tbuckley/cabot-search huggingface dataset:
Colonoscopy for Small Adenomas
Authors: Michael B. Wallace
Journal: Annals of Internal Medicine (1999)

Letters20 April 1999Colonoscopy for Small AdenomasNorton J. Greenberger, MDNorton J. Greenberger, MDUniversity of Kansas Medical Center; Kansas City, KS 66160 (Greenberger)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-130-8-199904200-00010 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Hurowitz and Stubbs raise the question of suitable management for patients known to have small polyps (≤ 5 mm) on flexible sigmoidoscopy. Controversy continues to surround management of patients who have a small tubular adenoma on screening flexible sigmoidoscopy and whether they should undergo colonoscopy of the proximal colon. It is not only the size of a polyp but also the underlying histologic characteristics that should determine appropriate management. Most authorities consider polyps to have advanced features if the polyps are greater than 1.0 cm or if they have a villous or tubulovillous structure. The seemingly disparate results ...References1. Read TE, Read JD, Butterly LF. Importance of adenomas 5 mm or less in diameter that are detected by sigmoidoscopy. N Engl J Med. 1997;336:8-12. CrossrefMedlineGoogle Scholar2. Wallace MB, Kemp JA, Trnka WM, Donovan JM, Farraye FA. Is colonoscopy indicated for small adenomas found by screening flexible sigmoidoscopy? Ann Intern Med. 1998;129:273-8. LinkGoogle Scholar3. Zarchy T, Ershoff D. Do characteristics of adenomas on flexible sigmoidoscopy predict advanced lesions on baseline colonoscopy? Gastroenterology. 1994;106:1501-4. CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAuthors: Norton J. Greenberger, MDAffiliations: University of Kansas Medical Center; Kansas City, KS 66160 (Greenberger) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoIs Colonoscopy Indicated for Small Adenomas Found by Screening Flexible Sigmoidoscopy? Michael B. Wallace , James Alan Kemp , Yvona M. Trnka , Joanne M. Donovan , and Francis A. Farraye Colonoscopy for Small Adenomas Michael B. Wallace , Francis A. Farraye , and James Alan Kemp Colonoscopy for Small Adenomas James C. Hurowitz Colonoscopy for Small Adenomas Kenneth W. Stubbs Colonoscopy for Small Adenomas Thomas E. Read , Julie D. Read , and Lynn F. Butterly Metrics Cited byScreening colonoscopy: option or preference?Screening flexible sigmoidoscopy: Effectiveness is not enough 20 April 1999Volume 130, Issue 8Page: 701KeywordsAdenomasColonColonoscopyFlexible sigmoidoscopyLesions ePublished: 15 August 2000 Issue Published: 20 April 1999 Copyright & PermissionsCopyright © 1999 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Bacterial adaptation to the gut environment favors successful colonization
Authors: Enea Rezzonico, Renaud Mestdagh, Michèle Delley, Séverine Combremont, Marc-Emmanuel Dumas, Elaine Holmes, Jeremy Nicholson, Rodrigo Bibiloni
Journal: Gut Microbes (2011)

Rodent models harboring a simple yet functional human intestinal microbiota provide a valuable tool to study the relationships between mammals and their bacterial inhabitants. In this study, we aimed to develop a simplified gnotobiotic mouse model containing 10 easy-to-grow bacteria, readily available from culture repositories, and of known genome sequence, that overall reflect the dominant commensal bacterial makeup found in adult human feces. We observed that merely inoculating a mix of fresh bacterial cultures into ex-germ free mice did not guarantee a successful intestinal colonization of the entire bacterial set, as mice inoculated simultaneously with all strains only harbored 3 after 21 d. Therefore, several inoculation procedures were tested and levels of individual strains were quantified using molecular tools. Best results were obtained by inoculating single bacterial strains into individual animals followed by an interval of two weeks before allowing the animals to socialize to exchange their commensal microbes. Through this procedure, animals were colonized with almost the complete bacterial set (9/10). Differences in the intestinal composition were also reflected in the urine and plasma metabolic profiles, where changes in lipids, SCFA, and amino acids were observed. We conclude that adaptation of bacterial strains to the host's gut environment (mono-colonization) may predict a successful establishment of a more complex microbiota in rodents.
Survival After Multiple Hospitalizations for Infections and Dehydration in Nursing Home Residents With Advanced Cognitive Impairment
Authors: Joan M. Teno, Pedro Gozalo, Susan L. Mitchell, Denise Tyler, Vincent Mor
Journal: JAMA (2013)

Multiple hospitalizations for complications from a terminal illness may be burdensome for elderly patients and reflect poor quality care.Infections and eating problems are 2 such complications characterizing the final stage of dementia. 1In a previous study, 1 burdensome health care transitions were defined as 2 or more hospitalizations for infections or dehydration during the last 90 days of life in nursing home (NH) residents with advanced cognitive impairment.The objective of this study was to examine a related issue: whether the occurrence of multiple hospitalizations for these complications was associated with survival. MethodsThe study population was identified using data from the national Minimum Data Set repository, 2 which includes standardized assessments regularly completed by staff on all NH residents in the United States between January 1, 2000, and December 31, 2008.We identified the first baseline assessment in which a resident had a Cognitive Performance Score 3 of 4, 5, or 6, indicating moderate to very severe cognitive impairment.
Airway versus transbronchial biopsy and BAL in lung transplant recipients: different but complementary
Authors: C Ward, GI Snell, B Orsida, L Zheng, TJ Williams, EH Walters
Journal: European Respiratory Journal (1997)

Lung transplantation is now an established therapeutic intervention for end-stage cardiopulmonary disease in humans. Chronic rejection, in the form of bronchiolitis obliterans syndrome (BOS), remains the commonest cause of morbidity and mortality in those surviving more than 3 months. The pathology of BOS involves airway changes. We have evaluated the potential for endobronchial biopsies (EBB) to complement existing sampling methods used in allograft monitoring and have compared the results of EBB findings with those of bronchoalveolar lavage (BAL) and transbronchial biopsy (TBB) in 18 clinically stable patients. We found that all the EBB had inflammatory cells present but that only five TBB specimens had evidence of inflammation, with airway material being present in 78% of the TBB. Paired BAL and EBB yielded different results, with no correlations between total macrophages, lymphocytes, CD4+ cells or CD8+ cells. We conclude that endobronchial biopsies are potentially useful as an additional sample for the monitoring of inflammation in lung allografts, since they yield different, and potentially complimentary, information to bronchoalveolar lavage and transbronchial biopsy.
The Molecular Biology of Laron Dwarfism and Medullary Thyroid Cancer
Authors: Charles E. Jackson, Robert A. Norum
Journal: New England Journal of Medicine (1989)

TWO elegant studies reported in this issue of the Journal 1 , 2 demonstrate the value of collaboration between clinicians and molecular biologists in applying the newer techniques of DNA analysis that increasingly permit us to understand disease at the molecular level. The studies of Amselem et al.1 on Laron-type dwarfism required accurate clinical diagnosis in patients of short stature who had high plasma levels of growth hormone and low levels of insulin-like growth factor I. Similarly, the linkage results in multiple endocrine neoplasia type 2a that are the basis of the screening reported by Sobol et al.2 depended on accurate clinical diagnosis . . .
Growth factor-dependent initiation of DNA replication in nuclei isolated from an interleukin 3-dependent murine myeloid cell line.
Authors: N C Munshi, T G Gabig
Journal: Journal of Clinical Investigation (1990)

To study the proliferative response of hematopoietic cells to growth factors at the molecular level, we developed a cell-free system for growth factor-dependent initiation of genomic DNA replication. Nuclei were isolated from the IL-3-dependent cell line NFS/N1-H7 after a 10-h period of IL-3 deprivation. Cytosolic and membrane-containing subcellular fractions were prepared from proliferating NFS/N1-H7 cells. Nuclei from the nonproliferating cells (+/- IL-3) showed essentially no incorporation of [3H]thymidine during a 16-h incubation with a mixture of unlabeled GTP, ATP, UTP, CTP, dGTP, dATP, dCTP, and [3H]dTTP. When the combination of IL-3, a cytosolic fraction, and a membrane-containing fraction from proliferating cells was added to nuclei from nonproliferating cells, a burst of [3H]thymidine incorporation into DNA began after a 12-h lag period, attained a maximal rate at 16 h, and reached a level of 860 pmol thymidine/10(6) nuclei at 24 h (corresponding to replication of approximately 56% total mouse genomic DNA). This DNA synthesis was inhibited approximately 90% by the specific DNA polymerase alpha inhibitor aphidicolin. Deletion of a single cellular component or IL-3 from the system resulted in a marked reduction of DNA replication (-membrane, 80 +/- 4%; -cytosol, 90% +/- 4%; -IL-3, 74 +/- 7% inhibition). This model requires a growth factor (IL-3), a sedimentable cell fraction containing its receptor and possibly additional membrane-associated components, and a cytosolic fraction. It appears to recapitulate the molecular events required for progression from early G1 to S phase of the cell cycle induced by IL-3 binding to its receptor.
Changing the Evaluation of Future Physicians—Reply
Authors: Rodrigo B. Cavalcanti
Journal: JAMA (2011)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Beware of Cells Bearing Gifts
Authors: Samuel C. Dudley
Journal: Circulation Research (2005)

eart failure is a major worldwide health problem that is growing in prevalence despite recent treatment advances.Patients with heart failure ultimately die from either pump failure or cardiac arrhythmia, and there is a link between the degree of contractile dysfunction and arrhythmic risk.Since the 1960s, the definitive therapy for heart failure has been cardiac transplantation, but the limited supply of organs has restricted the impact of this therapy.Starting in the mid-1990s, a series of observations has led to the concept that cells might be used to repair myocardial damage.Subsequently, this therapy has shown promise in ischemic and nonischemic forms of myocardial injury.
Expression of ras oncogenes in cultured human cells alters the transcriptional and posttranscriptional regulation of cytokine genes.
Authors: G D Demetri, T J Ernst, E S Pratt, B W Zenzie, J G Rheinwald, J D Griffin
Journal: Journal of Clinical Investigation (1990)

Autonomous production of cytokines such as the hematopoietic colony-stimulating factors (CSFs), IL-1, or IL-6 has been demonstrated in numerous human and murine neoplasms, and may be involved in the pathogenesis of several paraneoplastic syndromes such as leukocytosis, fever, and hypercalcemia. Because of the high frequency with which mutations in ras protooncogenes have been detected in human tumors, as well as evidence linking ras gene products to activation of certain cellular functions, we investigated whether ras mutations might influence the regulation of cytokine genes. Normal human fibroblasts transfected with a mutant val12 H-ras oncogene expressed increased levels of mRNA transcripts encoding granulocyte-CSF (G-CSF), granulocyte-macrophage-CSF (GM-CSF), and IL-1 beta compared with controls. Human mesothelioma cells transfected with a mutant asp12 N-ras oncogene exhibited similar alterations in cytokine gene expression. Estimates of transcriptional activity by nuclear run-on analysis revealed a selective increase in transcription only for the IL-1 gene. Analysis of mRNA half-life demonstrated a marked increase in the stability of numerous cytokine transcripts, including G-CSF, GM-CSF, IL-1, and IL-6. The addition of anti-IL-1 neutralizing antibody to cultures of cells expressing ras mutants did not block the expression of any of the cytokines examined, suggesting that the baseline expression of GM-CSF, G-CSF, and IL-6 was not a secondary event due to the increased transcription of IL-1. These results indicate that mutations in ras genes may alter expression of several cytokine genes through both transcriptional and posttranscriptional mechanisms.
Abstract 3418: Characterization of a survival pathway controlled by FGFR4 in alveolar Rhabdomyosarcoma
Authors: Marco Wachtel, Beat Schäfer
Journal: Cancer Research (2010)

Abstract The inefficiency of the currently used conventional treatment modalities for alveolar Rhabdomyosarcoma (aRMS) stimulate the search for alternative treatment approaches such as targeted therapies exploiting addiction of tumors cells to specific signalling pathways. Indeed, inhibition of specific nodal points in such pathways such as growth factor receptors (e.g. IGF1R) was effective in preclinical model systems of aRMS and might advance to early clinical studies. However, experience from clinical studies of adult tumors suggests that tumor cells can escape such therapies targeting solely one signalling molecule via (re)activation of alternative pathways. Therefore, the evolution of tumor resistance needs to be addressed already in preclinical studies and might then be targeted upfront by employing an evidence-based combination approach. Here, we describe a FGFR regulated survival pathway which is able to rescue aRMS cells from apoptosis induced by blocking other growth factor pathways. The relevant receptor is FGFR4, a direct target of the oncogenic PAX3/FKHR fusion protein, whose activation efficiently blocks apoptosis induced by an IGF1R inhibitor in different aRMS cell lines. On the other hand, combined inhibition of both FGFR4 and IGF1R pathways synergistically reduces aRMS cell viability, involving upregulation of Bcl-xl. Interestingly, the survival pathway downstream of FGFR4 does neither involve MEK/ERK nor Akt. Experiments defining the components of this pathway using genetic siRNA screens are currently underway. Taken together, our data hint to a potential escape mechanism of tumor cells from therapies targeting the IGF1R/AKT axis via FGFR4 and suggests that combined inhibition of the FGFR4 and IGF1R pathways might be superior to single treatments. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3418.
Allogeneic transplantation improves the overall and progression-free survival of Hodgkin lymphoma patients relapsing after autologous transplantation: a retrospective study based on the time of HLA typing and donor availability
Authors: Barbara Sarina, Luca Castagna, Lucia Farina, Francesca Patriarca, Fabio Benedetti, Angelo M. Carella, Michele Falda, Stefano Guidi, Fabio Ciceri, Alessandro Bonini, Samantha Ferrari, Michele Malagola, Enrico Morello, Giuseppe Milone, Benedetto Bruno, Nicola Mordini, Simonetta Viviani, Alessandro Levis, Laura Giordano, Armando Santoro, Paolo Corradini
Journal: Blood (2010)
Strategy for the assessment of neurobehavioral consequences of environmental factors.
Authors: H A Tilson, P A Cabe
Journal: Environmental Health Perspectives (1978)

One of the critical issues confronting the evolving discipline of behavioral and neurological toxicology is the general lack of test validation in animal models. This paper seeks to provide a strategy aimed at resolving this important problem. It is proposed that test validation be accomplished by evaluating known neurotoxins in a battery of tests chosen to assess in animal models a wide range of effects on the basis of reported human toxicosis symptomatology. We propose to measure ongoing home cage motor activity, food consumption, water consumption, clay consumption (and the diurnal cycling of these), neurological/physiological indices (reflexes, autonomic signs, equilibrium/gait, balance, tremor, reactivity, and muscular strength), and aspects of cognitive and associative behavior involving both endogenous and exogenous (sensory) control of responding. An integrated, time-efficient scheme, covering 90 days of chemical treatment and 30 days of post-dosing recovery will be used. Chemical substances to be evaluated were chosen with the view of representing classes of neurotoxic effects. For initial study, triethyltin was chosen as an agent producing demyelination of nerves, acrylamide as an agent producing "dying-back" neuropathy, and methylmercury as an agent producing mixed central and peripheral neuropathies. Agents which attack specific loci in the nervous system and those producing anoxia will not be assessed in the first stages of this research due to lack of species generality of known effects, present lack of appropriate exposure facilities, or other problems. In addition, two drugs (amphetamine and sodium salicylate) will be investigated to support the generality of the testing procedures. By comparing the observed results of the neurotoxins in the animal models with the predicted effects based on reported human symptomatology, some decision concerning the validity of each procedure will be made. It is expected that the validation of tests to be used in behavioral and neurological toxicology will permit the meaningful assessment of more complex issues, such as the mechanisms by which neurotoxins act.
Coagulation Blockade Prevents Sepsis-induced Respiratory and Renal Failure in Baboons
Authors: KAREN E. WELTY-WOLF, MARTHA S. CARRAWAY, DEBRA L. MILLER, THOMAS L. ORTEL, MIRELLA EZBAN, ANDREW J. GHIO, STEVEN IDELL, CLAUDE A. PIANTADOSI
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

Sepsis-induced tissue factor (TF) expression activates coagulation in the lung and leads to a procoagulant environment, which results in fibrin deposition and potentiates inflammation. We hypothesized that preventing initiation of coagulation at TF–Factor VIIa (FVIIa) complex would block fibrin deposition and control inflammation in sepsis, thereby limiting acute lung injury (ALI) and other organ damage in baboons. A model of ALI was used in which adult baboons were primed with killed Escherichia coli (1 × 109 CFU/kg), and bacteremic sepsis was induced 12 h later by infusion of live E. coli at 1 × 1010 CFU/kg. Animals in the treatment group were given a competitive inhibitor of TF, site-inactivated FVIIa (FVIIai), intravenously at the time of the infusion of live bacteria and monitored physiologically for another 36 h. FVIIai dramatically protected gas exchange and lung compliance, prevented lung edema and pulmonary hypertension, and preserved renal function relative to vehicle (all p < 0.05). Treatment attenuated sepsis-induced fibrinogen depletion (p < 0.01) and decreased systemic proinflammatory cytokine responses, for example, interleukin 6 (p < 0.01). The protective effects of TF blockade in sepsis-induced ALI were confirmed by using tissue factor pathway inhibitor. The results show that TF–FVIIa complex contributes to organ injury in septic primates in part through selective stimulation of proinflammatory cytokine release and fibrin deposition.
Autophagy and senescence in fibrosing cholangiopathies
Authors: Yasuni Nakanuma, Motoko Sasaki, Kenichi Harada
Journal: Journal of Hepatology (2014)

SummaryFibrosing cholangiopathy such as primary sclerosing cholangitis (PSC) and biliary atresia (BA) is characterized by biliary epithelial injuries and concentric fibrous obliteration of the biliary tree together with inflammatory cell infiltration. In these diseases, inappropriate innate immunity is reported to contribute more to bile duct pathology as compared with various aspects of "classical" autoimmune diseases. Primary biliary cirrhosis (PBC) is characterized by chronic cholangitis with bile duct loss and classical autoimmune features. Cellular senescence of cholangiocytes and a senescence-associated secretory phenotype lead to the production of proinflammatory cytokines and chemokines that may modify the milieu of the bile duct and then trigger fibroinflammatory responses in PSC and PBC. Furthermore, deregulated autophagy might be involved in cholangiocyte senescence and possibly in the autoimmune process in PBC, and the deregulated innate immunity against enteric microbes or their products that is associated with cholangiocyte senescence might result in the fibrosing cholangitis that develops in PBC and PSC. In BA, innate immunity against double-stranded RNA viruses might be involved in cholangiocyte apoptosis and also in the development of the epithelial-mesenchymal transition of cholangiocytes that results in fibrous obliteration of bile ducts. These recent advances in the understanding of immune-mediated biliary diseases represent a paradigm shift: the cholangiocyte is no longer viewed merely as a passive victim of injury; it is now also considered to function as a potential effector in bile duct pathology.