Search for the Decays B^0 -> D^{(*)+} D^{(*)-}

Using the CLEO-II data set we have searched for the Cabibbo-suppressed decays B^0 -> D^{(*)+} D^{(*)-}. For the decay B^0 -> D^{*+} D^{*-}, we observe one candidate signal event, with an expected background of 0.022 +/- 0.011 events. This yield corresponds to a branching fraction of Br(B^0 -> D^{*+} D^{*-}) = (5.3^{+7.1}_{-3.7}(stat) +/- 1.0(syst)) x 10^{-4} and an upper limit of Br(B^0 -> D^{*+} D^{*-}) D^{*\pm} D^\mp and B^0 -> D^+ D^-, no significant excess of signal above the expected background level is seen, and we calculate the 90% CL upper limits on the branching fractions to be Br(B^0 -> D^{*\pm} D^\mp) D^+ D^-) < 1.2 x 10^{-3}.Comment: 12 page postscript file also available through http://w4.lns.cornell.edu/public/CLNS, submitted to Physical Review Letter

Observation of the Decay Ds+→ωπ+D_{s}^{+}\to \omega\pi^{+}

Using e+e- annihilation data collected by the CLEO~II detector at CESR, we have observed the decay Ds+ to omega pi+. This final state may be produced through the annihilation decay of the Ds+, or through final state interactions. We find a branching ratio of [Gamma(Ds+ to omega pi+)/Gamma(Ds+ to eta pi+)]=0.16+-0.04+-0.03, where the first error is statistical and the second is systematic.Comment: 9 pages, postscript file also available through http://w4.lns.cornell.edu/public/CLN

Risk of metabolic syndrome among children living in metropolitan Kuala Lumpur: A case control study

Background With the increasing prevalence of childhood obesity, the metabolic syndrome has been studied among children in many countries but not in Malaysia. Hence, this study aimed to compare metabolic risk factors between overweight/obese and normal weight children and to determine the influence of gender and ethnicity on the metabolic syndrome among school children aged 9-12 years in Kuala Lumpur and its metropolitan suburbs. Methods A case control study was conducted among 402 children, comprising 193 normal-weight and 209 overweight/obese. Weight, height, waist circumference (WC) and body composition were measured, and WHO (2007) growth reference was used to categorise children into the two weight groups. Blood pressure (BP) was taken, and blood was drawn after an overnight fast to determine fasting blood glucose (FBG) and full lipid profile, including triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC). International Diabetes Federation (2007) criteria for children were used to identify metabolic syndrome. Results Participants comprised 60.9% (n = 245) Malay, 30.9% (n = 124) Chinese and 8.2% (n = 33) Indian. Overweight/obese children showed significantly poorer biochemical profile, higher body fat percentage and anthropometric characteristics compared to the normal-weight group. Among the metabolic risk factors, WC ≥90th percentile was found to have the highest odds (OR = 189.0; 95%CI 70.8, 504.8), followed by HDL-C≤1.03 mmol/L (OR = 5.0; 95%CI 2.4, 11.1) and high BP (OR = 4.2; 95%CI 1.3, 18.7). Metabolic syndrome was found in 5.3% of the overweight/obese children but none of the normal-weight children (p < 0.01). Overweight/obese children had higher odds (OR = 16.3; 95%CI 2.2, 461.1) of developing the metabolic syndrome compared to normal-weight children. Binary logistic regression showed no significant association between age, gender and family history of communicable diseases with the metabolic syndrome. However, for ethnicity, Indians were found to have higher odds (OR = 5.5; 95%CI 1.5, 20.5) compared to Malays, with Chinese children (OR = 0.3; 95%CI 0.0, 2.7) having the lowest odds. Conclusions We conclude that being overweight or obese poses a greater risk of developing the metabolic syndrome among children. Indian ethnicity is at higher risk compared to their counterparts of the same age. Hence, primary intervention strategies are required to prevent this problem from escalating

Up-Regulation of Hepatitis C Virus Replication and Production by Inhibition of MEK/ERK Signaling

BACKGROUND: Viruses interact with and exploit the host cellular machinery for their multiplication and propagation. The MEK/ERK signaling pathway positively regulates replication of many RNA viruses. However, whether and how this signaling pathway affects hepatitis C virus (HCV) replication and production is not well understood. METHODS AND RESULTS: In this study, we took advantage of two well-characterized MEK/ERK inhibitors and MEK/ERK dominant negative mutants and investigated the roles of the MEK/ERK signaling pathway in HCV gene expression and replication. We showed that inhibition of MEK/ERK signaling enhanced HCV gene expression, plus- and minus-strand RNA synthesis, and virus production. In addition, we showed that this enhancement was independent of interferon-alpha (IFN-alpha) antiviral activity and did not require prior activation of the MEK/ERK signaling pathway. Furthermore, we showed that only MEK and ERK-2 but not ERK-1 was involved in HCV replication, likely through regulation of HCV RNA translation. CONCLUSIONS: Taken together, these results demonstrate a negative regulatory role of the MEK/ERK signaling pathway in HCV replication and suggest a potential risk in targeting this signaling pathway to treat and prevent neoplastic transformation of HCV-infected liver cells

Multiplexed and scalable super-resolution imaging of three-dimensional protein localization in size-adjustable tissues

The biology of multicellular organisms is coordinated across multiple size scales, from the subnanoscale of molecules to the macroscale, tissue-wide interconnectivity of cell populations. Here we introduce a method for super-resolution imaging of the multiscale organization of intact tissues. The method, called magnified analysis of the proteome (MAP), linearly expands entire organs fourfold while preserving their overall architecture and three-dimensional proteome organization. MAP is based on the observation that preventing crosslinking within and between endogenous proteins during hydrogel-tissue hybridization allows for natural expansion upon protein denaturation and dissociation. The expanded tissue preserves its protein content, its fine subcellular details, and its organ-scale intercellular connectivity. We use off-the-shelf antibodies for multiple rounds of immunolabeling and imaging of a tissue's magnified proteome, and our experiments demonstrate a success rate of 82% (100/122 antibodies tested). We show that specimen size can be reversibly modulated to image both inter-regional connections and fine synaptic architectures in the mouse brain.United States. National Institutes of Health (1-U01-NS090473-01

Satellite Data-Based Phenological Evaluation of the Nationwide Reforestation of South Korea

Through the past 60 years, forests, now of various age classes, have been established in the southern part of the Korean Peninsula through nationwide efforts to reestablish forests since the Korean War (1950-53), during which more than 65% of the nation&apos;s forest was destroyed. Careful evaluation of long-term changes in vegetation growth after reforestation is one of the essential steps to ensuring sustainable forest management. This study investigated nationwide variations in vegetation phenology using satellite-based growing season estimates for 1982-2008. The start of the growing season calculated from the normalized difference vegetation index (NDVI) agrees reasonably with the ground-observed first flowering date both temporally (correlation coefficient, r = 0.54) and spatially (r = 0.64) at the 95% confidence level. Over the entire 27-year period, South Korea, on average, experienced a lengthening of the growing season of 4.5 days decade(-1), perhaps due to recent global warming. The lengthening of the growing season is attributed mostly to delays in the end of the growing season. The retrieved nationwide growing season data were used to compare the spatial variations in forest biomass carbon density with the time-averaged growing season length for 61 forests. Relatively higher forest biomass carbon density was observed over the regions having a longer growing season, especially for the regions dominated by young (&lt;30 year) forests. These results imply that a lengthening of the growing season related to the ongoing global warming may have positive impacts on carbon sequestration, an important aspect of large-scale forest management for sustainable development.open2

Constitutive activation of glycogen synthase kinase-3β correlates with better prognosis and cyclin-dependent kinase inhibitors in human gastric cancer

Background: Aberrant regulation of glycogen synthase kinase-3 beta (GSK-3 beta) has been implicated in several human cancers; however, it has not been reported in the gastric cancer tissues to date. The present study was performed to determine the expression status of active form of GSK-3 beta phosphorylated at Tyr(216) (pGSK-3 beta) and its relationship with other tumor-associated proteins in human gastric cancers. Methods: Immunohistochemistry was performed on tissue array slides containing 281 human gastric carcinoma specimens. In addition, gastric cancer cells were cultured and treated with a GSK-3 beta inhibitor lithium chloride (LiCl) for immunoblot analysis. Results: We found that pGSK-3 beta was expressed in 129 (46%) of 281 cases examined, and was higher in the early-stages of pathologic tumor-node-metastasis (P < 0.001). The expression of pGSK-3 beta inversely correlated with lymphatic invasion (P < 0.001) and lymph node metastasis (P < 0.001) and correlated with a longer patient survival (P < 0.001). In addition, pGSK-3 beta expression positively correlated with that of p16, p21, p27, p53, APC, PTEN, MGMT, SMAD4, or KAl1 (P < 0.05), but not with that of cyclin D1. This was confirmed by immunoblot analysis using SNU-668 gastric cancer cells treated with LiCl. Conclusions: GSK-3 beta activation was frequently observed in early-stage gastric carcinoma and was significantly correlated with better prognosis. Thus, these findings suggest that GSK-3 beta activation is a useful prognostic marker for the early-stage gastric cancer.Hirakawa H, 2009, ONCOL REP, V22, P481, DOI 10.3892/or_00000460Dar AA, 2009, ONCOGENE, V28, P866, DOI 10.1038/onc.2008.434Holmes T, 2008, STEM CELLS, V26, P1288, DOI 10.1634/stemcells.2007-0600Wang Q, 2008, CELL DEATH DIFFER, V15, P908, DOI 10.1038/cdd.2008.2Takahashi-Yanaga F, 2008, CELL SIGNAL, V20, P581, DOI 10.1016/j.cellsig.2007.10.018Pan MH, 2007, J AGR FOOD CHEM, V55, P7777, DOI 10.1021/jf071520hShakoori A, 2007, CANCER SCI, V98, P1388, DOI 10.1111/j.1349-7006.2007.00545.xZheng HC, 2007, ANTICANCER RES, V27, P3561Saegusa M, 2007, J PATHOL, V213, P35, DOI 10.1002/path.2198Ma C, 2007, CANCER RES, V67, P7756, DOI 10.1158/0008-5472.CAN-06-4665Forde JE, 2007, CELL MOL LIFE SCI, V64, P1930, DOI 10.1007/s00018-007-7045-7Li YW, 2007, J BIOL CHEM, V282, P21542, DOI 10.1074/jbc.M701978200Ding QQ, 2007, CANCER RES, V67, P4564, DOI 10.1158/0008-5472.CAN-06-1788Kunnimalaiyaan M, 2007, MOL CANCER THER, V6, P1151, DOI 10.1158/1535-7163.MCT-06-0665Soto-Cerrato V, 2007, MOL CANCER THER, V6, P362, DOI 10.1158/1535-7163.MCT-06-0266Cao Q, 2006, CELL RES, V16, P671, DOI 10.1038/sj.cr.7310078Yang CH, 2006, PRECIS AGRIC, V7, P33, DOI 10.1007/s11119-005-6788-0Crew KD, 2006, WORLD J GASTROENTERO, V12, P354Mai W, 2007, ONCOLOGY-BASEL, V71, P297, DOI 10.1159/000106429Tan J, 2005, CANCER RES, V65, P9012, DOI 10.1158/0008-5472.CAN-05-1226Shakoori A, 2005, BIOCHEM BIOPH RES CO, V334, P1365, DOI 10.1016/j.bbrc.2005.07.041Farago M, 2005, CANCER RES, V65, P5792Ghosh JC, 2005, CLIN CANCER RES, V11, P4580Liao XB, 2003, MOL CANCER THER, V2, P1215Lee HS, 2003, J PATHOL, V200, P39, DOI 10.1002/path.1288Doble BW, 2003, J CELL SCI, V116, P1175, DOI 10.1242/jcs.00384Gotoh J, 2003, CARCINOGENESIS, V24, P435Goto H, 2002, ORAL ONCOL, V38, P549Lee HS, 2001, INT J CANCER, V91, P619D`Amico M, 2000, J BIOL CHEM, V275, P32649, DOI 10.1074/jbc.M000643200Endoh Y, 2000, J PATHOL, V191, P257Wu LY, 1998, J NATL MED ASSOC, V90, P410WOODGETT JR, 1984, BIOCHIM BIOPHYS ACTA, V788, P339

Habitat and Host Indicate Lineage Identity in Colletotrichum gloeosporioides s.l. from Wild and Agricultural Landscapes in North America

Understanding the factors that drive the evolution of pathogenic fungi is central to revealing the mechanisms of virulence and host preference, as well as developing effective disease control measures. Prerequisite to these pursuits is the accurate delimitation of species boundaries. Colletotrichum gloeosporioides s.l. is a species complex of plant pathogens and endophytic fungi for which reliable species recognition has only recently become possible through a multi-locus phylogenetic approach. By adopting an intensive regional sampling strategy encompassing multiple hosts within and beyond agricultural zones associated with cranberry (Vaccinium macrocarpon Aiton), we have integrated North America strains of Colletotrichum gloeosporioides s.l. from these habitats into a broader phylogenetic framework. We delimit species on the basis of genealogical concordance phylogenetic species recognition (GCPSR) and quantitatively assess the monophyly of delimited species at each of four nuclear loci and in the combined data set with the genealogical sorting index (gsi). Our analysis resolved two principal lineages within the species complex. Strains isolated from cranberry and sympatric host plants are distributed across both of these lineages and belong to seven distinct species or terminal clades. Strains isolated from V. macrocarpon in commercial cranberry beds belong to four species, three of which are described here as new. Another species, C. rhexiae Ellis & Everh., is epitypified. Intensive regional sampling has revealed a combination of factors, including the host species from which a strain has been isolated, the host organ of origin, and the habitat of the host species, as useful indicators of species identity in the sampled regions. We have identified three broadly distributed temperate species, C. fructivorum, C. rhexiae, and C. nupharicola, that could be useful for understanding the microevolutionary forces that may lead to species divergence in this important complex of endophytes and plant pathogens