tbuckley/cabot-search huggingface dataset:
Abstract 2436: Regulation of breast cancer cell metabolism by the AMPK/ERR/PGC pathway
Authors: Étienne Audet-Walsh, David Papadopoli, Julie St-Pierre, Vincent Giguère
Journal: Cancer Research (2014)

Abstract Reprogramming of energy metabolism is now considered a hallmark of cancer. Deciphering molecular mechanisms underlying this process is therefore necessary to understand malignant transformation and cancer progression, but also to develop novel therapeutic tools. In the present study, our aim was to discover potential molecular links between two major pathways involved in energy metabolism in breast cancer cells: the energy sensor AMPK (AMP-activated protein kinase) in relationship with the estrogen-related receptors (ERRα and ERRγ) and their coactivators PGC-1α and PGC-1β (peroxisome-proliferator activated receptor γ coactivator-1). Using microarray analysis and qRT-PCR validation, we showed that activation of AMPK significantly altered the expression of the ERRs and the PGCs as well as their metabolic target genes. Moreover, pathway analysis revealed that a significant subset of genes regulated by AMPK pharmacological activation for 1 and 4 days were associated with the ERR/PGC transcriptional programs. Using metabolomics tools, we demonstrated that the energetic remodeling following AMPK pharmacological activation depends in part on ERR/PGC in breast cancer cells. Indeed, the induction in glucose and glutamine uptake and usage by activated AMPK was decreased by half following impairment of the ERR/PGC axis. Moreover, total, uncoupled and coupled respirations were also significantly decreased by ≈50% following ERR/PGC siRNA-mediated knock down. In order to understand the role of the ERRs in the transcriptional regulation of downstream targets of AMPK, we performed chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). Our results indicate that AMPK activation induces ERRs binding at the genomic scale, with the presence of 12,043 and 8,559 novel binding sites for ERRα and ERRγ, respectively. Basal, ERRs' binding to energy metabolism genes was already strong and did not change significantly after treatment. However, AMPK pharmacological activation induced ERRs binding to novel pathways such as numerous genes of the folate metabolism pathway. The biological consequence of the modulation of these pathways by the AMPK/ERR/PGC axis is presently under investigation. In conclusion, using transcriptomics, metabolomics and functional genomics, we revealed the interconnection of the AMPK with the ERR/PGC axis and the importance of this pathway in breast cancer cell metabolic states. Citation Format: Étienne Audet-Walsh, David Papadopoli, Julie St-Pierre, Vincent Giguère. Regulation of breast cancer cell metabolism by the AMPK/ERR/PGC pathway. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2436. doi:10.1158/1538-7445.AM2014-2436
Free-radical chemistry of cigarette smoke and its toxicological implications.
Authors: D F Church, W A Pryor
Journal: Environmental Health Perspectives (1985)

Cigarette smoke contains two very different populations of free radicals, one in the tar and one in the gas phase. The tar phase contains several relatively stable free radicals; we have identified the principal radical as a quinone/hydroquinone (Q/QH2) complex held in the tarry matrix. We suggest that this Q/QH2 polymer is an active redox system that is capable of reducing molecular oxygen to produce superoxide, eventually leading to hydrogen peroxide and hydroxyl radicals. In addition, we have shown that the principal radical in tar reacts with DNA in vitro, possibly by covalent binding. The gas phase of cigarette smoke contains small oxygen- and carbon-centered radicals that are much more reactive than are the tar-phase radicals. These gas-phase radicals do not arise in the flame, but rather are produced in a steady state by the oxidation of NO to NO2, which then reacts with reactive species in smoke such as isoprene. We suggest that these radicals and the metastable products derived from these radical reactions may be responsible for the inactivation of alpha 1-proteinase inhibitor by fresh smoke. Cigarette smoke oxidizes thiols to disulfides; we suggest the active oxidants are NO and NO2. The effects of smoke on lipid peroxidation are complex, and this is discussed. We also discuss the toxicological implications for the radicals in smoke in terms of a number of radical-mediated disease processes, including emphysema and cancer.
Zinc Metabolism in Hepatic Dysfunction
Authors: Bert L. Vallee, Warren E. C. Wacker, Anthony F. Bartholomay, Eugene D. Robin
Journal: New England Journal of Medicine (1956)

THE presence of zinc in living organisms and its essentiality as a nutrient for plants and animals have been recognized for many, ears.1 , 2 Normal persons take in about 10 to 15 mg. of zinc a day, most of it being excreted in the feces, which contain about 10 mg. a day; about 300 or 400 microgm. a day is excreted in the urine.3 Most human organs contain zinc, the amounts in different organs varying between 10 and 200 microgm. per gram of wet tissue.4 The serum zinc concentration has been reported to be decreased in several diseases, notably pernicious anemia. . . .
HHV-8 positive, HIV negative disseminated Kaposi's sarcoma complicating steroid dependent ulcerative colitis: a successfully treated case
Authors: A Bursics, K Morvay, K Ábrahám, M Marschalkó, M Kardos, B Járay, K Nagy
Journal: Gut (2005)

We present the case of a 49 year old man who had suffered histologically confirmed ulcerative colitis (UC) since 1998. He had been asymptomatic for four years when in August 2002 an acute relapse developed. Colonoscopy and histology of a superficial bowel specimen showed clear signs of active UC with no signs of malignancy. Despite adequate therapy he failed to improve and was referred for restorative proctocolectomy because of steroid dependency and end stage colon. By the time of his referral, violaceous reddish-brown nodules had developed on his extremities. Skin biopsy showed spindle cells and vascular slits. Histological diagnosis was Kaposi’s sarcoma (KS) of the skin. He underwent a restorative proctocolectomy with ileostomy in March 2003. The pathological examination of the colon showed features of UC and surprisingly, characteristic signs of KS also. Human immunodeficiency virus (HIV) tests …
Transfection-mediated expression of a dominant cAMP-resistant phenotype in the opossum kidney (OK) cell line prevents parathyroid hormone-induced inhibition of Na-phosphate cotransport. A protein kinase-A-mediated event.
Authors: J H Segal, A S Pollock
Journal: Journal of Clinical Investigation (1990)

Sodium-phosphate cotransport in the PTH-responsive opossum kidney (OK) cell line is inhibited by PTH, cAMP, and activators of protein kinase C. In order to probe the role of cAMP, we stably transfected OK cells with an expression vector for a cAMP-binding mutation of the murine protein kinase A regulatory subunit. Two-dimensional electrophoresis of cAMP-binding proteins from transfected cells indicated a 20-fold overexpression of the mutant regulatory unit. Protein kinase A from these cells had a 20-fold increase in the concentration of cAMP required for half-maximal activation, 2.8 microM vs. 0.15 microM for wild type cells. In the transfected cells, Na-phosphate cotransport was insensitive to up to 1 mM 8-Br-cAMP and 1 microM PTH, while these same agonists caused a significant inhibition of transport in the wild type cells. The effects on Na-phosphate cotransport of the protein kinase C activators oleoyl-acetyl glycerol and tetradecanoyl-phorbol acetate, which were marked in the wild type cells, were still present, although attenuated, in the transfected mutants. With prolonged passage, the cAMP-insensitive phenotype reverted to wild type cAMP sensitivity despite continued selection for the cotransfected neo marker. The revertant cells had a normal cAMP requirement for half-maximal activation of protein kinase A, 0.13 microM, and the PTH and cAMP-sensitive inhibition of Na-phosphate cotransport was restored. We suggest that an intact and normally cAMP-sensitive protein kinase A pathway is an absolute requirement for PTH inhibition of Na-phosphate cotransport in the OK cell.
Abstract 3161: Increased expression of MUC1 and claudin-10 is associated with poor prognosis of patients with gastric cancer
Authors: Keon Uk Park, Jin Young Kim, Young Rok Do, Hong Suk Song, Ilseon Hwang, Eunyoung Ha, Hun Mo Ryoo, Young Joo Min
Journal: Cancer Research (2011)

Abstract Background: Mucins are high molecular weight glycoproteins that play important roles in carcinogenesis and tumor invasion. Several studies have shown the aberrant expression profile of mucins in gastric cancer. Claudins are the proteins that participate in the formation of tight junctions. Tight junction proteins are believed to be involved in the regulation of proliferation, differentiation, and other cellular functions. Expression of claudin family in gastric cancers has been studied by many laboratories, but the results are conflicting. Therefore, we investigated the potential of MUC and claudin family to be used as a prognostic marker in gastric cancer. Methods: One-hundred eighty gastric adenocarcinoma patients who underwent surgical resection and had not received any pre- or -post surgery therapy, were selected for this study. Among the 180 gastric cancer samples tested here, 63 (34%) were early gastric cancer, and 117 (66%) were advanced. We made tissue microarrays with paraffin-embeded formalin fixed blocks of gastric cancer and these microarrays were evaluated for phenotypic expression of MUC1, MUC4, Claudin 1, 3, 4, 5, 7 and 10 using anti-human rabbit or mouse polyclonal antibody. The expression levels were correlated with key clinicopathologic features and patient outcomes. Results: There was no significant difference of MUC and claudin expression between early and advanced gastric cancer. Gastric cancer patients with increased MUC1 expression were significantly associated with shorter overall survival as compared to those with low expression of MUC1 (log rank, p=0.039). MUC4 expression were significantly associated with decreased overall survival only in N0 patients (log rank, p=0.046). Increased expression of Claudin-10 was significantly associated with shorter disease free survival (log rank, p=0.038). Claudin 1,3,4,5 and 7 expression was not associated with significant difference of overall survival or disease free survival.Conclusion: Our present findings show that the increased expression of MUC1 and claudin-10 is a prognostic indicator of poor survival of patients with early and advanced gastric cancer. 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 3161. doi:10.1158/1538-7445.AM2011-3161
INCREMENTAL PREDICTIVE VALUE FOR INCIDENT CARDIOVASCULAR DISEASE OF 4 SUBCLINICAL MARKERS COMBINED: LIPOPROTEIN PARTICLE CONCENTRATION, NT-PROBNP CONCENTRATION, CORONARY ARTERY CALCIFICATION SCORE AND SMALL ARTERY STIFFNESS IN ASYMPTOMATIC SUBJECTS IN THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS
Authors: Daniel A. Duprez, Na Zhu, David R. Jacobs Jr, Hossein Bahrami, Joao Lima, James Otvos, Lori B. Daniels, Alan Maisel
Journal: Journal of the American College of Cardiology (2011)
Halting the Progression of Chronic Nephropathy
Authors: Ruth C. Campbell, Piero Ruggenenti, Giuseppe Remuzzi
Journal: Journal of the American Society of Nephrology (2002)

ABSTRACT. The incidence of end-stage renal disease (ESRD) is increasing worldwide. In the United States alone, there were 372,000 patients requiring renal replacement therapy in the year 2000 and is expected to rise to 650,000 by the year 2010. The trends in Europe and Japan are forecasted to follow a similar path. These increases represent a significant burden to countries worldwide; not only due to the financial costs of providing ESRD care, but also because of lost productivity and significant morbidity and mortality for the affected patients. There is clearly a pressing need for the aggressive identification and early treatment of patients with nephropathy to prevent progression to ESRD. Research in the last 25 yr has made great advances in the understanding of the progression of chronic renal disease in diabetic and nondiabetic proteinuric nephropathy. There are now effective treatment options that can slow the progression of chronic nephropathies in many individuals, and ongoing research has raised the tantalizing prospect of the reversal of renal disease progression. E-mail: gremuzzi@marionegri.it
Porphyria cutanea tarda with menopausal exacerbation: the possible role of menstruation as natural phlebotomy
Authors: Eri Nishioka, Yoko Funasaka, Toshinori Bito, Akira Ito, Masahiro Tani, Akira Kawara, Seitetsu Yoon, Masao Kondo, Masamitsu Ichihashi
Journal: Journal of the American Academy of Dermatology (2003)
THE IMPACT OF BODY MASS INDEX ON THE ONE YEAR OUTCOME OF PATIENTS TREATED BY PCI WITH BIOLIMUS- AND SIROLIMUS- ELUTING STENTS FROM THE LEADERS TRIAL.
Authors: Giovanna Sarno, Scot Garg, Yoshinobu Onuma, Pawel Buszman, Axel Linke, Thomas Ischinger, Volker Klauss, Franz Eberli, Roberto Corti, William Wijns, Marie-Claude Morice, Carlo Di Mario, Pedro Eerdmans, Hector M. Garcia-Garcia, Gerrit-Anne van Es, Dick Goedhart, Ton de Vries, Peter Jüni, Bernhard Meier, Stephan Windecker, Patrick Serruys
Journal: Journal of the American College of Cardiology (2010)
Determination of hepatitis B virus DNA in serum using the polymerase chain reaction: Clinical significance and correlation with serological and biochemical markers
Authors: Bennie L. Baker, Adrian M. Di Bisceglie, Shuichi Kaneko, Roger Miller, Stephen M. Feinstone, Jeanne G. Waggoner, Jay H. Hoofnagle
Journal: Hepatology (1991)

Sera from 98 patients with various stages of chronic hepatitis B virus infection were studied to determine the clinical significance of hepatitis B virus DNA in serum detected by the polymerase chain reaction. Patients were divided into three groups according to their HBsAg and HBeAg status. Group I (n = 31) had detectable HBsAg and HBeAg, group II (n = 46) had HBsAg but not HBeAg and group III (n = 21) consisted of patients who were once chronic hepatitis B virus carriers but had lost HBsAg during follow-up. Group I patients usually had significant liver disease (raised serum aminotransferases), had higher titers of HBsAg and had been infected with hepatitis B virus for a shorter period than patients in the other two groups. All patients in group I had hepatitis B virus DNA detectable by polymerase chain reaction and 94% had sufficient hepatitis B virus DNA present for detection by dot-blot hybridization. Group II patients had lower mean serum aminotransferase activities and titers of HBsAg than those in group I. Serum hepatitis B virus DNA was detectable by polymerase chain reaction in 78% but in only 30% of group II patients by dot-blot hybridization. Group II patients who did not have hepatitis B virus DNA detectable by polymerase chain reaction had mean serum aminotransferase levels within the normal range and had a younger mean age than those with hepatitis B virus DNA. Group III patients generally had no evidence of active liver disease. Of five patients in this group seropositive for hepatitis B virus DNA by polymerase chain reaction on initial testing, all eventually became negative for hepatitis B virus DNA on subsequent testing. There was a tendency for those patients in group III with hepatitis B virus DNA detectable by polymerase chain reaction to have elevated serum aminotransferase levels (40% vs. 25%); however, these differences were not statistically significant. Taken together, these data show that the presence of hepatitis B virus DNA in serum as detected by polymerase chain reaction appears to be a good marker of the level of viremia, can be correlated with aminotransferase levels and parallels the presence of HBsAg in serum. (Hepatology 1991;13:632-636.)
Altitude and Health.
Authors: F. F. Roget
Journal: JAMA (1921)

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
PET ANIMAL INFESTATIONS AND HUMAN SKIN LESIONS
Authors: MARK HEWITT, GRAHAME S. WALTON, MARGARET WATERHOUSE
Journal: British Journal of Dermatology (1971)

SUMMARY.— A preliminary survey carried out in a Cornish rural population has revealed that animal ectoparasites are a common cause of human skin disease. The results of this investigation are described and their relative importance in human dermatology discussed.
Determining the number of psychiatric beds needed
Authors: D. Roy, M. Pierides, T. Craig
Journal: BMJ (1995)

EDITOR,—We support Graham Thornicroft and Geraldine Strathdee's view that it is not possible to debate the issue of how many psychiatric beds are needed without placing the emphasis firmly on the whole mental health system.1 But the notion that pressure on inpatient beds could be eased by more efficient management by “senior clinical gatekeepers” is too simplistic. The suggestion that the crisis in acute inpatient services would end if only clinicians managed their services properly is being repeated so often that it is beginning …
Clinical Experience with Dipaxin and with the Combined Use of Prothrombopenic Agents
Authors: RICARDO KATZ, HÉCTOR DUCCI, WERNER ROESCHMANN, LUCÍA TORIELLO
Journal: Circulation (1954)

The experience with a new prothrombopenic agent, Dipaxin, is presented. With a 30 mg. dose a prothrombin complex concentration under 30 per cent is reached in 41 hours or less. When associated with 1500 mg. of Tromexan the latent period is reduced to 24 hours. The prothrombopenic action of Dipaxin is readily counteracted with vitamin K 1 administered either orally or intravenously.
The Standing of American Ophthalmology.
Authors: H. V. Würdemann
Journal: JAMA (1896)

Milwaukee, March, 23, 1896. <h3>To the Editor:</h3> —Exception may well be taken to the arrangement of ophthalmic surgeons generally and of ophthalmology in the rather rambling editorial published in the issue of March 21, which is intended to impress the reader with the idea that American ophthalmic authors, particularly those of the American Ophthalmological Society are "ashamed of what they should be proud of." The innuendoes of this editorial are certainly distasteful to the majority of the 267 members of the Section on Ophthalmology of theAmerican Medical Association, and may be particularly so to a considerable number of those who are also members of the American Ophthalmological Society. Perhaps there may be cause to criticize the 1895 Transactions of the latter. I am, however, unwilling that such a stricture should be passed upon American Ophthalmology and upon that large and growing (!) class of pratitioners who are particularly interested in
Multidisciplinary Approaches to Biomedical Research
Authors: Adam T. Perzynski
Journal: JAMA (2010)

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
What is MRSA?
Authors: A. Pantosti, M. Venditti
Journal: European Respiratory Journal (2009)

For decades methicillin-resistant Staphylococcus aureus (MRSA) has been considered the prototype of multi-resistant nosocomial pathogens, causing infections in high-risk patients. Changes in the healthcare system, coupled with the evolution of this versatile microorganism, have transformed MRSA into a cause of community-onset infections, in both patients who have contact with the healthcare system and patients without such a risk factor. New lineages of MRSA, defined as community acquired (CA)-MRSA, have emerged that have a propensity to cause infections in young individuals without risk factors. CA-MRSA primarily causes skin infections and, rarely, necrotising pneumonia. In the USA, these strains belong to a single widespread clone, designated USA300, while in Europe they belong to a variety of clones. Most strains carry genes for the Panton–Valentine leukocidin, whose role in diseases is under debate. In subjects living in the community who have contact with the healthcare system, MRSA strains of the nosocomial type are a frequent cause of infection and of pneumonia in particular. The detection of a large MRSA reservoir in pigs and the finding that professionally exposed individuals are colonised, has further shown that it is necessary to closely follow the epidemiology of MRSA if we want to combat it effectively.