We present results of a large-scale simulation for the flavor non-singlet light hadron spectrum in quenched lattice QCD with the Wilson quark action. Hadron masses are calculated at four values of lattice spacing in the range a ≈ 0.1 -0.05 fm on lattices with a physical extent of 3 fm at five quark masses corresponding to m π /m ρ ≈ 0.75 -0.4. The calculated spectrum in the continuum limit shows a systematic deviation from experiment, though the magnitude of deviation is contained within 11%. Results for decay constants and light quark masses are also reported.

We investigate chiral and conformal properties of the lattice QCD with eight flavors (N f = 8) through meson spectrum using the Highly Improved Staggered Quark (HISQ) action. We also compare our results with those of N f = 12 and N f = 4 which we study on the same systematics. We find that the decay constant Fπ of the pseudoscalar meson "pion" π is non-zero, with its mass Mπ consistent with zero, both in the chiral limit extrapolation of the chiral perturbation theory (ChPT). We also measure other quantities which we find are in accord with the π data results: The ρ meson mass is consistent with non-zero in the chiral limit, and so is the chiral condensate, with its value neatly coinciding with that from the Gell-Mann-Oakes-Renner relation in the chiral limit. Thus our data for the N f = 8 QCD are consistent with the spontaneously broken chiral symmetry. Remarkably enough, while the N f = 8 data near the chiral limit are well described by the ChPT, those for the relatively large fermion bare mass m f away from the chiral limit actually exhibit a finite-size hyperscaling relation, suggesting a large anomalous dimension γm ∼ 1. This implies that there exists a remnant of the infrared conformality, and suggests that a typical technicolor ("onefamily model") as modeled by the N f = 8 QCD can be a walking technicolor theory having an approximate scale invariance with large anomalous dimension γm ∼ 1.2

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Immunoglobulin G4-related disease (IgG4-RD) is a recently discovered systemic condition, in which various organ manifestations are linked by a similar histological appearance. Our knowledge of this condition is still fragmented, as most studies have examined only a few dozen patients or focused on a particular organ manifestation. This study was conducted to learn the demography and patient characteristics of IgG4-RD using a large cohort. A total of 235 consecutive patients with IgG4-RD, diagnosed in 8 general hospitals in the same medical district, were identified by searching the institutions’ radiology database. Inclusion criteria were histology-proven IgG4-RD according to the Pathology Consensus Statement and/or definitive type 1 autoimmune pancreatitis meeting the International Consensus Diagnostic Criteria. Clinical notes and images of selected patients were retrospectively reviewed. All patients were adults (M/F = 4/1). The median age was 67 years (range 35–86). Nine tenths were diagnosed in their 50s to 70s. Among 486 manifestations identified in total, the most common was pancreatitis diagnosed in 142 patients (60%), followed by sialadenitis (34%), tubulointerstitial nephritis (23%), dacryoadenitis (23%), and periaortitis (20%). The majority of patients (95%) had at least 1 of the 5 most common manifestations. Male and female patients differed in their organ manifestations (periaortitis more common in males and sialodacryoadenitis more common in females). Serum IgG4 (normal ≤135 mg/dL) was elevated to >135 mg/dL in 208 patients (88%) and >270 mg/dL in 167 (71%). The IgG4 value was significantly higher in patients with multiorgan involvement than in those with a single manifestation (median 629 mg/dL vs 299 mg/dL, P < 0.01). Of 218 patients, for whom both IgG4 and IgG values were available, the IgG4/IgG ratio was raised to >10% in 194 (89%). Corticosteroids were effective, but the relapse rate was estimated to be 24% in the study period (median 37 months). During the follow-up, 15 malignant diseases were diagnosed in 13 patients (6%). This figure is similar to the incidence (12.9 cancers) expected from the Japanese nationwide study for cancer epidemiology (standardized incidence ratio 1.16). In conclusion, this reliable dataset could improve the characterization of IgG4-RD, particularly its unique demography and the frequency of each organ manifestation.

We present the first observation of a flavor-singlet scalar meson as light as the pion in N f = 8 QCD on the lattice, using the Highly Improved Staggered Quark action. Such a light scalar meson can be regarded as a composite Higgs with mass 125 GeV. In accord with our previous lattice results showing that the theory exhibits walking behavior, the light scalar may be a technidilaton, a pseudo Nambu-Goldstone boson of the approximate scale symmetry in walking technicolor. PACS numbers: 11.15.Ha, 12.39.Mk, 12.60.Nz, 14.80.Tt Recently, a Higgs boson with mass around 125 GeV has been discovered at the Large Hadron Collider (LHC) [1,2]. While the current LHC data show good agreement with the Standard model Higgs boson, there exists a possibility that the Higgs boson is a composite particle in an underlying strongly coupled gauge theory. A typical example is the walking technicolor theory, featuring approximate scale invariance and a large anomalous dimension, γ m ≈ 1 [3] (see also similar works [4][5][6]). Such a theory predicts a light composite Higgs, "technidilaton" [3], emerging as a pseudo Nambu-Goldstone (NG) boson of the spontaneously broken approximate scale symmetry. It was shown [7,8] that the technidilaton is phenomenologically consistent with the current LHC data.Thus, the most urgent theoretical task to test walking technicolor theories would be to check whether or not such a light flavor-singlet scalar bound state exists from first-principle calculations with lattice gauge theory. Since the composite Higgs should be associated with the electroweak symmetry breaking, it must be predominantly a bound state of technifermions carrying electroweak charges, but not of technigluons having no electroweak charges (up to some mixings between them). Thus we look for a light flavor-singlet scalar meson in the correlator of fermionic operators on the lattice.One of the most popular candidates for walking technicolor theories is QCD with a large number of (massless) flavors (N f ) in the fundamental representation. For the past few years, we have studied the SU(3) gauge theory with N f = 4, 8, 12, and 16, in a common lattice setup [9][10][11]. (For reviews of lattice studies in search for candidates for walking technicolor theories, see [12][13][14][15].)In N f = 12 QCD we actually observed [11, 16] a flavorsinglet scalar meson (σ) lighter than the "pion" having the quantum numbers corresponding to the NG pion (π) in the broken phase. (Recently a light flavor-singlet scalar meson consistent with ours was also observed by another group [17] using a different lattice action.)We found [9] that N f = 12 QCD is consistent with a conformal theory. If it is a conformal theory, it should have no bound states ("unparticle") in the exact chiral limit, and hence a light bound state can only be formed in the presence of a fermion mass m f which explicitly (not spontaneously) breaks the scale/chiral/electroweak symmetry.Hence such a light scalar meson in N f = 12 QCD would not be a composite Higgs associated with the spontaneou...

Summary Californian populations of Echinochloa phyllopogon have evolved multiple‐herbicide resistance (MHR), posing a threat to rice production in California. Previously, we identified two CYP81A cytochrome P450 genes whose overexpression is associated with resistance to acetolactate synthase (ALS) inhibitors from two chemical groups. Resistance mechanisms to other herbicides remain unknown. We analyzed the sensitivity of an MHR line to acetyl‐CoA carboxylase (ACCase) inhibitors from three chemical groups, followed by an analysis of herbicide metabolism and segregation of resistance of the progenies in sensitive (S) and MHR lines. ACCase herbicide metabolizing function was investigated in the two previously identified P450s. MHR plants exhibited resistance to all the ACCase inhibitors by enhanced herbicide metabolism. Resistance to the ACCase inhibitors segregated in a 3 : 1 ratio in the F2 generation and completely co‐segregated with ALS inhibitor resistance in F6 lines. Expression of the respective P450 genes conferred resistance to the three herbicides in rice, which is in line with the detection of hydroxylated herbicide metabolites in vivo in transformed yeast. CYP81As are super P450s that metabolize multiple herbicides from five chemical classes, and concurrent overexpression of the P450s induces metabolism‐based resistance to the three ACCase inhibitors in MHR E. phyllopogon, as it does to ALS inhibitors.

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Although (-)-epigallocatechin gallate (EGCG) has been reported to induce apoptosis in a variety of tumor cells, detailed mechanisms remain to be explored. In the present study, we investigated the antitumor mechanism of EGCG by using human T-cell acute lymphoblastic leukemia Jurkat cells. We focused on the involvement of reactive oxygen species, as we found previously that EGCG caused apoptotic cell death in osteoclastic cells due mainly to promotion of the reduction of Fe(III) to Fe(II) to trigger Fenton reaction, which affords hydroxyl radical from hydrogen peroxide [H(2)O(2) + Fe(II) --> (*)OH + OH(-) + Fe(III)]. EGCG (12.5-50 micro M) decreased the viability of Jurkat cells and caused concomitant increase in cellular caspase-3 activity. Catalase and the Fe(II)-chelating reagent o-phenanthroline suppressed the EGCG effects, indicating involvements of both H(2)O(2) and Fe(II) in the mechanism. Unexpectedly, epicatechin gallate (ECG), which has Fe(III)-reducing potency comparable with EGCG, failed to decrease the viability of Jurkat cells, while epigallocatechin (EGC), which has low capacity to reduce Fe(III), showed cytotoxic effects similar to EGCG. These results suggest that, unlike in osteoclastic cells, a mechanism other than Fe(III) reduction plays a role in catechin-mediated Jurkat cell death. We found that EGCG causes an elevation of H(2)O(2) levels in Jurkat cell culture, in cell-free culture medium and sodium phosphate buffer. Catechins with a higher ability to produce H(2)O(2) were more cytotoxic to Jurkat cells. Hydrogen peroxide itself exerted Fe(II)-dependent cytotoxicity. Amongst tumor and normal cell lines tested, cells exhibiting lower H(2)O(2)-eliminating activity were more sensitive to EGCG. From these findings, we propose the mechanism that make catechins cytotoxic in certain tumor cells is due to their ability to produce H(2)O(2) and that the resulting increase in H(2)O(2) levels triggers Fe(II)-dependent formation of highly toxic hydroxyl radical, which in turn induces apoptotic cell death.