373 research outputs found

    Crossed products by endomorphisms and reduction of relations in relative Cuntz-Pimsner algebras

    Full text link
    Starting from an arbitrary endomorphism \alpha of a unital C*-algebra A we construct a crossed product. It is shown that the natural construction depends not only on the C*-dynamical system (A,\alpha) but also on the choice of an ideal orthogonal to kernel of \alpha. The article gives an explicit description of the internal structure of this crossed product and, in particular, discusses the interrelation between relative Cuntz-Pimsner algebras and partial isometric crossed products. We present a canonical procedure that reduces any given C*-correspondence to the 'smallest' C*-correspondence yielding the same relative Cuntz-Pimsner algebra as the initial one. In the context of crossed products this reduction procedure corresponds to the reduction of C*-dynamical systems and allow us to establish a coincidence between relative Cuntz-Pimsner algebras and crossed products introduced.Comment: The article is based on papers arXiv:math.OA/0703801 and arXiv:math.OA/0704.3811, and in essence forms their unification, refinement and developmen

    Interleukin-6 and Associated Cytokine Responses to An Acute Bout of High-intensity Interval Exercise: the Effect of Exercise Intensity and Volume

    Get PDF
    Acute increases in interleukin (IL)-6 following prolonged exercise are associated with the induction of a transient anti-inflammatory state (e.g., increases in IL-10) that is partly responsible for the health benefits of regular exercise. The purposes of this study were to investigate the IL-6–related inflammatory response to high-intensity interval exercise (HIIE) and to determine the impact of exercise intensity and volume on this response. Ten participants (5 males and 5 females) completed 3 exercise bouts of contrasting intensity and volume (LOW, MOD, and HIGH). The HIGH protocol was based upon standard HIIE protocols, while the MOD and LOW protocols were designed to enable a comparison of exercise intensity and volume with a fixed duration. Inflammatory cytokine concentrations were measured in plasma (IL-6, IL-10) and also determined the level of gene expression (IL-6, IL-10, and IL-4R) in peripheral blood. The plasma IL-6 response to exercise (reported as fold changes) was significantly greater in HIGH (2.70 ± 1.51) than LOW (1.40 ± 0.32) (P = 0.04) and was also positively correlated to the mean exercise oxygen uptake (r = 0.54, P < 0.01). However, there was no change in anti-inflammatory IL-10 or IL-4R responses in plasma or at the level of gene expression. HIIE caused a significant increase in IL-6 and was greater than that seen in low-intensity exercise of the same duration. The increases in IL-6 were relatively small in magnitude, and appear to have been insufficient to induce the acute systemic anti-inflammatory effects, which are evident following longer duration exercise

    Innate immune responses to a single session of sprint interval training.

    Get PDF
    Sprint interval training (SIT) is a potent stimulus for physiological and metabolic adaptations comparable with those induced by traditional "aerobic" endurance training. There has been a great deal of recent research on SIT, which may lead to increased use of this type of training. The purpose of the present study was to determine the acute effects of SIT on aspects of innate immunity not previously researched in this context. Nine males completed 1 SIT and 1 resting control trial in a crossover design. Blood and saliva samples were obtained at pre-, post-, and 30 min postexercise to measure blood neutrophil oxidative burst activity (OBA) in addition to saliva secretary IgA (s-IgA) and lysozyme. SIT induced a significant depression of neutrophil fMLP-stimulated OBA (-30% for the 30-min postexercise time point, p  0.05). The main novel finding of the present study is that a single session of SIT causes significant exercise-induced immunodepression of some neutrophil functions but mucosal immunity was not depressed

    Designing a broad-spectrum integrative approach for cancer prevention and treatment

    Get PDF
    Targeted therapies and the consequent adoption of "personalized" oncology have achieved notablesuccesses in some cancers; however, significant problems remain with this approach. Many targetedtherapies are highly toxic, costs are extremely high, and most patients experience relapse after a fewdisease-free months. Relapses arise from genetic heterogeneity in tumors, which harbor therapy-resistantimmortalized cells that have adopted alternate and compensatory pathways (i.e., pathways that are notreliant upon the same mechanisms as those which have been targeted). To address these limitations, aninternational task force of 180 scientists was assembled to explore the concept of a low-toxicity "broad-spectrum" therapeutic approach that could simultaneously target many key pathways and mechanisms. Using cancer hallmark phenotypes and the tumor microenvironment to account for the various aspectsof relevant cancer biology, interdisciplinary teams reviewed each hallmark area and nominated a widerange of high-priority targets (74 in total) that could be modified to improve patient outcomes. For thesetargets, corresponding low-toxicity therapeutic approaches were then suggested, many of which werephytochemicals. Proposed actions on each target and all of the approaches were further reviewed forknown effects on other hallmark areas and the tumor microenvironment. Potential contrary or procar-cinogenic effects were found for 3.9% of the relationships between targets and hallmarks, and mixedevidence of complementary and contrary relationships was found for 7.1%. Approximately 67% of therelationships revealed potentially complementary effects, and the remainder had no known relationship. Among the approaches, 1.1% had contrary, 2.8% had mixed and 62.1% had complementary relationships. These results suggest that a broad-spectrum approach should be feasible from a safety standpoint. Thisnovel approach has potential to be relatively inexpensive, it should help us address stages and types ofcancer that lack conventional treatment, and it may reduce relapse risks. A proposed agenda for futureresearch is offered

    Associations of common breast cancer susceptibility alleles with risk of breast cancer subtypes in BRCA1 and BRCA2 mutation carriers

    Get PDF
    Introduction: More than 70 common alleles are known to be involved in breast cancer (BC) susceptibility, and several exhibit significant heterogeneity in their associations with different BC subtypes. Although there are differences in the association patterns between BRCA1 and BRCA2 mutation carriers and the general population for several loci, no study has comprehensively evaluated the associations of all known BC susceptibility alleles with risk of BC subtypes in BRCA1 and BRCA2 carriers. Methods: We used data from 15,252 BRCA1 and 8,211 BRCA2 carriers to analyze the associations between approximately 200,000 genetic variants on the iCOGS array and risk of BC subtypes defined by estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and triple-negative- (TN) status; morphologic subtypes; histological grade; and nodal involvement. Results: The estimated BC hazard ratios (HRs) for the 74 known BC alleles in BRCA1 carriers exhibited moderate correlations with the corresponding odds ratios from the general population. However, their associations with ER-positive BC in BRCA1 carriers were more consistent with the ER-positive as

    Assessing associations between the AURKAHMMR-TPX2-TUBG1 functional module and breast cancer risk in BRCA1/2 mutation carriers

    Get PDF
    While interplay between BRCA1 and AURKA-RHAMM-TPX2-TUBG1 regulates mammary epithelial polarization, common genetic variation in HMMR (gene product RHAMM) may be associated with risk of breast cancer in BRCA1 mutation carriers. Following on these observations, we further assessed the link between the AURKA-HMMR-TPX2-TUBG1 functional module and risk of breast cancer in BRCA1 or BRCA2 mutation carriers. Forty-one single nucleotide polymorphisms (SNPs) were genotyped in 15,252 BRCA1 and 8,211 BRCA2 mutation carriers and subsequently analyzed using a retrospective likelihood appr
    corecore