (40 mg/m2, intravenous bolus, day 1) and cyclophosphamide (600 mg/m2, intravenous bolus, day 1) every 3 weeks until maximum tumor response. Patients subsequently received surgery, adjuvant chemotherapy, radiotherapy and hormonal therapy as appropriate.Downstaging occurred in 71 of the 82 patients (86.6%). Seventy-two patients (67 patients with downstaging and five patients without downstaging) were resectable (resectability rate, 87.8%). The clinical response rate was 84.2%, with a complete response (CR) rate of 17.1% and a pathological CR rate of 7.8%. During 891 cycles of chemotherapy, the most common grade 3/4 hematological toxicity was leukopenia (36.0%). There were no treatment-related deaths. The median follow-up period was 51 months, with a median overall survival (OS) of 66 months, and a 5 year OS rate of 50.9% for all patients. The 5 year OS and disease-free survival (DFS) rates of the 64 patients who underwent surgery were 55.8% and 44.7%, respectively.Neoadjuvant chemotherapy with iFAC had a comparable response rate and DFS to the conventional bolus FAC regimen, with an acceptable toxicity in LABC using the AJCC 2002 staging system. An early response to neoadjuvant iFAC was a favorable prognostic factor.
The adverse influence of pregnancy upon sulphation: a clue to the pathogenesis of intrahepatic cholestasis of pregnancy?
Authors: Mervyn H. Davies, Josephine M. Ngong, Mehmet Yucesoy, Subrat K. Acharya, Charles O. Mills, Judith B. Weaver, Rosemary H. Waring, Elwyn Elias
Journal: Journal of Hepatology (1994)
Mechanisms of Membrane Transport of Folates into Cells and Across Epithelia
Authors: Rongbao Zhao, Ndeye Diop-Bove, Michele Visentin, I. David Goldman
Journal: Annual Review of Nutrition (2011)

Until recently, the transport of folates into cells and across epithelia has been interpreted primarily within the context of two transporters with high affinity and specificity for folates, the reduced folate carrier and the folate receptors. However, there were discrepancies between the properties of these transporters and characteristics of folate transport in many tissues, most notably the intestinal absorption of folates, in terms of pH dependency and substrate specificity. With the recent cloning of the proton-coupled folate transporter (PCFT) and the demonstration that this transporter is mutated in hereditary folate malabsorption, an autosomal recessive disorder, the molecular basis for this low-pH transport activity is now understood. This review focuses on the properties of PCFT and briefly addresses the two other folate-specific transporters along with other facilitative and ATP-binding cassette (ABC) transporters with folate transport activities. The role of these transporters in the vectorial transport of folates across epithelia is considered.
Experimental transmission of duck hepatitis B virus to pekin ducks and to domestic geese
Authors: Patricia L. Marion, John M. Cullen, Roberto R. Azcárraga, Mary Jo Van Davelaar, William S. Robinson
Journal: Hepatology (1987)

We investigated experimental transmission of duck hepatitis B virus to its original host, the domestic Pekin duck, and to three other avian species. Intramuscular injection of a standard inoculum of duck hepatitis B virus into 2- to 5-day-old Pekin ducklings hatched from a duck hepatitis B virus-free flock resulted in viremia in 100% of 107 animals, indicating that duck hepatitis B virus infection of young progeny of a defined duck hepatitis B virus-free flock occurs reproducibly. When the same inoculum was injected into chicks and Muscovy ducklings of the same age, no evidence of viral infection was detectable. In contrast, hatchlings of two domestic breeds of geese were readily infected by duck hepatitis B virus, developing viremia at a slower rate than Pekin ducklings, but a higher average titer of viremia 4 weeks or more after injection. Neither the pattern of restriction enzyme sites in the viral DNA nor the susceptibility of ducklings to the virus were detectably altered after passage in geese. As in duck hepatitis B virus-infected young ducklings, most of the experimentally infected goslings appeared to be persistently infected and those eventually laying eggs transmitted virus to the progeny. While ducklings exhibited a fairly uniform inflammatory response to the virus, duck hepatitis B virus inoculation of the goslings resulted in both inflammation and an altered hepatocellular morphology not seen in uninjected controls. The host range of duck hepatitis B virus appears to be limited to the primary host and a close taxonomic relative, similar to other members of the hepadnavirus family, hepatitis B virus and ground squirrel hepatitis virus.
Insulin Resistance After Renal Transplantation
Authors: Aiko P.J. de Vries, Stephan J.L. Bakker
Journal: Diabetes Care (2002)

Hjelmesaeth et al. (1) have validated the use of seven oral glucose tolerance test (OGTT)-derived insulin sensitivity indexes against the euglycemic-hyperinsulinemic clamp technique in a Caucasian renal transplant population. We agree with the authors that the availability of more cost- and time-efficient surrogate estimates of insulin sensitivity than the euglycemic-hyperinsulinemic clamp would greatly benefit the design of future …
Bilateral rupture of the Achilles tendon in patients on steroid therapy.
Authors: J F Haines
Journal: Annals of the Rheumatic Diseases (1983)

Three patients are presented who sustained bilateral rupture of the Achilles tendon while on systemic steroid therapy for chest disease; a fourth patient with polymyalgia rheumatica on steroids is also presented. This is further evidence that tendon rupture can be a direct complication of steroid treatment. The English-language literature on bilateral Achilles tendon rupture is reviewed.
Regulation of Oxygen Distribution in Tissues by Endothelial Nitric Oxide
Authors: Victor M. Victor, Cristina Nuñez, Pilar D'Ocón, Cormac T. Taylor, Juan V. Esplugues, Salvador Moncada
Journal: Circulation Research (2009)

Nitric oxide (NO) decreases cellular oxygen (O(2)) consumption by competitively inhibiting cytochrome c oxidase. Here, we show that endogenously released endothelial NO, either basal or stimulated, can modulate O(2) consumption both throughout the thickness of conductance vessels and in the microcirculation. Furthermore, we have shown that such modulation regulates O(2) distribution to the surrounding tissues. We have demonstrated these effects by measuring O(2) consumption in blood vessels in a hypoxic chamber and O(2) distribution in the microcirculation using the fluorescent oxygen-probe Ru(phen)(3)(2+). Removal of NO by physical or pharmacological means, or in eNOS(-/-) mice, abolishes this regulatory mechanism. Our results indicate that, in addition to its well-known effect on the regulation of vascular tone, endothelial NO plays a major role in facilitating the distribution of O(2), an action which is crucial for the adaptation of tissues, including the vessel wall itself, to hypoxia. It is possible that changes in the distribution of O(2) throughout the vessel wall may be implicated in the origin of vascular pathologies such as atherosclerosis.
Inhibitory Effect of Yogurt on Ehrlich Ascites Tumor-Cell Proliferation2
Authors: G. V. Reddy, K. M. Shahani, M. R. Banerjee
Journal: JNCI Journal of the National Cancer Institute (1973)

Journal Article Inhibitory Effect of Yogurt on Ehrlich Ascites Tumor-Cell Proliferation Get access G. V. Reddy, G. V. Reddy Department of Food Science and Technology and Institute for Cellular Research, University of Nebraska, Lincoln, Nebraska 68503 Search for other works by this author on: Oxford Academic PubMed Google Scholar K. M. Shahani, K. M. Shahani Department of Food Science and Technology and Institute for Cellular Research, University of Nebraska, Lincoln, Nebraska 68503 Search for other works by this author on: Oxford Academic PubMed Google Scholar M. R. Banerjee M. R. Banerjee Department of Food Science and Technology and Institute for Cellular Research, University of Nebraska, Lincoln, Nebraska 68503 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 50, Issue 3, March 1973, Pages 815–817, https://doi.org/10.1093/jnci/50.3.815 Published: 01 March 1973 Article history Received: 08 November 1972 Accepted: 12 January 1973 Published: 01 March 1973
Metabolic fingerprint of ischaemic cardioprotection: importance of the malate-aspartate shuttle
Authors: T. T. Nielsen, N. B. Stottrup, B. Lofgren, H. E. Botker
Journal: Cardiovascular Research (2011)

The convergence of cardioprotective intracellular signalling pathways to modulate mitochondrial function as an end-target of cytoprotective stimuli is well described. However, our understanding of whether the complementary changes in mitochondrial energy metabolism are secondary responses or inherent mechanisms of ischaemic cardioprotection remains incomplete. In the heart, the malate–aspartate shuttle (MAS) constitutes the primary metabolic pathway for transfer of reducing equivalents from the cytosol into the mitochondria for oxidation. The flux of MAS is tightly linked to the flux of the tricarboxylic acid cycle and the electron transport chain, partly by the amino acid l-glutamate. In addition, emerging evidence suggests the MAS is an important regulator of cytosolic and mitochondrial calcium homeostasis. In the isolated rat heart, inhibition of MAS during ischaemia and early reperfusion by the aminotransferase inhibitor aminooxyacetate induces infarct limitation, improves haemodynamic responses, and modulates glucose metabolism, analogous to effects observed in classical ischaemic preconditioning. On the basis of these findings, the mechanisms through which MAS preserves mitochondrial function and cell survival are reviewed. We conclude that the available evidence is supportive of a down-regulation of mitochondrial respiration during lethal ischaemia with a gradual 'wake-up' during reperfusion as a pivotal feature of ischaemic cardioprotection. Finally, comments on modulating myocardial energy metabolism by the cardioprotective amino acids glutamate and glutamine are given.
Expression of growth factor and chemokine receptors: new insights in the biology of inflammatory breast cancer
Authors: N. Cabioglu, Y. Gong, R. Islam, K.R. Broglio, N. Sneige, A. Sahin, A.M. Gonzalez-Angulo, P. Morandi, C. Bucana, G.N. Hortobagyi, M. Cristofanilli
Journal: Annals of Oncology (2007)
Proteasomal Degradation of Topoisomerase I Is Preceded by c-Jun NH2-Terminal Kinase Activation, Fas Up-Regulation, and Poly(ADP-Ribose) Polymerase Cleavage in SN38-Mediated Cytotoxicity against Multiple Myeloma
Authors: Laurence Catley, Yu-Tzu Tai, Reshma Shringarpure, Renate Burger, Moni Thi Son, Klaus Podar, Pierfrancesco Tassone, Dharminder Chauhan, Teru Hideshima, Louis Denis, Paul Richardson, Nikhil C. Munshi, Kenneth C. Anderson
Journal: Cancer Research (2004)

Abstract Topoisomerase I inhibitors are effective anticancer therapies and have shown activity in hematologic malignancies. Here we show for the first time that SN38, the potent active metabolite of irinotecan, induces c-Jun NH2-terminal kinase activation, Fas up-regulation, and caspase 8-mediated apoptosis in multiple myeloma (MM) cells. Proteasomal degradation of nuclear topoisomerase I has been proposed as a resistance mechanism in solid malignancies. SN38-induced proteasomal degradation of topoisomerase I was observed during SN38-mediated cytotoxicity against MM.1S myeloma cell line but occurred after c-Jun NH2-terminal kinase activation, Fas up-regulation, and poly(ADP-ribose) polymerase cleavage and failed to protect cells from apoptosis. Differential toxicity was observed against MM cells versus bone marrow stromal cells, and SN38 inhibited adhesion-induced up-regulation of MM cell proliferation when MM cells adhere to bone marrow stromal cells. In addition, SN38 directly inhibited constitutive and inducible interleukin 6 and vascular endothelial growth factor secretion by bone marrow stromal cells. Synergy was observed when SN38 was used in combination with doxorubicin, bortezomib, as well as poly(ADP-ribose) polymerase inhibitor NU1025 and Fas-activator CH11. These findings have clinical significance, because identification of downstream apoptotic signaling after topoisomerase I inhibition will both elucidate mechanisms of resistance and optimize future combination chemotherapy against MM.
Relation of Shyness in Grade School Children to the Genotype for the Long Form of the Serotonin Transporter Promoter Region Polymorphism
Authors: Shoshana Arbelle, Jonathan Benjamin, Moshe Golin, Ilana Kremer, Robert H. Belmaker, Richard P. Ebstein
Journal: American Journal of Psychiatry (2003)

Studies have shown that genetic factors are significant in predisposing individuals to shyness and social phobia. Toward further elucidating the genetic structure of shyness, the authors examined four functional polymorphisms that make biological sense for contributing to the development of this phenotype: serotonin transporter promoter region 44 base pair insertion/deletion (5-HTTLPR), dopamine D(4) receptor exon III repeat (DRD4), catechol O-methyltransferase (COMT), and monoamine oxidase A promoter region repeat (MAO(A)).The authors assessed shyness after recruitment of a nonclinical sample (N=118, unscreened second-grade children) using a composite scale derived from questionnaires administered to the children, parents, and teachers. DNA from buccal smears successfully obtained from 98 children was genotyped by polymerase chain reaction methods for the 5-HTTLPR, DRD4, COMT, and MAO(A) polymorphisms.Significant correlations were observed for parents', teachers', and children's ratings of shyness, and Cronbach's alpha reliability was high for all three scales. A significant association was observed between the long 5-HTTLPR polymorphism and shyness, both by the functional classification of Lesch as well as by consideration of all three genotypes. No significant association was observed for the DRD4, COMT, or MAO(A) polymorphisms.This study provisionally identifies a common genetic polymorphism, 5-HTTLPR, that modestly (effect size=7%) contributed to greater shyness scores in a nonclinical group of second-grade students. These first findings may be relevant to previous reports that have shown an association between the 5-HTTLPR long form and obsessive-compulsive disorder and autism.
Waiting list statistics. II: An estimate of inflation of waiting list length.
Authors: A Lee, B Don, M J Goldacre
Journal: BMJ (1987)

The discrepancy between the length of the waiting list and eventual admissions from the waiting list was investigated by comparing data from two different sources of routine statistics in the Oxford region. It was estimated that about 28% of the waiting list comprised patients who were not eventually admitted to hospital within the region.
Large-Scale Coding Sequence Change Underlies the Evolution of Postdevelopmental Novelty in Honey Bees
Authors: William Cameron Jasper, Timothy A. Linksvayer, Joel Atallah, Daniel Friedman, Joanna C. Chiu, Brian R. Johnson
Journal: Molecular Biology and Evolution (2014)

Whether coding or regulatory sequence change is more important to the evolution of phenotypic novelty is one of biology's major unresolved questions. The field of evo–devo has shown that in early development changes to regulatory regions are the dominant mode of genetic change, but whether this extends to the evolution of novel phenotypes in the adult organism is unclear. Here, we conduct ten RNA-Seq experiments across both novel and conserved tissues in the honey bee to determine to what extent postdevelopmental novelty is based on changes to the coding regions of genes. We make several discoveries. First, we show that with respect to novel physiological functions in the adult animal, positively selected tissue-specific genes of high expression underlie novelty by conferring specialized cellular functions. Such genes are often, but not always taxonomically restricted genes (TRGs). We further show that positively selected genes, whether TRGs or conserved genes, are the least connected genes within gene expression networks. Overall, this work suggests that the evo–devo paradigm is limited, and that the evolution of novelty, postdevelopment, follows additional rules. Specifically, evo–devo stresses that high network connectedness (repeated use of the same gene in many contexts) constrains coding sequence change as it would lead to negative pleiotropic effects. Here, we show that in the adult animal, the converse is true: Genes with low network connectedness (TRGs and tissue-specific conserved genes) underlie novel phenotypes by rapidly changing coding sequence to perform new-specialized functions.
Dynamic Mast Cell–Stromal Cell Interactions Promote Growth of Pancreatic Cancer
Authors: Ying Ma, Rosa F. Hwang, Craig D. Logsdon, Stephen E. Ullrich
Journal: Cancer Research (2013)

Pancreatic ductal adenocarcinoma (PDAC) exists in a complex desmoplastic microenvironment, which includes cancer-associated fibroblasts [also known as pancreatic stellate cells (PSC)] and immune cells that provide a fibrotic niche that impedes successful cancer therapy. We have found that mast cells are essential for PDAC tumorigenesis. Whether mast cells contribute to the growth of PDAC and/or PSCs is unknown. Here, we tested the hypothesis that mast cells contribute to the growth of PSCs and tumor cells, thus contributing to PDAC development. Tumor cells promoted mast cell migration. Both tumor cells and PSCs stimulated mast cell activation. Conversely, mast cell-derived interleukin (IL)-13 and tryptase stimulated PSC proliferation. Treating tumor-bearing mice with agents that block mast cell migration and function depressed PDAC growth. Our findings suggest that mast cells exacerbate the cellular and extracellular dynamics of the tumor microenvironment found in PDAC. Therefore, targeting mast cells may inhibit stromal formation and improve therapy.
Nondisjunction of chromosomes leading to hyperdiploid childhood B-cell precursor acute lymphoblastic leukemia is an early event during leukemogenesis
Authors: E. Renate Panzer-Grümayer, Karin Fasching, Simon Panzer, Klaudia Hettinger, Klaus Schmitt, Sylvia Stöckler-Ipsiroglu, Oskar A. Haas
Journal: Blood (2002)
Angiogenesis and Endothelial Cell Repair in Renal Disease and Allograft Rejection
Authors: Marlies E.J. Reinders, Ton J. Rabelink, David M. Briscoe
Journal: Journal of the American Society of Nephrology (2006)

This review discusses the concept that the turnover and replacement of endothelial cells is a major mechanism in the maintenance of vascular integrity within the kidney. CD133+CD34+KDR+ endothelial cell progenitor cells emigrate from the bone marrow and differentiate into CD34+KDR+ expressing cells, which are present in high numbers within the circulation. These progenitor cells are available for recruitment into normal or inflamed tissues to facilitate endothelial cell repair. In several forms of renal disease, proinflammatory insults mediate oxidative stress, senescence, and sloughing of endothelial cells. A lack of growth factors or an inefficient recruitment of endothelial cell progenitors results in hypoxic tissue injury and accelerates the process of chronic renal failure. Augmentation of vascular repair by the provision of growth factors such as vascular endothelial growth factor or by the transfer of progenitor cells directly into the kidney can be protective and prevent ongoing interstitial damage. In allografts, persistent injury results in excessive turnover of graft vascular endothelial cells. Moreover, chronic damage elicits a response that is associated with the recruitment of both leukocytes and endothelial cell progenitors, facilitating an overlapping process of inflammation and angiogenesis. Because the angiogenesis reaction itself is proinflammatory, this process becomes self-sustaining. Collectively, these data indicate that angiogenesis and endothelial cell turnover are important in renal inflammatory processes and allograft rejection. Manipulation of the response may have therapeutic implications to protect against injury and chronic disease processes.