bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inactivation of Pseudomonas aeruginosa by Direct Sunlight
Authors: Sagripanti Jose‐Luis , Grote Gudrun , Niederwöhrmeier Bärbel , Marschall Hans‐Jürgen 
Published: February 2013

AbstractWe determined the sensitivity of Pseudomonas aeruginosa to direct sunlight radiation, while maintaining the experimental temperature below levels harmful to the bacterium. The results presented here were similar to previous data on solar sensitivity obtained half a world away on another related bacterial species. The findings presented in this study suggest that related bacteria have a characteristic sensitivity to sunlight with their survival depending mainly on the fluence (photons) received in a dose‐dependent manner that is otherwise relatively independent from latitude, atmospheric ozone and other local conditions. Conditions that inactivated P. aeruginosa did not result in measurable impairment of specific polymerase chain reaction (PCR) or enzyme‐linked immunoassays (ELISA) tests suggesting that this germ could still be amenable to detection after inactivation by sunlight. The results presented in this study should assist in predicting the survival of P. aeruginosa outdoors and in monitoring the risk posed by this widespread organism in a variety of environmental settings.
Multiplexed, UVC‐Induced, Sequence‐Dependent DNA Damage Detection
Authors: Nair Sindhu G. , Loppnow Glen R. 
Published: February 2013

AbstractThe exposure of DNA to ultraviolet (UV) radiation causes sequence‐dependent damage. Thus, there is a need for an analytical technique that can detect damage in large numbers of DNA sequences simultaneously. In this study, we have designed an assay for UVC‐induced DNA damage in multiple oligonucleotides simultaneously by using a 96‐well plate and a novel automated sample mover. The UVC‐induced DNA damage is measured using smart probes, analogs of molecular beacons in which guanosine nucleotides act as the fluorescence quencher. Our results show that the oligonucleotide damage constants obtained with this method are reproducible and similar to those obtained in cuvettes. The calibration curve for poly‐dT shows good linearity (R2 = 0.96), with limits of detection (LOD) and quantification (LOQ) equal to 55 and 183 nm, respectively. The results show that the damage kinetics upon irradiation is sensitive to the different types of photoproducts formed in the different sequences used; i.e. poly‐A oligonucleotides containing guanine are damaged at a faster rate than poly‐A oligonucleotides containing either thymine or cytosine. Thus, detecting DNA damage in a 96‐well plate and quantifying the damage with smart probes are a simple, fast and inexpensive mix‐and‐read technique for multiplexed, sequence‐specific DNA damage detection.
Do We Practice What We Preach? Goal Setting for Ecological Restoration
Authors: Hallett Lauren M. , Diver Sibyl , Eitzel Melissa V. , Olson Jessica J. , Ramage Benjamin S. , Sardinas Hillary , Statman‐Weil Zoe , Suding Katharine N. 
Published: February 2013

AbstractOver the last decade, several research and opinion pieces have challenged the tenets of restoration ecology but a lack of centralized data has impeded assessment of how scientific developments relate to on‐the‐ground restoration. In response, the Society for Ecological Restoration (SER) launched the Global Restoration Network (GRN) to catalog worldwide restoration efforts. We reviewed over 200 GRN projects to identify the goals governing restoration and the frequency with which they are measured. We used the SER Primer on Ecological Restoration to frame our analysis, categorizing goals by SER's attributes of restored ecosystems. We developed additional attributes to characterize goals not encompassed by the SER‐defined attributes. Nearly all projects included goals related to ecosystem form, namely similarity to reference conditions and the presence of indigenous species, and these goals were frequently measured. Most projects included goals related to ecosystem function, and many highlighted interactions between abiotic and biotic factors by either modifying abiotic conditions to support focal species or manipulating species to achieve desired ecosystem functions. Few projects had goals related to ecosystem stability, whereas the majority of projects had goals related to social values. Although less frequently measured, social goals were described as important for long‐term project success. In conclusion, science and practice frequently aligned on goals related to ecosystem composition and function, but scientific guidelines on resilience and self‐sustainability appear insufficient to guide practice. In contrast, the common inclusion of goals for human well‐being indicates that, if intended to advise practice, restoration guidelines should give direction on social goals.
Restoration of Zooplankton Communities in Industrially Damaged Lakes: Influences of Residual Metal Contamination and the Recovery of Fish Communities
Authors: Webster Natalie I. , Keller Wendel B. , Ramcharan Charles W. 
Published: February 2013

AbstractThe Sudbury, Ontario, Canada area offers a unique opportunity to develop our understanding of biotic and abiotic lake recovery processes in industrially damaged natural systems. In recent decades, lakes in the Sudbury area have shown improvements in water quality due to decreases in sulfur (S) and metal emissions from area smelters, and reduced acid deposition from more distant sources. However, biological recovery is lagging and mechanisms controlling the lag are not yet clear. Our study examines the roles of two factors, residual metal contamination and altered fish predation, on zooplankton community recovery. Data collected over three decades on six study lakes were analyzed using redundancy analysis (RDA) and partial RDA's to assess historical and present relationships of water chemistry and fish abundance with zooplankton community recovery. Continuing metal toxicity appears to be the primary cause of the absence of some zooplankton species, particularly Daphnia spp. from metal‐contaminated lakes. Conversely, once water quality is suitable and abundant planktivores reestablish, fish planktivory becomes a factor affecting Daphnia spp. establishment. The introduction of piscivores into these lakes may be necessary to facilitate the return of many Daphnia species. Further reductions in metal toxicity will also assist with the complete recovery of zooplankton communities. Studying natural systems over several decades allows us to better understand the intricate steps involved with recovery of industrially damaged lakes, and this knowledge will greatly benefit future restoration efforts in other industrially damaged systems.
A variant of LEAFY reveals its capacity to stimulate meristem development by inducing RAX1
Authors: Chahtane Hicham , Vachon Gilles , Le Masson Marie , Thévenon Emmanuel , Périgon Sophie , Mihajlovic Nela , Kalinina Anna , Michard Robin , Moyroud Edwige , Monniaux Marie , Sayou Camille , Grbic Vojislava , Parcy Francois , Tichtinsky Gabrielle 
Published: February 2013

SummaryIn indeterminate inflorescences, floral meristems develop on the flanks of the shoot apical meristem, at positions determined by auxin maxima. The floral identity of these meristems is conferred by a handful of genes called floral meristem identity genes, among which the LEAFY (LFY) transcription factor plays a prominent role. However, the molecular mechanism controlling the early emergence of floral meristems remains unknown. A body of evidence indicates that LFY may contribute to this developmental shift, but a direct effect of LFY on meristem emergence has not been demonstrated. We have generated a LFY allele with reduced floral function and revealed its ability to stimulate axillary meristem growth. This role is barely detectable in the lfy single mutant but becomes obvious in several double mutant backgrounds and plants ectopically expressing LFY. We show that this role requires the ability of LFY to bind DNA, and is mediated by direct induction of REGULATOR OF AXILLARY MERISTEMS1 (RAX1) by LFY. We propose that this function unifies the diverse roles described for LFY in multiple angiosperm species, ranging from monocot inflorescence identity to legume leaf development, and that it probably pre‐dates the origin of angiosperms.
If the permanent deferral were lifted would men who have sex with men want to donate blood, and if so, who would be eligible?
Authors: Belanger Geoffrey A. , McFarland Willi , Raymond H. Fisher , Custer Brian 
Published: February 2013

BackgroundThe deferral of men who have sex with men (MSM) from blood donation is controversial worldwide, with national policies varying from no explicit deferral to permanent deferral. This study assesses whether MSM have donated and would be interested in donating if the US exclusion policy were removed and who would be eligible to donate if the policy were modified to a temporary or lower‐risk deferral criterion.Study Design and MethodsQuestions about previous blood donation and interest in future donation were added to the National HIV Behavioral Surveillance survey questionnaire, which periodically gathers risk behavior information from MSM in San Francisco.ResultsOverall, 77.3% of 475 MSM respondents expressed interest in donating. By lower‐risk criteria, 10.1% had no sexual contact in the past 6 months (2.3% in the past 12 months) and 1.9% had only lower‐risk sexual contact in the past 6 months (1.5% in the past 12 months). Of the 23.4% who answered yes to having donated in the past, at least 25.2% did not comply with the current deferral of no male–male sex since 1977.ConclusionThe majority of MSM are interested in donating blood. Depending on how the policy would be changed (i.e., either a temporary or a behavior‐based deferral criterion), substantial numbers of MSM would be eligible.
Regulation of Herpes Simplex Virus gB-Induced Cell-Cell Fusion by Mutant Forms of gH/gL in the Absence of gD and Cellular Receptors
Authors: Atanasiu Doina , Cairns Tina M. , Whitbeck J. Charles , Saw Wan Ting , Rao Samhita , Eisenberg Roselyn J. , Cohen Gary H. 
Published: February 2013

ABSTRACT
Herpesvirus entry requires the viral glycoprotein triad of gB and gH/gL to carry out fusion between the virion envelope and a cellular membrane in order to release the nucleocapsid into the target cell. Herpes simplex virus (HSV) also requires glycoprotein gD to initiate the fusion cascade by binding a cell receptor such as nectin 1 or herpesvirus entry mediator (HVEM). While the structure of gB is that of a class III fusion protein, gH/gL has no features that resemble other viral fusion proteins. Instead, it is suggested that gH/gL acts as a regulator of gB. The crystal structure of HSV-2 gH/gL was obtained with a functional protein that had a deletion of 28 residues at the gH N terminus (gHΔ48/gL). Unexplainably, monoclonal antibodies (MAbs) with virus-neutralizing activity map to these residues. To reconcile these two disparate observations, we studied the ability of gHΔ48/gL to regulate fusion. Here, we show that the protein induces low (constitutive) levels of fusion by gB in the absence of gD and/or receptor. However, when gD and receptor are present, this mutant functions as well as does wild-type (wt) gH/gL for fusion. We propose that gHΔ48/gL has an intermediate structure on the pathway leading to full regulatory activation. We suggest that a key step in the pathway of fusion is the conversion of gH/gL to an activated state by receptor-bound gD; this activated gH/gL resembles gHΔ48/gL.

IMPORTANCE
Herpes simplex viruses (HSVs) cause many human diseases, from mild cold sores to lethal neonatal herpes. As an enveloped virus, HSV must fuse its membrane with a host membrane in order for replication to take place. The virus uses four glycoproteins for this process, gD, gB, and gH/gL, and either of two cell receptors, herpesvirus entry mediator (HVEM) and nectin 1. Although the virus can enter the cell by direct fusion at the plasma membrane or via endocytosis, the same four glycoproteins are involved. The absence of any of these proteins abolishes the entry process. Here, we show that a mutant form of gH/gL, gHΔ48/gL, can induce fusion of gB-expressing cells in the absence of gD and a gD receptor. Our study supports the concept that gB is the HSV fusogen and its activity is regulated by gH/gL.
Thyroid Hormone Regulation of miR-21 Enhances Migration and Invasion of Hepatoma
Authors: Huang Ya-Hui , Lin Yang-Hsiang , Chi Hsiang-Cheng , Liao Chen-Hsin , Liao Chia-Jung , Wu Sheng-Ming , Chen Cheng-Yi , Tseng Yi-Hsin , Tsai Chung-Ying , Lin Sheng-Yen , Hung Yu-Ting , Wang Chih-Jen , Lin Crystal D. , Lin Kwang-Huei 
Published: February 2013

Abstract
Thyroid hormone (T3) signaling through the thyroid hormone receptor (TRα1) regulates hepatoma cell growth and pathophysiology, but the underlying mechanisms are unclear at present. Here, we have shown that the oncomir microRNA-21 (miR-21) is activated by T3 through a native T3 response element in the primary miR-21 promoter. Overexpression of miR-21 promoted hepatoma cell migration and invasion, similar to that observed with T3 stimulation in hepatoma cells. In addition, anti-miR-21–induced suppression of cell migration was rescued by T3. The Rac-controlled regulator of invasion and metastasis, T-cell lymphoma invasion and metastasis 1 (TIAM1), was identified as a miR-21 target additionally downregulated by T3. Attenuation and overexpression of miR-21 induced upregulation and downregulation of TIAM1, respectively. TIAM1 attenuation, in turn, enhanced migration and invasion via the upregulation of β-catenin, vimentin, and matrix metalloproteinase-2 in hepatoma cells. Notably, correlations between TRα1, miR-21, and TIAM1 expression patterns in animal models paralleled those observed in vitro. In the clinic, we observed a positive correlation (P = 0.005) between the tumor/nontumor ratios of TRα1 and miR-21 expression, whereas a negative correlation (P = 0.019) was seen between miR-21 and TIAM1 expression in patients with hepatoma. Our findings collectively indicate that miR-21 stimulation by T3 and subsequent TIAM1 suppression promotes hepatoma cell migration and invasion. Cancer Res; 73(8); 2505–17. ©2013 AACR.
Prospective Analysis of Body Mass Index, Physical Activity, and Colorectal Cancer Risk Associated with β-Catenin (CTNNB1) Status
Authors: Morikawa Teppei , Kuchiba Aya , Lochhead Paul , Nishihara Reiko , Yamauchi Mai , Imamura Yu , Liao Xiaoyun , Qian Zhi Rong , Ng Kimmie , Chan Andrew T. , Meyerhardt Jeffrey A. , Giovannucci Edward , Fuchs Charles S. , Ogino Shuji 
Published: February 2013

Abstract
Dysregulation of the WNT/β-catenin (CTNNB1) signaling pathway is implicated in colorectal carcinoma and metabolic diseases. Considering these roles and cancer prevention, we hypothesized that tumor CTNNB1 status might influence cellular sensitivity to obesity and physical activity. In clinical follow-up of 109,046 women in the Nurses' Health Study and 47,684 men in the Health Professionals Follow-up Study, there were 861 incident rectal and colon cancers with tissue immunohistochemistry data on nuclear CTNNB1 expression. Using this molecular pathological epidemiology database, we conducted Cox proportional hazards regression analysis using data duplication method to assess differential associations of body mass index (BMI) or exercise activity with colorectal cancer risk according to tumor CTNNB1 status. Greater BMI was associated with a significantly higher risk of CTNNB1-negative cancer [multivariate HR = 1.34; 95% confidence interval (CI), 1.18–1.53 for 5.0 kg/m2 increment; Ptrend = 0.0001] but not with CTNNB1-positive cancer risk (multivariate HR = 1.07; 95% CI, 0.92–1.25 for 5.0 kg/m2 increment; Ptrend = 0.36; Pheterogeneity = 0.027, between CTNNB1-negative and CTNNB1-positive cancer risks). Physical activity level was associated with a lower risk of CTNNB1-negative cancer (multivariate HR = 0.93; 95% CI, 0.87–1.00 for 10 MET-h/wk increment; Ptrend = 0.044) but not with CTNNB1-positive cancer risk (multivariate HR = 0.98; 95% CI, 0.91–1.05 for 10 MET-h/wk increment; Ptrend = 0.60). Our findings argue that obesity and physical inactivity are associated with a higher risk of CTNNB1-negative colorectal cancer but not with CTNNB1-positive cancer risk. Furthermore, they suggest that energy balance and metabolism status exerts its effect in a specific carcinogenesis pathway that is less likely dependent on WNT/CTNNB1 activation. Cancer Res; 73(5); 1600–10. ©2012 AACR.
β-1,4-Galactosyltransferase III Enhances Invasive Phenotypes Via β1-Integrin and Predicts Poor Prognosis in Neuroblastoma
Authors: Chang Hsiu-Hao , Chen Chia-Hua , Chou Chih-Hsing , Liao Yung-Feng , Huang Miao-Juei , Chen Ya-Hsin , Wang Wei-Jen , Huang John , Hung Ji-Shiang , Ho Wan-Ling , Jeng Yung-Ming , Che Mei-Ieng , Lee Hsinyu , Lu Meng-Yao , Yang Yung-Li , Jou Shiann-Tarng , Lin Dong-Tsamn , Lin Kai-Hsin , Hsu Wen-Ming , Huang Min-Chuan 
Published: February 2013

Abstract
Purpose: Neuroblastoma (NB) is a neural crest-derived tumor that commonly occurs in childhood. β-1,4-Galactosyltransferase III (B4GALT3) is highly expressed in human fetal brain and is responsible for the generation of poly-N-acetyllactosamine, which plays a critical role in tumor progression. We therefore investigated the expression and role of B4GALT3 in NB.
Experimental Design: We examined B4GALT3 expression in tumor specimens from 101 NB patients by immunohistochemistry and analyzed the correlation between B4GALT3 expression and clinicopathologic factors or survival. The functional role of B4GALT3 expression was investigated by overexpression or knockdown of B4GALT3 in NB cells for in vitro and in vivo studies.
Results: We found that B4GALT3 expression correlated with advanced clinical stages (P = 0.040), unfavorable Shimada histology (P &lt; 0.001), and lower survival rate (P &lt; 0.001). Multivariate analysis showed that B4GALT3 expression is an independent prognostic factor for poor survival of NB patients. B4GALT3 overexpression increased migration, invasion, and tumor growth of NB cells, whereas B4GALT3 knockdown suppressed the malignant phenotypes of NB cells. Mechanistic investigation showed that B4GALT3-enhanced migration and invasion were significantly suppressed by β1-integrin blocking antibody. Furthermore, B4GALT3 overexpression increased lactosamine glycans on β1-integrin, increased expression of mature β1-integrin via delayed degradation, and enhanced phosphorylation of focal adhesion kinase. Conversely, these properties were decreased by knockdown of B4GALT3 in NB cells.
Conclusions: Our findings suggest that B4GALT3 predicts an unfavorable prognosis for NB and may regulate invasive phenotypes through modulating glycosylation, degradation, and signaling of β1-integrin in NB cells. Clin Cancer Res; 19(7); 1705–16. ©2013 AACR.
Aflibercept
Authors: Ciombor Kristen K. , Berlin Jordan , Chan Emily 
Published: February 2013

Abstract
Aflibercept, an intravenously administered anti-VEGF and antiplacental growth factor (PlGF) agent, has recently been approved by the U.S. Food and Drug Administration in combination with 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI) for the treatment of patients with metastatic colorectal cancer who have previously received an oxaliplatin-containing chemotherapy regimen. In the phase III VELOUR trial, aflibercept plus FOLFIRI statistically significantly prolonged both progression-free survival (PFS; median PFS for the aflibercept plus FOLFIRI arm was 6.90 vs. 4.67 months for the placebo-plus-FOLFIRI arm) and overall survival (median overall survival for the aflibercept-plus-FOLFIRI arm was 13.50 vs. 12.06 months for the placebo plus FOLFIRI arm), but grade 3 or 4 adverse events were more common with the addition of aflibercept. However, the addition of aflibercept to 5-fluorouracil, leucovorin, and oxaliplatin (mFOLFOX6) in the phase II AFFIRM trial of first-line treatment of mCRC failed to improve PFS or response rate. As a decoy VEGF receptor, aflibercept (VEGF-Trap) has binding affinity for VEGF-A, VEGF-B, PlGF-1, and PlGF-2, and this is a mechanism of significant interest. Optimal strategies for incorporating aflibercept into treatment regimens that include other anti-VEGF and cytotoxic chemotherapeutic agents, as well as development of predictive biomarkers for treatment response, have yet to be defined. Clin Cancer Res; 19(8); 1920–5. ©2013 AACR.
Phase II Trial of MEK Inhibitor Selumetinib (AZD6244, ARRY-142886) in Patients with BRAFV600E/K-Mutated Melanoma
Authors: Catalanotti Federica , Solit David B. , Pulitzer Melissa P. , Berger Michael F. , Scott Sasinya N. , Iyriboz Tunc , Lacouture Mario E. , Panageas Katherine S. , Wolchok Jedd D. , Carvajal Richard D. , Schwartz Gary K. , Rosen Neal , Chapman Paul B. 
Published: February 2013

Abstract
Purpose: Test the hypothesis that in BRAF-mutated melanomas, clinical responses to selumetinib, a MEK inhibitor, will be restricted to tumors in which the PI3K/AKT pathway is not activated.
Experimental Design: We conducted a phase II trial in patients with melanoma whose tumors harbored a BRAF mutation. Patients were stratified by phosphorylated-AKT (pAKT) expression (high vs. low) and treated with selumetinib 75 mg per os twice daily. Pretreatment tumors were also analyzed for genetic changes in 230 genes of interest using an exon-capture approach.
Results: The high pAKT cohort was closed after no responses were seen in the first 10 patients. The incidence of low pAKT melanoma tumors was low (∼25% of melanomas tested) and this cohort was eventually closed because of poor accrual. However, among the five patients with melanoma accrued in the low pAKT cohort, there was one partial response (PR). Two other patients had near PRs before undergoing surgical resection of residual disease (one patient) or discontinuation of treatment due to toxicity (one patient). Among the two nonresponding, low pAKT patients with melanoma, co-mutations in MAP2K1, NF1, and/or EGFR were detected.
Conclusions: Tumor regression was seen in three of five patients with BRAF-mutated, low pAKT melanomas; no responses were seen in the high pAKT cohort. These results provide rationale for co-targeting MEK and PI3K/AKT in patients with BRAF mutant melanoma whose tumors express high pAKT. However, the complexity of genetic changes in melanoma indicates that additional genetic information will be needed for optimal selection of patients likely to respond to MEK inhibitors. Clin Cancer Res; 19(8); 2257–64. ©2013 AACR.
FOX(M1) News—It Is Cancer
Authors: Halasi Marianna , Gartel Andrei L. 
Published: February 2013

Abstract
FOXM1 is an oncogenic transcription factor of the Forkhead family and it has a well-defined role in cell proliferation and cell-cycle progression. Expression of FOXM1 is excluded in quiescent or differentiated cells, but its level is highly elevated in proliferating and malignant cells. Overexpression of FOXM1 has been reported in more than 20 types of human cancer. In recent years, FOXM1 has been implicated in diverse cellular processes and also a growing body of experimental data has underlined the relevance of FOXM1 in tumorigenesis. Although FOXM1 is under the control of three major tumor suppressors (RB, p53, and p19ARF), it is still active in the majority of human cancers. The oncogenic potential of FOXM1 is mainly based on its ability to transcriptionally activate genes that are involved in different facets of cancer development. In this review, the contribution of FOXM1 to each of the hallmarks of cancer will be summarized and discussed. Mol Cancer Ther; 12(3); 245–54. ©2012 AACR.