tbuckley/cabot-search huggingface dataset:
Differential expression of novel tyrosine kinase substrates during breast cancer development
Authors: Yunhao Chen, Lee Yee Choong, Qingsong Lin, Robin Philps, Chee Hong Wong, Boon Keong Ang, Marie Chiew Shia Loh, Choy Leong Hew, Nilesh Shah, Brian J Druker, Poh Kuan Chong, Yoon Pin Lim
Journal: Clinical Cancer Research (2007)

To identify novel tyrosine kinase substrates that have never been implicated in cancer, we studied the phosphoproteomic changes in the MCF10AT model of breast cancer progression using a combination of phosphotyrosyl affinity enrichment, iTRAQ TM technology, and LC-MS/MS. Using complementary MALDI- and ESI-based mass spectrometry, 57 unique proteins comprising tyrosine kinases, phosphatases, and other signaling proteins were detected to undergo differential phosphorylation during disease progression. Seven of these proteins (SPAG9, Toll-interacting protein (TOLLIP), WBP2, NSFL1C, SLC4A7, CYFIP1, and RPS2) were validated to be novel tyrosine kinase substrates. SPAG9, TOLLIP, WBP2, and NSFL1C were further proven to be authentic targets of epidermal growth factor signaling and Iressa (gefitinib). A closer examination revealed that the expression of SLC4A7, a bicarbonate transporter, was down-regulated in 64% of the 25 matched normal and tumor clinical samples. The expression of TOLLIP in clinical breast cancers was heterogeneous with 25% showing higher expression in tumor compared with normal tissues and 35% showing the reverse trend. Preliminary studies on SPAG9, on the other hand, did not show differential expression between normal and diseased states. This is the first time SLC4A7 and TOLLIP have been discovered as novel tyrosine kinase substrates that are also associated with human cancer development. Future molecular and functional studies will provide novel insights into the roles of TOLLIP and SLC4A7 in the molecular etiology of breast cancer. Molecular & Cellular Proteomics 6:2072–2087, 2007.
Abstract 17746: Differences of Serial Changes of Neointimal Coverage among 2.5, 3.0 and 3.5 Sirolimus-Eluting Stents: Follow-Up Optical Coherence Tomography Study
Authors: Daisuke Nakamura, Masami Nishino, Yasuharu Lee, Takahiro Yoshimura, Masayuki Taniike, Nobuhiko Makino, Hiroyasu Kato, Yasuyuki Egami, Ryu Shutta, Jun Tanouchi, Yoshio Yamada
Journal: Circulation (2010)

Background: Some reports showed serial changes of neointimal coverage after sirolimus-eluting stents (SES) implantation however, the differences among 2.5, 3.0 and 3.5 mm-sized SES have not been sufficiently evaluated. Thus, we investigated the differences of serial changes of neointimal coverage post SES implantation among 2.5, 3.0 and 3.5 mm-stents with a follow-up optical coherence tomography (OCT) study. Methods: Post-stent OCT evaluation at 6–8 and 18–20 months follow-up were performed in 12 patients (18 SESs). Differences of the percent of covered struts and neointimal hyperplasia thickness. (NIH), which were evaluated by serial OCT from 6–8 months to 18–20 months follow-up, were compared among 2.5, 3.0, and 3.5 mm-SESs. Results: We evaluated 458 struts in 2.5 mm-SESs, 1214 struts in 3.0 mm-SESs and 622 struts in 3.5 mm-SESs at 6–8 months and 487 struts in 2.5 mm-SESs, 931 struts in 3.0 mm-SESs and 352 struts in 3.5 mm-SESs at 18–20 months after stent implantation by OCT. Percent of covered struts w...
Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery
Authors: Mary C Corretti, Todd J Anderson, Emelia J Benjamin, David Celermajer, Francois Charbonneau, Mark A Creager, John Deanfield, Helmut Drexler, Marie Gerhard-Herman, David Herrington, Patrick Vallance, Joseph Vita, Robert Vogel
Journal: Journal of the American College of Cardiology (2002)
A Study of the Differential Blood Count in One Thousand Cases of Active Pulmonary Tuberculosis
Authors: John W. Flinn
Journal: Annals of Internal Medicine (1929)

Article1 January 1929A Study of the Differential Blood Count in One Thousand Cases of Active Pulmonary TuberculosisJOHN W. FLINNJOHN W. FLINNSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-2-7-622 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis study was prompted by the work of Cunningham, Sabin et al, at the Johns Hopkins Hospital, on the rôle of the monocyte in experimental tuberculosis. After the study was begun, its scope was influenced very materially by the conclusions of Medlar and his co-workers at the University of Wisconsin, regarding the different parts played by the monocyte, the neutrophile and the lymphocyte in the histopathological reaction in tuberculosis.Sabin and her associates, using supravital staining methods, traced the monocyte from its origin in the reticular cells of the spleen and of the bone-marrow to its consummation in the typical... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Prescott, Arizona*Presented before the American College of Physicians, New Orleans, March 6, 1928. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThe course of fever during treatment of pulmonary tuberculosis 1 January 1929Volume 2, Issue 7Page: 622-636KeywordsBlood countsCellsLymphocytesMonocytesSpleenStaining ePublished: 1 December 2008 Issue Published: 1 January 1929 PDF downloadLoading ...
474. The Barrier to Liposomal Transfection Is Enhanced by DNASES Lacking Lysosomal-Targetting Glycosylation
Authors: Andrew Wilber, Gary Armour, Michael C. Schneider
Journal: Molecular Therapy (2004)

Prior studies suggested that liposome-transfected plasmids, to achieve expression, had to evade post-endocytic lysosomal degradation by Dnase 1 (D1) and/or Dnase II; however, we have shown that the main circulating nuclease barrier to liposomal gene transfection is almost certainly the macrophage-secreted enzyme Dnase1-like 3 (Dnase1l3 or D3) [Wilber et al. Mol Ther 2002]. In addition, we found this barrier is not cell-autonomous, but is conveyed upon HeLa cells by media conditioned either by cells expressing transfected D3 or interferon-gamma induced macrophages. By immunoprecipitation, western, and zymogram, the only Dnase secreted by induced macrophages is the 28 kDa D3 enzyme. This innate immunity function is postulated to exist to protect cells against the entry and expression of potentially mutagenic or infectious extracellular DNA. While homologous to D1 over its core nuclease sequence, D3 has a distinct basic C-terminus. If this C-terminus is truncated from D3, the remaining protein retains its nuclease activity against naked or  DNA, yet loses barrier activity. In-frame fusion to D1 of this C-terminal domain creates a chimeric enzyme (D1-D3CT) with significantly increased barrier activity. Substitution of asparagines residues involved in N-linked glycosylation of D1 are known to diminish the targeting of this enzyme to lysosomes [Nishikawa et al. J Biol Chem 1999]. We find that for both D1 and D1-D3CT, N > S substitutions at these residues progressively increase the capacity of the nucleases to block transfection. As expected, the N > S substitutions in murine D1 and chimeric D1-D3CT translated smaller, sharper bands of nuclease activity in SDS-PAGE zymograms. Barrier to transfection activity was quantified by measuring the efficiency of transfection using FuGene-6 (Roche) reagent. of GFP-expression vectors Efficiency was measured by flow cytometry. No GFP expression is detectable by western in D3-exposed cells, and free DNA nuclease activity in the media by RDA was about half that found for D1. As measured by radial diffusion assays, levels of free-DNA nuclease activity in conditioned media were not significantly different between any of the D1 and D1-D3CT enzymes. In summary, D1-D3CT sans N-linked glycosylation erects a more potent a barrier to transfection when compared to both wild-type D1 or D1-D3CT. Results strongly suggest the majority of liposome-bound DNA achieves expression mainly by entering via a non-lysosomal pathway guarded by D3, and generally distinct from that targeted by a lysosomal enzyme like D1. Studies of this nuclease barrier will help explain the mechanism by which liposomal gene transfer occurs, and help devise methods to improve efficiency.
Abstract 102: KDM5B plays a central role in esophageal cancer progression
Authors: Naohiro Nishida, Yoshihiro Kano, Jun Koseki, Masamitsu Konno, Koichi Kawamoto, Yuichiro Doki, Masaki Mori, Hideshi Ishii
Journal: Cancer Research (2015)

Abstract Esophageal cancer is consists of highly heterogeneous populations, which include cancer initiating cells, so-called cancer stem cells. Although histone modification is shown to be an essential factor for normal stem cell maintenance, the involvement of histone demethylase in cancer progression has been poorly understood. We investigated the functional roles of the Histone H3 lysine 4 (H3K4) demethylase KDM5B, a crucial epigenetic regulator that is required for normal embryonic development and cell growth. KDM5B knockdown resulted in the suppression of esophageal cancer cell growth, sphere formation and invasion ability and was associated with loss of epithelial cell marker expression. These tumor inhibitory effects were reverted subsequent to subcutaneous inoculation of these cells into immune-deficient mice. These results indicated that KDM5B plays an important role in maintaining cancer stem cells and justifies the rationale for studying the effects of continuous inhibition of this epigenetic factor in esophageal cancer. Citation Format: Naohiro Nishida, Yoshihiro Kano, Jun Koseki, Masamitsu Konno, Koichi Kawamoto, Yuichiro Doki, Masaki Mori, Hideshi Ishii. KDM5B plays a central role in esophageal cancer progression. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 102. doi:10.1158/1538-7445.AM2015-102
The New Living Heart Michael E. DeBakey, MD, Antonio M. Gotto, Jr, MD, DPhil. 495 pp. Holbrook, Mass: Adams Media Corp; 1997. $17.95. ISBN 1-55850-722-1.
Authors: Lori Mosca, Ralph Mosca
Journal: Circulation (1998)

The end of this millennium will be remembered for many things. Chief among them will be that this was the era of the consumer, whose needs helped to ignite and continue to fuel an explosive information age. Slogans such as “An educated consumer is our best customer” epitomize the paradigm shift from gullery to tutelage in contemporary marketing, although some may view the latter as simply a more sophisticated form of mendacity. In part, the new strategy is a response to advances in communication technology coupled with the compulsions of discerning consumers. Parallel transitions have occurred in medicine, now known as the healthcare industry, in which the term client has become synonymous with patient, the concept of population served has been replaced by the number of lives covered, and in which a practice may not survive without an elaborate Web site or home page. The patient is now the commodity. The buyer’s market in medicine has stimulated efforts at outreach and information transfer at unprecedented levels.

Medical consumers have become efficient search engines. They can access the latest medical information on-line, they are intrigued by watching live operations on the Nova channel, and they are able to read the results of research studies in the New York Times, often long before medical journals ever hit our “in” boxes. With …
Abstract 4009: N-ras codon 61 mutation is associated with distant metastasis in patients with follicular thyroid carcinoma
Authors: MinJi Jeon, Eun Kyung Jang, Dong Eun Song, So Young Sim, Eui Young Kim, Yun M. Choi, Ji Min Han, Won G. Kim, Tae Yong Kim, Young Kee Shong, Won Bae Kim
Journal: Cancer Research (2014)

Abstract Distant metastasis is a main cause of death in follicular thyroid carcinoma (FTC) patients. Factors related to distant metastasis in FTC had been known as age, primary tumor size, and invasiveness. Ras mutations were also supposed to be associated with poor clinical outcomes. We analyzed Ras mutations in FTC with a distant metastasis (FTC M1, n=28), size matched-FTC without a distant metastasis (FTC M0, n=28), follicular adenoma (FA, n=17), and nodular hyperplasia (NH, n=12) to figure out the roles of Ras mutations in follicular thyroid carcinogenesis and metastasis. In addition, we assess the relationship between Ras mutations and clinical outcomes in FTC patients. NRAS, HRAS, and KRAS mutations were assessed using direct sequencing method. Among 85 patients, 39 patients (46%) had Ras mutations. NRAS codon 61 mutation (n=21; 25%) was the most common point mutation. HRAS codon 61, KRAS codon 12/13, and KRAS codon 61 mutations were found in 7, 6, and 4 patients, respectively. NRAS codon 12/13 mutation was found in only 1 patient, and HRAS codon 12/13 mutation was not found. Ras mutations were significantly more common in the FTC than FA or NH groups. Especially, NRAS codon 61 mutation was associated with distant metastasis in patients with FTC. However, there was no significant difference in survival between the Ras mutation positive-FTC and Ras mutation negative-FTC patients. Ras mutation, especially NRAS codon 61 mutation, was significantly associated with the presence of distant metastases. NRAS codon 61 mutation status might be a potential prognostic factor in FTC patients. Citation Format: MinJi Jeon, Eun Kyung Jang, Dong Eun Song, So Young Sim, Eui Young Kim, Yun Mi Choi, Ji Min Han, Won Gu Kim, Tae Yong Kim, Young Kee Shong, Won Bae Kim. N-ras codon 61 mutation is associated with distant metastasis in patients with follicular thyroid carcinoma. [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 4009. doi:10.1158/1538-7445.AM2014-4009
Abstract 1746: Novel and selective Axl inhibitors
Authors: Zaihui Zhang, Rick Li, Erica Lee, Yuxiang Hu, Jun Yan, Jasbinder Sanghera
Journal: Cancer Research (2014)

Abstract Axl is a member of the TAM tyrosine kinase family and is activated by products of Gas6 and Protein S genes. Axl is overexpressed or overactive in breast, renal, endometrial, ovarian, thyroid, non-small cell lung carcinoma, uveal melanoma as well as in myeloid leukemias. It has also been demonstrated that Axl expression is upregulated in drug-resistant cancer cells. Knock-down of Axl by RNAi repressed tumor formation in MDA-231 breast carcinoma model. Downregulation of Axl expression by RNAi led to a decrease of K562/ADR and MCF-7/ADR cells invasion, proliferation, and increased cell chemosensitivity in vitro. In a xenograft model of MDR cells, downregulation of Axl enhanced the anticancer activity of chemotherapeutic drugs. Therefore, Axl is a potential target for the development of chemotherapeutic agents for cancer therapy. During our endeavor of discovering and developing Axl kinase inhibitors for cancer therapy, we have discovered a series of potent and selective Axl inhibitors. These new compounds have demonstrated nM potency against Axl and good selectivity against other kinases in a selected panel of kinases. Many of these new compounds can reduce the pAkt levels in several cancer cell lines in a dose dependent manner and demonstrated inhibition of cell proliferation at sub-micromolar concentration in thymidine incorporation assay. Several selected compounds have demonstrated efficacy in colony formation assays. The most promising compounds are now being selected for in vivo proof-of-concept studies. The pharmaceutical properties of these compounds together with ADME profile were also evaluated and will be reported. These new Axl inhibitors represent a new approach for cancer therapy. Citation Format: Zaihui Zhang, Rick Li, Erica Lee, Yuxiang Hu, Jun Yan, Jasbinder Sanghera. Novel and selective Axl inhibitors. [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 1746. doi:10.1158/1538-7445.AM2014-1746
The World Health Organisation: WHO's special programmes: undermining from above
Authors: F. Godlee
Journal: BMJ (1995)

Despite the World Health Organisation's spoken commitment to developing integrated primary health care, its most visible and successful activities are not integrated within countries; they are its disease specific intervention programmes, such as the Global Programme on AIDS and the programmes for the control of diarrhoeal and acute respiratory diseases. The 10 or so special programmes, all but one of which (the onchocerciasis control programme) are based in Geneva, have found increasing favour among donors, but critics say that they undermine WHO's attempts to integrate its activities at country level and discourage countries from developing their own capacity.The World Health Organization (WHO) has affirmed its commitment to develop integrated primary health care. WHO's most visible and successful activities are, however, its disease and specific intervention programs such as the Global Program on AIDS and programs for the control of diarrheal and acute respiratory diseases. These special programs were established in response to the perceived need among donors for initiatives which were more comprehensive than WHO's regional and country-based activities. Donors want more accountability and transparency as well as more aggressive, concrete, solid work on important problems. The special programs therefore receive no funds from WHO's regular budget, but are funded from extrabudgetary contributions. Each special program has its own director and a management executive committee comprised of donors' representatives. The programs boost WHO's routine activities, using international and regional expertise and a project-based approach to attack specific diseases or health issues. Donor placement of funds outside of the control of WHO central management, however, points to the decline of WHO and the lack of faith among donors about its abilities. While the ten or so special programs have found increasing favor among donors, it is possible that they undermine WHO's attempts to integrate its activities at the country level and discourage countries from developing their own capacity. There is a great need for WHO to take stock of what is happening both within and to itself, and to make appropriate changes to facilitate achieving sustainable change at the country level.
Drug Reimportation Talks
Authors: Tracy Hampton
Journal: JAMA (2005)

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
Reference values for the 6 minute walk test in healthy Italian children aged 6-11 years
Authors: Diletta Innocenti, Eleonora Masi, Matteo Masolini, Simone Gambazza, Sergio Zuffo, Enrico Lombardi
Journal: European Respiratory Journal (2013)

Background -  The 6 minute walk test (6MWT) assesses the exercise capacity in children with chronic lung disease. Despite its widespread use, reference values for the 6MWT in children have only been published by 2 other groups in Europe and are currently not available for Italian children. Aim of the present study was to establish references values for the 6MWT in healthy Italian children aged 6 to 11 years.   Methods -  Children were recruited from two primary public schools. Parents were asked to provide clinical information about their children via questionnaires. The anthropometric data of all children were evaluated and the main outcome measure was the distance walked in 6 min. Tests were conducted according to the American Thoracic Society guidelines (1).   Results -  A total of 261 healthy Italian children (range 6-11 years) were recruited. Overall, the mean distance walked in 6 min was 612.9 m with no significant difference between boys and girls. Univariate analysis showed that age, height, weight and the weekly amount of physical activity were significantly correlated with the distance walked in 6 min. When adjusting for the other covariates, age, height and weight were independently correlated with the 6 min walk distance and explained 25% of the variability of the distance covered.   Conclusions -  We have assessed reference values for the 6MWT in 6-11 year old Italian children. These standards will provide useful references for the care of paediatric patients with chronic lung disease.  (1) ATS Statement: Guidelines for the Six-Minute Walk Test. Am J Respir Crit Care Med 2002;166:111-117
Nitric oxide generated by ionizing radiation facilitates egf receptor signaling in lung cancer cells
Authors: Hyung-Chahn Lee, Sang-Hyeok Woo, Hyeon-Ok Jin, Sung-Keum Seo, Su-Im Yoon, Myung-Jin Park, Doo-Hyun Yoo, Young-Joon Hong, Chang-Hun Rhee, Seok-Il Hong, In-Chul Park
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4414 

Ionizing radiation (IR) is utilized as a treatment to cure or manage cancer. Various components of IR-inducible signal transduction cascade can promote the survival of tumor cells and confer relative resistance to IR. Understanding the mechanisms of these responses should provide new molecular targets for tumor radiosensitization. In this present study, we investigate the roles of nitric oxide (NO) generated by IR in the signaling of EGF in A549 non-small cell lung carcinoma cells. A549 lung adenocarcinoma cells were exposed to IR, and NO level and NO synthase (NOS) activity was determined. NO scavenger, NO donor and NO synthase (NOS) inhibitor were used, and transfection of NOS cDNA and its siRNA was performed. Then, EGF receptor signal events were analyzed. exposure of cells to IR resulted in a transient induction of EGF receptor phosphorylation in dose-dependent manner. NO scavenger and NO synthase (NOS) inhibitor suppressed the IR-induced generation of NO, EGF receptor (EGFR) phosphorylation, and its downstream signal activation such as Shc binding, Akt and ERK1/2 phosphorylation. Furthermore, overexpression of NOS increased the IR-induced NO production and EGFR activation, and siRNA of NOS suppressed these events. These results indicate that NO produced by IR significantly contributes to the EGF receptor-mediated signaling. These study suggests that IR-induced NO formation is required in the EGF receptor phosphorylation and its signal activation. Detailed analysis of the mechanisms of cross-talk of IR-induced NO production via NOS and EGFR will yield new therapeutic interventions for EGFR signal-related diseases such as cancer. Acknowledgement: This work is supported by the National Nuclear R & D program of the Ministry of Science & Technoloy of Korea