bluuebunny/crossref_metadata_2025_split huggingface dataset:
School Nurses: Improve the Reception and Sharpen the Image
Authors: Seidenberg Arlene 
Published: October 2009

ABSTRACTMany educators and community members misunderstand the present‐day school nurses. These nurses' roles encompass a much broader range of health‐related activities than did their predecessors' roles. Continued education and professional autonomy have enabled school nurses to direct their attention to primary and secondary prevention and to the maintenance of health. By utilizing a systems approach, school nurses can plan strategies that promote visibility and clarify their images. The outcome could result in better understanding and cooperation between the nurses and other school personnel, resulting in an ultimate benefit to children. The organization of a city school district's health service program and the functions of some of its team members are described. Pertinent statistics regarding the district and the nurses working within it are provided. Examples are given of typical school nurses experiences and responsibilities. Numerous suggestions are made for establishing networks with those persons having formal and informal power in order to achieve visibility and credibility. Some of the suggestions include participation at parent association meetings, presidents' council, teacher‐faculty meetings, community council meetings and spreading the message via school and local newspapers.
Health‐Risk Behaviors Among Middle School Students In A Large Majority‐Minority School District
Authors: Fetro Joyce V. , Coyle Karin K. , Pham Phong 
Published: October 2009

ABSTRACTSince 1991, the Centers for Disease Control and Prevention has administered the Youth Risk Behavior Survey (YRBS) biennially to representative samples of high school students. YRBS results indicate that health‐risk behaviors often developed during middle school years. To date, few state and local education agencies have administered the YRBS‐Middle School. This study measured prevalence of health‐risk behaviors among middle school students in a large, majority‐minority school district (n=1,783). Results indicated that young adolescents (ages 11–14) are engaging in multiple health‐risk behaviors. For example, 24.4% seriously considered committing suicide in the previous year, 53.3% had been in a physical fight, 50.2% ever drank alcohol, 17.9% ever used marijuana, and 13.4% had already had sex. Such behaviors potentially could lead to serious consequences related to their educational achievement and overall health status. Health‐related policy and program applications are discussed.
Addition of an aerated iron‐rich waste‐activated sludge to control the soluble sulphide concentration in sewage
Authors: Zhang Lehua , De Gusseme Bart , Cai Lankun , De Schryver Peter , Marzorati Massimo , Boon Nico , Lens Piet , Verstraete Willy 
Published: October 2009

AbstractHydrogen sulphide emission in sewers is associated with toxicity, corrosion and odour and also yields considerable costs. The purpose of this study was to evaluate whether the soluble sulphide concentration in raw sewage can be controlled by dosing an iron‐rich waste‐activated sludge (WAS) or an iron‐rich aerated waste‐activated sludge (AWAS). An average soluble sulphide elimination of 99% was achieved at an iron‐rich AWAS to sewage ratio (v/v) of 16%, whereas dosage of iron‐poor AWAS at the same ratio decreased the soluble sulphide in the raw sewage by only 53%. Our lab‐scale tests suggest that dosing iron‐rich AWAS to sewage did not affect the chemical oxygen demand (COD) and total ammonia nitrogen (TAN) removal as well as the nitrification efficiency in the receiving activated sludge system. The results indicate that iron‐rich AWAS dosage is a feasible technique to remediate the sulphide problem in sewers.
The use of restaurant inspection disclosure systems as a means of communicating food safety information
Authors: Filion Katie , Powell Douglas A. 
Published: October 2009

AbstractThe World Health Organization estimates that up to 30% of individuals in developed countries become ill from food or water each year. Up to 70% of these illnesses are estimated to be linked to food prepared at foodservice establishments. Consumer confidence in the safety of food prepared in restaurants is fragile, varying significantly from year to year, with many consumers attributing foodborne illness to foodservice. One of the key drivers of restaurant choice is consumer perception of the hygiene of a restaurant. Restaurant hygiene information is something consumers desire, and when available, may use to make dining decisions.
Clean restrooms: how important are they to restaurant consumers?
Authors: Barber Nelson , Scarcelli Joseph M. 
Published: October 2009

AbstractThere are many choices to make in restaurant dining, and for experienced consumers, the expectation of safe, quality food has increased. The foodservice industry is in a challenging and competitive environment. Determining what factors of customer satisfaction are important to maintain or increase market share is critical to success. For consumers, there are few opportunities to evaluate food handling, safety and cleanliness practices of a restaurant. Research has shown that consumers are concerned with restroom cleanliness, with a functioning restroom having a positive influence on customers' perception of the restaurant; and has also been shown to impact the choice of where to eat or whether to return to a restaurant. This study tested these assumptions by using a data set from the southwestern US, finding that consumers are concerned with restaurant cleanliness and food safety, with restrooms an important factor to consumers when assessing the cleanliness of an eating establishment.
EBV-Induced Human CD8+ NKT Cells Suppress Tumorigenesis by EBV-Associated Malignancies
Authors: Yuling He , Ruijing Xiao , Li Li , Xiang Ji , Rui Zhou , Yujuan Wang , Lijun Zhang , Chunxian Du , Xinti Tan , Wei Xiao , Lang Chen , Yanping Jiang , Tao Xiong , Mengjun Wu , Jie Xiong , Youxin Jin , Jinquan Tan 
Published: October 2009

Abstract
The underlying mechanism of the protective and suppressive role of NKT cells in human tumor immunosurveillance remains to be fully elucidated. We show that the frequencies of CD8+ NKT cells in patients with EBV-associated Hodgkin's lymphoma or nasopharyngeal carcinoma are significantly lower than those in healthy EBV carriers. These CD8+ NKT cells in tumor patients are also functionally impaired. In human-thymus-severe combined immunodeficient (hu-thym-SCID) chimeras, EBV challenge efficiently promotes the generation of IFN-γ–biased CD8+ NKT cells. These cells are strongly cytotoxic, drive syngeneic T cells into a Th1 bias, and enhance T-cell cytotoxicity to EBV-associated tumor cells. Interleukin-4–biased CD4+ NKT cells are predominately generated in unchallenged chimeras. These cells are noncytotoxic, drive syngeneic T cells into a Th2 bias, and do not affect T-cell cytotoxicity. In humanized xenogeneic tumor-transplanted hu-thym-SCID chimeras, adoptive transfer with EBV-induced CD8+ NKT cells significantly suppresses tumorigenesis by EBV-associated malignancies. EBV-induced CD8+ NKT cells are necessary and sufficient to enhance the T-cell immunity to EBV-associated malignancies in the hu-thym-SCID chimeras. CD4+ NKT cells are synergetic with CD8+ NKT cells, leading to a more pronounced T-cell antitumor response in the chimeras cotransferred with CD4+ and CD8+ NKT cells. Thus, immune reconstitution with EBV-induced CD8+ NKT cells could be a useful strategy in management of EBV-associated malignancies. [Cancer Res 2009;69(20):7935–44]
A Modified Sleeping Beauty Transposon System That Can Be Used to Model a Wide Variety of Human Cancers in Mice
Authors: Dupuy Adam J. , Rogers Laura M. , Kim Jinsil , Nannapaneni Kishore , Starr Timothy K. , Liu Pentao , Largaespada David A. , Scheetz Todd E. , Jenkins Nancy A. , Copeland Neal G. 
Published: October 2009

Abstract
Recent advances in cancer therapeutics stress the need for a better understanding of the molecular mechanisms driving tumor formation. This can be accomplished by obtaining a more complete description of the genes that contribute to cancer. We previously described an approach using the Sleeping Beauty (SB) transposon system to model hematopoietic malignancies in mice. Here, we describe modifications of the SB system that provide additional flexibility in generating mouse models of cancer. First, we describe a Cre-inducible SBase allele, RosaSBaseLsL, that allows the restriction of transposon mutagenesis to a specific tissue of interest. This allele was used to generate a model of germinal center B-cell lymphoma by activating SBase expression with an Aid-Cre allele. In a second approach, a novel transposon was generated, T2/Onc3, in which the CMV enhancer/chicken β-actin promoter drives oncogene expression. When combined with ubiquitous SBase expression, the T2/Onc3 transposon produced nearly 200 independent tumors of more than 20 different types in a cohort of 62 mice. Analysis of transposon insertion sites identified novel candidate genes, including Zmiz1 and Rian, involved in squamous cell carcinoma and hepatocellular carcinoma, respectively. These novel alleles provide additional tools for the SB system and provide some insight into how this mutagenesis system can be manipulated to model cancer in mice. [Cancer Res 2009;69(20):8150–6]
Structural Basis for the Binding of the Anticancer Compound 6-(7-Nitro-2,1,3-Benzoxadiazol-4-Ylthio)Hexanol to Human Glutathione S-Transferases
Authors: Federici Luca , Lo Sterzo Carlo , Pezzola Silvia , Di Matteo Adele , Scaloni Flavio , Federici Giorgio , Caccuri Anna Maria 
Published: October 2009

Abstract
Glutathione S-transferases (GST) constitute a superfamily of enzymes with diversified functions including detoxification from xenobiotics. In many human cancers, Pi class GST (GSTP1-1) is overexpressed and contributes to multidrug resistance by conjugating chemotherapeutics. In addition, GSTP1-1 displays antiapoptotic activity by interacting with c-Jun NH2-terminal kinase, a key regulator of apoptosis. Therefore, GSTP1-1 is considered a promising target for pharmaceutical treatment. Recently, a potent inhibitor of GSTs, 6-(7-nitro-2,1,3-benzoxadiazol-4-ylthio)hexanol (NBDHEX), was identified and tested on several tumor cell lines demonstrating high antiproliferative activity. To establish the structural basis of NBDHEX activity, we determined the crystal structure of NBDHEX bound to either GSTP1-1 or GSTM2-2 (mu class). NBDHEX in both cases binds to the H-site but occupies different positions. Furthermore, the compound is covalently attached to the GSH sulfur in the GSTM2-2 crystal, forming a σ-complex, although it is bound but not conjugated in the GSTP1-1 crystal. Several differences in the H-sites of the two isozymes determine the higher affinity of NBDHEX for GSTM2-2 with respect to GSTP1-1. One such difference is the presence of Ile104 in GSTP1-1 close to the bound NBDHEX, whereas the corresponding position is occupied by an alanine in GSTM2-2. Mutation of Ile104 into valine is a frequent GSTP1-1 polymorphism and we show here that the Ile104Val and Ile104Ala variants display a 4-fold higher affinity for the compound. Remarkably, the GSTP1-1/Ile104Ala structure in complex with NBDHEX shows a considerable shift of the compound inside the H-site. These data might be useful for the development of new anticancer compounds. [Cancer Res 2009;69(20):8025–34]
Differences in Tumor Regulatory T-Cell Localization and Activation Status Impact Patient Outcome
Authors: Ménétrier-Caux Christine , Gobert Michael , Caux Christophe 
Published: October 2009

Abstract
The presence of regulatory T cells (Treg) has been described in a large panel of solid tumors. However, their impact on tumor progression differs according to the tumor type analyzed. We recently obtained evidence in breast carcinoma that Treg localized within lymphoid aggregates, but not in the tumor bed, have a negative impact on patients' survival. Moreover, we showed selective Treg recruitment through CCR4/CCL22 in the lymphoid aggregates upon contact with dendritic cells (DC), where they became strongly and selectively activated (ICOShigh) and block conventional T-cell response. Here, we discuss the meaning and potential implication of these novel findings. [Cancer Res 2009;69(20):7895–8]
Revving the Throttle on an Oncogene: CDK8 Takes the Driver Seat
Authors: Firestein Ron , Hahn William C. 
Published: October 2009

Abstract
The Wnt/β-catenin pathway plays an important role in initiation in most, if not all, colon cancers. Prior work has provided important insights into the regulation of β-catenin stability in the cytoplasm; however, relatively little is known about the mechanism by which β-catenin activates gene transcription in the nucleus. Using genetic approaches, studies in human colon cancers and Drosophila have identified CDK8 as a colon cancer oncogene that regulates β-catenin transcriptional activity. These convergent observations provide new insights into the regulation of nuclear β-catenin activity and identify a novel therapeutic target for β-catenin-driven malignancies. [Cancer Res 2009;69(20):OF7899–901]
The Cytoskeleton Protein Filamin-A Is Required for an Efficient Recombinational DNA Double Strand Break Repair
Authors: Yue Jingyin , Wang Qin , Lu Huimei , Brenneman Mark , Fan Feiyue , Shen Zhiyuan 
Published: October 2009

Abstract
The human actin-binding protein filamin-A (also known as ABP-280) cross-links actin into a dynamic three-dimensional structure. It interacts with &gt;45 proteins of diverse functions, serving as the scaffold in various signaling networks. BRCA2 is a protein that regulates RAD51-dependent recombinational repair of DNA double strand breaks (DSB). Proximate to the COOH terminus of the BRCA2 protein, a conserved and DNA binding domain (BRCA2-DBD) interacts with filamin-A and BCCIP. In this study, we sought to test the hypothesis that filamin-A influences homologous recombinational repair of DSB and the maintenance of genomic stability. We used three pairs of cell lines with normal and reduced filamin-A expression, including breast cancer and melanoma cells. We found that lack or reduction of filamin-A sensitizes cells to ionizing radiation, slows the removal of DNA damage–induced γH2AX nuclear foci, reduces RAD51 nuclear focus formation and recruitment to chromatin in response to irradiation, and results in a 2-fold reduction of homologous recombinational repair of DSB. Furthermore, filamin-A–deficient cells have increased frequencies of micronucleus formation after irradiation. Our data illustrate the importance of the cytoskeleton structure in supporting the homologous recombinational DNA repair machinery and genome integrity, and further implicate a potential of filamin-A as a marker for prognosis in DNA damage–based cancer therapy. [Cancer Res 2009;69(20):7978–85]
BH3-only proteins Mcl-1 and Bim as well as endonuclease G are targeted in spongistatin 1–induced apoptosis in breast cancer cells
Authors: Schneiders Uta M. , Schyschka Lilianna , Rudy Anita , Vollmar Angelika M. 
Published: October 2009

AbstractSpongistatin 1, a marine experimental substance with chemotherapeutic potential, induces apoptosis and inhibits clonogenic survival of MCF-7 cells. Regarding the apoptotic signaling pathways of spongistatin 1, we present two major facts. Firstly, spongistatin 1–induced cell death, mainly caspase-independent, involves the proapoptotic proteins apoptosis-inducing factor and endonuclease G. Both proteins translocate from mitochondria to the nucleus and contribute to spongistatin 1–mediated apoptosis as shown via gene silencing. Secondly, spongistatin 1 acts as a tubulin depolymerizing agent and is able to free the proapoptotic Bcl-2 family member Bim from its sequestration both by the microtubular complex and by the antiapoptotic protein Mcl-1. Silencing of Bim by small interfering RNA leads to a diminished translocation of apoptosis-inducing factor and endonuclease G to the nucleus and subsequently reduces apoptosis rate. Thus, we identified Bim as an important factor upstream of mitochondria executing a central role in the caspase-independent apoptotic signaling pathway induced by spongistatin 1. Taken together, spongistatin 1 is both a valuable tool for the characterization of apoptotic pathways and a promising experimental anticancer drug. [Mol Cancer Ther 2009;8(10):2914–25]
FLT3-ITD up-regulates MCL-1 to promote survival of stem cells in acute myeloid leukemia via FLT3-ITD–specific STAT5 activation
Authors: Yoshimoto Goichi , Miyamoto Toshihiro , Jabbarzadeh-Tabrizi Siamak , Iino Tadafumi , Rocnik Jennifer L. , Kikushige Yoshikane , Mori Yasuo , Shima Takahiro , Iwasaki Hiromi , Takenaka Katsuto , Nagafuji Koji , Mizuno Shin-ichi , Niiro Hiroaki , Gilliland Gary D. , Akashi Koichi 
Published: October 2009

Abstract
Myeloid cell leukemia-1 (MCL-1) is an essential survival factor for hematopoiesis. In humans, hematopoietic stem cells (HSCs) express MCL-1 at the highest level in response to FMS-like tyrosine kinase-3 (FLT3) signaling. We here show that this FLT3-dependent stem cell maintenance system also plays a critical role in survival of leukemic stem cells (LSCs) in acute myeloid leukemia (AML). The CD34+CD38− LSC fraction expresses high levels of FLT3 as well as MCL-1, even compared with normal HSCs. Treatment with FLT3 ligand induced further MCL-1 up-regulation in LSCs in all AML cases tested. Interestingly, the group of samples expressing the highest levels of MCL-1 constituted AML with FLT3–internal tandem duplications (ITD). In FLT3-ITD AML cell lines, cells expressed a high level of MCL-1, and an inhibition of MCL-1 induced their apoptotic cell death. A tyrosine kinase inhibitor suppressed MCL-1 expression, and induced apoptosis that was reversed by the enforced MCL-1 expression. Finally, transduction of FLT3-ITD into HSCs strongly activated MCL-1 expression through its signal transducer and activator of transcription 5 (STAT5)–docking domains. This effect was completely abrogated when STAT5 activation was blocked. Thus, the acquisition of FLT3-ITD ensures LSC survival by up-regulating MCL-1 via constitutive STAT5 activation that is independent of wild-type FLT3 signaling.
AML1/RUNX1 mutations in 470 adult patients with de novo acute myeloid leukemia: prognostic implication and interaction with other gene alterations
Authors: Tang Jih-Luh , Hou Hsin-An , Chen Chien-Yuan , Liu Chieh-Yu , Chou Wen-Chien , Tseng Mei-Hsuan , Huang Chi-Fei , Lee Fen-Yu , Liu Ming-Chih , Yao Ming , Huang Shang-Yi , Ko Bor-Sheng , Hsu Szu-Chun , Wu Shang-Ju , Tsay Woei , Chen Yao-Chang , Lin Liang-In , Tien Hwei-Fang 
Published: October 2009

AbstractSomatic mutation of the AML1/RUNX1(RUNX1) gene is seen in acute myeloid leukemia (AML) M0 subtype and in AML transformed from myelodysplastic syndrome, but the impact of this gene mutation on survival in AML patients remains unclear. In this study, we sought to determine the clinical implications of RUNX1 mutations in 470 adult patients with de novo non-M3 AML. Sixty-three distinct RUNX1 mutations were identified in 62 persons (13.2%); 32 were in N-terminal and 31, C-terminal. The RUNX1 mutation was closely associated with male sex, older age, lower lactic dehydrogenase value, French-American-British M0/M1 subtypes, and expression of HLA-DR and CD34, but inversely correlated with CD33, CD15, CD19, and CD56 expression. Furthermore, the mutation was positively associated with MLL/PTD but negatively associated with CEBPA and NPM1 mutations. AML patients with RUNX1 mutations had a significantly lower complete remission rate and shorter disease-free and overall survival than those without the mutation. Multivariate analysis demonstrated that RUNX1 mutation was an independent poor prognostic factor for overall survival. Sequential analysis in 133 patients revealed that none acquired novel RUNX1 mutations during clinical courses. Our findings provide evidence that RUNX1 mutations are associated with distinct biologic and clinical characteristics and poor prognosis in patients with de novo AML.
Identification of genes coding for B cell antigens of Mycoplasma mycoides subsp. mycoides Small Colony (Mmm SC) by using phage display
Authors: Miltiadou Dubravka R , Mather Arshad , Vilei Edy M , Du Plessis Dion H 
Published: October 2009

Abstract

Background
Contagious bovine pleuropneumonia (CBPP) is a mycoplasmal disease caused by Mycoplasma mycoides subsp. mycoides SC (Mmm SC). Since the disease is a serious problem that can affect cattle production in parts of Africa, there is a need for an effective and economical vaccine. Identifying which of the causative agent's proteins trigger potentially protective immune responses is an important step towards developing a subunit vaccine. Accordingly, the purpose of this study was to determine whether phage display combined with bioinformatics could be used to narrow the search for genes that code for potentially immunogenic proteins of Mmm SC. Since the production of IgG2 and IgA are associated with a Th1 cellular immune response which is implicated in protection against CBPP, antigens which elicit these immunoglobulin subclasses may be useful in developing a subunit vaccine.

Results
A filamentous phage library displaying a repertoire of peptides expressed by fragments of the genome of MmmSC was constructed. It was subjected to selection using antibodies from naturally- and experimentally-infected cattle. Mycoplasmal genes were identified by matching the nucleotide sequences of DNA from immunoselected phage particles with the mycoplasmal genome. This allowed a catalogue of genes coding for the proteins that elicited an immune response to be compiled. Using this method together with computer algorithms designed to score parameters that influence surface accessibility and hence potential antigenicity, five genes (abc, gapN, glpO, lppB and ptsG) were chosen to be expressed in Escherichia coli. After appropriate site-directed mutagenesis, polypeptides representing portions of each of these proteins were tested for immunoreactivity. Of these five, polypeptides representing expression products of abc and lppB were recognised on immunoblots by sera obtained from cattle during a natural outbreak of the disease.

Conclusion
Since phage display physically couples phenotype with genotype, it was used to compile a list of sequences that code for Mmm SC proteins bearing epitopes which were recognised by antibodies in the serum of infected animals. Together with the appropriate bioinformatic analyses, this approach provided several potentially useful vaccine or diagnostic leads. The phage display step empirically identified sequences by their interaction with antibodies which accordingly reduced the number of ORFs that had to be expressed for testing. This is a particular advantage when working with Mmm SC since the mycoplasmal codon for tryptophan needs to be mutated to prevent it from being translated as a stop in E. coli.