Chiral Anomaly for a New Class of Lattice Dirac Operators

A new class of lattice Dirac operators which satisfy the index theorem have been recently proposed on the basis of the algebraic relation $\gamma_{5}(\gamma_{5}D) + (\gamma_{5}D)\gamma_{5} = 2a^{2k+1}(\gamma_{5}D)^{2k+2}$. Here $k$ stands for a non-negative integer and $k=0$ corresponds to the ordinary Ginsparg-Wilson relation. We analyze the chiral anomaly and index theorem for all these Dirac operators in an explicit elementary manner. We show that the coefficient of anomaly is independent of a small variation in the parameters $r$ and $m_{0}$, which characterize these Dirac operators, and the correct chiral anomaly is obtained in the (naive) continuum limit $a\to 0$.Comment: 23 pages. Corrected typos and misprints. Made several sentences more precise, and references up-dated. (To appear in Nucl. Phys. B

Successful remission of ulcerative colitis flare-up during pregnancy with adsorptive granulomonocytapheresis plus tacrolimus

Ulcerative colitis (UC) is 1 of the 2 major phenotypes of chronic inflammatory bowel disease (IBD), which afflicts millions of individuals throughout the world with debilitating symptoms that impair function and quality of life. Further, IBD often affects women during childbearing age. Indeed, UC activity frequently increases during pregnancy, and the medications used to induce remission may adversely affect the health of the mother and the unborn child. We report successful induction of a remission in a UC case who experienced a flare-up in the first trimester of pregnancy. Upon relapse, she was treated with steroids and adsorptive granulomonocytapheresis (GMA) with the Adacolumn plus tacrolimus. This combination therapy induced a stable remission that was maintained during her entire pregnancy. She gave birth to a healthy child at 36 weeks of pregnancy with no maternal or fetal complications. Our experience indicates that GMA, as a non-drug therapeutic intervention with a favorable safety profile, plus tacrolimus might be a relevant treatment option for patients with active IBD during pregnancy. A future study of a large cohort of pregnant patients should strengthen our findings

Polychlorinated biphenyl (118) activates osteoclasts and induces bone resorption in goldfish

To analyze the effect of polychlorinated biphenyl (PCB) 118 on fish bone metabolism, we examined osteoclastic and osteoblastic activities, as well as plasma calcium levels, in the scales of PCB (118)-injected goldfish. In addition, effect of PCB (118) on osteoclasts and osteoblasts was investigated in vitro. Immature goldfish, in which the endogenous effects of sex steroids are negligible, were used. PCB (118) was solubilized in dimethyl sulfoxide at a concentration of 10 ppm. At 1 and 2 days after PCB (118) injection (100 ng/g body weight), both osteoclastic and osteoblastic activities, and plasma calcium levels were measured. In an in vitro study, then, both osteoclastic and osteoblastic activities as well as each marker mRNA expression were examined. At 2 days, scale osteoclastic activity in PCB (118)-injected goldfish increased significantly, while osteoblastic activity did not change significantly. Corresponding to osteoclastic activity, plasma calcium levels increased significantly at 2 days after PCB (118) administration. Osteoclastic activation also occurred in the marker enzyme activities and mRNA expressions in vitro. Thus, we conclude that PCB (118) disrupts bone metabolism in goldfish both in vivo and in vitro experiments. © 2012 The Author(s)

Stand and self-thinning dynamics in natural Abies stands in northern Hokkaido, Japan

Stand dynamics and self-thinning were analyzed in relation to the dynamics of above-ground biomass in natural Abies sachalinensis stands growing on sand dunes in northern Hokkaido, Japan. This was done in order to examine wave-type regeneration in the stands. Fifty-two plots were established in almost pure Abies stands that ranged from saplings to the mature and collapsing growth stages. Above-ground biomass and tree height reached asymptotic levels prior to the collapsing phase, unlike wave-regeneration Abies stands in central Japan and North America. Stand density was high in the young growth stages, but the self-thinning rate, that is, the density decrease per biomass growth in the study stands was greater than in wave-regeneration stands in central Japan, as indicated by a large self-thinning exponent (−1.26 by reduced major axis regression). The range of tree height distribution was very narrow, and the stands’ vertical structure was typically single-layered. The slenderness ratio of trees was large, except in young stands. In mature and collapsing stands, advanced seedling density increased markedly. These stand and tree characteristics were considered to be correlated with the wave-type regeneration in the study stands, and it is assumed that prevailing winds affect tree mortality

p66Shc has a pivotal function in impaired liver regeneration in aged mice by a redox-dependent mechanism

Liver regeneration involves complicated processes and is affected by various patho-physiological conditions. The present study was designed to examine the molecular mechanisms underlying the aging-associated impairment of liver regeneration. Male C57BL/6J mice were used as young and aged mice (20 months old, respectively). These mice were subjected to 70% partial hepatectomy (PH). Liver regeneration and liver injury/stresses were evaluated chronologically after PH. Post-hepatectomy liver regeneration was markedly impaired in aged mice. Though the extent of hepatocyte proliferation in the regenerating liver was similar in aged and young mice, cell growth was absent in aged mice. Oxidative stress (OS) was observed immediately after hepatectomy, followed by marked apoptosis in aged mice. Signaling molecules regarding cell proliferation (MAPK, STAT-3, p46/52Shc) and anti-oxidation (catalase, SOD, Ref-1, GPx) were expressed/activated after hepatectomy in livers of both aged and young mice. Akt was not activated in aged-mouse liver, but its expression was similar to that in young mice. p66Shc, known as an age-/oxidant-associated protein, was strongly phosphorylated. By knocking-down p66Shc, the impairment of liver regeneration was normalized. OS immediately after hepatectomy induced subsequent liver injury (apoptosis), and deletion of p66Shc suppressed both OS and hepatocyte apoptosis in the regenerating liver of aged mice. Though we need additional data in other animal models to fully understand the mechanism, p66Shc may play a pivotal role in the impairment of liver regeneration in aged mice by triggering OS and subsequent apoptosis. The present data may provide a clue to understanding the mechanism underlying the association between aging and the impairment of liver regeneration

Gene silencing of gelsolin in bladder cancer

We previously reported that gelsolin gene expression is reduced in various tumors. In an effort to gain further insights into the mechanism of gelsolin downregulation in tumors, we examined the in vivo properties of the gelsolin promoter in urinary bladder cancer cell lines. Neither mutation nor hypermethylation were responsible for gene silencing at the promoter. After exposure to trichostatin A (TSA), a histone deacetylase inhibitor, gelsolin promoter activity was markedly enhanced in the cancer cells not in cells derived from normal tissue. Chromatin immunoprecipitation (ChIP) assays revealed that both histones H3 and H4 were hypoacetylated in the promoter region of the cancer cells, and the accumulation of acetylated histones were detected by TSA treatment. In vivo footprinting analysis revealed the presence of dimethylsulfate (DMS) hypersensitive site in the untranslated region around nucleotide -35 only in the cancer cells but not in cells derived from normal tissue, and analysis of KMnO4 reactive nucleotides showed that the stem loop structure could be formed in vivo of the cancer cells. This novel stem loop structure may play a part in regulating the transcription of the gelsolin gene in the cancer cells. .. These results suggest that nucleosome accessibility through histone deacetylation and structural changes (DMS hypersensitivity and stem loop structure) in the promoter region form the basis of the mechanism leading to the silencing of gelsolin gene in human bladder cancer

Possible Involvement of Hepatitis B Virus Infection of Hepatocytes in the Attenuation of Apoptosis in Hepatic Stellate Cells.

The induction of apoptosis in hepatic stellate cells (HSCs) is a promising therapeutic strategy against hepatitis B virus (HBV)-related hepatic fibrosis. The underlying mechanisms of apoptosis in HSCs, however, are unknown under consideration of HBV infection. In this study, the effects of HBV on apoptosis and endoplasmic reticulum (ER) stress signaling in HSCs were examined.The effects of conditioned media (CM) from HepG2.2.15 on apoptosis induced by the proteasome inhibitor MG132 in LX-2 and HHSteC were studied in regard to c-Jun. In combination with c-Fos, c-Jun forms the AP-1 early response transcription factor, leading to AP-1 activation, signal transduction, endoplasmic reticulum (ER) stress and apoptosis.In LX-2 cells, MG132 treatment was associated with the phosphorylation of c-Jun, activation of AP-1 and apoptosis. However, in the presence of CM from HepG2.2.15, these phenomena were attenuated. In HHSteC cells, similar results were observed. HBV genomic DNA is not involved in the process of HSC apoptosis. It is possible that HBeAg has an inhibitory effect on MG132-induced apoptosis in LX-2. We also observed the upregulation of several ER stress-associated genes, such as cAMP responsive element binding protein 3-like 3, inhibin-beta A and solute carrier family 17-member 2, in the presence of CM from HepG2.2.15, or CM from PXB cells infected with HBV.HBV inhibits the activation of c-Jun/AP-1 in HSCs, contributing to the attenuation of apoptosis and resulting in hepatic fibrosis. HBV also up-regulated several ER stress genes associated with cell growth and fibrosis. These mechanistic insights might shed new light on a treatment strategy for HBV-associated hepatic fibrosis