bluuebunny/crossref_metadata_2025_split huggingface dataset:
Optimization of Hot Water Treatment for Removing Microbial Colonies on Fresh Blueberry Surface
Authors: Kim Tae Jo , Corbitt Melody P. , Silva Juan L. , Wang Dja Shin , Jung Yean‐Sung , Spencer Barbara 
Published: May 2011

Abstract:  Blueberries for the frozen market are washed but this process sometimes is not effective or further contaminates the berries. This study was designed to optimize conditions for hot water treatment (temperature, time, and antimicrobial concentration) to remove biofilm and decrease microbial load on blueberries. Scanning electron microscopy (SEM) image showed a well‐developed microbial biofilm on blueberries dipped in room temperature water. The biofilm consisted of yeast and bacterial cells attached to the berry surface in the form of microcolonies, which produced exopolymer substances between or upon the cells. Berry exposure to 75 and 90 °C showed little to no microorganisms on the blueberry surface; however, the sensory quality (wax/bloom) of berries at those temperatures was unacceptable. Response surface plots showed that increasing temperature was a significant factor on reduction of aerobic plate counts (APCs) and yeast/mold counts (YMCs) while adding Boxyl® did not have significant effect on APC. Overlaid contour plots showed that treatments of 65 to 70 °C for 10 to 15 s showed maximum reductions of 1.5 and 2.0 log CFU/g on APCs and YMCs, respectively; with acceptable level of bloom/wax score on fresh blueberries. This study showed that SEM, response surface, and overlaid contour plots proved successful in arriving at optima to reduce microbial counts while maintaining bloom/wax on the surface of the blueberries.Practical Application:  Since chemical sanitizing treatments such as chlorine showed ineffectiveness to reduce microorganisms loaded on berry surface (Beuchat and others 2001, Sapers 2001), hot water treatment on fresh blueberries could maximize microbial reduction with acceptable quality of fresh blueberries.
Muscle characteristics in young Norwegian‐Swedish Coldblooded Trotters and associations with breeding index, body size and early training
Authors: REVOLD T. , IHLER C. F. , KARLSTRÖM K. , LARSEN S. , ESSÉN‐GUSTAVSSON B. 
Published: May 2011

SummaryReasons for performing study:The trotting speed of Norwegian‐Swedish Coldblooded Trotters (NSCTs) is, although inferior to Standardbred speeds, gradually increasing. This development is mainly attributed to breeding progresses. Characteristics of the middle gluteal muscle have recently been described in a small number of these horses but the actual spread in muscle parameters within the population is unknown.Objectives:To describe the characteristics of the middle gluteal muscle and their naturally occurring variability in young NSCT horses and investigate possible association with body size, individual breeding index and early training.Methods:Biopsies of the middle gluteal muscle of 144 NSCT horses born in 2005 were collected at age 17–24 months. The horses were randomly selected by stratified sampling with gender and paternal progeny as stratification factors. The muscle samples were analysed for fibre type composition, fibre type areas, capillary supply and the activity of the key metabolic enzymes citrate synthase, 3‐OH‐acyl‐CoA‐dehydrogenase and lactate dehydrogenase. Correlation analysis including muscle parameters and body size, individual breeding index and early training was performed.Results:Large interindividual differences were identified in muscle characteristics. Male horses had higher percentages oftype IIAfibres and lower percentages oftype IIXfibres than age‐matched females. Fibre type areas followed the ordertype IIX>IIAX>IIA>I,while the capillary supply per fibre type area increased in the opposite order. No gender‐related differences were found in fibre type areas or capillary supply. Height was correlated to the relative area oftype Ifibres. Early training was associated with increased oxidative capacity and increased percentage oftype IIAfibres. The lowest breeding index was found in untrained horses.Conclusions:Muscle characteristics differ among young NSCT horses, but the innate oxidative capacity seems to be lower than in Standardbreds of comparable age. Early training may influence on these parameters.
Direct Antibody Access to the HIV-1 Membrane-Proximal External Region Positively Correlates with Neutralization Sensitivity
Authors: Chakrabarti B. K. , Walker L. M. , Guenaga J. F. , Ghobbeh A. , Poignard P. , Burton D. R. , Wyatt R. T. 
Published: June 2011

ABSTRACT
On the prereceptor-engaged HIV-1 envelope glycoprotein (Env) spike, epitope access by the membrane-proximal external region (MPER)-directed broadly neutralizing antibodies 2F5 and 4E10 remains unresolved. Data on binding to cell surface Env and entry data using primary isolates suggest inaccessibility of the 2F5 and 4E10 epitopes on the viral spike prior to receptor engagement, but trimer gel shift analysis and slow kinetics of shedding induced by 2F5 and 4E10 indicate otherwise. Therefore, it remains unclear if the epitopes themselves are formed in their antibody-bound state (or at least sampled) prior to receptor/coreceptor engagement or if receptor interactions both expose and form the MPER epitopes, presumably in the putative prefusion transitional intermediate. Here, we performed antibody-virus “washout experiments” using both lab-adapted and a panel of clade B primary isolates to analyze MPER accessibility. The neutralization activity of 2F5 and 4E10 against lab-adapted viruses and sensitive and moderately resistant viruses was largely unaffected by relatively rapid antibody-virus washing, suggesting direct interaction with the “static” spike. However, for more neutralization-resistant viruses, the 2F5 and 4E10 antibodies could neutralize only under the “no antibody-virus wash” conditions, implying that the MPER epitopes were not accessible prior to receptor engagement. Accessibility in the washout conditions could be precisely predicted by the relative resistance to neutralization in a standard neutralization format. These data are consistent with a model in which the local MPER antibody epitope conformations may be sampled on the native spike but are occluded to antibody by local steric or distal quaternary constraints adopted by highly resistant HIV-1 isolates.
THE FIVE-HUNDRED-METER APERTURE SPHERICAL RADIO TELESCOPE (FAST) PROJECT
Authors: NAN RENDONG , LI DI , JIN CHENGJIN , WANG QIMING , ZHU LICHUN , ZHU WENBAI , ZHANG HAIYAN , YUE YOULING , QIAN LEI 
Published: May 2011

Five-hundred-meter Aperture Spherical radio Telescope (FAST) is a Chinese mega-science project to build the largest single dish radio telescope in the world. Its innovative engineering concept and design pave a new road to realize a huge single dish in the most effective way. FAST also represents Chinese contribution in the international efforts to build the square kilometer array (SKA). Being the most sensitive single dish radio telescope, FAST will enable astronomers to jump-start many science goals, such as surveying the neutral hydrogen in the Milky Way and other galaxies, detecting faint pulsars, looking for the first shining stars, hearing the possible signals from other civilizations, etc. The idea of sitting a large spherical dish in a karst depression is rooted in Arecibo telescope. FAST is an Arecibo-type antenna with three outstanding aspects: the karst depression used as the site, which is large to host the 500-meter telescope and deep to allow a zenith angle of 40 degrees; the active main reflector correcting for spherical aberration on the ground to achieve a full polarization and a wide band without involving complex feed systems; and the light-weight feed cabin driven by cables and servomechanism plus a parallel robot as a secondary adjustable system to move with high precision. The feasibility studies for FAST have been carried out for 14 years, supported by Chinese and world astronomical communities. Funding for FAST has been approved by the National Development and Reform Commission in July of 2007 with a capital budget ~ 700 million RMB. The project time is 5.5 years from the commencement of work in March of 2011 and the first light is expected to be in 2016. This review intends to introduce the project of FAST with emphasis on the recent progress since 2006. In this paper, the subsystems of FAST are described in modest details followed by discussions of the fundamental science goals and examples of early science projects.
Suppression of Apoptosis by PIF1 Helicase in Human Tumor Cells
Authors: Gagou Mary E. , Ganesh Anil , Thompson Ruth , Phear Geraldine , Sanders Cyril , Meuth Mark 
Published: May 2011

Abstract
Defining the processes that sustain telomere maintenance is critical to our understanding of cancer and longevity. PIF1 is a nonprocessive 5′-&gt;3′ human DNA helicase that exhibits broad substrate specificity. In vitro studies have implicated PIF1 in maintaining telomeres and processing stalled DNA replication forks, but disruption of the murine Pif1 gene did not yield any apparent phenotype. In this study, we evaluated the function of the PIF1 gene in human cells by using siRNA knockdown strategies to gauge its role in the response to DNA replication stress. We found that PIF1 depletion reduced the survival of both p53-deficient and p53-proficient human tumor cells by triggering apoptosis. In contrast, nonmalignant cells were unaffected by PIF1 depletion. Apoptosis induction in tumor cells was augmented by cotreatment with replication inhibitors (thymidine, hydroxyurea, or gemcitabine). When sensitive PIF1-depleted cells were released from a thymidine-induced S-phase arrest, there remained a subpopulation of cells that failed to enter S-phase. This cell subpopulation displayed an increase in levels of cyclin E and p21, as well as a deficiency in S-phase checkpoint markers that were induced with thymidine in PIF1 expressing cells. Specifically, CHK1 activation was suppressed and we detected no consistent changes in ATM S1981 autophosphorylation, γH2AX induction, or RPA hyperphosphorylation. Death in PIF1-depleted cells was detected in late G1/early S-phase and was dependent on caspase-3 activity. Taken together, our findings suggest roles for PIF1 in S-phase entry and progression that are essential to protect human tumor cells from apoptosis. Cancer Res; 71(14); 4998–5008. ©2011 AACR.
Elevated Plasma Growth Differentiation Factor-15 Correlates with Lymph Node Metastases and Poor Survival in Endometrial Cancer
Authors: Staff Anne Cathrine , Trovik Jone , Zahl Eriksson Ane Gerda , Wik Elisabeth , Wollert Kai C. , Kempf Tibor , Salvesen Helga B. 
Published: May 2011

Abstract
Purpose: The study objective was to investigate and validate plasma growth differentiation factor-15 (GDF-15) as a predictor of lymph node metastasis and a poor prognosis in primary endometrial cancer.
Experimental Design: Plasma samples from 510 women treated for endometrial cancer in a primary investigation cohort (n = 44) and a secondary validation cohort (n = 466) were analyzed for GDF-15. Plasma from healthy premenopausal (n = 20) and postmenopausal (n = 20) women, women with borderline (n = 43), benign (n = 144), and malignant ovarian tumors (n = 125) were used for comparison.
Results: Median plasma GDF-15 concentration for the endometrial cancer group was elevated (1,077 ng/L) as compared with pre- and postmenopausal controls (590 and 684 ng/L) and women with benign (591 ng/L) or borderline ovarian tumors (718 ng/L; all P &lt; 0.001), but similar to the ovarian cancer group. In the large validation cohort of endometrial carcinomas, high plasma GDF-15 was significantly associated with International Federation of Gynecology and Obstetrics (FIGO) stage III/IV disease, nonendometrioid histology, high grade, older age, postmenopausal status, and lymph node metastases (all P ≤ 0.001). High GDF-15 was also an independent predictor of poor disease-specific and recurrence-free survival.
Conclusions: Based on findings indicated in a primary investigation set and confirmed in the large secondary validation set, we report for the first time plasma GDF-15 as a biomarker for endometrial cancer phenotype, including presence of lymph node metastasis and reduced survival. Its applicability as a predictor of metastatic nodes and in monitoring treatment of endometrial cancer needs to be further studied. Clin Cancer Res; 17(14); 4825–33. ©2011 AACR.
SRSF1 Regulates the Alternative Splicing of Caspase 9 Via A Novel Intronic Splicing Enhancer Affecting the Chemotherapeutic Sensitivity of Non–Small Cell Lung Cancer Cells
Authors: Shultz Jacqueline C. , Goehe Rachel W. , Murudkar Charuta S. , Wijesinghe Dayanjan S. , Mayton Eric K. , Massiello Autumn , Hawkins Amy J. , Mukerjee Prabhat , Pinkerman Ryan L. , Park Margaret A. , Chalfant Charles E. 
Published: May 2011

Abstract
Increasing evidence points to the functional importance of alternative splice variations in cancer pathophysiology with the alternative pre-mRNA processing of caspase 9 as one example. In this study, we delve into the underlying molecular mechanisms that regulate the alternative splicing of caspase 9. Specifically, the pre-mRNA sequence of caspase 9 was analyzed for RNA cis-elements known to interact with SRSF1, a required enhancer for caspase 9 RNA splicing. This analysis revealed 13 possible RNA cis-elements for interaction with SRSF1 with mutagenesis of these RNA cis-elements identifying a strong intronic splicing enhancer located in intron 6 (C9-I6/ISE). SRSF1 specifically interacted with this sequence, which was required for SRSF1 to act as a splicing enhancer of the inclusion of the 4 exon cassette. To further determine the biological importance of this mechanism, we employed RNA oligonucleotides to redirect caspase 9 pre-mRNA splicing in favor of caspase 9b expression, which resulted in an increase in the IC50 of non–small cell lung cancer (NSCLC) cells to daunorubicin, cisplatinum, and paclitaxel. In contrast, downregulation of caspase 9b induced a decrease in the IC50 of these chemotherapeutic drugs. Finally, these studies showed that caspase 9 RNA splicing was a major mechanism for the synergistic effects of combination therapy with daunorubicin and erlotinib. Overall, we have identified a novel intronic splicing enhancer that regulates caspase 9 RNA splicing and specifically interacts with SRSF1. Furthermore, we showed that the alternative splicing of caspase 9 is an important molecular mechanism with therapeutic relevance to NSCLCs. Mol Cancer Res; 9(7); 889–900. ©2011 AACR.
Comparison of thalidomide and lenalidomide as therapy for myelofibrosis
Authors: Jabbour Elias , Thomas Deborah , Kantarjian Hagop , Zhou Lingsha , Pierce Sherry , Cortes Jorge , Verstovsek Srdan 
Published: May 2011

Abstract
With the use of the International Working Group for Myelofibrosis Treatment and Research consensus criteria, we re-assessed the efficacy of thalidomide and lenalidomide in 125 patients with myelofibrosis treated in 3 consecutive phase 2 trials: 44 received single-agent thalidomide, 41 single-agent lenalidomide, and 40 a combination of lenalidomide plus prednisone. The thalidomide group included significantly more untreated patients and patients with performance status of 2. The Lenalidomide-based therapy produced higher efficacy (34%-38%) than thalidomide (16%; P = .06). Responses to thalidomide were seen within 3-15 weeks, whereas responses to the lenalidomide-based therapy were also seen after a prolonged course of therapy (range, 2-45 weeks). Lenalidomide plus prednisone therapy resulted in significantly longer response duration (median, 34 months) than single-agent lenalidomide or thalidomide (median, 7 and 13 months, respectively; P = .042). Fewer patients (P = .001) discontinued the lenalidomide plus prednisone therapy (13%) because of side effects then patients on single-agents therapy (32%-39%). In conclusion, the combination of lenalidomide plus prednisone appears to be more ef-fective and safer than single-agent thalidomide or lenalidomide.
Context-dependent codon partition models provide significant increases in model fit in atpB and rbcL protein-coding genes
Authors: Baele Guy , Van de Peer Yves , Vansteelandt Stijn 
Published: May 2011

Abstract

Background
Accurate modelling of substitution processes in protein-coding sequences is often hampered by the computational burdens associated with full codon models. Lately, codon partition models have been proposed as a viable alternative, mimicking the substitution behaviour of codon models at a low computational cost. Such codon partition models however impose independent evolution of the different codon positions, which is overly restrictive from a biological point of view. Given that empirical research has provided indications of context-dependent substitution patterns at four-fold degenerate sites, we take those indications into account in this paper.

Results
We present so-called context-dependent codon partition models to assess previous empirical claims that the evolution of four-fold degenerate sites is strongly dependent on the composition of its two flanking bases. To this end, we have estimated and compared various existing independent models, codon models, codon partition models and context-dependent codon partition models for the atpB and rbcL genes of the chloroplast genome, which are frequently used in plant systematics. Such context-dependent codon partition models employ a full dependency scheme for four-fold degenerate sites, whilst maintaining the independence assumption for the first and second codon positions.

Conclusions
We show that, both in the atpB and rbcL alignments of a collection of land plants, these context-dependent codon partition models significantly improve model fit over existing codon partition models. Using Bayes factors based on thermodynamic integration, we show that in both datasets the same context-dependent codon partition model yields the largest increase in model fit compared to an independent evolutionary model. Context-dependent codon partition models hence perform closer to codon models, which remain the best performing models at a drastically increased computational cost, compared to codon partition models, but remain computationally interesting alternatives to codon models. Finally, we observe that the substitution patterns in both datasets are drastically different, leading to the conclusion that combined analysis of these two genes using a single model may not be advisable from a context-dependent point of view.
Indole and 3-indolylacetonitrile inhibit spore maturation in Paenibacillus alvei
Authors: Kim Yong-Guy , Lee Jin-Hyung , Cho Moo Hwan , Lee Jintae 
Published: May 2011

Abstract

Background
Bacteria use diverse signaling molecules to ensure the survival of the species in environmental niches. A variety of both Gram-positive and Gram-negative bacteria produce large quantities of indole that functions as an intercellular signal controlling diverse aspects of bacterial physiology.

Results
In this study, we sought a novel role of indole in a Gram-positive bacteria Paenibacillus alvei that can produce extracellular indole at a concentration of up to 300 μM in the stationary phase in Luria-Bertani medium. Unlike previous studies, our data show that the production of indole in P. alvei is strictly controlled by catabolite repression since the addition of glucose and glycerol completely turns off the indole production. The addition of exogenous indole markedly inhibits the heat resistance of P. alvei without affecting cell growth. Observation of cell morphology with electron microscopy shows that indole inhibits the development of spore coats and cortex in P. alvei. As a result of the immature spore formation of P. alvei, indole also decreases P. alvei survival when exposed to antibiotics, low pH, and ethanol. Additionally, indole derivatives also influence the heat resistance; for example, a plant auxin, 3-indolylacetonitrile dramatically (2900-fold) decreased the heat resistance of P. alvei, while another auxin 3-indoleacetic acid had a less significant influence on the heat resistance of P. alvei.

Conclusions
Together, our results demonstrate that indole and plant auxin 3-indolylacetonitrile inhibit spore maturation of P. alvei and that 3-indolylacetonitrile presents an opportunity for the control of heat and antimicrobial resistant spores of Gram-positive bacteria.
Histone deacetylase inhibitors SAHA and sodium butyrate block G1-to-S cell cycle progression in neurosphere formation by adult subventricular cells
Authors: Zhou Qiong , Dalgard Clifton L , Wynder Christopher , Doughty Martin L 
Published: May 2011

Abstract

Background
Histone deacetylases (HDACs) are enzymes that modulate gene expression and cellular processes by deacetylating histones and non-histone proteins. While small molecule inhibitors of HDAC activity (HDACi) are used clinically in the treatment of cancer, pre-clinical treatment models suggest they also exert neuroprotective effects and stimulate neurogenesis in neuropathological conditions. However, the direct effects of HDACi on cell cycle progression and proliferation, two properties required for continued neurogenesis, have not been fully characterized in adult neural stem cells (NSCs). In this study, we examined the effects of two broad class I and class II HDACi on adult mouse NSCs, the hydroxamate-based HDACi suberoylanilide hydroxamic acid (vorinostat, SAHA) and the short chain fatty acid HDACi sodium butyrate.

Results
We show that both HDACi suppress the formation of neurospheres by adult mouse NSCs grown in proliferation culture conditions in vitro. DNA synthesis is significantly inhibited in adult mouse NSCs exposed to either SAHA or sodium butyrate and inhibition is associated with an arrest in the G1 phase of the cell cycle. HDACi exposure also resulted in transcriptional changes in adult mouse NSCs. Cdk inhibitor genes p21 and p27 transcript levels are increased and associated with elevated H3K9 acetylation levels at proximal promoter regions of p21 and p27. mRNA levels for notch effector Hes genes and Spry-box stem cell transcription factors are downregulated, whereas pro-neural transcription factors Neurog1 and Neurod1 are upregulated. Lastly, we show HDAC inhibition under proliferation culture conditions leads to long-term changes in cell fate in adult mouse NSCs induced to differentiate in vitro.

Conclusion
SAHA and sodium butyrate directly regulate cdk inhibitor transcription to control cell cycle progression in adult mouse NSCs. HDAC inhibition results in G1 arrest in adult mouse NSCs and transcriptional changes associated with activation of neuronal lineage commitment programs and a reduction of stem/progenitor state. Changes in differentiated cell state in adult mouse NSCs treated with HDACi under proliferation culture conditions suggests an intrinsic relationship between multipotency, cell cycle progression and HDAC activity in these cells.