The link between market orientation and performance in the Australian public sector

Marketing academics and practitioners assume a direct link between market orientation and performance and argue that this applies to both business and non-business organisations. While this aspect has been studied in the business sector, this paper discusses the concepts of market orientation and performance and investigates this relationship in the Australian public sector. The conceptualization of market orientation used is that by Jaworski and Kohli (1993) on which basis MARKOR was developed. This instrument together with an instrument to measure the perceptions of performance of senior managers in the Australian public sector are used to investigate the hypothesized link. The findings confirm a positive relationship between market orientation and performance. The size and type of public sector organisation involved are also found to affect the levels of market orientation together with its components and performance. From the findings, implication are drawn and directions for future research discussed.peer-reviewe

Decomposition cross-correlation for analysis of collagen matrix deformation by single smooth muscle cells

Microvascular remodeling is known to depend on cellular interactions with matrix tissue. However, it is difficult to study the role of specific cells or matrix elements in an in vivo setting. The aim of this study is to develop an automated technique that can be employed to obtain and analyze local collagen matrix remodeling by single smooth muscle cells. We combined a motorized microscopic setup and time-lapse video microscopy with a new cross-correlation based image analysis algorithm to enable automated recording of cell-induced matrix reorganization. This method rendered 60–90 single cell studies per experiment, for which collagen deformation over time could be automatically derived. Thus, the current setup offers a tool to systematically study different components active in matrix remodeling

The Redox State of Transglutaminase 2 Controls Arterial Remodeling

While inward remodeling of small arteries in response to low blood flow, hypertension, and chronic vasoconstriction depends on type 2 transglutaminase (TG2), the mechanisms of action have remained unresolved. We studied the regulation of TG2 activity, its (sub) cellular localization, substrates, and its specific mode of action during small artery inward remodeling. We found that inward remodeling of isolated mouse mesenteric arteries by exogenous TG2 required the presence of a reducing agent. The effect of TG2 depended on its cross-linking activity, as indicated by the lack of effect of mutant TG2. The cell-permeable reducing agent DTT, but not the cell-impermeable reducing agent TCEP, induced translocation of endogenous TG2 and high membrane-bound transglutaminase activity. This coincided with inward remodeling, characterized by a stiffening of the artery. The remodeling could be inhibited by a TG2 inhibitor and by the nitric oxide donor, SNAP. Using a pull-down assay and mass spectrometry, 21 proteins were identified as TG2 cross-linking substrates, including fibronectin, collagen and nidogen. Inward remodeling induced by low blood flow was associated with the upregulation of several anti-oxidant proteins, notably glutathione-S-transferase, and selenoprotein P. In conclusion, these results show that a reduced state induces smooth muscle membrane-bound TG2 activity. Inward remodeling results from the cross-linking of vicinal matrix proteins, causing a stiffening of the arterial wall

Transglutaminases in vascular biology: relevance for vascular remodeling and atherosclerosis

The transglutaminase (Tgase) family consists of nine known members of whom at least three are expressed in the vascular system: type 1 Tgase, type 2 Tgase and factor XIII. The cross-linking of proteins is a characteristic feature of Tgases, of well-known importance for stabilizing the blood clot and providing mechanical strength to tissues. However, recent data suggest that Tgases play a role in several other processes in vascular biology. These newly discovered areas include endothelial barrier function, small artery remodeling, and atherosclerosi

Smooth Muscle Biomechanics and Plasticity: Relevance for Vascular Calibre and Remodelling

Blood vessel structure and calibre are not static. Rather, vessels remodel continuously in response to their biomechanical environment. Vascular calibre is dictated by the amount, composition and organization of the elastic extracellular matrix. In addition, the amount and organization of contractile smooth muscle cell (SMC) also need to be regulated. The SMCs are organized such that maximum contractile force generally occurs at diameters slightly below the diameter at full dilation and physiological pressure. Thus, in a remodelling vessel, not only the matrix but also the SMCs need to undergo structural adaptation. Surprisingly little is known on the adaptation of SMC contractile properties in the vasculature. The purpose of this review is to explore this SMC plasticity in the context of vascular remodelling. While not much work on this has been carried out on blood vessels, SMC plasticity is more extensively studied on other hollow structures such as airway and bladder. We therefore include studies on bladder and airway SMCs because of their possible relevance for vascular SMC behaviour. Here, plasticity is thought to form an adaptation allowing maintained function despite large volume changes. In blood vessels, the general match of active and passive diameter-tension relations suggests that SMC plasticity is part of normal vascular physiological adaptation. Vascular SMCs display similar processes and forms of adaptation as seen in nonvascular SMCs. This may become particularly relevant under strong vasoconstriction, when inward cytoskeletal adaptation possibly prevents immediate full dilation. This may contribute to structural inward remodelling as seen in hypertension and flow reductio

Relation between active and passive biomechanics of small mesenteric arteries during remodeling

Small artery remodeling involves matrix reorganization, but may also encompass changed smooth muscle cell biomechanical properties. Here we study the temporal relationship between such contractile plasticity and matrix remodeling in small rat mesenteric arteries subjected to 1 or 3 days of altered flow or acute interventions on matrix structure; cross-linking by transglutaminase and matrix digestion by elastase. Diameter-tension relations were made in the passive state and upon full activation (125 mM K+ and 10⁻⁵ M norepinephrine). In low flow (LF), inward matrix remodeling occurred after 1 day, when the distended diameter at full dilation (D₁₀₀) was reduced from 351±15μm to 299±14μm (SEM, n=8, p <0.05). The optimal diameter for force development (D(opt)) was reduced after 3 days, from 291±10μm to 247±5μm (LF, p <0.05). As a result, a mismatch of D(opt)/D₁₀₀ existed after 1 day of LF, which normalized after 3 days. Dynamics of contraction were studied following quick isometric release by 0.2∙D₁₀₀; tension recovery was faster in anatomically smaller vessels following normal flow. This association was partly lost after 1 day of LF, while after 3 days the vessels became not only smaller but also faster, re-establishing this association. High flow vessels demonstrated similar contractile plasticity. Active diameter-tension relations at low distension did not change following transglutaminase or elastase. However, at high distension, any alteration in passive tension coincided with an opposite change in active tension. These data demonstrate an intrinsic interaction between passive and active biomechanics that occurs instantaneously during matrix remodeling at high distensions while contractile plasticity lags matrix remodeling after flow intervention

Paravascular spaces: entry to or exit from the brain?

New Findings: What is the topic of this review? In this symposium report, we review the glymphatic clearance from the brain. What advances does it highlight? Evaluation of the evidence indicates that cerebrospinal fluid flows along paravascular spaces at the surface of the brain. However, bulk flow along penetrating arteries into the brain, followed by exit along veins, requires further confirmation. Clearance from the brain, based on mixing, might provide an alternative explanation for experimental findings. Abstract: The interstitial fluid of the brain provides the environment for proper neuronal function. Maintenance of the volume and composition of interstitial fluid requires regulation of the influx and removal of water, ions, nutritive and waste products. The recently described glymphatic pathway might contribute to some of these functions. It is proposed that cerebrospinal fluid enters the brain via paravascular spaces along arteries, mixes with interstitial fluid, and leaves the brain via paravascular spaces along veins. In this symposium report, we review the glymphatic concept, its concerns, and alternative views on interstitial fluid–cerebrospinal fluid exchange

Remodeling of resistance arteries in organoid culture is modulated by pressure and pressure pulsation and depends on vasomotion

The hypothesis was tested that pressure and pressure pulsation modulate vascular remodeling. Arterioles (similar to200 mum lumen diameter) were dissected from rat cremaster muscle and studied in organoid culture. In the first series, arterioles were kept at a stable pressure level of either 50 or 100 mmHg for 3 days. Both groups showed a progressive increase in myogenic tone during the experiment. Arterioles kept at 50 mmHg showed larger endothelium-dependent dilation, compared with vessels kept at 100 mmHg on day 3. Remodeling, as indicated by the reduction in maximally dilated diameter at 100 mmHg, was larger in arterioles kept at 50 mmHg compared with 100 mmHg: 34 +/- 4.5 versus 10 +/- 4.8 mum (P <0.05). In the second series, arterioles were subjected to a stable pressure of 60 mmHg or oscillating pressure of 60 &PLUSMN; 10 mmHg (1.5 Hz) for 4 days. Pressure pulsation induced partial dilation and was associated with less remodeling: 34 &PLUSMN; 4.0 versus 19 &PLUSMN; 4.5 μm (P <0.01) for stable pressure versus oscillating pressure. Vasomotion was frequently observed in all groups, and inward remodeling was larger in vessels with vasomotion: 30 +/- 2.5 mum compared with vessels that did not exhibit vasomotion: 8.0 +/- 5.0 mum (P <0.01). In conclusion, these results indicate that remodeling is not enhanced by high pressure. Pressure pulsation causes partial dilation and reduces inward remodeling. The appearance of vasomotion is associated with enhanced inward remodelin

Activation of resistance arteries with endothelin-1: From vasoconstriction to functional adaptation and remodeling

Remodeling of resistance arteries is a key feature in hypertension. We studied the transition of vasoconstriction to remodeling in isolated rat skeletal muscle arterioles. Arterioles activated with 10 nM endothelin-1 showed functional adaptation when kept at low distension in a wire myograph setup, where contractile properties shifted towards a smaller lumen diameter after 1 day. Pressurized arteries kept in organoid culture showed physical inward remodeling after 3-day activation with 10 nM endothelin-1, characterized by a reduction in relaxed diameter without a change in the wall cross-sectional area (eutrophic remodeling). The relaxed lumen diameter (at 60 mm Hg) decreased from 169 +/- 5 (day 0) to 155 +/- 4 mum (day 3). An antibody directed to the beta(3)-integrin subunit (but not one directed to the beta(1)-integrin subunit) enhanced remodeling, from a reduction in relaxed diameter at 60 mm Hg of 15 +/- 2.4 to 22 +/- 1.8 mum (both on day 3). Collagen gel contraction experiments showed that the antibody directed to the beta(3)-integrin subunit enhanced the compaction of collagen by smooth muscle cells, from 83 +/- 1.5 to 68 +/- 1.5% of the initial gel diameter. In conclusion, these data show that inward eutrophic remodeling is a response to sustained contraction, which may involve collagen reorganization through beta(3)-integrins. Copyright (C) 2004 S. Karger AG, Base