Open University

About: Open University is a education organization based out in Milton Keynes, United Kingdom. It is known for research contribution in the topics: Context (language use) & Population. The organization has 11702 authors who have published 35020 publications receiving 1110835 citations. The organization is also known as: Open University, The & Open University.

We recruit attitude : the selection and shaping of call centre labour

Abstract: Call centres are growing rapidly and are receiving attention from politicians, policy makers and academics. While most of the latter focus on work relations, notably patterns of control and surveillance, this paper explores the role of recruitment, selection and training in the shaping call centre labour. The paper uses data from a case study of a call centre (Telebank) to argue that the increased significance of social competencies within interactive service work gives these procedures greater salience and that they are used by management to address the indeterminacy of labour, in part, outside the labour process. Primary data from management and customer service representatives is used to examine and contrast their respective perceptions of recruitment, selection and training. The paper shows the contested and contradictory tendencies associated with how a particular company identifies and then uses social competencies. Tensions in the labour process between the mobilization of employee attributes and the deliberate moulding and standardization of such competencies is merely part of wider and unresolved tensions concerning the contested nature of emotional labour and the demands of quantity and quality in the management of call centre work.

Open Innovation Practices in SMEs and Large Enterprises

Abstract: Few studies on open innovation (OI) have addressed OI practices in small and medium sized enterprises (SMEs) and how their use of OI and resulting benefits differ from large enterprises. The lack of resources in SMEs to engage in looking outward is said to be a barrier to OI, but at the same time this shortage is cited as a motive for looking beyond organizational boundaries for technological knowledge. We investigate how OI dimensions have an impact on the innovative performance of SMEs in comparison to large companies. The key finding is that the effects of OI practices in SMEs often differ from those in large firms. SMEs are more effective in using different OI practices simultaneously when they introduce new products on the market whereas this is less the case for large firms. Turnover from new products in SMEs is driven by IP protection mechanisms while large firms in this case benefit more from their search strategies. However, the strengths of these differences between SMEs and large firms.

Postmitotic neurons develop a p21-dependent senescence-like phenotype driven by a DNA damage response.

Abstract: Summary In senescent cells, a DNA damage response drives not only irreversible loss of replicative capacity but also production and secretion of reactive oxygen species (ROS) and bioactive peptides including pro-inflammatory cytokines. This makes senescent cells a potential cause of tissue functional decline in aging. To our knowledge, we show here for the first time evidence suggesting that DNA damage induces a senescence-like state in mature postmitotic neurons in vivo. About 40‐80% of Purkinje neurons and 20‐40% of cortical, hippocampal and peripheral neurons in the myenteric plexus from old C57Bl ⁄6 mice showed severe DNA damage, activated p38MAPkinase, high ROS production and oxidative damage, interleukin IL-6 production, heterochromatinization and senescence-associated b-galactosidase activity. Frequencies of these senescence-like neurons increased with age. Short-term caloric restriction tended to decrease frequencies of positive cells. The phenotype was aggravated in brains of late-generation TERC) ⁄ ) mice with dysfunctional telomeres. It was fully rescued by loss of p21(CDKN1A) function in late-generation TERC) ⁄ )CDKN1A) ⁄ ) mice, indicating p21 as the necessary signal transducer between DNA damage response and senescence-like phenotype in neurons, as in senescing fibroblasts and other proliferationcompetent cells. We conclude that a senescence-like phenotype is possibly not restricted to proliferation-competent cells. Rather, dysfunctional telomeres and ⁄or accumulated DNA damage can induce a DNA damage response leading to a phenotype in postmitotic neurons that resembles cell senescence in multiple features. Senescence-like neurons might be a source of oxidative and inflammatory stress and a contributor to brain aging.