tbuckley/cabot-search huggingface dataset:
Abstract A40: The incorporation of PTEN/EGFR (DNA) FISH and quantitative biomarker immunofluorescence identifies a phenotype associated with survival in patients with malignant glioma
Authors: Michael Joseph Donovan, Nadina Erill, Pere Puig, Anna Colomer, Susana Boluda, Isidre Ferrer
Journal: Clinical Cancer Research (2010)

Abstract Introduction: Glioblastoma multiforme (GBM) is the most common and malignant of adult glial tumors. Despite best standard of care including surgical resection, radiation and chemotherapy (e.g. temozolomide), the median survival remains approximately 12 – 15 months, with fewer than 25% of patients surviving up to 2 years and less than 10% of patients surviving up to 5 years. We sought to identify a preliminary set of baseline tissue-based DNA and protein features which may reflect growth mechanisms responsible for disease progression, and overall survival (OS). Methods: Formalin fixed paraffin embedded specimens from 54 patients (44 Astrocytoma (including 14 GBM), 6 oligodendroglioma and 4 mixed) with outcome data and a median follow-up of 3 years were evaluated using dual-color DNA FISH for PTEN and EGFR. A multispectral immunofluorescent (IF) assay was used as previously described (Cordon-Cardo et al., 2007) to evaluate Ki67, PTEN, and P-AKT. Feature performance was univariately assessed using Kaplan-Meier survival curves. Results: A &amp;gt;10% Loss of heterozygosity (LOH) for PTEN (p-value &amp;lt;0.05) but not EGFR amplification / polysomy was associated with decreased OS in the total cohort. By comparison, the combination of PTEN LOH and EGFR amplification/polysomy in the GBM-only group (n=12, complete data files) was associated with improved survival (p-value 0.03). By quantitative IF, increasing levels of KI67 were associated with shortened OS (p-value 0.004) in the total cohort. Conclusions: The incorporation of DNA FISH and quantitative IF is useful for developing a biologic baseline for understanding disease course in malignant gliomas. PTEN LOH and EGFR amplification / polysomy in GBM may suggest a pathway mechanism for favorable response. Citation Information: Clin Cancer Res 2010;16(7 Suppl):A40
Cystinuria caused by mutations in rBAT, a gene involved in the transport of cystine
Authors: María Julia Calonge, Paolo Gasparini, Josep Chillarón, Miguel Chillón, Michele Gallucci, Ferran Rousaud, Leopoldo Zelante, Xavier Testar, Bruno Dallapiccola, Franco Di Silverio, Pedro Barceló, Xavier Estivill, Antonio Zorzano, Virginia Nunes, Manuel Palacín
Journal: Nature Genetics (1994)
Vaccine related poliomyelitis in non-immunised relatives and household contacts.
Authors: D E Bateman, G Elrington, P Kennedy, M Saunders
Journal: BMJ (1987)

A propos de 2 observations: la paliomyelite avec paralysie peut etre contractee par les sujets non immunises, lors de la vaccination d'enfants de leur famille. La vaccination devrait etre appliquee a tous les membres de la maisonnee
635. Experimental Study on Changes of the Revascularization and Expression of VEGF and Its Receptors in Ischemic Skeletal Muscle
Authors: Wei Liang, Baigen Zhang, Hao Zhang, Jiwei Zhang, Zhaoxiong Zhou
Journal: Molecular Therapy (2005)

Background: Vascular endothelial growth factor (VEGF) may become the candidate for the treatment of the refractory arterial occlusive disease. The angiogenesis value of VEGF depends on the expression of its specific receptors that include Flt-1 and Flk-1. However, excessive quantity of VEGF may cause tumor. So the exogenous VEGF should be used under the condition of VEGF deficiency and VEGF receptors sufficiency. The aim of this study was to investigate dynamic expression of endogenous VEGF and its receptors in skeletal muscle under limb ischemia condition.
Cardiovascular Risk Factors Are Associated With Increased Arterial Stiffness in Youth With Type 1 Diabetes
Authors: Dana Dabelea, Jennifer W. Talton, Ralph D’Agostino, R. Paul Wadwa, Elaine M. Urbina, Lawrence M. Dolan, Stephen R. Daniels, Santica M. Marcovina, Richard F. Hamman
Journal: Diabetes Care (2013)

OBJECTIVE To evaluate if presence of cardiovascular (CV) risk factors and their clustering as metabolic syndrome (MetS) is associated with increased arterial stiffness and accelerated progression over time among youth with type 1 diabetes. RESEARCH DESIGN AND METHODS Longitudinal study of 298 youth with type 1 diabetes (age 14.5 years; 46.3% female; duration 4.8 years), with two research visits conducted 5 years apart. CV factors included: waist circumference, blood pressure (BP), fasting lipids (HDL cholesterol, LDL cholesterol [LDL-c], triglycerides), albumin/creatinine ratio, and HbA1c. MetS was based on Adult Treatment Panel III criteria modified for youth. Pulse wave velocity (PWV) in the carotid–femoral segment was measured by tonometry. Mixed models were used to assess the rate of progression in PWV and the association between CV factors and PWV over time. RESULTS PWV increased significantly over time (0.145 m/s/year; P &amp;lt; 0.0001). MetS (P = 0.0035), large waist (P &amp;lt; 0.0001), and elevated BP (P = 0.0003) at baseline were each associated with worse PWV over time. These baseline factors, however, did not significantly influence the rate of progression. Increases in waist circumference (P &amp;lt; 0.0001), LDL-c levels (P = 0.0156), and declining glucose control (HbA1c; P = 0.0419) were independently associated with higher PWV over time. CONCLUSIONS Presence, clustering, and worsening of CV risk factors are associated with increased arterial stiffness over time in youth with type 1 diabetes. Whether improvement in CV risk factors early in life will slow the progression of arterial stiffness and reduce the burden of CV disease in this population requires further study.
A rapid drug release system with a NIR light-activated molecular switch for dual-modality photothermal/antibiotic treatments of subcutaneous abscesses
Authors: Wei-Lun Chiang, Tzu-Tsen Lin, Radhakrishnan Sureshbabu, Wei-Tso Chia, Hsu-Chan Hsiao, Hung-Yi Liu, Chih-Man Yang, Hsing-Wen Sung
Journal: Journal of Controlled Release (2014)
Virus receptor trap neutralizes coxsackievirus in experimental murine viral myocarditis
Authors: B LIM, J CHOI, J NAM, C GIL, J SHIN, S YUN, D KIM, E JEON
Journal: Cardiovascular Research (2006)

The coxsackie and adenovirus receptor (CAR) and the decay-accelerating factor (DAF) are receptors for coxsackievirus B3 (CVB3), which is known as the major cause of human viral myocarditis. We investigated the potential for therapeutic use of soluble virus receptor fusion proteins.We designed and generated a novel virus receptor trap (hCAR-hDAF:Fc) consisting of both CVB3 receptors and the Fc portion of human IgG1 and evaluated its antiviral effects in experimental CVB3 myocarditis.Among four soluble virus receptor fusion proteins (hCAR:Fc, hDAF:Fc, hCAR-hDAF:Fc and hDAF-hCAR:Fc), hCAR:Fc and hCAR-hDAF:Fc in the supernatant of transfected cells neutralized echovirus, adenovirus, and various serotypes of CVB in a dose-dependent manner. Both soluble viral receptor proteins bound to the VP0 and VP1 capsid proteins of CVB3. The in vivo efficacy of viral receptor proteins was evaluated by intramuscular injection of plasmid (hCAR:Fc or hCAR-hDAF:Fc) followed by electroporation in a murine model of CVB3 myocarditis. Serum levels of the virus receptor proteins increased relative to baseline values from day 3 and peaked on day 14 at 12.9-fold for hCAR:Fc and 7.1-fold for hCAR-hDAF:Fc. The 3-week survival rate was significantly higher in hCAR-hDAF:Fc-treated mice (61%) than in hCAR:Fc-treated mice (29%) and in controls (15%; p<0.05). Myocardial inflammation, fibrosis, and myocardial virus titers were all significantly reduced in the hCAR:Fc and hCAR-hDAF:Fc groups compared to the controls.Our soluble virus receptor trap, hCAR-hDAF:Fc, attenuated viral infection, myocardial inflammation, and fibrosis, resulting in higher survival rates in mice with coxsackieviral myocarditis. Furthermore, it consists exclusively of human components, and we demonstrated that this soluble virus receptor trap may be used as a potential candidate for a novel therapeutic agent for the treatment of acute viral myocarditis during the viremic phase.
Functional Roles of Ca <sub>v</sub> 1.3 (α <sub>1D</sub> ) Calcium Channel in Sinoatrial Nodes
Authors: Zhao Zhang, Yanfang Xu, Haitao Song, Jennifer Rodriguez, Dipika Tuteja, Yoon Namkung, Hee-Sup Shin, Nipavan Chiamvimonvat
Journal: Circulation Research (2002)

We directly examined the role of the Ca v 1.3 (α 1D ) Ca 2+ channel in the sinoatrial (SA) node by using Ca v 1.3 Ca 2+ channel-deficient mice. A previous report has shown that the null mutant (Ca v 1.3 −/− ) mice have sinus bradycardia with a prolonged PR interval. In the present study, we show that spontaneous action potentials recorded from the SA nodes show a significant decrease in the beating frequency and rate of diastolic depolarization in Ca v 1.3 −/− mice compared with their heterozygous (Ca v 1.3 +/− ) or wild-type (WT, Ca v 1.3 +/+ ) littermates, suggesting that the deficit is intrinsic to the SA node. Whole-cell L-type Ca 2+ currents ( I Ca,L s) recorded in single isolated SA node cells from Ca v 1.3 −/− mice show a significant depolarization shift in the activation threshold. The voltage-dependent activation of Ca v 1.2 (α 1C ) versus Ca v 1.3 Ca 2+ channel subunits was directly compared by using a heterologous expression system without β coexpression. Similar to the I Ca,L recorded in the SA node of Ca v 1.3 −/− mutant mice, the Ca v 1.2 Ca 2+ channel shows a depolarization shift in the voltage-dependent activation compared with that in the Ca v 1.3 Ca 2+ channel. In summary, using gene-targeted deletion of the Ca v 1.3 Ca 2+ channel, we were able to establish a role for Ca v 1.3 Ca 2+ channels in the generation of the spontaneous action potential in SA node cells.
Abstract 2211: Accessible chromatin structure permits factors Sp1 and Sp3 to regulate human TGFBI gene expression
Authors: Jong-Joo Lee, Joo-Hong Park, Keunhee Park, Min-Ji Song, Wook-Jin Yang, Hyoung-Pyo Kim
Journal: Cancer Research (2012)

Abstract Transforming growth factor beta 1-induced (TGFBI) protein is an extracellular matrix (ECM) protein expressed widely in human tissues. The gene encoding this protein was first described as a major TGF-b-responsive gene in the lung adenocarcinoma cell line A549. TGFBI appears to mediate cell adhesion and migration through interaction with integrin, and increased TGFBI expression has been associated with inflammatory diseases including rheumatoid arthritis, atherosclerosis, cyclosporine nephropathy, and stab wound healing. TGFBI is ubiquitously expressed in healthy tissues, while disrupted TGFBI expression has been described in human tumor cell lines and in human primary tumor samples. A general function of this protein appears to be as a promoter or suppressor of cancer progression, depending on the tissue. Regulation of TGFBI expression by epigenetic mechanism such as DNA methylation and microRNA has been reported, but few studies have focused on how chromatin structure affects transcriptional activity relating to TGFBI expression. We show that both chromatin structure and regulatory elements in the TGFBI promoter region that bind factors Sp1 and Sp3 regulate constitutive expression of TGFBI. In this study, we investigated how human TGFBI expression is regulated in lung and breast cancer cells. We observed that the TGFBI promoter in A549 and MBA-MD-231 cells, which constitutively express TGFBI, existed in an open chromatin conformation associated with transcriptionally permissive histone modifications. Moreover, we found that TGFBI expression required Sp1 transcription elements that can bind transcription factors Sp1 and Sp3 in vitro. Occupancy of the TGFBI promoter by Sp1 and Sp3 in vivo was only observed in TGFBI-expressing cells, indicating that open chromatin conformation might facilitate the binding of Sp1 and Sp3 to the TGFBI promoter region. TGFBI promoter activity was impaired when Sp1 elements were mutated, but was increased when Sp1 or Sp3 factors was overexpressed. Furthermore, Sp1 inhibition in vivo by mithramycin A, as well as knockdown of Sp1 and/or Sp3 expression by short interfering RNA, significantly reduced TGFBI mRNA and protein levels. Thus, our data demonstrated that the expression of TGFBI is well correlated with chromatin conformation at the TGFBI promoter, and that factors Sp1 and Sp3 are the primary determinants for the control of constitutive expression of TGFBI gene. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2211. doi:1538-7445.AM2012-2211
Abstract P1-04-01: X-Linked Inhibitor of Apoptosis Protein (XIAP) Regulates TRAIL-Induced Apoptosis in Inflammatory Breast Cancer Cells
Authors: JL Allensworth, KM Aird, MB Murray, GR. Devi
Journal: Cancer Research (2010)

Abstract TRAIL, a proapoptotic receptor agonist, is a promising tool for anticancer therapy due to its selective triggering of death receptor-mediated apoptosis in cancer cells while sparing the majority of normal cells. Overexpression of X-linked inhibitor of apoptosis protein (XIAP) has been identified as a major mechanism of TRAIL resistance as a result of its ability to inhibit caspase activity, the effector arm of apoptotic cell death. Previous studies in our laboratory in preclinical models of inflammatory breast cancer (IBC), a highly invasive and lethal subtype, have revealed that apoptotic dysregulation mediated by XIAP is a key factor in IBC pathogenesis and acquired therapeutic resistance to epidermal growth factor receptor (ErbB1/2) targeting agents. Characterization of TRAIL efficacy in IBC cell lines derived from primary tumors revealed that SUM149, a triple negative, EGFR activated cell line, is sensitive to TRAIL-induced apoptosis and exhibits a corresponding decrease in XIAP and an increase in caspase3 activation compared to TRAIL-resistant SUM190, ErbB2 overexpressing cells in which XIAP levels are unchanged by TRAIL treatment. Profile from an apoptotic proteomic array revealed that SUM190 cells have low basal levels of the TRAIL receptors DR4 and DR5 in comparison to SUM149 cells. Stable overexpression of XIAP in the TRAIL-sensitive SUM149 cells resulted in a two fold decrease in sensitivity to TRAIL with decreased caspase3 activation. Further, SUM149wtXIAP cells showed low levels of TRAIL receptor expression similar to the TRAIL-insensitive SUM190 line. Conversely, increased cell death was observed in SUM190 cells in which XIAP was knocked down using a lentiviral shRNA expression construct. In order to examine therapeutic strategies aimed at restoring function to the apoptotic pathways in IBC cells, we used the small molecule inhibitor Embelin to modulate XIAP action. Treatment of SUM149wtXIAP cells with Embelin in combination with TRAIL enhanced cell death compared to treatment with TRAIL or Embelin alone. Assessment of the interaction using a derivation of the Chou-Talalay method revealed a combination index of 0.054 in SUM149wtXIAP cells, which is indicative of strong synergism between the two agents. These results reveal that knockdown or antagonism of XIAP allows TRAIL to induce activation of effector caspases efficiently and establishes the feasibility of use of XIAP inhibitors to enhance therapeutic apoptosis in IBC therapy. Funded by American Cancer Society-RSG-08-290-01-CCE (GRD), predoctoral DOD BCRP award (KMA), and the Duke University Chancellor's Scholarship (JLA). Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P1-04-01.
Scrotal ulceration during induction therapy of acute promyelocytic leukemia with ATRA
Authors: Keechilat Pavithran, Rajalakshmi Arjun, Raman Aruna, Mathew Thomas
Journal: American Journal of Hematology (2004)

Abstract all‐trans ‐Retinoic acid (ATRA) has been shown to improve survival in patients with acute promyelocytic leukemia (APML). It is a well‐tolerated drug except for the serious side effect of ATRA syndrome. Dryness of the skin, cheilitis, and xerostomia are the common mucocutaneous side effects. Occurrence of scrotal ulceration is very rare. We report a 13‐year‐old boy who had scrotal ulceration caused by ATRA during the induction therapy of APML. Am. J. Hematol. 75:260–261, 2004. © 2004 Wiley‐Liss, Inc.
THROMBOCYTOPENIC PURPURA AND HYPERTHYROIDISM
Authors: TOMÁS GONZÁLEZ
Journal: Annals of Internal Medicine (1967)

Letters and Comments1 December 1967THROMBOCYTOPENIC PURPURA AND HYPERTHYROIDISMTOMÁS GONZÁLEZ, M.D.TOMÁS GONZÁLEZ, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-67-6-1350_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor: Drs. Marshall, Weisberger, Levy, and Breckenridge in their article "Coexistent Idiopathic Thrombocytopenic Purpura and Hyperthyroidism," which appeared on p. 411 of the August 1967 issue of the ANNALS OF INTERNAL MEDICINE, reviewed 42 cases of thrombocytopenic purpura considered to be idiopathic, and they found 4 cases of manifest hyperthyroidism and 2 cases of latent Graves' disease. On this basis, the authors admitted that idiopathic thrombocytopenic purpura and hyperthyroidism may be related.The authors do not taken into account the possibility of thrombocytopenic purpura secondary to hyperthyroidism. Woodruff (1), and Darenskii (2) corrected the thrombocytopenic purpura in two...References1. WOODRUFF P: The behaviour of the blood platelets in thyrotoxicosis. Med. J. Aust. 2: 190, 1940. CrossrefGoogle Scholar2. DARENSKII DI: [Thrombopenic purpura in thyrotoxicosis.] (Rus.) Klin. Med. (Moskva) 38: 146, 1960. MedlineGoogle Scholar3. PAULINGONZALEZ CT: Purpura thrombocytopénique secondaire à hyperthyroidie. Canad. Med. Ass. J. 97: 229, 1967. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Hôtel-Dieu de Montréal Montreal Canada PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byIdiopathic thrombocytopenic purpura and graves disease 1 December 1967Volume 67, Issue 6Page: 1350-1351KeywordsHyperthyroidismIdiopathic thrombocytopenic purpura Issue Published: 1 December 1967 PDF downloadLoading ...
Colchicine, Serum Albumin, and Alkaline Phosphatase
Authors: David Kershenobich, MlSAEL Uribe, Gloria Irene Suárez, Ruy Pérez Tamayo, Marcos Rojkind
Journal: Annals of Internal Medicine (1978)

Letters and Corrections1 July 1978Colchicine, Serum Albumin, and Alkaline PhosphataseDAVID KERSHENOBICH, M.D., PH.D., MlSAEL URIBE, M.D., GLORIA IRENE SUÁREZ, M.B., RUY PÉREZ TAMAYO, M.D., MARCOS ROJKIND, M.D., PH.D.DAVID KERSHENOBICH, M.D., PH.D.Search for more papers by this author, MlSAEL URIBE, M.D.Search for more papers by this author, GLORIA IRENE SUÁREZ, M.B.Search for more papers by this author, RUY PÉREZ TAMAYO, M.D.Search for more papers by this author, MARCOS ROJKIND, M.D., PH.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-89-1-144_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Although colchicine has been used in humans for several centuries as an anti-inflammatory agent in acute gout, its pharmacologic properties as well as its metabolism and toxicity are not yet completely know.Two recent reports, one by Dr. Ravid and colleagues (1) in which colchicine given to patients with amyloidosis produced gradual remission of the nephrotic syndrome and a rise of serum albumin to normal levels, and another by Wilfred (2) in which colchicine administered in vivo to rats increased hepatic alkaline phosphatase activity, are interesting and provocative observations.We are conducting a double-blind trial designed to...References1. RAVID M, ROBSON M, and KEDAR (KEIZMAN) I: Prolonged colchicine treatment in four patients with amyloidosis. Ann Intern Med 87:568-570, 1977 LinkGoogle Scholar2. WILFRED G: Colchicine increases hepatic alkaline phosphatase activity. Biochim Biophys Acta 500:209-212, 1977 CrossrefMedlineGoogle Scholar3. KERSHENOBICH D, URIBE M, SUAREZ G, and ROJKIND M: Treatment of cirrhosis with colchicine: a randomized trial (abstract). Gastroenterology 70:986, 1976 Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: DAVID KERSHENOBICH, M.D., PH.D.; MlSAEL URIBE, M.D.; GLORIA IRENE SUÁREZ, M.B.; RUY PÉREZ TAMAYO, M.D.; MARCOS ROJKIND, M.D., PH.D. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byColchicine for alcoholic and non-alcoholic liver fibrosis and cirrhosisColchicine for alcoholic and non-alcoholic liver fibrosis and cirrhosisColchicine for alcoholic and non-alcoholic liver fibrosis or cirrhosisColchicine improves the alterations in the liver adenylate cyclase system of cirrhotic ratsReply 1 July 1978Volume 89, Issue 1Page: 144-144KeywordsAmyloidosisColchicineGoutPhosphatasesSerum albuminToxicity ePublished: 1 December 2008 Issue Published: 1 July 1978 PDF downloadLoading ...
Genes can disconnect the social brain in more than one way
Authors: André Aleman, René S. Kahn
Journal: Behavioral and Brain Sciences (2004)

Burns proposes an intriguing hypothesis by suggesting that the “schizophrenia genes” might not be regulatory genes themselves, but rather closely associated with regulatory genes directly involved in the proper growth of the social brain. We point out that this account would benefit from incorporating the effects of localized lesions and aberrant hemispheric asymmetry on cortical connectivity underlying the social brain. In addition, we argue that the evolutionary framework is superfluous.
Carotid baroreflex function in young men with borderline blood pressure elevation.
Authors: D L Eckberg
Journal: Circulation (1979)

Carotid baroreflex function was assessed in 10 normotensive young men and 20 age-matched subjects with borderline hypertension (successive blood pressures above and below 140/90 mm Hg) by measuring sinus node responses to brief neck suction. Subjects with borderline hypertension were divided into two equal groups according to their average systolic arterial pressures. Baroreflex responses were reset to function at higher pressure levels than normal in subjects with mild borderline hypertension, but reflex sensitivity was normal. Responses were also reset in subjects with more severe borderline hypertension, but reflex was subnormal. The results suggest that a gradation of baroreflex responsiveness exists among patients classified as having borderline hypertension: Subnormal responsiveness was found in those subjects whose resting average systolic arterial pressure was greater than or equal to 140 mm Hg.