@titmeister Twitterissä. Henkilöbrändin rakentuminen Arman Alizadin Twitter-profiilissa.

Tutkielmassa perehdytään esiintyjänä ja tuottajana tunnetun Arman Alizadin henkilöbrändiin ja sen rakentumiseen hänen Twitter-profiilinsa kautta. Henkilöbrändäys voidaan tässä käsittää itsensä esilletuonnin strategiaksi, joka tähtää esimerkiksi näkyvyyden ja taloudellisen hyödyn saavuttamiseen. Tarkoitukseni on selvittää millaisena Alizadin henkilöbrändi Twitterissä näyttäytyy ja millaisia keinoja hän käyttää henkilöbrändinsä rakentamiseksi ja ylläpitämiseksi. Tarkastelen myös sitä, miten Alizadin henkilöbrändi suhteutuu henkilöbrändäykseen liitettyihin vaatimuksiin ja ominaisuuksiin. Lisäksi käsittelen henkilöbrändäyksen suhdetta työhön ja mediatyön murrokseen. Pohdin Alizadin ja hänen Twitter-seuraajiensa välistä vuorovaikutusta ja sen vaikutusta Alizadin henkilöbrändiin. Tutkimusaihettani kehystää mediakonvergenssin käsite, joka voidaan ymmärtää medioiden, tuottajien ja vastaanottajien lähentymisenä ja yhdentymisenä. Tutkielman aineisto koostuu Alizadin twiiteistä ja uudelleentwiittauksista kolmen kuukauden ajalta keväältä 2015. Aineisto on käyty läpi ja kategorisoitu käyttäen metodina sisällönanalyysia.

Integrated genomic characterization of endometrial carcinoma

We performed an integrated genomic, transcriptomic and proteomic characterization of 373 endometrial carcinomas using array- and sequencing-based technologies. Uterine serous tumours and ∼25% of high-grade endometrioid tumours had extensive copy number alterations, few DNA methylation changes, low oestrogen receptor/progesterone receptor levels, and frequent TP53 mutations. Most endometrioid tumours had few copy number alterations or TP53 mutations, but frequent mutations in PTEN, CTNNB1, PIK3CA, ARID1A and KRAS and novel mutations in the SWI/SNF chromatin remodelling complex gene ARID5B. A subset of endometrioid tumours that we identified had a markedly increased transversion mutation frequency and newly identified hotspot mutations in POLE. Our results classified endometrial cancers into four categories: POLE ultramutated, microsatellite instability hypermutated, copy-number low, and copy-number high. Uterine serous carcinomas share genomic features with ovarian serous and basal-like breast carcinomas. We demonstrated that the genomic features of endometrial carcinomas permit a reclassification that may affect post-surgical adjuvant treatment for women with aggressive tumours.

Analytical Field-Effect Method for Extraction of Subgap States in Thin-Film Transistors

We present an analytical field-effect method to extract the density of subgap states (subgap DOS) in amorphous semiconductor thin-film transistors (TFTs), using a closed-form relationship between surface potential and gate voltage. By accounting the interface states in the subthreshold characteristics, the subgap DOS is retrieved, leading to a reasonably accurate description of field-effect mobility and its gate voltage dependence. The method proposed here is very useful not only in extracting device performance but also in physically based compact TFT modeling for circuit simulation.

Fourier spectrum based extraction of an equivalent trap state density in indium gallium zinc oxide transistors

Segregating the dynamics of gate bias induced threshold voltage shift, and in particular, charge trapping in thin film transistors (TFTs) based on time constants provides insight into the different mechanisms underlying TFTs instability. In this Letter we develop a representation of the time constants and model the magnitude of charge trapped in the form of an equivalent density of created trap states. This representation is extracted from the Fourier spectrum of the dynamics of charge trapping. Using amorphous In-Ga-Zn-O TFTs as an example, the charge trapping was modeled within an energy range of Delta E-t approximate to 0.3 eV and with a density of state distribution as D-t(Et-j) = D-t0 exp(-Delta E-t/kT) with D-t0 = 5.02 x 10(11) cm(-2) eV(-1). Such a model is useful for developing simulation tools for circuit design. (C) 2014 AIP Publishing LLC.

祖国力学事业辛勤的耕耘者——恭贺挚友伟长先生九秩华诞

<正> 今年正值我的老朋友钱伟长先生九十华诞,我愿在此向他表示最诚挚的祝贺,祝愿他健康长寿、老当益壮、诸事顺遂! 我与伟长先生的相识、相知可追溯到半个多世纪之前. 1946年初我赴美留学, 2月间到了加州理工学院的喷气推进研究室(JPL),那时在Th.von Karman教授周围可谓人才济济,特别是集中着几位出类拔萃的中国青年学者:钱学森、钱伟长、郭永怀、林家翘等等,我很快就与他们熟悉了.青年钱伟长给我留下了

Irteerak ikaskuntza baliabide bezala: Armañon Interpretazio Zentroa

[eus] Haur Hezkuntzan zientziaren ikaskuntzarako baliabide aberasgarrienetako bat irteerak dira, hauek beharrezkoak baitira haurraren garapen integralerako. Horretarako, irteerak eskolaren parte izan behar dute eta irakasleek bisitaldiak proposatu behar dituzte. Hainbat toki daude bisitak egiteko HHko haurrekin eta lan honetan Armañongo Interpretazio Zentroaren hezkuntza eskaintza aztertuko da, adin txikiko umeen kasuan bertako baliabideen eragina ikusi ahal izateko. Zentroaren arduradunen iritziak ezagututa eta HHko haurren bisitaldia aztertuta, emaitzak eta ondorioak aterako dira.

mtDNA Data Indicate a Single Origin for Dogs South of Yangtze River, Less Than 16,300 Years Ago, from Numerous Wolves

There is no generally accepted picture of where, when, and how the domestic dog originated. Previous studies of mitochondrial DNA (mtDNA) have failed to establish the time and precise place of origin because of lack of phylogenetic resolution in the so fa

Instrumentos musicales en diversos materiales y estilos formales.

7 hojas : ilustraciones, fotografías a color

HDAC Inhibition Overcomes Acute Resistance to MEK Inhibition in BRAF-Mutant Colorectal Cancer by Downregulation of c-FLIPL

Purpose: Activating mutations in the BRAF oncogene are found in 8% to 15% of colorectal cancer patients and have been associated with poor survival. In contrast with BRAF-mutant (MT) melanoma, inhibition of the MAPK pathway is ineffective in the majority of BRAFMT colorectal cancer patients. Therefore, identification of novel therapies for BRAFMT colorectal cancer is urgently needed.

Experimental Design: BRAFMT and wild-type (WT) colorectal cancer models were assessed in vitro and in vivo. Small-molecule inhibitors of MEK1/2, MET, and HDAC were used, overexpression and siRNA approaches were applied, and cell death was assessed by flow cytometry, Western blotting, cell viability, and caspase activity assays.

Results: Increased c-MET-STAT3 signaling was identified as a novel adaptive resistance mechanism to MEK inhibitors (MEKi) in BRAFMT colorectal cancer models in vitro and in vivo. Moreover, MEKi treatment resulted in acute increases in transcription of the endogenous caspase-8 inhibitor c-FLIPL in BRAFMT cells, but not in BRAFWT cells, and inhibition of STAT3 activity abrogated MEKi-induced c-FLIPL expression. In addition, treatment with c-FLIP–specific siRNA or HDAC inhibitors abrogated MEKi-induced upregulation of c-FLIPL expression and resulted in significant increases in MEKi-induced cell death in BRAFMT colorectal cancer cells. Notably, combined HDAC inhibitor/MEKi treatment resulted in dramatically attenuated tumor growth in BRAFMT xenografts.

Conclusions: Our findings indicate that c-MET/STAT3-dependent upregulation of c-FLIPL expression is an important escape mechanism following MEKi treatment in BRAFMT colorectal cancer. Thus, combinations of MEKi with inhibitors of c-MET or c-FLIP (e.g., HDAC inhibitors) could be potential novel treatment strategies for BRAFMT colorectal cancer.

Vitamin D3 suppresses morphological evolution of the cribriform cancerous phenotype

Development of cribriform morphology (CM) heralds malignant change in human colon but lack of mechanistic understanding hampers preventive therapy. This study investigated CM pathobiology in three-dimensional (3D) Caco-2 culture models of colorectal glandular architecture, assessed translational relevance and tested effects of 1,25(OH)2D3, the active form of vitamin D. CM evolution was driven by oncogenic perturbation of the apical polarity (AP) complex comprising PTEN, CDC42 and PRKCZ (phosphatase and tensin homolog, cell division cycle 42 and protein kinase C zeta). Suppression of AP genes initiated a spatiotemporal cascade of mitotic spindle misorientation, apical membrane misalignment and aberrant epithelial configuration. Collectively, these events promoted “Swiss cheese-like” cribriform morphology (CM) comprising multiple abnormal “back to back” lumens surrounded by atypical stratified epithelium, in 3D colorectal gland models. Intestinal cancer driven purely by PTEN-deficiency in transgenic mice developed CM and in human CRC, CM associated with PTEN and PRKCZ readouts. Treatment of PTEN-deficient 3D cultures with 1,25(OH)2D3 upregulated PTEN, rapidly activated CDC42 and PRKCZ, corrected mitotic spindle alignment and suppressed CM development. Conversely, mutationally-activated KRAS blocked 1,25(OH)2D3 rescue of glandular architecture. We conclude that 1,25(OH)2D3 upregulates AP signalling to reverse CM in a KRAS wild type (wt), clinically predictive CRC model system. Vitamin D could be developed as therapy to suppress inception or progression of a subset of colorectal tumors.