Heavy Quark Effects in the Virtual Photon Structure Functions

We investigate the heavy quark mass effects in the virtual photon structure functions $F_{2}^{\gamma}(x, Q^2, P^2)$ and $F_{L}^{\gamma}(x, Q^2, P^2)$ in the framework of the mass-independent renormalization group equation (RGE). We study a formalism in which the heavy quark mass effects are treated based on parton picture as well as on the operator product expansion (OPE), and perform the numerical evaluation of $F_{\rm eff}^{\gamma}(x, Q^2, P^2)$ to the next-leading order (NLO) in QCD.Comment: 19 pages, LaTeX, 4 eps figures, PTPTe

Wnt-4 and Ets-1 signaling pathways for regeneration after acute renal failure

Ischemic acute renal failure (ARF) is the most common form of ARF in the adult population. The molecular mechanisms of tubular regeneration after ischemic renal injury remain largely unknown. An understanding of the mechanisms that lead to renal cell proliferation and regeneration will be necessary for the exploration of novel therapeutic strategies for the treatment of ARF. It has been suggested that regeneration processes may recapitulate developmental processes in order to restore organ or tissue function. The adult tubular epithelial cells have a potent ability of regenerate after cellular damage. We examined functional role of two developmental genes, Wnt-4 and Ets-1, in renal tubular regeneration in ARF. The Wnt-β-catenin pathway plays key roles in embryogenesis. Wnt-4 is known to be expressed in the mesonephric duct in the embryonic development. To clarify the significance of the Wnt-4-β-catenin pathway in ARF, we used a rat ARF model in vivo and LLC-PK1 cells as an in vitro model. After clamping left rat renal artery for 1 hour, we examined whole kidney homogenate and total RNA extracted at 3, 6, 12, 24, 48, and 72 hours after reperfusion by Western blot analysis and real-time reverse transcription-polymerase chain reaction (RT-PCR). Wnt-4 mRNA and protein expression were strongly increased at 3 to 12 hours and 6 to 24 hours after ischemia, respectively. In immunohistologic examination, Wnt-4 was expressed in the proximal tubules and coexpressed with aquaporin 1 and proliferating cell nuclear antigen (PCNA). Cyclin D1 and cyclin A were expressed at 12 to 48 hours after reperfusion. Furthermore, overexpression of Wnt-4 and β-catenin promoted the cell cycle and increased the promoter activity and protein expression of cyclin D1 and cyclin A in LLC-PK1 cells. These data suggest that the Wnt-4-β-catenin pathway plays a key role in the cell cycle progression of renal tubules in ARF. The Ets family of transcription factors is defined by a conserved DNA-binding Ets domain that forms a winged helix-turn-helix structure motif. The Ets family is involved in a diverse array of biologic functions, including cellular growth, migration, and differentiation. To clarify the significance of Ets-1 in ARF, we used a rat ARF model in vivo and LLC-PK1 cells as an in vitro model. Ets-1 mRNA and protein expression were strongly increased at 3 to 12 hours and 6 to 24 hours after the ischemia, respectively. In the immunohistologic examination, Ets-1 was expressed in the proximal tubules and coexpressed with PCNA. Furthermore, overexpression of Ets-1 promoted the cell cycle and increased the promoter activity and protein expression of cyclin D1 in LLC-PK1 cells. Ets-1 promoter activity increased between 3 hours and 6 hours in hypoxia, and hypoxia also induced changes in the Ets-1 protein level in LLC-PK1 cells. Taken together, these data suggest that Ets-1 plays a key role in the cell cycle progression of renal tubules in ARF. Our data suggest that Wnt-4-β-catenin and Ets-1 pathways regulate the transcription of cyclin D1 and control the regeneration of renal tubules in ARF. These developmental genes may play key roles in dedifferentiation and regeneration of the renal tubular cells after ARF

Heavy quark effects on parton distribution functions in the unpolarized virtual photon up to the next-to-leading order in QCD

We investigate the heavy quark mass effects on the parton distribution functions in the unpolarized virtual photon up to the next-to-leading order in QCD. Our formalism is based on the QCD-improved parton model described by the DGLAP evolution equation as well as on the operator product expansion supplemented by the mass-independent renormalization group method. We evaluate the various components of the parton distributions inside the virtual photon with the massive quark effects, which are included through the initial condition for the heavy quark distributions, or equivalently from the matrix element of the heavy quark operators. We discuss some features of our results for the heavy quark effects and their factorization-scheme dependence.Comment: 16 pages, 16 figures, version to appear in Phys. Rev.

On the 16.5 T Superconducting Magnet Operation(Part II. Several Instruments and Techniques Developed in HFLSM)

A 16.5 T superconducting magnet employing a surface diffusion processed Nb_3Sn tape was installed in High Field Laboratory for Superconducting Materials at Tohoku University in 1982. The magnet generates high fields up to 16.5 T in a 57 mm diameter bore and has the maximum stored energy of 660 kJ. Since 1982, the magnet has been used for 622 days and charged up about 1070 times up to the field higher than 14 T without serious troubles. In this paper, results of 16.5 T superconducting magnet operations in the last 4 years are described

Target Mass Corrections for the Virtual Photon Structure Functions to the Next-to-next-to-leading Order in QCD

We investigate target mass effects in the unpolarized virtual photon structure functions $F_2^\gamma(x,Q^2,P^2)$ and $F_L^\gamma(x,Q^2,P^2)$ in perturbative QCD for the kinematical region $\Lambda^2 \ll P^2 \ll Q^2$, where $-Q^2(-P^2)$ is the mass squared of the probe (target) photon and $\Lambda$ is the QCD scale parameter. We obtain the Nachtmann moments for the structure functions and then, by inverting the moments, we get the expressions in closed form for $F_2^\gamma(x,Q^2,P^2)$ up to the next-to-next-to-leading order and for $F_L^\gamma(x,Q^2,P^2)$ up to the next-to-leading order, both of which include the target mass corrections. Numerical analysis exhibits that target mass effects appear at large $x$ and become sizable near $x_{\rm max}(=1/(1+\frac{P^2}{Q^2}))$, the maximal value of $x$, as the ratio $P^2/Q^2$ increases.Comment: 24 pages, LaTeX, 7 eps figures, REVTeX

Regulation of cyclin D1 expression and cell cycle progression by mitogen-activated protein kinase cascade

Regulation of cyclin D1 expression and cell cycle progression by mitogen-activated protein kinase cascade. Mitogen-activated protein kinases (MAPKs) have been shown to play an important role in transducing extracellular signals into cellular responses. The classic MAPK pathway is commonly activated by growth factors and has been shown to play a crucial role in cell proliferation. Transforming growth factor-β (TGF-β)–activating kinase-1 (TAK1) is a novel MAPK kinase kinase that is reported to stimulate the MKK6-p38K pathway. To elucidate the functional roles of the TAK1 pathway, we transfected its constitutive active form (TAKdN) and negative form (TAKK63W) to LLC-PK1 cells. TAKdN stimulated MKK6 phosphorylation and p38K activity and inhibited the percentages of the S and G2/M phases. TAKK63W, the constitutive negative form, reduced TGF-β–stimulated MKK6 phosphorylation and p38K activity and increased the percentages of the S and G2/M phases. The cyclin D1 protein level is reduced by the TAK1 pathway. We also examined the effects of the TAK1 pathway on cyclin D1 promoter-luciferase assay. The overexpression of TAKdN or p38K inhibited cyclin D1 promoter activity. In contrast, overexpression of the active form of MKK1, the classic MAPK-activator, MKK1 increased cyclin D1 promoter activity and protein level, as well as the percentages of S and G2/M phases

TGF-βbgr-activating kinase-1 inhibits cell cycle and expression of cyclin D1 and A in LLC-PK1 cells

TGF-βbgr-activating kinase-1 inhibits cell cycle and expression of cyclin D1 and A in LLC-PK1 cells.BackgroundTransforming growth factor-βbgr (TGF-βbgr) is known to play an important role in the pathophysiology of renal tubular disease. Researchers have recently identified a novel mitogen-activated protein kinase kinase kinase (MAPKKK), TAK (TGF-βbgr activated kinase)1, which stimulates the MKK3/6-p38K pathway. The purpose of our study was to investigate the functional role of the TAK1-MKK3/6-p38K pathway and classical MAPK cascades in the progression of the cell cycle in renal tubular cells.MethodsThe constitutive active form and negative form of TAK1 (TAK1dN and TAK1K63W, respectively), and active and negative forms of the p42/44 MAPK-activator, MKK1 (S222E and S222A, respectively) were transfected to LLC-PK1 cells. Western blot analyses and promoter-luciferase assay of cyclins D1, D2, D3, E, and A were performed, and cell cycle progression was analyzed by FACS scan.ResultsTAK1dN stimulated MKK6 and p38K activity and inhibited the percentage of the S and G2/M phases. TAK1K63 W inhibited TGF-βbgr-stimulated MKK6 and p38K activity. Cyclin D1 and cyclin A protein levels and promoter activities were negatively regulated by TAK1dN. In contrast, overexpression of the active form of p42/44 MAPK-activator, MKK1, increased cyclin D1 and A promoter activity and protein levels.ConclusionThe growth-inhibitory effects of TGF-βbgr are at least partially mediated by the TAK1-MKK6-p38K pathway. Cyclin D1 and A promoter activity and cell cycle progression in renal tubular cells are negatively regulated by the TAK1-MKK6-p38K pathway and positively regulated by the MKK1-p42/44MAPK pathway