BC200 is a long noncoding RNA expressed at high levels in the Alzheimer's disease (AD), and blocking of BC200 by siRNA is assumed to be an effective method for various disease therapy. We have established an AD cell model overexpressing amyloid β-peptide (Aβ)1-42 to observe the effects of BC200 on the cell viability and apoptosis, and to investigate the associated underlying mechanisms. Efficient knockdown and overexpression of BC200 were established using BC200 siRNA and BC200 mimics, respectively. Cell viability following BC200 knockdown and overexpression was assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyltetrazolium bromide assay, and cell apoptosis was monitored by flow cytometry. We successfully established an AD cell model overexpressing Aβ1-42 gene, and reported the results of change of BC200 on Aβ1-42 levels. Knockdown of BC200 significantly suppressed b-site amyloid precursor protein-cleaving enzyme 1 (BACE1) expression, and overexpression of BC200 increased BACE1 expression. Besides, inhibition of BC200 significantly increased cell viability and reduced cell apoptosis in the AD model via directly targeting BACE1, which can be increased by overexpression of BC200. BC200 regulated AD cell viability and apoptosis via targeting BACE1, and it may be one of the putative target in AD development and provides potential new insights into genetic therapy against AD.

The afterglow problem has been preventing CsI:Tl single crystal scintillators from being used for applications in the field of computer tomography and high-speed imaging. We show that Yb 2+ codoping in CsI:Tl can reduce it at least by one order of magnitude after 50 ms from X-ray cut-off compared to ordinary CsI:Tl. and higher effective atomic number (Z eff = 54) and allows the fabrication of micro-columnar films. Given its low cost, CsI:Tl materials became widely used for radiological imaging, 3 X-ray and gamma ray spectroscopy, homeland security and nuclear medicine applications. However, due to the persistent afterglow in CsI:Tl attributed to thermal ionization of trapped electrons (Tl 0 ) followed by radiative recombination with trapped holes [V KA (Tl + )], 4 which causes the pulse pile up in high count-rate applications, its usage in computer tomography (CT) and high-speed imaging applications is thus not possible. 5,6Thus, ways to suppress the afterglow in CsI:Tl have been researched intensively over the last two decades. In general, co-doping by an appropriate ion was found to be an effective method to suppress the afterglow in scintillators and phosphors as has been shown e.g. Therefore, despite the success of the afterglow suppression in CsI:Tl the codoping strategies mentioned above have simultaneously deteriorated the other important scintillation characteristics such as light yield and energy resolution which points to the complex character of the scintillation mechanism. Impurities (doped ions) may introduce energy levels in the band gap of the host crystal which interfere with the charge 3312 | CrystEngComm, 2014, 16, 3312-3317This journal is

Platelet aggregation is crucial for the development of cerebral infarction (CI) and it is markedly increased due to the binding of thromboxane A2 (TXA2) to its receptor (TXA2R). Therefore, TXA2R plays a central role in the pathogenesis of atherosclerosis and thrombosis. This study aimed to investigate the relationship between human TXA2R gene single nucleotide polymorphisms (SNPs) and non-cardiogenic CI in a Chinese cohort. Two SNPs, rs768963 and rs4523, located in the regulatory and coding regions of TXA2R gene, respectively, were examined in DNA samples from 407 Chinese patients with CI and 270 controls. 407 CI was categorized into subtypes using Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification. There was no significant association between rs4523 variants and CI. However, there was a significant difference in the overall distribution of genotypes and dominant/recessive models of rs768963 between CI and control groups. In addition, multiple logistic regression analysis revealed that the C allele of rs768963 was significantly associated with total CI (P = 0.023), large artery atherosclerosis subtype (P = 0.009), small artery occlusion subtype (P = 0.044) after adjusting for confounding factors (odds ratio = 1.533, 1.918 and 1.573, respectively). We conclude that TXA2R rs768963 polymorphism is associated with CI in a Chinese population.

Purpose. Alzheimer’s disease (AD) is considered to be the most common neurodegenerative disease and also one of the major fatal diseases affecting the elderly, thus bringing a huge burden to society. Therefore, identifying AD-related hub genes is extremely important for developing novel strategies against AD. Materials and Methods. Here, we extracted the gene expression profile GSE63061 from the National Center for Biotechnology Information (NCBI) GEO database. Once the unverified gene chip was removed, we standardized the microarray data after quality control. We utilized the Limma software package to screen the differentially expressed genes (DEGs). We conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of DEGs. Subsequently, we constructed a protein-protein interaction (PPI) network using the STRING database. Result. We screened 2169 DEGs, comprising 1313 DEGs with upregulation and 856 DEGs with downregulation. Functional enrichment analysis showed that the response of immune, the degranulation of neutrophils, lysosome, and the differentiation of osteoclast were greatly enriched in DEGs with upregulation; peptide biosynthetic process, translation, ribosome, and oxidative phosphorylation were dramatically enriched in DEGs with downregulation. 379 nodes and 1149 PPI edges were demonstrated in the PPI network constructed by upregulated DEGs; 202 nodes and 1963 PPI edges were shown in the PPI network constructed by downregulated DEGs. Four hub genes, including GAPDH, RHOA, RPS29, and RPS27A, were identified to be the newly produced candidates involved in AD pathology. Conclusion. GAPDH, RHOA, RPS29, and RPS27A are expected to be key candidates for AD progression. The results of this study can provide comprehensive insight into understanding AD’s pathogenesis and potential new therapeutic targets.