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S. aureus is associated with atopic dermatitis (AD). Several staphylococcal products including cell wall components, protease, and exotoxins, are thought to be involved in allergic inflammation of AD via activating immune cells such as T cells and mast cells. None of the staphylococcal exotoxins has been reported to activate a primary IL-4 inducer, basophils, that are known to produce large amounts of IL-4 in response to allergens as well as IgE-independent stimuli such as mites and helminth proteases. In this study, we investigated the ability of staphylococcal superantigen-like (SSL) family to activate basophils. [https://www.selleckchem.com/products/mk-4827.html selleckchem] SSL12, reported its activity to activate mast cells, induced the production of IL-4 in bone marrow derived basophils. SSL12 also evoked the release of IL-4 in freshly isolated murine basophils in bone marrow cells, as the depletion of basophils by basophils-specific antibodies against high-affinity IgE receptor and CD49b diminished the responsiveness of bone marrow cells for SSL12. These results propose the novel immune regulatory activity of SSL12 by inducing IL-4 in basophils, that contributes to the development of allergic inflammation disorders and the immune evasion of the cocci.GOLPH3, an oncoprotein, plays crucial roles in tumor etiology. Compelling evidences have demonstrated that GOLPH3 contributes to regulate tumor cell growth, migration and invasion under normal nutrient condition. However, the oncogenic activity of GOLPH3 under serum starvation remains largely unknown. In this study, we reported that GOLPH3 depletion led to marked reduction in adhesion of glioma U251 cells, particularly under serum deprivation. We found that silencing of GOLPH3 expression reduced the protein amount of ITGB1 only in serum-free medium. Further insights into the mechanism between GOLPH3 and ITGB1, we applied proteasome or lysosome inhibitor to block the degradation of ITGB1, and identified GOLPH3 silencing can prompt ITGB1 lysosomal degradation under serum starvation. Finally, we found the reductions in glioma cell adhesion and ITGB1 protein amount could be rescued by ITGB1 overexpression. Taken together, these results show that GOLPH3 contributes to the adhesion of glioma cells by regulating the lysosomal degradation of ITGB1 under serum starvation.<br /><br /> Cancer nurse specialists are advanced practitioners who offer continuity of care and expert support for people diagnosed with specific cancers. Health Education England's Cancer Workforce Plan prioritises expansion of cancer nurse specialist numbers by 2021 as part of the Cancer Taskforce Strategy for England.<br /><br /> To assess whether working practices of advanced practice specialist nurses are associated with clinical outcomes for people with lung cancer.<br /><br /> Adults with non-small cell lung cancer followed from 30 days post-diagnosis in English secondary care were obtained from the English National Lung Cancer Audit, 2007 to 2011. A national survey of lung cancer nurse specialists provided information on self-reported working practices. Mortality and unplanned admissions from 30 days to 12 months post diagnosis were respectively analysed using Cox and Poisson regression. Outcomes were assessed according to patients' receipt of initial assessments by a lung cancer nurse specialist and according to trust-level repoung cancer. These were not limited to a single treatment pathway, but do indicate discrete relationships within pathways. Our study provides initial measures of overall lung cancer nurse specialist working practices at trusts, however, more detailed studies with longitudinal measurement of lung cancer nurse specialist-patient interaction are needed to better ascertain impacts on long-term patient outcomes. The findings highlight opportunities for potential improvement in effectiveness of service and care management.Cytoskeletal proteins are beginning to be considered as key regulators of nuclear function. Among them, actin and myosin have been implicated in numerous tasks, including chromatin regulation, transcription and assembly of nascent ribonucleoprotein complexes. We also know from work performed by several labs that influx of actin and myosin into the nucleus and out of the nucleus is tightly regulated. In particular, in the case of actin, its nucleocytoplasmic import/export cycle is controlled by the importin/exportin system and it correlates with the transcriptional state of the cell. These basic molecular functions of both actin and myosin seem to impact key cellular functions, including development and differentiation as well as the cellular response to DNA damage by directly affecting transcriptional reprograming. These observations are beginning to suggest that actin and myosin could play an important role in consolidating the organization of the mammalian genome and that loss of actin and myosin likely leads to a general instability of the genome. In this chapter, we provide a general background on evidence that actin and myosin are important in key nuclear functions. Following this, we will focus on evidence supporting of a role in genome organization and finally we will discuss increasingly striking results on the role of actin and myosin in the maintenance of genome integrity.The presence of actin in the nucleus has been a matter of debate for many years. In recent years many important roles of actin in the nucleus (transcriptional regulation, chromatin remodeling, DNA repair, cell division, maintenance of nuclear architecture) have been identified, and the precise control of nuclear actin levels has been demonstrated. The vital importance of the actin driven processes in the cell make it highly likely that dysregulation of nuclear actin dynamics and structure can be linked to tumor induction and -progression. In this chapter I summarize our current knowledge about nuclear actin in the cancer context.Cancer, as a major cause of mortality, is highly related to alterations in the structure and behavior of cells of cancerous tissues. The invasive nature of cancer cells is correlated with their increased traction force, high deformability and altered cell adhesion. These changes are directly attributed to the remodeling of cell cytoskeleton mostly in actin structure. While microtubules and intermediate filaments are mostly involved in mechanical properties of cytoskeleton, actin fibers actively contribute to not only mechanical properties, but also other aspects. Hence study of actin mechanics assists in a deeper understanding of cancer related events. Here, with a biomechanical perspective, we describe the cytoskeleton changes in cancer onset and progress in fiber and protein levels, with focus on actin structure in terms of content and arrangement. Cytoskeleton remodeling and particularly alterations in the content and arrangement of actin structure, highly influence cell mechanical properties, force generation and adhesion potentials.