Relevant bibliographies by topics / HDIC

Academic literature on the topic 'HDIC'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "HDIC"

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Uzun, Fatih, and Alexander M. Korsunsky. "The Use of Surface Topography for the Identification of Discontinuous Displacements Due to Cracks." Metals 10, no. 8 (August 2, 2020): 1037. http://dx.doi.org/10.3390/met10081037.

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The determination of three components of displacements at material surfaces is possible using surface topography information of undeformed (reference) and deformed states. The height digital image correlation (hDIC) technique was developed and demonstrated to achieve micro-level in-plane resolution and nanoscale out-of-plane precision. However, in the original formulation hDIC and other topography-based correlation techniques perform well in the determination of continuous displacements. In the present study of material deformation up to cracking and filan failure, the ability to identify discontinuous triaxial displacements at emerging discontinuities is important. For this purpose, a new method reported herein was developed based on the hDIC technique. The hDIC solution procedure comprises two stages, namely, integer-pixel level correlation and sub-pixel level correlation. In order to predict the displacement and height changes in discontinuous regions, a smoothing stage was inserted between the two main stages. The proposed method determines accurately the discontinuous edges, and the out-of-plane displacements become sharply resolved without any further intervention in the algorithm function. High computational demand required to determine discontinuous displacements using high density topography data was tackled by employing the graphics processing unit (GPU) parallel computing capability with the paging approach. The hDIC technique with GPU parallel computing implementation was applied for the identification of discontinuous edges in an aluminium alloy dog bone test specimen subjected to tensile testing up to failure.
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Uzun, Fatih, and Alexander M. Korsunsky. "The height Digital Image Correlation (hDIC) technique for the identification of triaxial surface deformations." International Journal of Mechanical Sciences 159 (August 2019): 417–23. http://dx.doi.org/10.1016/j.ijmecsci.2019.06.014.

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Uzun, Fatih, Alexey I. Salimon, Eugene S. Statnik, Cyril Besnard, Jingwei Chen, Thomas Moxham, Enrico Salvati, Zifan Wang, and Alexander M. Korsunsky. "Polar transformation of 2D X-ray diffraction patterns and the experimental validation of the hDIC technique." Measurement 151 (February 2020): 107193. http://dx.doi.org/10.1016/j.measurement.2019.107193.

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Bradbury, Charlotte A., Farhat L. Khanim, Priyanka Mehta, Rachel E. Hayden, Charles F. Craddock, Chris M. Bunce, and Bryan M. Turner. "Characterisation of Histone Deacetylase (HDAC) Expression Profiles in Acute Myeloid Leukaemia: A Basis for the Development of Targeted Therapy Using Histone Deacetylase Inhibitors." Blood 104, no. 11 (November 16, 2004): 1123. http://dx.doi.org/10.1182/blood.v104.11.1123.1123.

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Abstract Post-translational modifications of chromatin structure are recognised as having a potential role in the pathogenesis of acute myeloid leukaemia (AML). Histone deacetylases play a central role in determining the acetylation status of histones and are emerging as novel targets in AML therapy. Histone deacetylase inhibitors (HDIs) inhibit growth of primary AML blasts in vitro and demonstrate clinical activity in patients with relapsed AML. To date, three major classes of HDACs have been characterised which differ in their susceptibility to HDIs. However, little is known of the pattern of HDAC expression in AML and this limits the rational use of HDIs in this disease. We have analysed the pattern of class I, II and III HDAC expression in AML cell lines, primary AML blasts and CD34+ selected progenitors from cord blood and normal donors by real time quantitative PCR(RT-PCR). RT-PCR analyses demonstrated consistently increased expression in AML blasts of two HDACs compared with proliferating CD34+ve cells from cord blood (n=5) . HDAC2 (class I HDAC) was more highly expressed in 3/3 myeloid cell lines and 20/24 primary AML samples, compared to cord blood CD 34+ve cells. SIRT1 (class III HDAC) was also more highly expressed in 3/3 myeloid cell lines and 24/24 primary AMLs. In contrast, no marked differences were detected in expression of HDAC1, 3, 4, 5, 6, 7, 9, 10, 11 and SIRT 2–6. We therefore studied the impact of sodium valproate (SV), an HDI with reported activity in AML, on HDAC activity and expression. SV treatment resulted in time and dose dependent increases in histone acetylation and specific methylation at H3K4, in both AML cell lines and primary AML cells. We have shown that the mechanism of the increased methylation at H3K4 is partly a result of the preference of the methyltransferase enzyme for acetylated histones. Using quantitative RT-PCR we found that SV treatment of HL-60 cells resulted in increased expression of the gene for MLL, an enzyme known to be capable of methylating H3K4. These changes in chromatin were associated with dose dependent cell killing. Significant (p<0.001, n=10) in vitro killing of primary AML blasts was observed at 1 mM SV and killing was enhanced by the addition of ATRA. However, histone modifications were observed in HL-60 cells at doses that had little effect upon cell viability or proliferation. We have immunoprecipitated complexes containing HDACs 1, 2 and 3 and assayed their enzymatic activity using a tritium labelled H4 peptide substrate. By this method, 1mM SV was potent at inhibiting HDACs 1, 2 and 3 activity. We have also studied the effects of SV on HDAC expression (all three classes) by RT-PCR in HL60 cells at 15 mins, 1h, 4h and 8h. A small number of HDACs were consistently and significantly upregulated by treatment with SV, TSA, Butyrate and SAHA. In contrast, the expression levels of HDAC2 and SIRT1 were relatively unchanged. These changes in HDAC expression may contribute to HDI resistance with continuous therapy. These data provide information which may be of value in determining choice of HDACis in Phase I/II studies in AML. They also identify increased histone methylation as a potentially important outcome of HDI treatment.
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Fiskus, Warren, Rekha Rao, Pravina Fernandez, Bryan Herger, Yonghua Yang, Jianguang Chen, Ravindra Kolhe, et al. "Molecular and biologic characterization and drug sensitivity of pan-histone deacetylase inhibitor–resistant acute myeloid leukemia cells." Blood 112, no. 7 (October 1, 2008): 2896–905. http://dx.doi.org/10.1182/blood-2007-10-116319.

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Abstract Hydroxamic acid analog pan-histone deacetylase (HDAC) inhibitors (HA-HDIs) have shown preclinical and clinical activity against human acute leukemia. Here we describe HA-HDI–resistant human acute myeloid leukemia (AML) HL-60 (HL-60/LR) cells that are resistant to LAQ824, vorinostat, LBH589, and sodium butyrate. HL-60/LR cells show increased expression of HDACs 1, 2, and 4 but lack HDAC6 expression, with concomitant hyperacetylation of heat shock protein 90 (hsp90). Treatment with HA-HDI failed to further augment hsp90 acetylation, or increase the levels of p21 or reactive oxygen species (ROSs), in HL-60/LR versus HL-60 cells. Although cross-resistant to antileukemia agents (eg, cytarabine, etoposide, and TRAIL), HL-60/LR cells are collaterally sensitive to the hsp90 inhibitor 17-AAG. Treatment with 17-AAG did not induce hsp70 or deplete the hsp90 client proteins AKT and c-Raf. HL-60/LR versus HL-60 cells display a higher growth fraction and shorter doubling time, along with a shorter interval to generation of leukemia and survival in nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. Thus, resistance of AML cells to HA-HDIs is associated with loss of HDAC6, hyperacetylation of hsp90, aggressive leukemia phenotype, and collateral sensitivity to 17-AAG. These findings suggest that an hsp90 inhibitor-based antileukemia therapy may override de novo or acquired resistance of AML cells to HA-HDIs.
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Schioppa, Tiziana, Hoang Oanh Nguyen, Laura Tiberio, Francesca Sozio, Carolina Gaudenzi, Mauro Passari, Annalisa Del Prete, Daniela Bosisio, and Valentina Salvi. "Inhibition of Class I Histone Deacetylase Activity Blocks the Induction of TNFAIP3 Both Directly and Indirectly via the Suppression of Endogenous TNF-α." International Journal of Molecular Sciences 23, no. 17 (August 28, 2022): 9752. http://dx.doi.org/10.3390/ijms23179752.

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Histone deacetylase inhibitors (HDIs) are promising drugs for the treatment of inflammatory diseases. However, their therapeutical exploitation is slowed down by severe adverse manifestations that can hardly be foreseen, mainly due to incomplete knowledge of how HDIs impact the delicate balance of inflammatory mediators. In this work, we characterized the effects of the HDI trichostatin A (TSA) on the expression of TNFAIP3, which is a crucial inhibitor of the classical NF-kB pathway and an LPS-induced negative feedback regulator. The accumulation of TNFAIP3 mRNA after LPS stimulation showed biphasic behavior, with one wave within the first hour of stimulation and a second wave several hours later, which were both reduced by TSA. By using inhibition and knockdown approaches, we identified two temporally and mechanistically distinct modes of action. The first wave of TNAIP3 accumulation was directly blunted by the histone deacetylase (HDAC) blockade. By contrast, the second wave was decreased mainly because of the lack of endogenous TNF-α induction, which, in turn, depended on the intact HDAC activity. In both cases, class I HDACs appeared to play a nonredundant role, with HDAC3 required, but not sufficient, for TNF-α and TNFAIP3 induction. In addition to TNFAIP3, TNF-α is known to induce many response genes that orchestrate the inflammatory cascade. Thus, suppression of TNF-α may represent a general mechanism through which HDIs regulate a selected set of target genes.
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Feng, Mei. "Towards a cultural model of qi in TCM." Review of Cognitive Linguistics 19, no. 1 (April 28, 2021): 1–25. http://dx.doi.org/10.1075/rcl.00074.fen.

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Abstract This paper aims to construct a cultural model of qi in Traditional Chinese Medicine (TCM) by probing into its conceptual metaphors based on a contextualized semantic analysis of qi in Huang Di’s Inner Classic (HDIC). It is found that there are eight conceptual metaphors of qi, each involving experiential correlation between source and target concept. To be specific, cause for effect builds up a major metonymic basis for the metaphorical mappings from the source concept of qi (i.e., substance) to the target concepts, including physiological function, breathing, climate, pathogenic factor, disease/syndrome, odor, property of drugs and time. It is worth special noting that time is understood in terms of the motion of qi in TCM. The conceptual metaphor time is qi is Chinese culture-specific. On the whole, conceptual metaphors of qi form a conceptual network and further constitute a cultural model: qi as the substance origin of human life is believed in TCM to function by ceaseless motion, giving rise to wellness or illness. This cultural model reflects a pair of inseparable concepts in ancient Chinese philosophy, viz. substance and (its) function, with the former being primary, essential and original, while the latter, secondary, concomitant and derivational.
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이케다 쇼주. "『新撰字鏡』本文解読上の諸問題 -HDICの紹介とその活用-." Kugyol Studies ll, no. 38 (February 2017): 39–56. http://dx.doi.org/10.17001/kugyol.2017..38.003.

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Li, Wenbo, and Zheng Sun. "Mechanism of Action for HDAC Inhibitors—Insights from Omics Approaches." International Journal of Molecular Sciences 20, no. 7 (April 1, 2019): 1616. http://dx.doi.org/10.3390/ijms20071616.

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Histone deacetylase inhibitors (HDIs) are a class of prominent epigenetic drugs that are currently being tested in hundreds of clinical trials against a variety of diseases. A few compounds have already been approved for treating lymphoma or myeloma. HDIs bind to the zinc-containing catalytic domain of the histone deacetylase (HDACs) and they repress the deacetylase enzymatic activity. The broad therapeutic effect of HDIs with seemingly low toxicity is somewhat puzzling when considering that most HDIs lack strict specificity toward any individual HDAC and, even if they do, each individual HDAC has diverse functions under different physiology scenarios. Here, we review recent mechanistic studies using omics approaches, including epigenomics, transcriptomics, proteomics, metabolomics, and chemoproteomics, methods. These omics studies provide non-biased insights into the mechanism of action for HDIs.
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Lasdiyanti, Mita, Eka N. Kencana, and Putu Suciptawati. "Modeling Human Development Index of Bali with Spatial Panel Data Regression." European Journal of Engineering Research and Science 4, no. 5 (May 28, 2019): 132–37. http://dx.doi.org/10.24018/ejers.2019.4.5.1312.

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Human development index (HDI) is an index that represents the successfulness of human development in a region. For Bali, one of 34 provinces in Indonesia, the progress of HDI in the period 2010–2017 showed an increasing trend. In the year 2010, the Bali’s HDI is accounted for 70.10, gradually increase to 74.30 in the year 2017. However, in 2017 there are some regions with their HDIs are below of Bali’s HDI, namely Jembrana, Buleleng, Klungkung, Bangli, and Karangasem. The aim of this work is to model the HDI of 9 regencies of Bali so that the main determinant to increase the HDIs especially for the regencies with lower HDIs could be determined. The model consists of one dependent variable (HDI) with three indicators as the independent ones, there are (a) life expectancy, (b) education, and (b) standard of living. By applying spatial panel data analysis, five models were built i.e. CEM, FEM (individual), FEM (time), REM, and spatial error FEM to determine the effect of each indicator. The result shows the best model is spatial error FEM in which education has the biggest influence compare than the others.
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Dissertations / Theses on the topic "HDIC"

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Toffoli, Valeria. "Superhydrophobic BIOMEMS sensor arrays: development of actuation and readout electronic strategies." Doctoral thesis, Università degli studi di Trieste, 2014. http://hdl.handle.net/10077/9993.

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2012/2013
La tecnologia dei sistemi micro-elettro-meccanici (MEMS) ha dimostrato d’avere grandi potenzialità in molti campi, in particolare nei sistemi bio-medicali. Essa si basa infatti su processi di fabbricazione ad altro volume produttivo, permettendo una considerevole riduzione dei costi per dispositivo. Un ulteriore beneficio di questa tecnologia risiede nella possibilità di dimensionare i dispositivi fino a raggiungere l’ordine del submicron, così da consentire l’integrazione e il monitoraggio in tempo reale di sistemi sensibili a biomarker di tipo medicale e biologici. Tra gli obiettivi futuri dei MEMS biomedicali (BioMEMS) vi è la realizzazione di dispositivi in grado di interfacciarsi direttamente con il paziente e definirne lo stato di salute grazie alla rilevazione del livello di centinaia di diversi biomarker (siano essi chimici o fisici). La medicina assumerebbe in questa visione una configurazione ad personam nella quale al paziente verrebbe prontamente somministrato un quantitativo di medicinale adatto alle risposte del suo organismo. A tale scopo i dispositivi MEMS devono essere in grado di effettuare analisi multiple operando in un ambiente liquido. Tuttavia è proprio l’ambiente liquido a comportare la riduzione di sensibilità e, quindi, di performance dei sensori MEMS. La presente ricerca si pone lo scopo di sviluppare nuovi sistemi elettronici di misurazione e attuazione di due distinte tipologie di BioMEMS risonanti operanti in liquido, i cantilever e i pillar. In particolare verrano trattati tre argomenti: la realizzazione di setup ottici per applicazione dei MEMS in liquido ed in aria, la progettazione di sistemi elettronici di attuazione e lettura di singoli pillar nel loro comportamento in frequenza e lo sviluppo di un software LabVIEW in grado di programmare un FPGA ed ottenere un PLL digitale da impiegarsi nell’analisi in tempo reale del comportamento in frequenza di RF-MEMS. Il primo progetto è stato sviluppato in collaborazione l'Università di Kaiserslautern (Germania) e prevedeva la realizzazione di sistemi microfluidici e setups ottici, interfacciati in modo tale da permettere la rilevazione della risposta in frequenza di molteplici MEMS operanti in parallelo. Nel secondo progetto l’obiettivo era la realizzazione di un sistema elettronico in grado di integrare in un unico dispositivo i sistemi di attuazione e lettura dei pillar. In particolare siamo stati in grado di modulare l’ampiezza di risonanza dei nostri dispositivi risonanti mediante l’applicazione della forza di polarizzazione Kelvin mentre lo sviluppo del sistema di lettura richiede ulteriore lavoro di indagine. Infine, nell'ultimo progetto è stato realizzato un sistema PLL digitale con 10 MHz di banda passante utilizzando la tecnologia della National Instruments (FlexRIO NI5781R). Mediante questo PLL si è potuto identificare la frequenza di risonanza di diverse tipologie di MEMS e se ne è seguite le variazioni in tempo reale . Le attività di ricerca sperimentale sono state eseguite presso il laboratorio CNR- IOM a Trieste.
XXVI Ciclo
1985
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Zagni, Chiara. "Progettazione e sintesi di nuovi inibitori delle istone deacetilasi." Thesis, Università degli Studi di Catania, 2011. http://hdl.handle.net/10761/253.

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Il controllo epigenetico dell'espressione genica e' operato da modifiche post-translazionali della cromatina, quali acetilazione e deacetilazione. Due enzimi sono respinsabili di questo processo: le HAT (istone acetiltransferasi) e le HDAC (istone deacetilasi). Le HDAC sono un gruppo di enzimi coinvoilti nella regolazione dell'espressione genica, nella riparazione de DNA e nella risposta allo stress. L'acetilazione gioca un ruolo importante nella trascrizione poiche' responsabile del rimodellamento della cromatina aumentando l'accesso dei fattori di trascrizione al DNA. Una diminuzione dei livelli dell'acetilazione istonica sono associate con un aumento dell'attivita' di trascrizione, mentre un decremento dei livelli di acetilazione e associate con le repression della repressione genica. Infatti nelle cellule tumoralisi osserva frequentemente un'anormale espressione genica. Gli inibitori delle HDAC (HDI) sono potenti induttori dell'arresto della crescita, della differenzione e della morte dellulare per apoptosis in cellule trasformate sia in vitro che in vivo. Ad oggi vi sono sette classi distinte di inibitori delle HDAC e tutti contengono tre elementi strutturali chiave del farmacoforo: a) un gruppo legante lo zinco (R), che coordina gli ioni zinco al fondo della lunga e stretta cavita' del sito attivo; b) un cappuccio o à ¢ capà ¢ (la funzione solfonammidica), che interagisce sia con gli aminoacidi sul margine del sito di legame sia con la superficie della proteina. c) un dominio di legame, il cui ruolo e' assicurare il corretto posizionamento dei gruppi precedenti e di interagire con il canale di legame lipofilo. Seguendo il nostro recente interesse nella ricerca di HDI piu' potenti, ho progettato e sintetizzato una nuova serie di composti contenenti quattro nuove porzioni chelanti lo zinco, quali formilidrazonometilica, 2-formilidrazinocarbonilica, 2,2,2-trifluoro-N-metilencetammidica e 2,2,2-trifluoro-N-metilacetammidica, legate attraverso uno spaziatore ad una solfonammide (Schema 1), responsabile dell'interazione idrofobica con l'HDAC. Studi di docking hanno mostrato che queste molecule si inseriscono perfettamente nella tasca enzimatica dell'HDAC con un ottimo à ¯ Gbind di à ¢ 7,9 kcal/mol che e' una 1 kcal/mol piu' bassa del SAHA, un ottimo inibitore.
The epigenetic control of gene expression is operated through post-translational modifications of chromatin such as acetylation and deacetylation. Two enzymes are responsable for these processes: HAT (histone acetyl transferase) and HDAC (histone deacetylase). HDAC is a group of enzymes involved in regulating gene expression, DNA repair and stress response. Acetylation plays an important role in trascription because it remodels chromatin structure enhancing access to DNA-binding factors. In general, increased levels of histone acetylation are associated with increased transcriptional activity, whereas decreased levels of acetylation are associated with repression of gene expression. In tumor cells abnormal gene expression is frequently observed. HDAC inhibitors have been shown to be potent inducers of growth arrest, differentiation, and apoptotic cell death both in vitro and in vivo transformed cells. To date there are seven distinct classes of HDAC inhibitors and all contain three key structural elements to their pharmacophore: a) a zinc-binding group which coordinates the zinc ion at the bottom of the long narrow active site cavity; b) a capping group which interacts both with the amino acids on the rim of the binding cavity and the protein surface; c) a linker domain whose role is to ensure the correct positioning of the two former groups and to in-teract with the lipophilic binding tunnel. Following our recent interest in the research of more potent HDAC inhibitors, we have projected and synthesized a new series of compounds containing four new zinc chelant moieties, i.e. formylhydrazonomethyl, 2-formylhydrazinocarbonyl, 2,2,2-trifluoro-N-methylideneacetamidic and N-(trifluoroacetyl)amidic, linked by an aromatic spacer to an aromatic sulfonamide, that is responsible of hydrophobic interaction with HDAC. Docking studies have shown that these new molecules fit very good in the HDAC enzymatic pocket with a best ï Gbind of â 7,9 kcal/mol that is 1 kcal/mol lower of the corresponding one for SAHA, a good HDAC.
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Ozdarska, Katarzyna. "Synthèses d’inhibiteurs de HDAC et leurs tests biologiques (Cytotoxicité, HDAC inhibition)." Thesis, Reims, 2020. http://www.theses.fr/2020REIMS023.

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L’épigénétique représente les modifications de l’expression génique, sans altérer la séquence nucléique de l'ADN. L'un des mécanismes de régulation est le remodelage de la chromatine qui s’effectue via les histones acétyltransférases et les histones désacétylases (HDAC) permettant ou non la transcription de gènes. Une expression anormale des HDAC est corrélée à de nombreuses maladies (dépendance à l'alcool, inflammation ainsi que les maladies cardiovasculaires et neurodégénératives, cancers…). Il est primordial de cibler la sélectivité d’une isoforme parmi les 11 connues des HDAC zinc dépendantes pour éviter les effets secondaires. Le but de la recherche était de concevoir et de synthétiser de nouveaux composés, de vérifier leur activité inhibitrice vis-à-vis des HDAC de classe I ou II et leur cytotoxicité sur quatre lignées cellulaires: HaCaT, V79-4, SH-SY5Y et PC12. Ainsi, nous nous sommes concentrés sur les pharmacomodulations du ZBG, de l’espaceur et de la tête de molécules connues tels que le MS-275 (sélectif de la classe I des HDAC), les SAHA et TSA (espaceur en C5 ou C6) avec une forte activité inhibitrice vis-à-vis des HDAC, mais non sélectifs. Nous nous sommes concentrés sur les pharmacomodulations de l'HDACI connu modifiant le domaine de liaison au zinc ZBG (sulfonylhydrazide, catéchol), la nature de l’espaceur (alkyl, aryl) et le groupe de reconnaissance de surface (bis-aryl, adamantyl, indolopyridazinone). Une bibliothèque de 57 nouveaux composés a été créée en trois séries. Aucun d'entre eux n'a montré d'activité inhibitrice satisfaisante. Les composés sélectionnés n'ont pas montré d'activité cytotoxique sur les lignées de cellules neuronales. Sur la base de cette recherche, il est possible de créer de nouveaux composés dans la série indolopyridazinone afin de les tester
Epigenetics represents changes in gene expression without altering the nucleic sequence of DNA. One of the main mechanisms of regulation of gene expression is chromatin remodeling via histone acetyltransferases and histone deacetylases (HDAC), which may or may not allow gene transcription. An abnormal expression of HDACs is correlated with many diseases (alcohol dependence, inflammation as well as cardiovascular and neurodegenerative diseases, cancers...). It is essential to target the selectivity of one isoform among the 11 known zinc-dependent HDACs to avoid side effects. The aim of the research was to design and synthesize new compounds, verify their inhibitory activity against class I or II HDACs and their cytotoxicity on four cell lines: HaCaT, V79-4, SH-SY5Y and PC12. We focused on the pharmacomodulations of ZBG, the linker and the cap of known molecules such as MS-275 (selective for class I of HDACs), SAHA and TSA (spacer in C5 or C6) with a strong inhibitory activity towards HDACs, but not selective. We concentrated on the pharmacomodulations of known HDACI modifying the zinc binding domain (sulfonylhydrazide, catechol), the nature of the spacer (alkyl, aryl) and the surface recognition group (bis-aryl, adamantyl, indolopyridazinone). A library of 57 new compounds was designed in three series. None of them showed satisfactory inhibitory activity. The selected compounds did not show cytotoxic activity on neuronal cell lines. Based on this research, it is possible to create new compounds in the indolopyridazinone series in order to test them
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Khan, Omar Ali. "HR23B, a biomarker for HDAC inhibitors." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:9cd76c0b-e70e-43f7-a92d-a99f403a077e.

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As our understanding of cancer biology increases and novel therapies are developed, an increasing number of predictive biomarkers are becoming clinically available. Aberrant acetylation has been strongly linked to tumourigenesis and the modulation of acetylation through targeting histone deacetylase (HDAC) has led to the introduction of many HDAC inhibitors. To date, two have had regulatory approval for the treatment of cutaneous T cell lymphoma (CTCL). Modifications in chromatin control underpin the mechanism of action of HDAC inhibitors. A genome wide loss-of-function screen identified HR23B as a gene that governs sensitivity to HDAC inhibitors. HR23B shuttles ubiquitinated cargo proteins to the proteasome and elevated levels may contribute to cell death mediated by this pathway. It also governs cell sensitivity to drugs that act directly on the proteasome. HDAC inhibitors influence proteasome activity and there may be a synergistic interaction with proteasome inhibitors. HR23B and HDAC6 interact and HDAC6 may be a negative regulator of apoptosis and a positive regulator of autophagy and through its ability to down-regulate HR23B, may impact on the cellular outcome of HDAC inhibitor treatment. Expression of HR23B has been correlated with clinical response to HDAC inhibitors in a retrospective analysis of CTCL patients. The tissue expression of HR23B and the autophagy marker LC3 has been investigated and there may be a reciprocal relationship in their expression in some tumours which may provide prognostic information and patients with low HR23B expression but high levels of autophagy appear to have a particularly poor prognosis. Well designed, biomarker-driven prospective clinical trials are needed to clarify the predictive and prognostic roles of HR23B.
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Polášek, Jaromír. "Implementace protokolu HDLC v síťových simulátorech." Master's thesis, Vysoké učení technické v Brně. Fakulta elektrotechniky a komunikačních technologií, 2018. http://www.nusl.cz/ntk/nusl-377008.

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This diploma thesis deals with the possibility of using HDLC (High-Level Data Link Control) protocol for communication and addressing of smart metering devices with a data concentrator. The HDLC protocol is used in two DLMS/COSEM (Device Language Message Specification/Companion Specification for Energy Metering) communication profiles. To simulate these communication profiles, the most appropriate simulation program is selected. Using this simulator, the first communication profile is implemented and the second one is designed. Communication profile based on TCP/IP (Transmission Control Protocol/Internet Protocol) has been fully implemented. To implement the three-layer HDLC communication profile, all options have been thoroughly explored. Using these findings, a process was designed to guide the full implementation. For the first communication profile the qualitative parameters are measured, which are then plotted and evaluated.
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Schreiner, Lindsay Marie. "HDAC Mediated Integration of NF-¿B Transcriptional Regulation." University of Toledo / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1404744801.

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Alqahtani, Abdulateef Alqarni. "Synthesis and Biological Evaluation of New HDAC Inhibitors." University of Toledo / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1525448898248748.

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Sindi, Shaimaa Hesham. "Guanidine- Based HDAC-Inhibitors as Anti-Cancer Agents." University of Toledo / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1564676186975875.

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Perin, Stefano <1995&gt. "Sintesi di inibitori peptidici per interazione MEF2-HDAC." Master's Degree Thesis, Università Ca' Foscari Venezia, 2021. http://hdl.handle.net/10579/19004.

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I peptidi sono sempre più impiegati come agenti terapeutici per diverse malattie. Possiedono caratteristiche intermedie tra i farmaci chimici e biologici come dimensioni inferiori, sintetizzabili chimicamente, facilmente modificabili, con bassa tossicità, antigenicità ridotta, affinità di legame e specificità. Queste caratteristiche uniche li rendono una modalità attraente per lo sviluppo di inibitori di interazioni proteina-proteina. Lo scopo del progetto è sviluppare nuovi inibitori a base di peptidi in grado di bloccare l’interazione del fattore di trascrizione “myocyte enhancer 2” (MEF2) con alcuni membri della classe IIa delle istone deacetilasi (HDAC), una sottofamiglia di quattro proteine (HDAC4, HDAC5, HDAC7 e HDAC9) che sono state collegate ad una varietà di tumori solidi ed ematologici. A tal fine sono stati prodotti una serie di peptidi HDAC della classe II impiegando un sistema automatizzato di sintesi peptidica su fase solida, purificati con HPLC su fase inversa e caratterizzati via spettroscopia di massa e dicroismo circolare. L’affinità di legame dei peptidi verso MEF2 è stata testata con saggi di Polarizzazione di Fluorescenza. Infine l’affinità di legame di un peptide è stata incrementata inserendo una struttura sintetica intramolecolare (un braccio), che aiuta a bloccare il peptide in una conformazione specifica, in modo tale da ridurre l’entropia conformazionale.
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Sodji, Quaovi Hemeka. "Improving histone deacetylase inhibition therapy through isoform selectivity and targeted delivery." Diss., Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/53445.

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Histone deacetylase (HDAC) inhibition has recently emerged as a novel therapy for cancer treatment. However, currently approved histone deacetylase inhibitors (HDACi) are pan-inhibitors thus inhibiting all 11 zinc dependent HDAC isoforms including those not involved in tumorigenesis. These inhibitors are also associated with various side effects including a potentially fatal cardiotoxicity. To address these issues, isoform selective HDACi were designed and synthesized. The use of 3-hydroxy-pyridin-2-thione (3HPT) as zinc chelation group resulted in small molecules devoid of HDAC1 inhibition but active against HDAC6 and/or 8. Selected 3HPT containing HDACi displayed anticancer activity against various cancer cell lines including DU145, LNCaP and Jurkat. Surprisingly, the lead-compounds were very potent against Jurkat Jγ cells which are resistant to SAHA-induced apoptosis. HDACi were also targeted to cancer cells using folic or pteroic acids as targeting groups. Incorporation of the folic acid into the HDACi pharmacophoric model resulted in inhibitors selective for HDAC6, whereas pteroic-based HDACi inhibited both HDAC1 and 6. Only the pteroic-based inhibitors displayed anticancer activities against folate receptor overexpressing tumors such KB and HeLa. Furthermore, cell-based studies established the inhibition of HDAC1 as the basis for the anticancer activities of the pteroic-based HDACi.
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Books on the topic "HDIC"

1

Koudouta, Paul. Prukutunzuma hdi. Mokolo [Cameroon]: Comité d'étude et de traduction en langue Hide a Tourou, 2005.

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Frajzyngier, Zygmunt. A grammar of Hdi. Berlin: Mouton de Gruyter, 2002.

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Erin, Shay, ed. A grammar of Hdi. Berlin: Mouton de Gruyter, 2002.

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Krämer, Oliver H., ed. HDAC/HAT Function Assessment and Inhibitor Development. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2788-4.

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Krämer, Oliver H., ed. HDAC/HAT Function Assessment and Inhibitor Development. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6527-4.

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Farley, Mark. A computer assisted learning package for the HDLC protocol. [s.l: The author], 1999.

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Bramlett, Lee. Lexique he̳di-français-anglais: Provisoire. Yaoundé, République du Cameroun: Société internationale de linguistique, 1996.

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Comité d'étude de langue et de traduction hedi à Tourou., ed. Laha nda gwa d̳a h e̳di. Mokolo, République du Cameroun: Comité d'étude de langue et de traduction hedi à Tourou, 1994.

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Bramlett, Lee. Lexique he̳di-français-anglais: Provisoire. Yaoundé, République du Cameroun: Société internationale de linguistique, 1996.

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Nanggroe Aceh Darussalam (Indonesia). Badan Perencanaan Pembangunan Daerah. and Indonesia. Badan Rehabilitasi & Rekonstruksi. Satuan Kerja Perencanaan Umum, Perencanaan Teknis, dan Manajemen Rantai Pengadaan., eds. Perhitungan dan analisis human development index (HDI) kabupaten-kota yang dilanda tsunami. Banda Aceh: Badan Perencanaan Pembangunan Daerah, Pemerintah Provinsi Nanggroe Aceh Darussalam, 2006.

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Book chapters on the topic "HDIC"

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Buchanan, W. J. "HDLC." In The Complete Handbook of the Internet, 451–59. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-0-306-48331-8_20.

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Buchanan, Bill. "HDLC." In Handbook of Data Communications and Networks, 571–79. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4757-0905-6_44.

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Buchanan, W. J. "HDLC." In The Handbook of Data Communications and Networks, 867–75. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7870-5_52.

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Schwab, Manfred. "HDAC Inhibitors." In Encyclopedia of Cancer, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2591-2.

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Olzscha, Heidi, Mina E. Bekheet, Semira Sheikh, and Nicholas B. La Thangue. "HDAC Inhibitors." In Methods in Molecular Biology, 281–303. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3667-0_19.

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Kokubo, Tetsuro. "Mammalian HDAC." In Encyclopedia of Systems Biology, 1173–74. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1622.

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Ito, Akihiro, Norikazu Nishino, and Minoru Yoshida. "HDAC Inhibitors." In Histone Deacetylases, 271–97. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1385/1-59745-024-3:271.

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Kwon, Paul, Meier Hsu, Dalia Cohen, and Peter Atadja. "HDAC Inhibitors." In Histone Deacetylases, 315–32. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1385/1-59745-024-3:315.

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Unger, Keith R., Mira Jung, and Anatoly Dritschilo. "Histone Deacetylases (HDAC)." In Cancer Therapeutic Targets, 1007–17. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_10.

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Unger, Keith R., Mira Jung, and Anatoly Dritschilo. "Histone Deacetylases (HDAC)." In Cancer Therapeutic Targets, 1–11. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6613-0_10-3.

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Conference papers on the topic "HDIC"

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Suh, Allison Y., Sung-Chang Lee, and Andreas A. Polycarpou. "Textured Sliders as Means to Reduce Adhesion in Ultra Low Flying Head Disk Interfaces." In ASME/STLE 2002 International Joint Tribology Conference. ASMEDC, 2002. http://dx.doi.org/10.1115/2002-trib-0256.

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A means of avoiding the negative consequences of ultra low flying super smooth Head/Disk Interfaces (HDIs) is to use textured sliders while still maintaining super smooth magnetic media. In this paper, the effect of preferential texturing (roughening) of slider air-bearing surfaces (ABS) on the intermolecular/adhesion forces at HDIs is investigated using a quasi-dynamic adhesion model. Super smooth (untextured), preferentially textured and rough sliders were investigated in this study. First, they were measured using an Atomic Force Microscope (AFM) and subsequently roughness parameters were extracted and used in the modeling. Preferential texturing provides a unique roughening of the ABS, where parts of the original surface are not affected, thus maintaining the initial roughness, with other parts of the surface being removed. This texturing has the net effect of reducing the effective or nominal area of contact between the slider and media surfaces, which plays an important role in the adhesion forces at the HDI. The simulation results indicate that preferential texturing can alleviate the problem of high adhesion forces in ultra-low flying HDI’s.
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Carbone, Carmine, Elena Di Gennaro, Biagio Pucci, Geny Piro, Monica Marra, Michele Caraglia, Alberto Abbruzzese, and Alfredo Budillon. "Abstract 2609: Tissue transglutaminase (TG2) promotes resistance to HDAC inhibitor (HDI) vorinostat in cancer cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2609.

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Prado, Bruno, Edna Barros, Thiago Figueiredo, and André Aziz. "HdSC." In the 24th symposium. New York, New York, USA: ACM Press, 2011. http://dx.doi.org/10.1145/2020876.2020917.

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Kupcho, Kevin R., Nathan J. Evans, Andrew L. Niles, Thomas A. Kirkland, and Dan F. Lazar. "Abstract 4784: Selective bioluminogenic HDAC activity assays for profiling HDAC inhibitors." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4784.

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Marinos, Alexandros, Erik Wilde, and Jiannan Lu. "HTTP database connector (HDBC)." In the 19th international conference. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1772690.1772852.

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Kaliszczak, Maciej, Meg Perumal, and Eric Aboagye. "Abstract 2608: HDAC-C1A: An irreversible HDAC inhibitor with significant anti-tumor activity." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2608.

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Suzart, Gabriel Souza, Ingrid Sanchez, Daniel Guimarães, Pedro Augusto Assis Lopes, and Pedro Antonio Pereira de Jesus. "Association between Human Development Index and Delay on Arrival to Stroke Unit." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.668.

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Background: Stroke outcomes depend somehow on the time taken from the symptoms onset until arrival to the specialized service. However, as it lacks literature exploring the impact of socio-demographics factors on this time, we investigated the association between Human Development Index and delay on arrival to specialized service. Design and setting: Cross-sectional study from a prospective cohort (PMID=33719516) at Hospital Geral Roberto Santos. Methods: From a total of 454 stroke patients, 156 were included in this study because they had registered address, time of admission and of symptoms onset. Patients had HDI defined by their address and were grouped into HDI categories. Results: In our sample, 57 (36,5%) individuals had medium HDI, 70 (44,9%) high HDI and 29 (18,6%) very high HDI. Very high HDI patients’ delay (2:01; 1:22-2:57) was lower than high HDI (3:05; 2:05-5:26) and medium HDI (2:25;1:45-4:04) patients. There was statistical significance comparing these groups (X²=11,41;p<0,05), but a post-hoc test revealed statistical difference just between the very high HDI and high HDI groups (p<0.05). Conclusions: We expected to find a direct relation between delay on arrival to the stroke service and HDI categories. However, this was not observed. *Authors contributed equally.
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Duchateau, Ruediger, Jens-Rainer Hoefft, Gunther Kuerbitz, and Hans-Ulrich Wieland. "HDIR: very high resolution thermal imager." In International Symposium on Optical Science and Technology, edited by Bjorn F. Andresen, Gabor F. Fulop, and Marija Strojnik. SPIE, 2000. http://dx.doi.org/10.1117/12.409869.

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Shi, Justin Y. "Use HDLC Principles for Distributed Applications." In 2015 IEEE International Conference on Computer and Information Technology; Ubiquitous Computing and Communications; Dependable, Autonomic and Secure Computing; Pervasive Intelligence and Computing (CIT/IUCC/DASC/PICOM). IEEE, 2015. http://dx.doi.org/10.1109/cit/iucc/dasc/picom.2015.297.

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Ebert, E., and N. Damaschke. "6.1.5 - HDNC-Messtechnik zu optischen Partikelcharakterisierung." In 18. GMA/ITG-Fachtagung Sensoren und Messsysteme 2016. AMA Service GmbH, Von-Münchhausen-Str. 49, 31515 Wunstorf, Germany, 2016. http://dx.doi.org/10.5162/sensoren2016/6.1.5.

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Reports on the topic "HDIC"

1

Simpson, W., ed. PPP in HDLC Framing. RFC Editor, December 1993. http://dx.doi.org/10.17487/rfc1549.

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Simpson, W., ed. PPP in HDLC-like Framing. RFC Editor, July 1994. http://dx.doi.org/10.17487/rfc1662.

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Bormann, C. PPP in a Real-time Oriented HDLC-like Framing. RFC Editor, September 1999. http://dx.doi.org/10.17487/rfc2687.

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Laine, Vivien E. Polarimetry of the polarized hydrogen deuteride HDice target under an electron beam. Office of Scientific and Technical Information (OSTI), October 2013. http://dx.doi.org/10.2172/1190862.

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Haßler, Björn, Taskeen Adam, Meaghan Brugha, Kalifa Damani, Zoe Allier-Gagneur, Sara Hennessy, David Hollow, et al. Country list with HDI, iHDI, MPI and Gini (version 1). EdTech Hub, September 2019. http://dx.doi.org/10.53832/edtechhub.0017.

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This is pdf of a country list with HDI, iHDI, MPI and Gini. This file is now superseeded by DOI: 10.5281/zenodo.3908363, see https://docs.edtechhub.org/lib/55A44ZRB (which will also be available as a data file).
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Pignataro, C., and M. Townsley. High-Level Data Link Control (HDLC) Frames over Layer 2 Tunneling Protocol, Version 3 (L2TPv3). RFC Editor, February 2006. http://dx.doi.org/10.17487/rfc4349.

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Martini, L., E. Rosen, G. Heron, and A. Malis. Encapsulation Methods for Transport of PPP/High-Level Data Link Control (HDLC) over MPLS Networks. RFC Editor, September 2006. http://dx.doi.org/10.17487/rfc4618.

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Ronald W. Smith. High Density Infrared (HDI) Transient Liquid Coatings for Improved Wear and Corrosion Resistance. Office of Scientific and Technical Information (OSTI), July 2007. http://dx.doi.org/10.2172/909431.

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Chinnaiyan, Prakash, and Paul M. Harari. Enhancing the Anti-Tumor Activity of ErbB Blockers with Histone Deaccetylase (HDAC) Inhibition in Prostate Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, November 2005. http://dx.doi.org/10.21236/ada458444.

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Chinnaiyan, Prakash, and Paul M. Harari. Enhancing the Anti-tumor Activity of ErbB Blockers with Histone Deaccetylase(HDAC)Inhibition in Prostate Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, May 2007. http://dx.doi.org/10.21236/ada472066.

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