ИССЛЕДОВАНИЕ ВЛИЯНИЯ ИГРОВОГО БИОУПРАВЛЕНИЯ НА ПСИХОФИЗИОЛОГИЧЕСКИЕ ПОКАЗАТЕЛИ СПОРТСМЕНОВ-ЕДИНОБОРЦЕВ С НАРУШЕНИЕМ ВЕГЕТАТИВНОГО СТАТУСА

106 single-combat sportsmen took part in this study: 76 sportsmen with dominant activity of sympathetic part of vegetative nervous system and pronounced strain and overstrain of regulatory systems. Control group consists of 30 healthy sportsmen. Game biofeedback showed considerable advantages over methods of pedagogical correction in improving psycho-physiological parameters.В исследовании приняли участие 106 спортсменов-единоборцев: 76 спортсменов с преобладанием активности симпатического отдела вегетативной нервной системы и выраженным напряжением и перенапряжением регуляторных систем, группу контроля составили 30 практически здоровых спортсменов. Игровое биоуправление показало преимущества по сравнению с методами педагогической коррекции в улучшении психофизиологических показателей

Нарушения вегетативного статуса у спортсменов ациклических видов спорта и их коррекция средствами технологии игрового биоуправления и транскраниальной стимуляции

Examining 37 sportsmen with the predominant activity of sympathetic unit of the vegetative nervous system, we detected the switch of bloodstream regulation control to the higher vegetative centers. We showed the effectiveness of the transcranial electrostimulation and gaming biofeedback methods for complex correction of vegetative status disorders.У 37 спортсменов с преобладанием активности симпатического отдела вегетативной нервной системы описан переход управления регуляцией кровообращения к высшим вегетативным центрам. Доказана эффективность комплексной коррекции нарушений вегетативного статуса методами транскраниальной электростимуляции и с помощью технологии игрового биоуправления

Gene products of chromosome 11q and their association with CCND1 gene amplification and tamoxifen resistance in premenopausal breast cancer

Introduction: The amplification event occurring at chromosome locus 11q13, reported in several different cancers, includes a number of potential oncogenes. We have previously reported amplification of one such oncogene, namely CCND1, to be correlated with an adverse effect of tamoxifen in premenopausal breast cancer patients. Over-expression of cyclin D-1 protein, however, confers tamoxifen resistance but not a tamoxifen-induced adverse effect. Potentially, co-amplification of an additional 11q13 gene, with a resulting protein over-expression, is required to cause an agonistic effect. Moreover, during 11q13 amplification a deletion of the distal 11q region has been described. In order to assess the potential impact of the deletion we examined a selected marker for this event. Method: Array comparative genomic hybridization analysis was employed to identify and confirm changes in the gene expression of a number of different genes mapping to the 11q chromosomal region, associated with CCND1 amplification. The subsequent protein expression of these candidate genes was then examined in a clinical material of 500 primary breast cancers from premenopausal patients who were randomly assigned to either tamoxifen or no adjuvant treatment. The protein expression was also compared with gene expression data in a subset of 56 breast cancer samples. Results: Cortactin and FADD (Fas-associated death domain) over-expression was linked to CCND1 amplification, determined by fluorescence in situ hybridization, but was not associated with a diminished effect of tamoxifen. However, deletion of distal chromosome 11q, defined as downregulation of the marker Chk1 (checkpoint kinase 1), was associated with an impaired tamoxifen response, and interestingly with low proliferative breast cancer of low grade. For Pak1 (p21-activated kinase 1) and cyclin D-1 the protein expression corresponded to the gene expression data. Conclusions: The results indicate that many 11q13 associated gene products are over-expressed in conjunction with cyclin D-1 but not linked to an agonistic effect of tamoxifen. Finally, the deletion of distal 11q, linked to 11q13 amplification, might be an important event affecting breast cancer outcome and tamoxifen response

Type I insulin-like growth factor receptor over-expression induces proliferation and anti-apoptotic signaling in a three-dimensional culture model of breast epithelial cells

INTRODUCTION: Activation of the type I insulin-like growth factor receptor (IGFIR) promotes proliferation and inhibits apoptosis in a variety of cell types. Transgenic mice expressing a constitutively active IGFIR or IGF-I develop mammary tumors and increased levels of IGFIR have been detected in primary breast cancers. However, the contribution of IGFIR activation in promoting breast cancer progression remains unknown. Mammary epithelial cell lines grown in three-dimensional cultures form acinar structures that mimic the round, polarized, hollow and growth-arrested features of mammary alveoli. We used this system to determine how proliferation and survival signaling by IGFIR activation affects breast epithelial cell biology and contributes to breast cancer progression. METHODS: Pooled, stable MCF-10A breast epithelial cells expressing wild-type IGFIR or kinase-dead IGFIR (K1003A) were generated using retroviral-mediated gene transfer. The effects of over-expression of wild-type or kinase-dead IGFIR on breast epithelial cell biology were analyzed by confocal microscopy of three-dimensional cultures. The contribution of signaling pathways downstream of IGFIR activation to proliferation and apoptosis were determined by pharmacological inhibition of phosphatidylinositol 3' kinase (PI3K) with LY294002, MAP kinase kinase (MEK) with UO126 and mammalian target of rapamycin (mTOR) with rapamycin. RESULTS: We found that MCF-10A cells over-expressing the IGFIR formed large, misshapen acinar structures with filled lumina and disrupted apico-basal polarization. This phenotype was ligand-dependent, occurring with IGF-I or supraphysiological doses of insulin, and did not occur in cells over-expressing the kinase-dead receptor. We observed increased proliferation, decreased apoptosis and increased phosphorylation of Ser(473 )of Akt and Ser(2448 )of mTOR throughout IGFIR structures. Inhibition of PI3K with LY294002 or MEK with UO126 prevented the development of acinar structures from IGFIR-expressing but not control cells. The mTOR inhibitor rapamycin failed to prevent IGFIR-induced hyperproliferation and survival signaling. CONCLUSION: Increased proliferation and survival signaling as well as loss of apico-basal polarity by IGFIR activation in mammary epithelial cells may promote early lesions of breast cancer. Three-dimensional cultures of MCF-10A cells over-expressing the IGFIR are a useful model with which to study the role of IGFIR signaling in breast cancer progression and for characterizing the effects of chemotherapeutics targeted to IGFIR signaling

Computational analysis of expression of human embryonic stem cell-associated signatures in tumors

<p>Abstract</p> <p>Background</p> <p>The cancer stem cell model has been proposed based on the linkage between human embryonic stem cells and human cancer cells. However, the evidences supporting the cancer stem cell model remain to be collected. In this study, we extensively examined the expression of human embryonic stem cell-associated signatures including core genes, transcription factors, pathways and microRNAs in various cancers using the computational biology approach.</p> <p>Results</p> <p>We used the class comparison analysis and survival analysis algorithms to identify differentially expressed genes and their associated transcription factors, pathways and microRNAs among normal vs. tumor or good prognosis vs. poor prognosis phenotypes classes based on numerous human cancer gene expression data. We found that most of the human embryonic stem cell- associated signatures were frequently identified in the analysis, suggesting a strong linkage between human embryonic stem cells and cancer cells.</p> <p>Conclusions</p> <p>The present study revealed the close linkage between the human embryonic stem cell associated gene expression profiles and cancer-associated gene expression profiles, and therefore offered an indirect support for the cancer stem cell theory. However, many interest issues remain to be addressed further.</p

Analysis of the vegetative status disoders of acyclic sportsmen and its correction with the technology of gaming biofeedback and transcranial electrostimulation

Examining 37 sportsmen with the predominant activity of sympathetic unit of the vegetative nervous system, we detected the switch of bloodstream regulation control to the higher vegetative centers. We showed the effectiveness of the transcranial electrostimulation and gaming biofeedback methods for complex correction of vegetative status disorders

ANALYSIS ON HOW GAME BIOFEEDBACK AFFECTS PSYCHO-PHYSIOLOGICAL PARAMETERS OF SINGLE-COMBAT SPORTSMEN WITH VEGETATIVE STATUS FAILURE

106 single-combat sportsmen took part in this study: 76 sportsmen with dominant activity of sympathetic part of vegetative nervous system and pronounced strain and overstrain of regulatory systems. Control group consists of 30 healthy sportsmen. Game biofeedback showed considerable advantages over methods of pedagogical correction in improving psycho-physiological parameters

IGF-IR: a new prognostic biomarker for human glioblastoma.

Glioblastomas (GBMs) are the most common malignant primary brain tumours in adults and are refractory to conventional therapy, including surgical resection, radiotherapy and chemotherapy. The insulin-like growth factor (IGF) system is a complex network that includes ligands (IGFI and IGFII), receptors (IGF-IR and IGF-IIR) and high-affinity binding proteins (IGFBP-1 to IGFBP-6). Many studies have reported a role for the IGF system in the regulation of tumour cell biology. However, the role of this system remains unclear in GBMs.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Identification of Insulin Receptor Substrate 1 (IRS-1) and IRS-2 as Signaling Intermediates in the α6β4 Integrin-Dependent Activation of Phosphoinositide 3-OH Kinase and Promotion of Invasion

Expression of the α6β4 integrin increases the invasive potential of carcinoma cells by a mechanism that involves activation of phosphoinositide 3-OH kinase (PI3K). In the present study, we investigated the signaling pathway by which the α6β4 integrin activates PI3K. Neither the α6 nor the β4 cytoplasmic domain contains the consensus binding motif for PI3K, pYMXM, indicating that additional proteins are likely to be involved in the activation of this lipid kinase by the α6β4 integrin. We identified insulin receptor substrate 1 (IRS-1) and IRS-2 as signaling intermediates in the activation of PI3K by the α6β4 integrin. IRS-1 and IRS-2 are cytoplasmic adapter proteins that do not contain intrinsic kinase activity but rather function by recruiting proteins to surface receptors, where they organize signaling complexes. Ligation of the α6β4 receptor promotes tyrosine phosphorylation of IRS-1 and IRS-2 and increases their association with PI3K, as determined by coimmunoprecipitation. Moreover, we identified a tyrosine residue in the cytoplasmic domain of the β4 subunit, Y1494, that is required for α6β4-dependent phosphorylation of IRS-2 and activation of PI3K in response to receptor ligation. Most importantly, Y1494 is essential for the ability of the α6β4 integrin to promote carcinoma invasion. Taken together, these results imply a key role for the IRS proteins in the α6β4-dependent promotion of carcinoma invasion