tbuckley/cabot-search huggingface dataset:
Differential Effect of Thioacetamide on Hepatic Methionine Adenosyltransferase Expression in the Rat
Authors: Zong-Zhi Huang, José M. Mato, Gary Kanel, Shelly C. Lu
Journal: Hepatology (1999)

Liver–specific and non-liver–specific methionine adenosyltransferase (MAT) are products of two genes, MAT1A and MAT2A, respectively, that catalyze the formation of S –adenosylmethionine (SAM), the principal methyl donor. Mature liver expresses mainly MAT1A. We showed a switch from MAT1A to MAT2A gene expression in human liver cancer cells that may offer a growth advantage. To gain a better understanding of the chronology and significance of the change in MAT expression, we examined changes in hepatic MAT expression after acute treatment of rats with a hepatocarcinogen, thioacetamide (TAA). TAA treatment for 3 weeks did not change the MAT1A mRNA level but reduced the liver–specific MAT protein level to below 30% of control. TAA also acutely reduced the activity of liver–specific MAT when added to normal liver homogenates. In contrast, both the mRNA and protein levels of non-liver–specific MAT were induced. Because liver–specific MAT exhibits a much higher K m for methionine (mmol/L) than non-liver–specific MAT (≈10 μmol/L), MAT activity was decreased at 5 mmol/L but increased at 20 μmol/L methionine concentration. The SAM level, SAM–to- S –adenosylhomocysteine (SAH) ratio, and DNA methylation all fell during treatment. In summary, TAA treatment induced differential changes in hepatic MAT expression. The reduction in liver–specific MAT protein level represents a novel mechanism of inactivation of liver–specific MAT. This along with induction in MAT2A contributed to a fall in the SAM–to–SAH ratio. The resulting DNA hypomethylation may be important in the process of hepatocarcinogenesis.
Fragmentation of bile duct stones by extracorporeal shock-wave lithotripsy: A five-year experience
Authors: Tilman Sauerbruch, Joseph Holl, Michael Sackmann, Gustav Paumgartner
Journal: Hepatology (1992)

Over 5 yr, 103 elderly patients (mean age = 70 yr) with bile duct stones (mainly not amenable to endoscopic extraction) underwent adjuvant extracorporeal shock-wave lithotripsy using a first-generation kidney lithotripter. Disintegration of stones was achieved after a mean of 1.4 sessions in 92% of the patients. Spontaneous passage of fragments into the duodenum occurred in one fourth of the patients, and endoscopic extraction of fragments was necessary in 75% of the patients, resulting in complete clearance of the bile duct stones in 91 (88%) of 103 patients. The most important adverse effect was septic disease after extracorporeal shock-wave lithotripsy in 4% of the patients. The 30-day mortality rate was 1% (one patient), and another 15 patients died during a mean follow-up of 26 +/- 14 mo (mainly of causes unrelated to biliary tract disease). Two of 91 patients who had been rendered stone free were readmitted because of recurrent stone disease during the follow-up period. Of the 43 patients who still had their gallbladders during extracorporeal shock-wave lithotripsy, 14% subsequently underwent cholecystectomy. These data show that extracorporeal shock-wave lithotripsy of bile duct stones is a useful and safe adjunct to nonsurgical procedures for the removal of calculi in the biliary tree.
From the authors
Authors: J. E. Brussee, H. A. Smit, B. Brunekreef, J. C. de Jongste
Journal: European Respiratory Journal (2005)

Exhaled nitric oxide in 4-year-old children: relationship with asthma and atopyTo the Editors:The paper by BRUSSEE et al. [1] describes the first large survey of the fraction of exhaled nitric oxide (FeNO) in a young population.The authors should be congratulated for undertaking such a study in an age range where great patience and persistence are required to obtain data.
Melanoma in people aged 65 and over.
Authors: C. C. Harland, R. A. Marsden, M. E. Fallowfield
Journal: BMJ (1992)

24 10O.'The difference between this figure and the estimate quoted in my editorial is attributable to the inclusion of additional charges for extended acute hospital care and different assumptions about the life expectancy of survivors (5 v 10 years).Even so, the cost of HA-lA still compares favourably with that of many other widely accepted medical mterventions.
Reforming Medicine: Lessons of the Last Quarter Century
Authors: Odin W. Anderson
Journal: JAMA (1984)

In this book the Sidels continue to coordinate and produce useful articles espousing left liberal ideas to reform the American health services. The book is a sophisticated polemic; the writers have personal experiences in the reform fringe of health services and draw on well-organized supporting data. Many of the 19 contributors were in the middle of the Civil Rights and War on Poverty movements of the latter 1960s. There is new and useful background material that has not been published before, such as community health centers in poverty areas; the urban hospital, particularly Cook County Hospital in Chicago; Medicaid; occupational health and the Occupational Safety and Health Administration; the women's health movement and affirmative action for admission to medical schools; the National Health Service Corps; and the status of the new health professionals, physician assistants, and nurse practitioners. The authors are appalled at the difficulties they personally encountered when attempting
Abstract 5337: The role of Eya3 as a target of EWS/Fli1 in Ewing's sarcoma
Authors: Tyler Robin, Lisa Reaves, Erin Mckinsey, Paul Jedlicka, Heide Ford
Journal: Cancer Research (2011)

Abstract Ewing's sarcoma is an aggressive pediatric bone cancer most commonly affecting patients between 10 and 20 years of age. The vast majority of Ewing's sarcomas harbor a characteristic translocation between chromosomes 11 and 22, encoding the EWS/Fli1 fusion protein. Fli1 is an Ets transcription factor with a DNA-binding domain, whereas the EWS portion of the fusion contributes a transcriptional activation domain. EWS/Fli1 acts as a potent oncogenic transcription factor that is critical in the development of Ewing's sarcoma. EWS/Fli1 knockdown and rescue microarray data suggest that Eya3 may be a downstream target of EWS/Fli1, which we have validated using EWS/Fli1 overexpression and knockdown systems. Eya3 is important in DNA repair, and can interact with the Six family of homeoproteins as a bipartite transcription factor. The Six-Eya complex promotes proliferation and survival to facilitate the proper development of many tissues, but these features can also lead to aggressive cancers when re-expressed in adult tissues. We have shown that Eya3 knockdown in the human tumor-derived Ewing's sarcoma cells line, A673, decreases the rate of proliferation of these cells. Additionally Eya3 knockdown sensitizes Ewing's sarcoma cells to chemotherapeutics currently used to treat Ewing's sarcoma: doxorubicin, etoposide, and vincristine. Furthermore, clonal isolates of A673 Eya3 knockdown cells, expressing very low levels of Eya3, morphologically resemble their presumed cell of origin, the mesenchymal stem cell. These data suggest that Eya3 is an important target of EWS/Fli1 that may serve as a clinically significant novel therapeutic target for the treatment of Ewing's sarcoma patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5337. doi:10.1158/1538-7445.AM2011-5337
Abstract A15: Distinct gene expression profiles in Lynch syndrome-associated ovarian cancer
Authors: Jenny-Maria Jönsson, Katarina Bartuma, Mev Dominguez Valentin, Katja Harbst, Zoreh Ketabi, Susanne Malander, Mats Jönsson, Ana Carneiro, Anna Måsbäck, Göran Jönsson, Mef Nilbert
Journal: Clinical Cancer Research (2013)

Abstract Background: Ovarian cancers linked to Lynch syndrome represent a rare subset that typically present at young age as early-stage tumors with an overrepresentation of endometrioid and clear cell histologies. We aimed to identify molecular profiles of Lynch syndrome-associated ovarian cancer for application in refined diagnostics and targeted therapeutics. Methods: Global gene expression profiling using whole-genome c-DNA-mediated Annealing, Selection, extension, and Ligation (WG-DASL) was applied to 48 histopathologically matched ovarian cancers, which represented Lynch syndrome-associated tumors and sporadic tumors. The results were validated by application of an external ovarian cancer data set and by immunohistochemistry. Results: Lynch syndrome-associated and sporadic ovarian cancers differed by 349 significantly deregulated genes, predominantly involved in the mTOR and MAPK/ERK signaling pathways. Conclusion: The distinct genetic signatures in Lynch syndrome-associated and sporadic ovarian cancers point to different tumorigenic routes and suggest that targets within the mTOR and MAPK/ERK signaling pathways may be relevant to consider for molecular diagnostics and targeted therapeutics. Citation Format: Jenny-Maria Jönsson, Katarina Bartuma, Mev Dominguez Valentin, Katja Harbst, Zoreh Ketabi, Susanne Malander, Mats Jönsson, Ana Carneiro, Anna Måsbäck, Göran Jönsson, Mef Nilbert. Distinct gene expression profiles in Lynch syndrome-associated ovarian cancer. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: From Concept to Clinic; Sep 18-21, 2013; Miami, FL. Philadelphia (PA): AACR; Clin Cancer Res 2013;19(19 Suppl):Abstract nr A15.
Quantitative <b> <i>TP73</i> </b> Transcript Analysis in Hepatocellular Carcinomas
Authors: Thorsten Stiewe, Sebastian Tuve, Martin Peter, Andrea Tannapfel, Ahmet H. Elmaagacli, Brigitte M. Pützer
Journal: Clinical Cancer Research (2004)

Abstract Purpose: The p53 family member p73 displays significant homology to p53, but data from primary tumors demonstrating increased expression levels of p73 in the absence of any gene mutations argue against a classical tumor suppressor function. A detailed analysis of the p73 protein in tumor tissues has revealed expression of two classes of p73 isoforms. Whereas the proapoptotic, full-length, transactivation-competent p73 protein (TA-p73) has a putative tumor suppressor activity similar to p53, the antiapoptotic, NH2-terminally truncated, transactivation-deficient p73 protein (ΔTA-p73) has been shown to possess oncogenic activity. The oncogenic proteins can be generated by the following two different mechanisms: (a) aberrant splicing (p73Δex2, p73Δex2/3, ΔN′-p73) and (b) alternative promoter usage of a second intronic promoter (ΔN-p73). The purpose of our study was to elucidate the origin of ΔTA-p73 isoforms in hepatocellular carcinomas. Experimental Design: We analyzed the underlying mechanisms of p73 overexpression in cancer cells by quantification of p73 transcripts from 10 hepatocellular carcinoma patients using isoform-specific real-time reverse transcription-PCR. Results: Our data demonstrate that only aberrantly spliced ΔTA-p73 transcripts from the TA promoter show significantly increased expression levels in the tumor whereas the ΔN-p73 transcript generated from the second promoter is not significantly up-regulated. Conclusions: Although we only analyzed 10 patient samples the results strongly suggest that the elevated activity of the first promoter (TA promoter) accounts for high-level expression of both full-length TA-p73 and aberrantly spliced ΔTA-p73 isoforms in hepatocellular carcinoma tissues.
Comparative effect of somatostatin-14 and somatostatin-28 on glucagon-induced glycogenolysis from the perfused rat liver
Authors: Michiyo Seno, Yutaka Seino, Tomohiko Taminato, Kinsuke Tsuda, Norikazu Kitano, Jun Takeda, Hirofumi Fukumoto, Gyohan Koh, Hiroo Imura
Journal: Metabolism (1988)
Correction of hypercoagulability and amelioration of pulmonary arterial hypertension by chronic blood transfusion in an asplenic hemoglobin E/β-thalassemia patient
Authors: Vichai Atichartakarn, Suporn Chuncharunee, Pakorn Chandanamattha, Khanchit Likittanasombat, Katcharin Aryurachai
Journal: Blood (2003)
IN VITRO PYRROLE AND PORPHYRIN SYNTHESIS IN LEAD POISONING AND IRON DEFICIENCY*
Authors: Herbert C. Lichtman, Felix Feldman
Journal: Journal of Clinical Investigation (1963)

synthesis was determined in the normal and the lead-poisoned erythrocyte. METHODSBlood was collected with heparin as the anticoagulant and kept at 0°C until incubation.Hemoglobin concen- tration, hematocrit, and erythrocyte, reticulocyte, nucle- ated erythrocyte, and leukocyte counts were determined on each specimen.The plasma was removed and the cells were washed twice with ice-cold 0.85% saline.The
STUDIES ON PNEUMONIA VIRUS OF MICE (PVM) IN CELL CULTURE
Authors: Richard W. Compans, Donald H. Harter, Purnell W. Choppin
Journal: The Journal of Experimental Medicine (1967)

Pneumonia virus of mice (PVM) particles are spheres 80-120 mmicro in diameter, or filaments of similar diameter with lengths up to 3 micro. The particles possess an outer spike-covered envelope and helical internal component 120-150 A in diameter. Virus particles acquire their envelope by a budding process at the cell membrane; mature particles are seen only extracellularly. Dense inclusions are prominent in the cytoplasm of PVM-infected BHK21 cells by 48 hr after inoculation. The inclusions appear to consist of aggregates of the internal component of PVM, and the helical component has been isolated in a cesium chloride gradient from extracts of osmotically shocked cells. Murine erythrocytes, which are agglutinated by PVM, adsorb to the surface of infected cells and to budding and extracellular PVM particles. On the basis of its structure and morphogenesis, PVM appears to be a myxovirus; however, it does not fit into either of the established subgroups of myxoviruses. The 120-150 A diameter of the PVM internal component differs from the diameters of the internal components of the two established subgroups of myxoviruses, and suggests that a third subgroup of these viruses may exist.
Age at menarche and non-alcoholic fatty liver disease
Authors: Seungho Ryu, Yoosoo Chang, Yuni Choi, Min-Jung Kwon, Chan-Won Kim, Kyung Eun Yun, Hyun-Suk Jung, Bo-Kyoung Kim, Yoo Jin Kim, Jiin Ahn, Yong Kyun Cho, Kye-Hyun Kim, Eun Chul Chung, Hocheol Shin, Juhee Cho
Journal: Journal of Hepatology (2014)
Progressive unilateral lung collapse in cystic fibrosis-a therapeutic challenge
Authors: William G Flight, Janet Hildage, A Kevin Webb
Journal: Journal of the Royal Society of Medicine (2012)

Progressive collapse and destruction of an entire lung is an uncommon but recognized manifestation of cystic fibrosis (CF).1 This devastating complication presents a considerable challenge to both the CF multi-disciplinary team and the transplant surgeon. The evidence base to guide management of this condition is sparse, and in our clinical experience it has proved impossible to reverse the underlying process. Case reports of surgical intervention for complete lung collapse have demonstrated a high incidence of adverse outcomes.1–3 We report, in detail, the case of one patient with progressive unilateral lung collapse followed by a summary of a seven comparable cases encountered at our unit.
Choline uptake into renal phospholipids following renal ischemia in rats.
Authors: M B Siegel, L M Lowenstein, N G Levinsky
Journal: Circulation Research (1979)

Renal phospholipid metabolism was studied after ischemia was induced by occlusion of the left renal artery in the rat. There was no change in the rate of cellular [14C]choline uptake after 25 or 60 minutes of ischemia. However, [14C]choline incorporation into phospholipid was two to three times greater in slices from the ischemic kidney than in slices from the contralateral control kidney. The increase occurred after 25 minutes of ischemia plus 15 minutes of reflow, and after 60 minutes of ischemia with or without reflow. When [14C]choline was injected into rats after a 60-minute period of renal ischemia, the rate of incorporation into phospholipid in the ischemic kidney was almost twice that of the control kidney. These results were similar to those of the in vitro experiments. Since virtually all of the cellular phospholipids of the kidney are present in cellular membranes, renal ischemia affects membrane metabolism. The mean distribution ratio of alpha-aminoisobutyric acid in slices of kidneys ischemic for 60 minutes was similar to that of control slices: 4.11 +/- 0.2 (SEM) vs. 4.30 +/- 0.30. The normal uptake of alpha-aminoisobutyric acid indicates that the increased incorporation of choline is associated with functional integrity of the membrane.
Human immune cells' behavior and survival under bioenergetically restricted conditions in an in vitro fracture hematoma model
Authors: Paula Hoff, Patrick Maschmeyer, Timo Gaber, Tabea Schütze, Tobias Raue, Katharina Schmidt-Bleek, René Dziurla, Saskia Schellmann, Ferenz Leonard Lohanatha, Eric Röhner, Andrea Ode, Gerd-Rüdiger Burmester, Georg N Duda, Carsten Perka, Frank Buttgereit
Journal: Cellular and Molecular Immunology (2013)
Prolonged Zidovudine Therapy: Confounded by Pneumocystis carinii Prophylaxis?
Authors: Timothy W. Odell
Journal: JAMA (1990)

<h3>To the Editor.—</h3> Zidovudine was shown to enhance survival and decrease the frequency of opportunistic infections in patients with acquired immunodeficiency syndrome and acquired immunodeficiency syndrome—related complex in the short-term 24-week phase II study published in 1987.<sup>1</sup>This benefit was obtained in the absence of chemoprophylaxis for opportunistic infections. During the subsequent uncontrolled continuation study,<sup>2</sup>all subjects received zidovudine. Chemoprophylaxis for the prevention of<i>Pneumocystis carinii</i>pneumonia (PCP) was left up to the discretion of each investigator. Fischl et al concluded that long-term zidovudine therapy continued to enhance survival and decrease the frequency of opportunistic infections. Some or all of the apparent benefit of zidovudine, however, may be due to prophylaxis for PCP. The number of patients who received PCP prophylaxis was not specified and comparisons were made against historical controls. Since the phase II trial in 1987, there has not been a single study, to our
Targeted Immunotherapy for Hairy Cell Leukemia
Authors: Jae H. Park, Ross L. Levine
Journal: Journal of Clinical Oncology (2012)

Article Tools UNDERSTANDING THE PATHWAY Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2011.39.8313 Journal of Clinical Oncology - published online before print February 21, 2012 PMID: 22355051 Targeted Immunotherapy for Hairy Cell Leukemia Jae H. ParkxJae H. ParkSearch for articles by this author , Ross L. LevinexRoss L. LevineSearch for articles by this author Show More Memorial Sloan-Kettering Cancer Center, New York, NY https://doi.org/10.1200/JCO.2011.39.8313 First Page Full Text PDF Figures and Tables © 2012 by American Society of Clinical Oncology
Phosphodiesterase 5 inhibition protects against increased intra‐abdominal pressure‐induced renal dysfunction in experimental congestive heart failure
Authors: Bishara Bishara, Niroz Abu‐Saleh, Hoda Awad, Nabil Ghrayeb, Ilia Goltsman, Doron Aronson, Iyad Khamaysi, Suhair Assady, Zaher Armaly, Saleem Haddad, Elias Haddad, Zaid Abassi
Journal: European Journal of Heart Failure (2012)
Treatment of Bacterial Meningitis
Authors: Jacob J. Schlesinger, Everett B. Cooper
Journal: Annals of Internal Medicine (1976)

Comments and Corrections1 July 1976Treatment of Bacterial MeningitisJACOB J. SCHLESINGER, M.D., EVERETT B. COOPER, M.D., F.A.C.P.JACOB J. SCHLESINGER, M.D.Search for more papers by this author, EVERETT B. COOPER, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-85-1-127 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The recent "Letter" by Farid and associates (Ann Intern Med 84:50-51, 1976) describes the use of trimethoprim-sulfamethoxazole in the treatment of bacterial meningitis. Although cure was effected in each of the cases described, we question the advisability of trimethoprim-sulfamethoxazole as the initial choice of chemotherapy.Optimal in-vitro synergy between trimethoprim and sulfamethoxazole depends in part on the degree of sensitivity to each component of the drug pair, with relative sensitivity to sulfamethoxazole of particular importance (1, 2). In this regard we wonder whether theNeisseria meningitidisrecovered was of serogroup A. These are prevalent in Egypt and...1. BUSHBY S: Trimethoprim-sulfamethoxazole: in-vitro microbiological aspects. J lnfec Dis (suppl) 128:442-462, 1973 CrossrefGoogle Scholar2. SCHIFFMAN D: Evaluation of an anti-infective combination. Trimethoprim-sulfamethoxazole (Bactrim, Septra). JAMA 231: 635-637, 1975 CrossrefMedlineGoogle Scholar3. GOTSCHLICH E: Development of polysaccharide vaccines for the prevention of meningococcal diseases. Monogr Allergy 9: 245-258, 1975 MedlineGoogle Scholar4. Surveillance summary. Meningococcal disease. Morbid Mortal Weekly Rep 22:58-59, 1973 Google Scholar5. CHERRYSHEENAN JC: Bacteriologic relapse in Haemophilus influenzae meningitis. Inadequate ampicillin therapy. N. Engl J Med 278:1001-1003, 1968 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 July 1976Volume 85, Issue 1Page: 127-128KeywordsBacterial meningitisChemotherapyDrugsNeisseria meningitidis Issue Published: 1 July 1976 PDF downloadLoading ...
Hepatic encephalopathy: Lack of changes of γ-aminobutyric acid content in plasma and cerebrospinal fluid
Authors: Flavio Moroni, Oliviero Riggio, Vincenzo Carlà, Vittorio Festuccia, Florio Ghinelli, Ignazio R. Marino, Manuela Merli, Laura Natali, Giovanni Pedretti, Franco Fiaccadori, Livio Capocaccia
Journal: Hepatology (1987)

The aim of the study was to verify the role of γ-aminobutyric acid in the pathogenesis of hepatic encephalopathy occurring in cirrhotic patients by attempting to correlate plasma and cerebrospinal fluid content of authentic γ-aminobutyric acid with the neurological manifestations of hepatic encephalopathy. For this purpose, plasma and cerebrospinal fluid γ-aminobutyric acid levels were measured by means of mass fragmentography in 17 cirrhotic patients with hepatic encephalopathy and in 6 cirrhotics without neurological symtoms. Moreover, in all patients, a second sample was obtained during the clinical course of hepatic encephalopathy. The mean plasma and cerebrospinal fluid γ-aminobutyric acid levels were not different in patients with or without hepatic encephalopathy and did not change during the evolution of the neurological symptoms. The lack of changes in the γ-aminobutyric acid content in plasma and cerebrospinal fluid during hepatic encephalopathy is in contrast with the hypothesized importance of increased entry into the brain of γ-aminobutyric acid in the pathogenesis of hepatic encephalopathy.