The Madison plasma dynamo experiment (MPDX) is a novel, versatile, basic plasma research device designed to investigate flow driven magnetohydrodynamic instabilities and other high-b phenomena with astrophysically relevant parameters. A 3 m diameter vacuum vessel is lined with 36 rings of alternately oriented 4000 G samarium cobalt magnets, which create an axisymmetric multicusp that contains $14 m 3 of nearly magnetic field free plasma that is well confined and highly ionized (>50%). At present, 8 lanthanum hexaboride (LaB 6 ) cathodes and 10 molybdenum anodes are inserted into the vessel and biased up to 500 V, drawing 40 A each cathode, ionizing a low pressure Ar or He fill gas and heating it. Up to 100 kW of electron cyclotron heating power is planned for additional electron heating. The LaB 6 cathodes are positioned in the magnetized edge to drive toroidal rotation through J Â B torques that propagate into the unmagnetized core plasma. Dynamo studies on MPDX require a high magnetic Reynolds number Rm > 1000, and an adjustable fluid Reynolds number 10 < Re < 1000, in the regime where the kinetic energy of the flow exceeds the magnetic energy (M 2 A ¼ ðv=v A Þ 2 > 1). Initial results from MPDX are presented along with a 0-dimensional power and particle balance model to predict the viscosity and resistivity to achieve dynamo action. V C 2014 AIP Publishing LLC.

Protein kinase C (PKC), a family of phospholipid-dependent serine/threonine kinases, is not only the major intracellular receptor for the mouse skin tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) but also is activated by a variety of stress factors including ultraviolet radiation (UVR). PKCepsilon is among six isoforms (alpha, delta, epsilon, eta, mu and zeta) expressed in the mouse skin. To determine the in vivo functional specificity of PKCepsilon in mouse skin carcinogenesis, we generated PKCepsilon transgenic mouse (FVB/N) lines 224 and 215 that overexpress PKCepsilon protein approximately 8- and 18-fold, respectively, over endogenous levels in the basal epidermal cells and cells of the hair follicle. PKCepsilon transgenic mice were observed to be highly sensitive to the development of papilloma-independent metastatic squamous cell carcinoma (mSCC) elicited either by repeated exposure to UVR or by the 7,12-Dimethylbenzanthracene-TPA tumor promotion protocol. The development of squamous cell carcinoma (SCC) appears to be linked to the PKCepsilon-mediated induction of cytokine tumor necrosis factor-alpha(TNFalpha). Immunohistochemical analysis for the expression of PKCepsilon in the SCC of PKCepsilon transgenic mice revealed that PKCepsilon was not expressed in the tumor itself; however, the uninvolved tissue surrounding the SCC exhibited intense PKCepsilon expression. Also, human SCC, similar to mouse SCC, did not express PKCepsilon in the tumor, whereas the surrounding uninvolved epidermis revealed strong PKCepsilon expression. These findings in both the PKCepsilon mouse model and human SCC indicate that overexpression of PKCepsilon in epidermis may lead to a microenvironment, which is suitable for enhancing the development of mSCC by a paracrine mechanism involving specific cytokines including TNFalpha.

Protein kinase C (PKC), a family of phospholipid‐dependent serine/threonine kinases, is not only the major intracellular receptor for the mouse skin tumor promoter 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) but also is activated by a variety of stress factors including ultraviolet radiation (UVR). PKCɛ is among six isoforms (α, δ, ɛ, η, μ and ζ) expressed in the mouse skin. To determine the in vivo functional specificity of PKCɛ in mouse skin carcinogenesis, we generated PKCɛ transgenic mouse (FVB/N) lines 224 and 215 that overexpress PKCɛ protein approximately 8‐ and 18‐fold, respectively, over endogenous levels in the basal epidermal cells and cells of the hair follicle. PKCɛ transgenic mice were observed to be highly sensitive to the development of papilloma‐independent metastatic squamous cell carcinoma (mSCC) elicited either by repeated exposure to UVR or by the 7,12‐Dimethylbenzanthracene–TPA tumor promotion protocol. The development of squamous cell carcinoma (SCC) appears to be linked to the PKCɛ‐mediated induction of cytokine tumor necrosis factor–α(TNFα). Immunohistochemical analysis for the expression of PKCɛ in the SCC of PKCɛ transgenic mice revealed that PKCɛ was not expressed in the tumor itself; however, the uninvolved tissue surrounding the SCC exhibited intense PKCɛ expression. Also, human SCC, similar to mouse SCC, did not express PKCɛ in the tumor, whereas the surrounding uninvolved epidermis revealed strong PKCɛ expression. These findings in both the PKCɛ mouse model and human SCC indicate that overexpression of PKCɛ in epidermis may lead to a microenvironment, which is suitable for enhancing the development of mSCC by a paracrine mechanism involving specific cytokines including TNFα.

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