Current status of e-learning systems in the Russian Federation on the example of the electronic information educational environment in the Tomsk polytechnic university

The article examines the concepts of e-learning and online courses. It analyzes status of e-learning systems in the Russia on the example of the Tomsk Polytechnic University. Also outlined are necessary conditions for its successful development in Russia

YB-1 And CTCF Differentially Regulate The 5-HTT Polymorphic Intron 2 Enhancer Which Predisposes To A Variety Of Neurological Disorders.

Mutation or inappropriate expression of the serotonin transporter (5-HTT) gene has been postulated as a possible predisposing factor in many CNS-related disorders, including numerous studies of affective disorders. The human gene encompasses 15 exons spanning -31 kb on chromosome 17qll (Lesch et aI., 1994)

Nucleolin as Activator of Human Papillomavirus Type 18 Oncogene Transcription in Cervical Cancer

High risk human papillomaviruses (HPVs) are central to the development of cervical cancer and the deregulated expression of high risk HPV oncogenes is a critical event in this process. Here, we find that the cell protein nucleolin binds in a sequence-specific manner to the HPV18 enhancer. The DNA binding activity of nucleolin is primarily S phase specific, much like the transcription of the E6 and E7 oncoproteins of HPV18 in cervical cancer cells. Antisense inactivation of nucleolin blocks E6 and E7 oncogene transcription and selectively decreases HPV18+ cervical cancer cell growth. Furthermore, nucleolin controls the chromatin structure of the HPV18 enhancer. In contrast, HPV16 oncogene transcription and proliferation rates of HPV16+ SiHa cervical cancer cells are independent of nucleolin activity. Moreover, nucleolin expression is altered in HPV18+ precancerous and cancerous tissue from the cervix uteri. Whereas nucleolin was homogeneously distributed in the nuclei of normal epithelial cells, it showed a speckled nuclear phenotype in HPV18+ carcinomas. Thus, the host cell protein nucleolin is directly linked to HPV18-induced cervical carcinogenesis

Identification of Y-Box Binding Protein 1 As a Core Regulator of MEK/ERK Pathway-Dependent Gene Signatures in Colorectal Cancer Cells

Transcriptional signatures are an indispensible source of correlative information on disease-related molecular alterations on a genome-wide level. Numerous candidate genes involved in disease and in factors of predictive, as well as of prognostic, value have been deduced from such molecular portraits, e.g. in cancer. However, mechanistic insights into the regulatory principles governing global transcriptional changes are lagging behind extensive compilations of deregulated genes. To identify regulators of transcriptome alterations, we used an integrated approach combining transcriptional profiling of colorectal cancer cell lines treated with inhibitors targeting the receptor tyrosine kinase (RTK)/RAS/mitogen-activated protein kinase pathway, computational prediction of regulatory elements in promoters of co-regulated genes, chromatin-based and functional cellular assays. We identified commonly co-regulated, proliferation-associated target genes that respond to the MAPK pathway. We recognized E2F and NFY transcription factor binding sites as prevalent motifs in those pathway-responsive genes and confirmed the predicted regulatory role of Y-box binding protein 1 (YBX1) by reporter gene, gel shift, and chromatin immunoprecipitation assays. We also validated the MAPK-dependent gene signature in colorectal cancers and provided evidence for the association of YBX1 with poor prognosis in colorectal cancer patients. This suggests that MEK/ERK-dependent, YBX1-regulated target genes are involved in executing malignant properties

Liposomal cisplatin can overcome chemotherapy resistance of A2780 ovarian cancer cells by inducing the extrinsic apoptotic pathway

Liposomes have been considered as promising, but passive carriers in medical sciences to mediate a controlled transport of a drug cargo to target sites or into target cells. Here, we provide evidence that a liposomal drug transport into cells might have stronger consequences for directing the drug activity beyond a simple transport function. Liposomal CDDP induces programmed cell death via the extrinsic pathway of apoptosis, which is in contrast to the drug taken up in free form. It thus appears that this is the key to explain, why liposomal CDDP overcomes cellular resistance regimes in A2780cis cells. These findings shed new light on liposomal drug carrier approaches in cancer and suggest liposomal CDDP as promising strategy for the treatment of CDDP resistant ovarian carcinomas