How valuable are your customers in the brand value co-creation process? The development of a Customer Co-Creation Value (CCCV) scale.

Despite an increasing amount of research on co-creation of value, in general, research on brand value co-creation remains limited. Particularly, how much value customers contribute to the brand value co-creation process remains unclear. This research develops in a series of eight studies the Customer Co-Creation Value (CCCV) measurement scale that helps firms assess the value of customers in the brand value co-creation process. The findings reveal that CCCV is a multidimensional construct consisting of two higher-order factors and seven dimensions: customer-owned resources (including brand knowledge, brand skills, brand creativity, and brand connectedness) and customer motivation (comprising brand passion, brand trust, and brand commitment). Further, the CCCV scale reliably and validly gauges the value customers contribute to a firm's brand. The CCCV framework helps marketing managers understand how customers can contribute to a firm's brand value cocreation efforts and how much value customers contribute to a brand in the co-creation process

<i>Egfl7</i> Is Differentially Expressed in Arteries and Veins during Retinal Vascular Development

<div><p>The vasculature of the central nervous system (CNS) is composed of vascular endothelial and mural cells which interact closely with glial cells and neurons. The development of the CNS vascularisation is a unique process which requires the contribution of specific regulators in addition to the classical angiogenic factors. The <i>egfl7</i> gene is mainly detected in endothelial cells during physiological and pathological angiogenesis. Egfl7 codes for a secreted protein which predominantly accumulates into the extracellular space where it controls vascular elastin deposition or the Notch pathway. <i>Egfl7</i> is the host gene of the microRNA miR126 which is also expressed in endothelial cells and which plays major functions during blood vessel development. While the expression of <i>egfl7</i> and that of miR126 were well described in endothelial cells during development, their pattern of expression during the establishment of the CNS vasculature is still unknown. By analysing the expression of <i>egfl7</i> and miR126 during mouse retina vascularisation, we observed that while expression of miR126 is detected in all endothelia, <i>egfl7</i> is initially expressed in all endothelial cells and then is progressively restricted to veins and to their neighbouring capillaries. The recruitment of mural cells around retina arteries coincides with the down-regulation of <i>egfl7</i> in the arterial endothelial cells, suggesting that this recruitment could be involved in the loss of <i>egfl7</i> expression in arteries. However, the expression pattern of <i>egfl7</i> is similar when mural cell recruitment is prevented by the injection of a PDGFRβ blocking antibody, suggesting that vessel maturation is not responsible for <i>egfl7</i> down-regulation in retinal arteries.</p></div

miR126 expression in mural cell deficient retinal vasculature.

<p><b>A</b>: miR126 expression detected by in situ hybridization in P9 whole mount retina from pups injected with vehicle or with the blocking antibody directed against PDGFRβ (αPDGFRβ). <b>B</b>: higher magnification of miR126 expression detected by in situ hybridization in P9 whole mount retina from pups injected with vehicle or with the blocking antibody directed against the PDGFRβ (αPDGFRβ).</p

<i>Egfl7</i> expression in mural cell deficient retinal vasculature.

<p><b>A</b>: Co-immunodetection of pericytes (NG2) and smooth muscle cells (SMA) in P9 retina from pups injected with vehicle or with the blocking antibody directed against the PDGFRβ (αPDGFRβ). <b>B</b>: Co-immunodetection at higher magnification of endothelial cells (isolectin B4), pericytes (NG2) and smooth muscle cells (SMA) in P9 retina from pups injected with vehicle or with the blocking antibody directed against the PDGFRβ (αPDGFRβ). <b>C</b>: Type IV collagen immunostaining showing the vasculature of P9 retina from pups injected with vehicle or with the blocking antibody directed against the PDGFRβ (αPDGFRβ). <b>D</b>: Combined collagen IV (Coll IV) immunostaining and <i>egfl7</i> in situ hybridization in P9 retina from pups injected with vehicle or with the blocking antibody directed against the PDGFRβ (αPDGFRβ). a, artery; v, vein. Magnifications are indicated.</p

<i>Egfl7</i> and miR126 expression in HUVEC and HUAEC primary endothelial cells.

<p><b>A</b>: Relative quantification by RT-qPCR of EphrinB2 and Dll4 in venous HUVEC and arterial HUAEC primary endothelial cells. Levels were normalized to those of HUVEC arbitrarily set to 1. <b>B</b>: Relative quantification by RT-qPCR of COUP-TFII and EphB4 in HUVEC and HUAEC primary endothelial cells. Levels were normalized to those of HUVEC arbitrarily set to 1. <b>C</b>: Relative quantification by RT-qPCR of <i>egfl7</i> and miR126 in HUVEC and HUAEC primary endothelial cells. Levels were normalized to those of HUVEC arbitrarily set to 1.</p

miR126 expression in adult retina.

<p>Left panel: miR126 expression detected by in situ hybridization in flat mounted adult retina. Right panel: higher magnification of the left panel; miR126 expression detected by in situ hybridization (upper panel); collagen IV immunostaining of the same retina area (lower panel). Magnifications are indicated.</p

<i>Egfl7</i> expression during retinal vascular development.

<p><b>A</b>: <i>egfl7</i> expression detected by in situ hybridization (blue staining) in flat mounted retinas of two- (P2), five- (P5), nine (P9) and fourteen- (P14) day old mouse pups. <b>B</b>: Left panel: <i>egfl7</i> expression detected by in situ hybridization in flat mounted adult retina. Right panel: higher magnification of the left panel; <i>egfl7</i> expression detected by in situ hybridization (upper panel), collagen IV immunostaining of the same retina area (lower panel). <b>C</b>: Relative quantification by RT-qPCR of <i>egfl7</i> transcripts in retina of nine- (P9), fourteen- (P14) day old mouse pups and adult mice. Levels were normalized to those of P9 retina arbitrarily set to 1. Magnifications are indicated.</p

Specific <i>Egfl7</i> expression pattern in the retinal developing vasculature.

<p><b>A</b>: Combined collagen IV (Coll IV) immunostaining and <i>egfl7</i> in situ hybridization in flat mounted retinas of five- (P5) and nine- (P9) day old mouse pups. a, artery; v, vein. <b>B</b>: Combined isolectin B4 staining (middle panel) and <i>egfl7</i> in situ hybridization (left panel) at the leading edge of the P5 retinal developing vasculature. DAPI staining is also shown in the right panel. *, Tip-cell. Magnifications are indicated.</p

Parvocellular expression of AVPmRNA, CRHmRNA and iNOS in control and septic shock patients and in sham, septic and septic ED rats.

<p>Abbreviations: AVP, Vasopressin; CRH, Corticotropin Releasing Hormone; mRNA, messenger RNA; iNOS, inducible nitric oxide synthase; ED, Early death.</p><p>Results are expressed as median (IQR).The index of labelling CRH and AVP <i>in-situ</i> hybridization and iNOS immunohistochemistry ranged from 0 to 3.</p><p>Comparison between the following animal groups:</p>a<p>Sham <i>versus</i> Sepsis,</p>b<p>Sepsis <i>versus</i> Septic Shock,</p>c<p>Sham <i>versus</i> Septic Shock.</p

Ante-hypophysis of patients who died from non-septic causes (A–C–E) or septic shock (B–D–F).

<p>Labelling of CRHR1 (A–B) and V1b receptor (C–D) after immunohistochemistry (ABC peroxidase/DAB) did not vary among the two groups. ACTH (E–F) immunostaining (ABC peroxidase/DAB) was decreased in septic shock patients.</p