40,187 research outputs found
Faculty recital: Tong-Il Han, September 30, 1994
Full text linkThis is the concert program of the Faculty recital: Tong-Il Han performance on Friday, September 30, 1994 at 8:00 p.m., at the Tsai Performance Center, 685 Commonwealth Avenue, Boston, Massachusetts. Works performed were Sonata in E major, Op. 109, Sonata in A-flat major, Op. 110, and Sonata in C minor, Op. 111 by Ludwig van Beethoven. Digitization for Boston University Concert Programs was supported by the Boston University Humanities Library Endowed Fund
IL-6, through p-STAT3 rather than p-STAT1, activates hepatocarcinogenesis and affects survival of hepatocellular carcinoma patients: a cohort study
No full textBackground: Biologic activities of functional mediators activate downstream transducers regulating inflammation and carcinogenesis. Correlation among mediators (IL-6, IL-27, TNF-alpha, and VEGF) with STAT proteins at diverse clinical-pathologic stages of hepatocellular carcinoma (HCC) remains limited.
Methods: Serum mediators assayed from 147 untreated HCC cases (HCC-total group) included 70 HBV-infected (HCC-HBV group), 64 HCV-infected (HCC-HCV group), and 13 without HBV-/HCV-infection (HCC-NBNC group). Another 156 non-HCC individuals comprised 54 healthy individuals (HG) and 102 chronic hepatitis patients (CH-total group) as control group. To correlate with serum mediators, 86-paired liver tissues (CH: 52 and HCC: 34 cases) served for p-STATs proteins immunostain.
Results: Although four mediators (IL-6, IL-27, TNF-alpha, and VEGF) significantly over-expressed, IL-6 presented the strongest correlation in HCC-total versus CH-total or HG groups (HCC-total versus CH-total: P < 0.001; HCC-total versus HG: P < 0.001). Over-expressed IL-6 concentration linked with poor liver function (Albumin: r = -0.383, P < 0.001; Bilirubin: r = 0.280, P = 0.001; INR: r = 0.299, P < 0.001; AST: 0.212, P = 0.016), tumor progression (TNM system: r = 0.370; P < 0.001), clinical condition severity (BCLC system: r = 0.471; P < 0.001; terminal-versus early-stage HCC, P = 0.001; advanced-versus early-stage HCC, P = 0.007; terminal-versus intermediate-stage HCC P = 0.003; advanced-versus intermediate-stage HCC P = 0.019), and 6-month mortality (P = 0.024). Likewise, serum IL-6 (r = 0.501, P = 0.003) as compared to IL-27 (r = 0.052, P = 0.770), TNF-alpha (r = 0.019, P = 0.917), and VEGF (r = 0.096, P = 0.595) expression reflected positive correlation with activation of tissues p-STAT3 rather than p-STAT1.
Conclusions: Serum IL-6, through p-STAT3 rather than p-STAT1 signal pathway, affected hepatic function, tumor progression, and determine HCC patient survival
Faculty recital: Tong-Il Han, September 21, 1989
Full text linkThis is the concert program of Faculty Recital: Tong-Il Han performance on Thursday, September 21, 1989 at 8:00 p.m., at the Tsai Performance Center, 685 Commonwealth Avenue, Boston, Massachusetts. Works performed were Sonata in B-flat Major, K. 281 by Wolfgang Amadeus Mozart, Sonata No 6 by Serge Prokofiev, and Sonata in F minor, Op. 5 by Johannes Brahms. Digitization for Boston University Concert Programs was supported by the Boston University Humanities Library Endowed Fund
Faculty recital: Tong-Il Hang, March 23, 2004
Full text linkThis is the concert program of the faculty recital of Tong-Il Han on Tuesday, March 23, 2004 at 8:00 p.m., at the Tsai Performance Center, 685 Commonwealth Avenue, Boston, Massachusetts. Works performed were Klavierstucke, Op. 119 by Johannes Brahms, Sonata in C Major, Op. 2 No. 3 by Ludwig van Beethoven, and Fantasy in C Major, Op. 17 by Robert Schumann. Digitization for Boston University Concert Programs was supported by the Boston University Center for the Humanities Library Endowed Fund
IL-8 confers resistance to EGFR inhibitors by inducing stem cell properties in lung cancer
No full textEpidermal growth factor receptor (EGFR)-targeted strategy is limited by resistance. We identify the potential genes involved in EGFR TKI (tyrosine kinase inhibitor) resistance and study the therapeutic mechanism in the non-small cell lung cancers. Potential genes involved in resistance were examined by analyzing datasets from a pair of EGFR TKI-sensitive (PC9) and TKI-resistant cells (PC9/gef). Blood specimens from patients taking EGFR TKI as first-line treatment were used to examine the correlation between drug's efficacy and IL-8 level. The effects of IL-8 on gefitinib-induced apoptosis, stemness, and in vivo tumorigenicity were investigated using established cell lines. We identified IL-8 was up-regulated in gefitinib-resistant cells, and high plasma IL-8 level was correlated with shorter progression-free-survival time. IL-8 overexpression suppressed gefitinib-induced apoptosis in gefitinib-sensitive cells. By contrast, suppression of IL-8 enhanced gefitinib-induced cell death in gefitinib-resistant cells. IL-8 also increased stem-like characteristics including aldehyde dehydrogenase activity, expression of stemness-related genes, clonogenic activity, side-population, and in vivo tumorigenicity. Consistently, knockdown of IL-8 leads to loss of stem cell-like characteristics in gefitinib-resistant cells. Our study demonstrates an important role for IL-8, and suggests IL-8 is a potential therapeutic target for overcoming EGFR TKI resistance
Tong-Il Han, piano, October 20, 1992
Full text linkThis is the concert program of the Tong-Il Han, piano performance on Tuesday, October 20, 1992 at 8:00 p.m., at the Tsai Performance Center, 685 Commonwealth Avenue. Works performed were Sonata No. 31 in A-flat major, Op. 110 by Ludwig van Beethoven, Sonata in E-flat major, Op. 26 by Samuel Barber, Variations and Fugue on a Theme by G. F. Handel, Op. 24 by Johannes Brahms. Digitization for Boston University Concert Programs was supported by the Boston University Humanities Library Endowed Fund
Copyright, contratto e accesso alla conoscenza: un’analisi comparata = Copyright, contract and access to knowledge: a comparative analysis.
Full text linkIl processo di digitalizzazione e lo sviluppo dei media, stravolgendo il paradigma tradizionale del copyright/diritto d’autore conducono a reazioni opposte. Da un lato, estendendo in vario modo l’ampiezza dell’esclusiva autorale favoriscono l’adozione di regole restrittive di accesso e uso dei contenuti; dall’altro, alimentano le logiche di condivisione, specie in alcune aree di produzione del sapere.
Il contratto, pur mutata la propria natura nella dimensione digitale, rappresenta la prima leva per l’affermazione di tali divergenti dinamiche, che, in entrambe le direzioni, riguardano anche la circolazione della conoscenza scientifica. Nel senso dell’apertura, lo strumento negoziale consente di perseguire i principi affermati dal movimento dell’Open Access (OA), abbattendo le barriere economiche e giuridiche all’accesso e utilizzo dei contenuti.
Dal deposito e pubblicazione su archivi istituzionali e disciplinari di opere transitate già attraverso i canali editoriali convenzionali, comunemente definita green road, alla pubblicazione su riviste ad accesso aperto, gold road, il fenomeno si sviluppa dal basso verso l’alto grazie alle dichiarazioni di principio e alle norme informali che hanno sin ora guidato le comunità accademiche nell’affermazione dell’OA. Di recente, tuttavia, i principi dell’OA sono oggetto di attenzione da parte del decisore pubblico che, pur timidamente, ne “impone” l’attuazione a tutte le comunità accademiche. Eppure, il diritto formale non sembra da solo sufficiente: è soltanto il primo tassello di una disciplina organica tesa a definire regole e incentivi per la produzione e la disseminazione della conoscenza scientifica, allo scopo di bilanciare la libertà “accademica” con il diritto di accesso alla conoscenza. = ENGLISH VERSION = Along with a comparative perspective that takes account of the U.S. and Italian law, this work aims to explore the interface between copyright and contract lae in publishing process.
In the current publishing environment, contracts and technology play a dominant role in the exploitation of copyrighted works. Publishers are granted by assignment of all copyright rights to reproduce and publish the work, but also to exercise control over its contents through technological protection measures. At the same time, mass digitization allows libraries and other organizations to make contents available online, which it entails a redefinition of the traditional publishing process and introduces new players to the scene (e.g., Google Books).
Hence, technology proves to be a powerful instrument for the spread of knowledge and it is on this pattern that Open Access (OA) is rapidly gaining ground.
Mostly based on a bottom-up approach that is on soft law, institutional policies and contracts, OA designs a new legal environment targeting the objectives of free accessibility, further distribution, and proper archiving of publications. These aims can be achieved through the creation of new open access business models to publish on OA journals (gold road) or to self-archive in institutional or disciplinary repositories works that have been originally published in conventional journals (green road).
However, in order for OA to be fully developed it is necessary to devise a principled and feasible approach to the dissemination of scholarly works against the current social, economic and legal background.
Indeed, the importance of OA is steadily recognized by legislators who integrate OA provisions into their legal system. This is an innovation of great significance, which was first fostered in the USA, and then extended in some European countries such as Italy and Germany in the European framework. Nevertheless, considering the different law systems, the formal law need to be combined with national strategies and institutional policies providing adequate incentives to the authors, while also promoting academic freedom and the right to knowledge access
Pro-inflammatory signaling by IL-10 and IL-22: bad habit stirred up by interferons?
No full textInterleukin (IL)-10 and IL-22 are key members of the IL-10 cytokine family that share characteristic properties such as defined structural features, usage of IL-10R2 as one receptor chain, and activation of signal transducer and activator of transcription (STAT)-3 as dominant signaling mode. IL-10, formerly known as cytokine synthesis inhibitory factor, is key to deactivation of monocytes/macrophages and dendritic cells. Accordingly, pre-clinical studies document its anti-inflammatory capacity. However, the outcome of clinical trials assessing the therapeutic potential of IL-10 in prototypic inflammatory disorders has been disappointing. In contrast to IL-10, IL-22 acts primarily on non-leukocytic cells, in particular epithelial cells of intestine, skin, liver, and lung. STAT3-driven proliferation, anti-apoptosis, and anti-microbial tissue protection is regarded a principal function of IL-22 at host/environment interfaces. In this hypothesis article, hidden/underappreciated pro-inflammatory characteristics of IL-10 and IL-22 are outlined and related to cellular priming by type I interferon. It is tempting to speculate that an inherent inflammatory potential of IL-10 and IL-22 confines their usage in tissue protective therapy and beyond that determines in some patients efficacy of type I interferon treatment
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