Perturbative Renormalization Factors of Bilinear Quark Operators for Improved Gluon and Quark Actions in Lattice QCD

We calculate one-loop renormalization factors of bilinear quark operators for gluon action including six-link loops and $O(a)$-improved quark action in the limit of massless quark. We find that finite parts of one-loop coefficients of renormalization factors diminish monotonically as either of the coefficients $c_1$ or $c_2+c_3$ of the six-link terms are decreased below zero. Detailed numerical results are given, for general values of the clover coefficient, for the tree-level improved gluon action in the Symanzik approach $(c_1=-1/12, c_2=c_3=0)$ and for the choices suggested by Wilson $(c_1=-0.252, c_2=0, c_3=-0.17)$ and by Iwasaki $(c_1=-0.331, c_2=c_3=0$ and $c_1=-0.27, c_2+c_3=-0.04)$ from renormalization-group analyses. Compared with the case of the standard plaquette gluon action, finite parts of one-loop coefficients are reduced by 10--20% for the Symanzik action, and approximately by a factor two for the renormalization-group improved gluon actions.Comment: 19 pages, REVTeX, with 3 epsf figure

Application of heavy-quark effective theory to lattice QCD: II. Radiative corrections to heavy-light currents

We apply heavy-quark effective theory to separate long- and short-distance effects of heavy quarks in lattice gauge theory. In this approach, the inverse heavy-quark mass and the lattice spacing are treated as short distances, and their effects are lumped into short-distance coefficients. We show how to use this formalism to match lattice gauge theory to continuum QCD, order by order in the heavy-quark expansion. In this paper, we focus on heavy-light currents. In particular, we obtain one-loop results for the matching factors of lattice currents, needed for heavy-quark phenomenology, such as the calculation of heavy-light decay constants, and heavy-to-light transition form factors. Results for the Brodsky-Lepage-Mackenzie scale $q^*$ are also given.Comment: 32 pages, 8 figures. v2 corrects Eqs. (4.9) and (4.10) and adds a reference. Program LatHQ2QCD to compute matching one-loop coefficients available at http://theory.fnal.gov/people/kronfeld/LatHQ2QCD

In vitro anticancer effects of a RAGE inhibitor discovered using a structure-based drug design system.

金沢大学医薬保健研究域医学系Receptor for advanced glycation end-products (RAGE) is a pattern recognition receptor implicated in the pathogenesis of certain types of cancer. In the present study, papaverine was identified as a RAGE inhibitor using the conversion to small molecules through optimized‑peptide strategy drug design system. Papaverine significantly inhibited RAGE‑dependent nuclear factor κ‑B activation driven by high mobility group box‑1, a RAGE ligand. Using RAGE‑ or dominant‑negative RAGE‑expressing HT1080 human fibrosarcoma cells, the present study revealed that papaverine suppressed RAGE‑dependent cell proliferation and migration dose‑dependently. Furthermore, papaverine significantly inhibited cell invasion. The results of the present study suggested that papaverine could inhibit RAGE, and provided novel insights into the field of RAGE biology, particularly anticancer therapies.Embargo Period 6 month

A new portable monitor for measuring odorous compounds in oral, exhaled and nasal air

<p>Abstract</p> <p>Background</p> <p>The B/B Checker^®, a new portable device for detecting odorous compounds in oral, exhaled, and nasal air, is now available. As a single unit, this device is capable of detecting several kinds of gases mixed with volatile sulfur compounds (VSC) in addition to other odorous gasses. The purpose of the present study was to evaluate the effectiveness of the B/B Checker^®for detecting the malodor level of oral, exhaled, and nasal air.</p> <p>Methods</p> <p>A total of 30 healthy, non-smoking volunteers (16 males and 14 females) participated in this study. The malodor levels in oral, exhaled, and nasal air were measured using the B/B Checker^®and by organoleptic test (OT) scores. The VSCs in each air were also measured by gas chromatography (GC). Associations among B/B Checker^®measurements, OT scores and VSC levels were analyzed using Spearman correlation coefficients. In order to determine the appropriate B/B Checker^®level for screening subjects with malodor, sensitivity and specificity were calculated using OT scores as an identifier for diagnosing oral malodor.</p> <p>Results</p> <p>In oral and nasal air, the total VSC levels measured by GC significantly correlated to that measured by the B/B Checker^®. Significant correlation was observed between the results of OT scores and the B/B Checker^®measurements in oral (r = 0.892, p < 0.001), exhaled (r = 0.748, p < 0.001) and nasal air (r = 0.534, p < 0.001). The correlation between the OT scores and VSC levels was significant only for oral air (r = 0.790, p < 0.001) and nasal air (r = 0.431, p = 0.002); not for exhaled air (r = 0.310, p = 0.096). When the screening level of the B/B Checker^®was set to 50.0 for oral air, the sensitivity and specificity were 1.00 and 0.90, respectively. On the other hand, the screening level of the B/B Checker^®was set to 60.0 for exhaled air, the sensitivity and specificity were 0.82 and 1.00, respectively.</p> <p>Conclusion</p> <p>The B/B Checker^®is useful for objective evaluation of malodor in oral, exhaled and nasal air and for screening subjects with halitosis.</p> <p>Trial registration</p> <p>ClinicalTrials.gov: <a href="http://www.clinicaltrials.gov/ct2/show/NCT01139073">NCT01139073</a></p

Loss of runt-related transcription factor 3 expression leads hepatocellular carcinoma cells to escape apoptosis

Background: Runt-related transcription factor 3 (RUNX3) is known as a tumor suppressor gene for gastric cancer and other cancers, this gene may be involved in the development of hepatocellular carcinoma (HCC). Methods: RUNX3 expression was analyzed by immunoblot and immunohistochemistry in HCC cells and tissues, respectively. Hep3B cells, lacking endogenous RUNX3, were introduced with RUNX3 constructs. Cell proliferation was measured using the MTT assay and apoptosis was evaluated using DAPI staining. Apoptosis signaling was assessed by immunoblot analysis. Results: RUNX3 protein expression was frequently inactivated in the HCC cell lines (91%) and tissues (90%). RUNX3 expression inhibited 90 +/- 8% of cell growth at 72 h in serum starved Hep3B cells. Forty-eight hour serum starvation-induced apoptosis and the percentage of apoptotic cells reached 31 +/- 4% and 4 +/- 1% in RUNX3-expressing Hep3B and control cells, respectively. Apoptotic activity was increased by Bim expression and caspase-3 and caspase-9 activation. Conclusion: RUNX3 expression enhanced serum starvation-induced apoptosis in HCC cell lines. RUNX3 is deleted or weakly expressed in HCC, which leads to tumorigenesis by escaping apoptosis

Dual Functions of ASCIZ in the DNA Base Damage Response and Pulmonary Organogenesis

Zn2+-finger proteins comprise one of the largest protein superfamilies with diverse biological functions. The ATM substrate Chk2-interacting Zn2+-finger protein (ASCIZ; also known as ATMIN and ZNF822) was originally linked to functions in the DNA base damage response and has also been proposed to be an essential cofactor of the ATM kinase. Here we show that absence of ASCIZ leads to p53-independent late-embryonic lethality in mice. Asciz-deficient primary fibroblasts exhibit increased sensitivity to DNA base damaging agents MMS and H2O2, but Asciz deletion or knock-down does not affect ATM levels and activation in mouse, chicken, or human cells. Unexpectedly, Asciz-deficient embryos also exhibit severe respiratory tract defects with complete pulmonary agenesis and severe tracheal atresia. Nkx2.1-expressing respiratory precursors are still specified in the absence of ASCIZ, but fail to segregate properly within the ventral foregut, and as a consequence lung buds never form and separation of the trachea from the oesophagus stalls early. Comparison of phenotypes suggests that ASCIZ functions between Wnt2-2b/ß-catenin and FGF10/FGF-receptor 2b signaling pathways in the mesodermal/endodermal crosstalk regulating early respiratory development. We also find that ASCIZ can activate expression of reporter genes via its SQ/TQ-cluster domain in vitro, suggesting that it may exert its developmental functions as a transcription factor. Altogether, the data indicate that, in addition to its role in the DNA base damage response, ASCIZ has separate developmental functions as an essential regulator of respiratory organogenesis

Leptospirosis in the Asia Pacific region

<p>Abstract</p> <p>Background</p> <p>Leptospirosis is a worldwide zoonotic infection that has been recognized for decades, but the problem of the disease has not been fully addressed, particularly in resource-poor, developing countries, where the major burden of the disease occurs. This paper presents an overview of the current situation of leptospirosis in the region. It describes the current trends in the epidemiology of leptospirosis, the existing surveillance systems, and presents the existing prevention and control programs in the Asia Pacific region.</p> <p>Methods</p> <p>Data on leptospirosis in each member country were sought from official national organizations, international public health organizations, online articles and the scientific literature. Papers were reviewed and relevant data were extracted.</p> <p>Results</p> <p>Leptospirosis is highly prevalent in the Asia Pacific region. Infections in developed countries arise mainly from occupational exposure, travel to endemic areas, recreational activities, or importation of domestic and wild animals, whereas outbreaks in developing countries are most frequently related to normal daily activities, over-crowding, poor sanitation and climatic conditions.</p> <p>Conclusion</p> <p>In the Asia Pacific region, predominantly in developing countries, leptospirosis is largely a water-borne disease. Unless interventions to minimize exposure are aggressively implemented, the current global climate change will further aggravate the extent of the disease problem. Although trends indicate successful control of leptospirosis in some areas, there is no clear evidence that the disease has decreased in the last decade. The efficiency of surveillance systems and data collection varies significantly among the countries and areas within the region, leading to incomplete information in some instances. Thus, an accurate reflection of the true burden of the disease remains unknown.</p

Optimal-Foraging Predator Favors Commensalistic Batesian Mimicry

BACKGROUND:Mimicry, in which one prey species (the Mimic) imitates the aposematic signals of another prey (the Model) to deceive their predators, has attracted the general interest of evolutionary biologists. Predator psychology, especially how the predator learns and forgets, has recently been recognized as an important factor in a predator-prey system. This idea is supported by both theoretical and experimental evidence, but is also the source of a good deal of controversy because of its novel prediction that in a Model/Mimic relationship even a moderately unpalatable Mimic increases the risk of the Model (quasi-Batesian mimicry). METHODOLOGY/PRINCIPAL FINDINGS:We developed a psychology-based Monte Carlo model simulation of mimicry that incorporates a "Pavlovian" predator that practices an optimal foraging strategy, and examined how various ecological and psychological factors affect the relationships between a Model prey species and its Mimic. The behavior of the predator in our model is consistent with that reported by experimental studies, but our simulation's predictions differed markedly from those of previous models of mimicry because a more abundant Mimic did not increase the predation risk of the Model when alternative prey were abundant. Moreover, a quasi-Batesian relationship emerges only when no or very few alternative prey items were available. Therefore, the availability of alternative prey rather than the precise method of predator learning critically determines the relationship between Model and Mimic. Moreover, the predation risk to the Model and Mimic is determined by the absolute density of the Model rather than by its density relative to that of the Mimic. CONCLUSIONS/SIGNIFICANCE:Although these predictions are counterintuitive, they can explain various kinds of data that have been offered in support of competitive theories. Our model results suggest that to understand mimicry in nature it is important to consider the likely presence of alternative prey and the possibility that predation pressure is not constant