tbuckley/cabot-search huggingface dataset:
Abstract 4079: Control of survivin expression by IGF-I in prostate epithelial cells.
Authors: David Danielpour, Kyung Song, Eswar Shankar, Jiayi Yang, Kara L. Bane
Journal: Cancer Research (2013)

Abstract Survivin, a unique member of the inhibitor of apoptosis (IAP) proteins, is overexpressed in numerous cancers through poorly defined mechanisms. We show that insulin-like growth factor-I (IGF-I), which is implicated in the etiology of prostate cancer, induces the expression of Survivin in a variety of pre-neoplastic and malignant prostate cell lines. Using the pre-neoplastic NRP-152 rat prostate cell line as a model, we showed that silencing Survivin by lentiviral-mediated shRNA represses IGF-I-stimulated cell growth, suggesting that the induction of Survivin is critical to this growth response. Moreover, we show that IGF-I induces the expression of Survivin through a transcriptional mechanism that is mediated in part by the PI3K/Akt/mTORC1 pathway. The CDE and CHR response elements in the proximal region of the Survivin promoter are decisive for this IGF-I response. TGF-β signaling antagonists similarly induced this promoter activity and rendered cells refractory to further promoter activation by IGF-I. Suppression of TGF-β signaling, either by TGF-β receptor kinase inhibitors or by silencing Smads 2 and 3, induced Survivin expression and promoted cell growth similar to that induced by IGF-I. TGF-β receptor antagonists also rescued cells from down-regulation of Survivin expression and growth suppression by pharmacological inhibitors of PI3K, Akt, MEK and mTORC1. Sh-RNA gene silencing studies suggest that mTORC1 induces while mTORC2 represses the expression of Survivin. We conclude that IGF-I signaling through a PI3K/Akt/mTORC1-dependent mechanism elevates expression of Survivin and promotes growth of prostate epithelial cells by suppressing Smad-dependent autocrine TGF-β signaling. Citation Format: David Danielpour, Kyung Song, Eswar Shankar, Jiayi Yang, Kara L. Bane. Control of survivin expression by IGF-I in prostate epithelial cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4079. doi:10.1158/1538-7445.AM2013-4079
Abstract 179: Identification of novel targets for aberrant methylation in pancreatic cancer by a newly developed method “methyl-CpG targeted transcriptional activation (MeTA)”
Authors: Shinichi Fukushige, Hideyuki Shimizu, Yuko Sato, Akira Horii
Journal: Cancer Research (2010)

Abstract Identification and characterization of genes selectively hypermethylated in cancer may improve our understanding of the role of epigenetic alterations in tumorigenesis. In addition, genes frequently methylated in a tumor-specific manner could be used as tumor markers. DNA methylation inhibitors such as 5-aza-cytidine or 5-aza-2’-deoxycytidine have been widely used to search epigenetically silenced genes. However, these inhibitors frequently upregulate genes whose promoters remain unmethylated. We tried to improve the specificity and sensitivity in detecting methylation-mediated silenced genes in cancer and successfully developed a new method termed “methyl-CpG targeted transcriptional activation (MeTA)” by using a transcriptional activating fragment with a methyl-CpG binding domain (MBD). Because MBD proteins in fact mediate transcriptional repression of tumor suppressor genes associated with promoter hypermethylation in cancer, MeTA is thought to be one of the ideal methods to search such genes. In the preliminary experiments using human embryonic kidney cell line 293T, we found that the combination of MeTA with gene expression microarray is useful; genes containing CpG islands can be efficiently identified (93.5% by MeTA vs. 66.8% by 5-aza-cytidine) even those that are difficult to find by the conventional DNA methylation inhibitors. We applied this method to twelve typical pancreatic cancer cell lines with a normal pancreatic ductal epithelial cell line HPDE as the control, and have searched for genes commonly upregulated after MeTA. Thirty-one genes were upregulated by two-folds or more in six pancreatic cancer cell lines or more. Among these, 26 genes have not been reported previously using the conventional DNA methylation inhibitors. Methylation statuses of three genes, NEFL, NEFM, and IRX4 were further examined by methylation-specific PCR and found that these three genes were aberrantly methylated in all of the analyzed tumors, 11 resected primary pancreatic cancer specimens and 22 pancreatic cancer cell lines. Our results suggest that “MeTA” is a highly efficient method to identify methylation-mediated transcriptionally silenced genes in human pancreatic cancer and that this method can be applied to other types of human cancer. 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 179.
Government was wrong to prioritise "gold" route for open access, say MPs
Authors: Z. Kmietowicz
Journal: BMJ (2013)

The UK government acted too quickly in favouring a “gold” model of open access that risked curbing access and increasing costs to universities, a committee of MPs has said.

The government and Research Councils UK (RCUK) should reconsider their current policies and review the evidence on how the alternative, “green” open access and repositories could help the United Kingdom move towards full open access, the House of Commons’ Business, Innovation and Skills Committee has said in a report published on 10 September.1

Last June the report of the Working Group on Expanding Access to Published Research Findings, led by the academic administrator Janet Finch, recommended that the best way to expand access to reports of publicly funded research was to adopt a system where the cost of publication …
The role of microRNA expression pattern in human intrahepatic cholangiocarcinoma
Authors: Lei Chen, He-Xin Yan, Wen Yang, Liang Hu, Le-Xin Yu, Qiong Liu, Liang Li, Dan-Dan Huang, Jin Ding, Feng Shen, Wei-Ping Zhou, Meng-Chao Wu, Hong-Yang Wang
Journal: Journal of Hepatology (2008)
Types of Radiation: The Journal Flunks Physics
Authors: H. Wick
Journal: JAMA (1987)

<h3>To the Editor.—</h3> In the table entitled "Types of Radiation" on page 560 of the Aug 1, 1986, issue of<i>JAMA</i>,<sup>1</sup>an accumulation of mistakes is found that could not have been surpassed even by intent. Alpha radiation is not the emission of two protons and two neutrons, ie, four particles, but of one alpha particle that may be regarded as a nucleus of the element helium, consisting of two neutrons and two protons. In alpha decay, the energy is strictly defined. This leads to well-defined traveling distances in air, which differ in the case of different alpha emitters. Beta radiation consists of electrons or positrons. As Einstein proved, the speed of light cannot be reached by such radiation! In the case of positron radiation, secondary gamma radiation resulting from the annihilation energy of a positron with its antiparticle, the electron, is observed. The energy spectrum of beta radiation
Pregnancy Following Closed Mitral Valvuloplasty
Authors: Wayne A. Wallace
Journal: JAMA (1971)

One hundred and thirty-nine women who underwent closed mitral valvuloplasty and subsequently became pregnant have been followed up for 1 to 17 years (mean, 10 years) following surgery. The overall postoperative course of these women was not altered by childbearing, when compared with the courses of the other patients in the series of which they are a part, and when a subgroup of 113 of the 139 women was compared with a matched control group. A review of five deaths which occurred in relation to pregnancy revealed that in at least three cardiac management was inadequate. Physicians as well as patients often wrongly consider surgery for valvular disease curative and do not apply the usual careful treatment that all patients with cardiac disease should receive.
Analysis of the Human G Protein–Coupled Receptor Kinase 2 (GRK2) Gene Promoter
Authors: Ricardo Ramos-Ruiz, Petronila Penela, Raymond B. Penn, Federico Mayor
Journal: Circulation (2000)

Desensitization of G protein-coupled receptors (GPCR) is emerging as an important feature of several cardiovascular diseases. G protein-coupled receptor kinase 2 (GRK2) plays a key role in the regulation of a variety of these receptors, and its cardiac expression levels are altered in pathological situations such as chronic heart failure. However, very little is known about the signals and mechanisms that modulate GRK2 expression in cardiovascular cells.We have studied the transcriptional activity of the 1.6-kb-long proximal genomic region of the human GRK2 gene. In an aortic smooth muscle cell line, agents that lead to physiological vasoconstriction and hypertrophy, such as phorbol esters, increased GRK2 promoter activity. Activation of signaling pathways by cotransfected G(alphaq) subunits or alpha(1)-adrenergic receptors also markedly enhanced the expression of the GRK2 promoter constructs. Conversely, proinflammatory cytokines, such as interleukin-1beta, tumor necrosis factor-alpha, or interferon-gamma, led to the opposite effect, decreasing the activity of the GRK2 promoter.Our results suggest that the expression of GRK2 in vascular cells is tightly controlled at the transcriptional level by the interplay between several extracellular messengers, which may trigger alterations of normal GRK2 levels in some physiopathological circumstances, thus promoting changes in the efficacy of the GPCR signal transduction.
A novel mechanism for mitogenic signaling via pro-transforming growth factor α within hepatocyte nuclei
Authors: Bettina Grasl-Kraupp, Elisabeth Schausberger, Karin Hufnagl, Christopher Gerner, Alexandra Löw-Baselli, Walter Rossmanith, Wolfram Parzefall, Rolf Schulte-Hermann
Journal: Hepatology (2002)

Transforming growth factor (TGF) α, an important mediator of growth stimulation, is known to act via epidermal growth factor receptor (EGF-R) binding in the cell membrane. Here we show by immunohistology, 2-dimensional immunoblotting, and mass spectrometry of nuclear fractions that the pro-protein of wild-type TGF-α occurs in hepatocyte nuclei of human, rat, and mouse liver. Several findings show a close association between nuclear pro-TGF-α and DNA synthesis. (1) The number of pro-TGF-α+ nuclei was low in resting liver and increased dramatically after partial hepatectomy and after application of hepatotoxic chemicals or the primary mitogen cyproterone acetate (CPA); in any case, S phase occurred almost exclusively in pro-TGF-α + nuclei. The same was found in human cirrhotic liver. (2) In primary culture, 7% of hepatocytes synthesized pro-TGF-α, which then translocated to the nucleus; 70% of these nuclei subsequently entered DNA replication, whereas only 2% of pro-TGF-α − hepatocytes were in S phase. (3) The frequency of hepatocytes coexpressing pro-TGF-α and DNA synthesis was increased by the hepatomitogens CPA or prostaglandin E 2 and was decreased by the growth inhibitor TGF-β1. (4) Treatment with mature TGF-α increased DNA synthesis exclusively in pro-TGF-α − hepatocytes, which was abrogated by the EGF-R tyrosine kinase inhibitor tyrphostin A25. In conclusion, TGF-α gene products may exert mitogenic effects in hepatocytes via 2 different signaling mechanisms: (1) the “classic” pathway of mature TGF-α via EGF-R in the membrane and (2) a novel pathway involving the presence of pro-TGF-α in the nucleus.
Give patients a second chance before striking them off, says ombudsman
Authors: A. Vass
Journal: BMJ (2002)

Patients should be given the chance to “rectify their behaviour” before being removed from a GP's list, warned the health service ombudsman for England, Michael Buckley (pictured), in his annual report published this week.

Nine complaints over unfair removal of patients were investigated during 2001-2—more than about any other aspect of the general practitioner service, said the report. In eight of the nine cases, …
Allergen immunotherapy with heat‐killed <i>Listeria monocytogenes</i> alleviates peanut and food‐induced anaphylaxis in dogs
Authors: O. L. Frick, S. S. Teuber, B. B. Buchanan, S. Morigasaki, D. T. Umetsu
Journal: Allergy (2004)

Background: Heat‐killed Listeria monocytogenes (HKL) potently stimulates interferon (IFN)‐ γ production in CD4 T‐lymphocytes, and when used as adjuvant for immunotherapy, reduces immunoglobulin (Ig)E production and reverses established allergen‐induced airway hyperreactivity (AHR) in a murine model of asthma. We asked if such treatment could decrease established peanut‐induced anaphylaxis or cow's milk‐induced food allergy in highly food‐allergic dogs. Methods: We therefore studied four 4‐year‐old atopic colony dogs extremely allergic to peanut (Group I), as well as five 7‐year‐old dogs very allergic to wheat, milk and other foods (Group II). All dogs experienced marked allergic symptoms, including vomiting and diarrhea on oral challenge with the relevant foods. The dogs were then vaccinated once subcutaneously with peanut or milk and wheat with HKL emulsified in incomplete Freund's adjuvant. Results: Following vaccination of the allergic dogs with HKL and allergen, oral challenges with peanut (Group I) or milk (Group II) elicited only minor or no symptoms. In addition, skin test end‐point titrations showed marked reductions for &gt;10 weeks after treatment, and levels of Ara h 1‐specific IgE in serum of peanut sensitive dogs, as demonstrated by immunoblotting, were greatly reduced by treatment with HKL plus peanut allergen. Conclusions: Thus, HKL plus allergen treatment markedly improved established food allergic responses in dogs, suggesting that such an immunotherapy strategy in humans might greatly improve individuals with food allergy and anaphylaxis.
Role of reproductive factors in hepatocellular carcinoma: Impact on hepatitis B- and C-related risk
Authors: Ming-Whei Yu, Hung-Chuen Chang, Shun-Chiao Chang, Yun-Fan Liaw, Shi-Ming Lin, Chun-Jen Liu, Shou-Dong Lee, Chih-Lin Lin, Pei-Jer Chen, Shee-Chan Lin, Chien-Jen Chen
Journal: Hepatology (2003)

Hepatocellular carcinoma (HCC) is more prevalent in men than in women. Estrogen may play some role in the development of HCC. We conducted a multicenter case–control study to evaluate the effects of reproductive factors on HCC risk, and to assess whether the association between each factor and HCC differs between hepatitis B surface antigen (HBsAg)–positive and –negative women, in which hepatitis C virus (HCV) is the major cause of HCC. The study included 218 women with HCC and 729 control women selected from nonbiological and first–degree female relatives of patients with HCC. The risk of HCC was inversely related to the number of full–term pregnancies (FTP) ( P trend = .0216) and age at natural menopause ( P trend = .0251 among women aged 45–55 without prior surgical menopause). Oophorectomy at age ≤50 during premenopausal years was also a risk factor (multivariate–adjusted OR, 2.57; 95% CI, 1.42–4.63). Use of hormone replacement therapy (HRT) (multivariate–adjusted OR, 0.46; 95% CI, 0.27–0.79) was associated with a lower risk of HCC, and there was a trend in the risk with increasing duration of HRT ( P trend = 0.0013). All reproductive factors had a similar impact on HBsAg–positive and –negative women except for an early menarche (≤12 vs. ≥16 years), which increased HCC risk in HBsAg carriers (multivariate–adjusted OR, 6.96; 95% CI, 2.52–19.18) but posed no increased risk in noncarriers ( P interaction = .0053). In conclusion, increased exposure to estrogen during adulthood may provide a protective effect against HCC. Nevertheless, an early menarche, which results in early estrogen exposure, does not confer protection for HBsAg carriers.
Newly Discovered Mechanism Points to Diabetes Prevention Strategy
Authors: Tracy Hampton
Journal: JAMA (2013)

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
Role of thyroid hormones in apolipoprotein A-I gene expression in rat liver.
Authors: W Strobl, N L Gorder, Y C Lin-Lee, A M Gotto, W Patsch
Journal: Journal of Clinical Investigation (1990)

To study the regulation of hepatic apo A-I gene expression, we measured synthesis and abundance of cellular apo A-I mRNA and its nuclear precursors in livers of hypothyroid and hyperthyroid rats. In hypothyroid animals, both synthesis and abundance of apo A-I mRNA was reduced to half of control values. After injection of a receptor-saturating dose of triiodothyronine into euthyroid rats, apo A-I gene transcription increased at 20 min, reached a maximum of 179% of control (P less than 0.01) at 3.5 h, and remained elevated for up to 48 h. The abundance of nuclear and total cellular apo A-I mRNA increased at 1 and 2 h, respectively, and exceeded the levels expected from enhanced transcription more than two fold at 24 h after hormone injection. Upon chronic administration of thyroid hormones, levels of nuclear and cytoplasmic apo A-I mRNA remained elevated but transcription of the apo A-I gene fell to 42% of control (P less than 0.01). Thus, thyroid hormones rapidly stimulate apo A-I gene transcription. Posttranscriptional events leading to increased stability of nuclear apo A-I RNA precursors become the principal mechanism for enhanced gene expression in chronic hyperthyroidism and may cause feedback inhibition of apo A-I gene transcription. Our results furthermore imply that the majority of hepatic nuclear apo A-I RNA precursors are degraded in euthyroid animals.
Unnecessary hospital referral data
Authors: K C Harvey
Journal: BMJ (1991)

sizes: fewer than 1500 patients per doctor.This has major implications for our resourcing, worse since the new contract's encouragement of higher list sizes.We serve one of the two most deprived areas in Bristol, but UPA(8) anomalies mean we receive no deprivation payments at all.Talbot' and Carr- Hill and Sheldon' have clearly shown this range of issues.
Hypothyroidism After Small Doses of Radioiodine in Hyperthyroidism.
Authors: Joseph A. Glennon
Journal: Annals of Internal Medicine (1971)

Meeting Abstracts1 May 1971Hypothyroidism After Small Doses of Radioiodine in Hyperthyroidism.Joseph A. Glennon, M.D., F.A.C.P., Clark T. Sawin, M.D., Edgar S. Gordon, M.D., F.A.C.P.Joseph A. Glennon, M.D., F.A.C.P.Search for more papers by this author, Clark T. Sawin, M.D.Search for more papers by this author, Edgar S. Gordon, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-74-5-823_5 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptSome have suggested that the incidence of hypothyroidism after treatment of hyperthyroidism with radioiodine may be lessened by using a lower dose of radioiodine. We traced 64 hyperthyroid patients who were successfully treated with 3 mc of radioiodine or less before 1951. Nine were lost to follow-up shortly after treatment. The remaining 55 were found, their thyroid status at last examination noted, and the data analyzed with the life-table method. The incidence of hypothyroidism was low (4%) at the end of the first year, as others have noted with lower doses of radioiodine. The cumulative incidence of hypothyroidism remained low... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Joseph A. Glennon, M.D., F.A.C.P.; Clark T. Sawin, M.D.; Edgar S. Gordon, M.D., F.A.C.P.Affiliations: Boston, Mass., and Madison, Wis. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1971Volume 74, Issue 5Page: 823-824KeywordsHyperthyroidismHypothyroidismThyroid ePublished: 1 December 2008 Issue Published: 1 May 1971 PDF downloadLoading ...
Effects of naloxone on myocardial ischemic preconditioning in humans
Authors: Fabrizio Tomai, Filippo Crea, Achille Gaspardone, Francesco Versaci, Anna S Ghini, Claudio Ferri, Giovambattista Desideri, Luigi Chiariello, Pier A Gioffré
Journal: Journal of the American College of Cardiology (1999)
Unusual extramedullary relapses under imatinib mesylate treatment in chronic myeloid leukemia
Authors: Yavuz Beyazit, Salih Aksu, Murat Kekilli, Ibrahim C. Haznedaroglu, Sadettin Kilickap, Hakan Goker
Journal: American Journal of Hematology (2005)

To the Editor: Imatinib mesylate has tremendously changed the clinical course of chronic myeloid leukemia (CML).Higashi and co-workers reported two CML patients who had imatinib-sensitive blast crisis immediately after discontinuation of the drug due to neutropenia in a recent issue of the this journal [1].Herein we report two CML cases that developed extramedullary collection of myeloblasts during the imatinib treatment.
Successful Treatment with Steroids of Upper Gastrointestinal Acute Graft vs. Host Disease After Hematopoietic Stem Cell Transplantation
Authors: T. Nishi, K. Okazaki, S. Fujii, K. Uchida, S. Uose, H. Nakase, M. Ohana, T. Nishihara, T. Chiba
Journal: Endoscopy (2001)

A 39-year-old man with acute myeloid leukemia underwent completely matched related hematopoietic stem cell transplantation. On post-transplantation day 83 he was diagnosed as having upper gastrointestinal graft-versus-host disease (GVHD) by endoscopic examination and pathological examination of endoscopic biopsy specimens, and daily administration of 60 mg of water-soluble prednisolone and 50 mg of cyclosporine was started. After steroid therapy, the symptoms of upper gastrointestinal GVHD disappeared completely and endoscopic findings dramatically improved.
Acute Febrile Reaction to Mephenesin Carbamate
Authors: David T. Schwartz, Charles F. Schetlin, Harold A. Zintel
Journal: JAMA (1964)

UNTOWARD REACTIONS to mephenesin carbamate (Tolseram) or to the parent compound, mephenesin, have been rare<sup>1</sup>and have occurred only after prolonged administration or overdose.<sup>2</sup>Mephenesin is an aromatic glycerol ether which decreases polysynaptic transmission in the spinal cord and brain stem and is used as a skeletal muscle relaxant in the treatment of multiple sclerosis, Parkinsonism, acute anxiety, and acute muscle strain. The patient described here represents, as far as we know, the first reported case of acute toxic reaction occurring soon after administration of mephenesin carbamate in small oral doses. <h3>Report of a Case</h3> A 39-year-old white male college professor was first seen at St. Luke's Hospital, New York, on May 8, 1964, complaining of low back pain five days after carrying heavy objects. His past history included suffering from "hay fever," but was otherwise noncontributory. He presented with a temperature of 98.6 F (37 C), respirations,