Turning points: the personal and professional circumstances that lead academics to become middle managers

In the current higher education climate, there is a growing perception that the pressures associated with being an academic middle manager outweigh the perceived rewards of the position. This article investigates the personal and professional circumstances that lead academics to become middle managers by drawing on data from life history interviews undertaken with 17 male and female department heads from a range of disciplines, in a post-1992 UK university. The data suggests that experiencing conflict between personal and professional identities, manifested through different socialization experiences over time, can lead to a ‘turning point’ and a decision that affects a person’s career trajectory. Although the results of this study cannot be generalized, the findings may help other individuals and institutions move towards a firmer understanding of the academic who becomes head of department—in relation to theory, practice and research.

Thromboxane A2 inhibition of SKCa after NO synthase block in rat middle cerebral artery

NO/prostanoid independent, EDHF-mediated hyperpolarization and dilation in rat middle cerebral arteries is mediated solely by endothelial cell IK(Ca). However, when the NO-pathway is also active, both SK(Ca) and IK(Ca) contribute to EDHF responses. As the SK(Ca) component can be inhibited by stimulation of thromboxane A(2) (TxA(2)) TP receptors and NO has the potential ability to inhibit thromboxane synthesis, we investigated whether TxA(2) might explain loss of functional input from SK(Ca) during NOS inhibition in cerebral arteries. EXPERIMENTAL APPROACH: Rat middle cerebral arteries were mounted in a wire myograph. Endothelium-dependent responses to the PAR2 agonist, SLIGRL were assessed as simultaneous changes in smooth muscle membrane potential and tension. KEY RESULTS: Responses were obtained in the presence of L-NAME as appropriate. Inhibition of TP receptors with either ICI 192,605 or SQ 29,548, did not affect EDHF mediated hyperpolarization and relaxation, but in their presence neither TRAM-34 nor apamin (to block IK(Ca) and SK(Ca) respectively) individually affected the EDHF response. However, in combination they virtually abolished it. Similar effects were obtained in the presence of the thromboxane synthase inhibitor, furegrelate, which additionally revealed an iberiotoxin-sensitive residual EDHF hyperpolarization and relaxation in the combined presence of TRAM-34 and apamin. CONCLUSIONS AND IMPLICATIONS: In the rat middle cerebral artery, inhibition of NOS leads to a loss of the SK(Ca) component of EDHF responses. Either antagonism of TP receptors or block of thromboxane synthase restores an input through SK(Ca). These data indicate that NO normally enables SK(Ca) activity in rat middle cerebral arteries.

Evidence for involvement of both IKCa and SKCa channels in hyperpolarizing responses of the rat middle cerebral artery

Endothelium-derived hyperpolarizing factor responses in the rat middle cerebral artery are blocked by inhibiting IKCa channels alone, contrasting with peripheral vessels where block of both IKCa and SKCa is required. As the contribution of IKCa and SKCa to endothelium-dependent hyperpolarization differs in peripheral arteries, depending on the level of arterial constriction, we investigated the possibility that SKCa might contribute to equivalent hyperpolarization in cerebral arteries under certain conditions. METHODS: Rat middle cerebral arteries (approximately 175 microm) were mounted in a wire myograph. The effect of KCa channel blockers on endothelium-dependent responses to the protease-activated receptor 2 agonist, SLIGRL (20 micromol/L), were then assessed as simultaneous changes in tension and membrane potential. These data were correlated with the distribution of arterial KCa channels revealed with immunohistochemistry. RESULTS: SLIGRL hyperpolarized and relaxed cerebral arteries undergoing variable levels of stretch-induced tone. The relaxation was unaffected by specific inhibitors of IKCa (TRAM-34, 1 micromol/L) or SKCa (apamin, 50 nmol/L) alone or in combination. In contrast, the associated smooth-muscle hyperpolarization was inhibited, but only with these blockers in combination. Blocking nitric oxide synthase (NOS) or guanylyl cyclase evoked smooth-muscle depolarization and constriction, with both hyperpolarization and relaxation to SLIGRL being abolished by TRAM-34 alone, whereas apamin had no effect. Immunolabeling showed SKCa and IKCa within the endothelium. CONCLUSIONS: In the absence of NO, IKCa underpins endothelium-dependent hyperpolarization and relaxation in cerebral arteries. However, when NOS is active SKCa contributes to hyperpolarization, whatever the extent of background contraction. These changes may have relevance in vascular disease states where NO release is compromised and when the levels of SKCa expression may be altered.

Inter-hemispheric mesospheric coupling in a comprehensive middle atmosphere model

Observations of noctilucent clouds have revealed a surprising coupling between the winter stratosphere and the summer polar mesopause region. In spite of the great distance involved, this inter-hemispheric link has been suggested to be the principal reason for both the year-to-year variability and the hemispheric differences in the frequency of occurrence of these high-altitude clouds. In this study, we investigate the dynamical influence of the winter stratosphere on the summer mesosphere using simulations from the vertically extended version of the Canadian Middle Atmosphere Model (CMAM). We find that for both Northern and Southern Hemispheres, variability in the summer polar mesopause region from one year to another can be traced back to the planetary-wave flux entering the winter stratosphere. The teleconnection pattern is the same for both positive and negative wave-flux anomalies. Using a composite analysis to isolate the events, it is argued that the mechanism for interhemispheric coupling is a feedback between summer mesosphere gravity-wave drag (GWD) and zonal wind, which is induced by an anomaly in mesospheric cross-equatorial flow, the latter arising from the anomaly in winter hemisphere GWD induced by the anomaly in stratospheric conditions.

Vertical propagation of information in a middle atmosphere data assimilation system by gravity-wave drag feedbacks

The mesospheric response to the 2002 Antarctic Stratospheric Sudden Warming (SSW) is analysed using the Canadian Middle Atmosphere Model Data Assimilation System (CMAM-DAS), where it represents a vertical propagation of information from the observations into the data-free mesosphere. The CMAM-DAS simulates a cooling in the lowest part of the mesosphere which is accomplished by resolved motions, but which is extended to the mid- to upper mesosphere by the response of the model's non-orographic gravity-wave drag parameterization to the change in zonal winds. The basic mechanism is that elucidated by Holton consisting of a net eastward wave-drag anomaly in the mesosphere during the SSW, although in this case there is a net upwelling in the polar mesosphere. Since the zonal-mean mesospheric response is shown to be predictable, this demonstrates that variations in the mesospheric state can be slaved to the lower atmosphere through gravity-wave drag.

Transnational urbanism in Port of Spain: returning middle-class urban elites

Port of Spain, Trinidad offers an ideal context in which to analyze pre-retirement return migration to a Global South urban realm, expanding transnational urban research beyond the conventional focus on Global North metropolitan destinations. In this article, we draw on the transnational narratives of a selected sample of relatively youthful Trinidadians, who have spent many years abroad acquiring education and professional experience, but who have then decided to return in mid-career to the capital region of the island nation of their birth, or of their parent(s). Theoretically, we position these returning professionals as members of a "middling" transnational urban class whose return is at least partly motivated by a desire to "make a difference." Our results contribute to a growing literature that documents the role of transnational middle-class urban elites returning elsewhere in the Carribbean: "middling" transnational urbanism is reshaping key facets of urbanization in the Global South.

Possible role for K+ in endothelium-derived hyperpolarizing factor–linked dilatation in rat middle cerebral artery

Background and Purpose— Endothelium-derived hyperpolarizing factor (EDHF) and K+ are vasodilators in the cerebral circulation. Recently, K+ has been suggested to contribute to EDHF-mediated responses in peripheral vessels. The EDHF response to the protease-activated receptor 2 ligand SLIGRL was characterized in cerebral arteries and used to assess whether K+ contributes as an EDHF. Methods— Rat middle cerebral arteries were mounted in either a wire or pressure myograph. Concentration-response curves to SLIGRL and K+ were constructed in the presence and absence of a variety of blocking agents. In some experiments, changes in tension and smooth muscle cell membrane potential were recorded simultaneously. Results— SLIGRL (0.02 to 20 μmol/L) stimulated concentration and endothelium-dependent relaxation. In the presence of NG-nitro-L-arginine methyl ester, relaxation to SLIGRL was associated with hyperpolarization and sensitivity to a specific inhibitor of IKCa, 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (1μmol/L), reflecting activation of EDHF. Combined inhibition of KIR with Ba2+ (30μmol/L) and Na+/K+-ATPase with ouabain (1 μmol/L) markedly attenuated the relaxation to EDHF. Raising extracellular [K+] to 15 mmol/L also stimulated smooth muscle relaxation and hyperpolarization, which was also attenuated by combined application of Ba2+ and ouabain. Conclusions— SLIGRL evokes EDHF-mediated relaxation in the rat middle cerebral artery, underpinned by hyperpolarization of the smooth muscle. The profile of blockade of EDHF-mediated hyperpolarization and relaxation supports a pivotal role for IKCa channels. Furthermore, similar inhibition of responses to EDHF and exogenous K+ with Ba2+ and ouabain suggests that K+ may contribute as an EDHF in the middle cerebral artery.