bluuebunny/crossref_metadata_2025_split huggingface dataset:
An Air-Based Cavity-Receiver for Solar Trough Concentrators
Authors: Bader Roman , Barbato Maurizio , Pedretti Andrea , Steinfeld Aldo 
Published: July 2010

Abstract
A cylindrical cavity-receiver containing a tubular absorber that uses air as the heat transfer fluid is proposed for a novel solar trough concentrator design. A numerical heat transfer model is developed to determine the receiver’s absorption efficiency and pumping power requirement. The 2D steady-state energy conservation equation coupling radiation, convection, and conduction heat transfer is formulated and solved numerically by finite volume techniques. The Monte Carlo ray-tracing and radiosity methods are applied to establish the solar radiation distribution and radiative exchange within the receiver. Simulations were conducted for a 50 m-long and 9.5 m-wide collector section with 120°C air inlet temperature, and air mass flows in the range 0.1–1.2 kg/s. Outlet air temperatures ranged from 260°C to 601°C, and corresponding absorption efficiencies varied between 60% and 18%. Main heat losses integrated over the receiver length were due to reflection and spillage at the receiver’s windowed aperture, amounting to 13% and 9% of the solar power input, respectively. The pressure drop along the 50 m module was in the range 0.23–11.84 mbars, resulting in isentropic pumping power requirements of 6.45×10−4−0.395% of the solar power input.
Evaluation of Extracellular Subviral Particles of Dengue Virus Type 2 and Japanese Encephalitis Virus Produced bySpodoptera frugiperdaCells for Use as Vaccine and Diagnostic Antigens
Authors: Kuwahara Miwa , Konishi Eiji 
Published: July 2010

ABSTRACTNew or improved vaccines against dengue virus types 1 to 4 (DENV1 to DENV4) and Japanese encephalitis virus (JEV), the causative agents of dengue fever and Japanese encephalitis (JE), respectively, are urgently required. The use of noninfectious subviral extracellular particles (EPs) is an inexpensive and safe strategy for the production of protein-based flavivirus vaccines. Although coexpression of premembrane (prM) and envelope (E) proteins has been demonstrated to produce EPs in mammalian cells, low yields have hindered their commercial application. Therefore, we used an insect cell expression system withSpodoptera frugiperda-derived Sf9 cells to investigate high-level production of DENV2 and JEV EPs. Sf9 cells transfected with theprMandEgenes of DENV2 or JEV secreted corresponding viral antigens in a particulate form that were biochemically and biophysically equivalent to the authentic antigens obtained from infected C6/36 mosquito cells. Additionally, equivalent neutralizing antibody titers were induced in mice immunized either with EPs produced by transfected Sf9 cells or with EPs produced by transfected mammalian cells, in the context of coimmunization with a DNA vaccine that expresses EPs. Furthermore, the results of an enzyme-linked immunosorbent assay (ELISA) using an EP antigen derived from Sf9 cells correlated significantly with the results obtained by a neutralization test and an ELISA using an EP antigen derived from mammalian cells. Finally, Sf9 cells could produce 10- to 100-fold larger amounts of E antigen than mammalian cells. These results indicate the potential of Sf9 cells for high-level production of flavivirus protein vaccines and diagnostic antigens.
Virulence Genes and Genotypic Associations in Nasal Carriage, Community-Associated Methicillin-Susceptible and Methicillin-Resistant USA400
Staphylococcus aureus
Isolates
Authors: Shukla Sanjay K. , Karow Mary E. , Brady Jennifer M. , Stemper Mary E. , Kislow Jennifer , Moore Natalie , Wroblewski Katherine , Chyou Po-Huang , Warshauer David M. , Reed Kurt D. , Lynfield Ruth , Schwan William R. 
Published: July 2010

ABSTRACT

It is not well understood why strains of community-associated methicillin-resistant
Staphylococcus aureus
(CA-MRSA), a major cause of skin and soft tissue infections, became successful so quickly, overtaking the place of methicillin-sensitive
S. aureus
(MSSA) in many communities. To evaluate the genetic basis of differences in their virulence traits, 293
S. aureus
isolates consisting of three cohorts, genotypically defined clinical CA-MRSA (
n
= 77), clinical MSSA (
n
= 103), and nasal carriage MSSA (
n
= 113), collected over a 19-year period in two Midwestern states in the United States, were (i) extensively genotyped and (ii) screened for 40 known virulence genes which included those for enterotoxins, leukocidins, hemolysins, and surface proteins and several newly identified putative toxin genes from the USA400 lineage of CA-MRSA. Genotypically, nasal carriage and clinical MSSA isolates were much more diverse than was the CA-MRSA group, which was found to be of USA400 lineage only. Virulence gene profiles of the three groups showed that CA-MRSA strains harbored significantly higher percentages (≥95%;
P
value, <0.05) of the
sea
,
sec
,
sec4
,
seg2
,
seh
,
sek
,
sel
,
sel2
,
ear
,
ssl1
,
lpl10
,
lukSF-PV
,
lukD
,
lukE
, and
clfA
genes than did the carriage and the clinical MSSA group (range, 0% to 58%). Genes of the enterotoxin gene cluster,
seg
,
sei
,
sem
,
sen
, and
seo
, were present in the clinical and carriage isolates but not in the CA-MRSA group. These results suggest that the presence of additional virulence factors in USA400 CA-MRSA strains compared to the nasal carriage and clinical MSSA strains probably contributed to their enhanced virulence.
Membrane Uncoating of Intact Enveloped Viruses
Authors: Haywood Anne M. 
Published: July 2010

ABSTRACT
Experiments in the 1960s showed that Sendai virus, a paramyxovirus, fused its membrane with the host plasma membrane. After membrane fusion, the virus spontaneously “uncoated” with diffusion of the viral membrane proteins into the host plasma membrane and a merging of the host and viral membranes. This led to deposit of the viral ribonucleoprotein (RNP) and interior proteins in the cell cytoplasm. Later work showed that the common procedure then used to grow Sendai virus produced damaged, pleomorphic virions. Virions, which were grown under conditions that were not damaging, made a connecting structure between virus and cell at the region where the fusion occurred. The virus did not release its membrane proteins into the host membrane. The viral RNP was seen in the connecting structure in some cases. Uncoating of intact Sendai virus proceeds differently from uncoating described by the current standard model developed long ago with damaged virus. A model of intact paramyxovirus uncoating is presented and compared to what is known about the uncoating of other viruses.
Cellular MicroRNAs 200b and 429 Regulate the Epstein-Barr Virus Switch between Latency and Lytic Replication
Authors: Ellis-Connell Amy L. , Iempridee Tawin , Xu Iris , Mertz Janet E. 
Published: July 2010

ABSTRACT

We previously showed that the cellular proteins ZEB1 and ZEB2/SIP1 both play key roles in regulating the latent-lytic switch of Epstein-Barr Virus (EBV) by repressing
BZLF1
gene expression. We investigated here the effects of cellular microRNA (miRNA) 200 (miR200) family members on the EBV infection status of cells. We show that miR200b and miR429, but not miR200a, can induce EBV-positive cells into lytic replication by downregulating expression of ZEB1 and ZEB2, leading to production of infectious virus. The levels of miR200 family members in EBV-infected cells strongly negatively correlated with the levels of the ZEBs (e.g., −0.89 [
P
< 0.001] for miR429 versus ZEB1) and positively correlated with the degree of EBV lytic gene expression (e.g., 0.73 [
P
< 0.01] for miR429 versus BZLF1). The addition of either miR200b or miR429 to EBV-positive cells led to EBV lytic reactivation in a ZEB-dependent manner; inhibition of these miRNAs led to decreased EBV lytic gene expression. The degree of latent infection by an EBV mutant defective in the primary ZEB-binding site of the EBV BZLF1 promoter was not affected by the addition of these miRNAs. Furthermore, EBV infection of primary blood B cells led to downregulation of these miRNAs and upregulation of ZEB levels. Thus, we conclude that miRNAs 200b and 429 are key regulators via their effects on expression of ZEB1 and ZEB2 of the switch between latent and lytic infection by EBV and, therefore, potential targets for development of new lytic induction therapeutics with which to treat patients with EBV-associated malignancies.
Characterization of the Envelope Glycoproteins Associated with Infectious Hepatitis C Virus
Authors: Vieyres Gabrielle , Thomas Xavier , Descamps Véronique , Duverlie Gilles , Patel Arvind H. , Dubuisson Jean 
Published: July 2010

ABSTRACTHepatitis C is caused by an enveloped virus whose entry is mediated by two glycoproteins, namely, E1 and E2, which have been shown to assemble as a noncovalent heterodimer. Despite extensive research in the field of such an important human pathogen, hepatitis C virus (HCV) glycoproteins have only been studied so far in heterologous expression systems, and their organization at the surfaces of infectious virions has not yet been described. Here, we characterized the envelope glycoproteins associated with cell-cultured infectious virions and compared them with their prebudding counterparts. Viral particles were analyzed by ultracentrifugation, and the envelope glycoproteins were characterized by coimmunoprecipitation and receptor pulldown assays. Furthermore, their oligomeric state was determined by sedimentation through sucrose gradients and by separation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) under nonreducing conditions. In sucrose gradient analyses, HCV envelope glycoproteins were associated with fractions containing the most infectious viral particles. Importantly, besides maturation of some of their glycans, HCV envelope glycoproteins showed a dramatic change in their oligomeric state after incorporation into the viral particle. Indeed, virion-associated E1 and E2 envelope glycoproteins formed large covalent complexes stabilized by disulfide bridges, whereas the intracellular forms of these proteins assembled as noncovalent heterodimers. Furthermore, the virion-associated glycoprotein complexes were recognized by the large extracellular loop of CD81 as well as conformation-sensitive antibodies, indicating that these proteins are in a functional conformation. Overall, our study fills a gap in the description of HCV outer morphology and should guide further investigations into virus entry and assembly.
Oncogenic Wip1 Phosphatase Is Inhibited by miR-16 in the DNA Damage Signaling Pathway
Authors: Zhang Xinna , Wan Guohui , Mlotshwa Sizolwenkosi , Vance Vicki , Berger Franklin G. , Chen Hexin , Lu Xiongbin 
Published: July 2010

Abstract
Wild-type p53-induced phosphatase 1 (Wip1) was identified as an oncogene amplified and overexpressed in several human cancers. Recent evidence suggested that Wip1 is a critical inhibitor in the ATM/ATR-p53 DNA damage signaling pathway. Wip1 dephosphorylates several key DNA damage–responsive proteins and reverses DNA damage–induced cell cycle checkpoints. Previous reports showed that Wip1 was transcriptionally induced by p53 at the early stage of the DNA damage response. To investigate the temporal and functional regulation of Wip1, we identified a microRNA, miR-16, that specifically targets the mRNA of Wip1 and thus negatively regulates the expression level of Wip1. miR-16 itself is induced immediately after DNA damage. Therefore, the increase in Wip1 protein level is significantly postponed compared with that of its mRNA level, preventing a premature inactivation of ATM/ATR signaling and allowing a functional completion of the early DNA damage response. To better understand miR-16 biological functions in the context of cancer cells, we examined its expression in mammary tumor stem cells and found it to be markedly downregulated in mammary tumor stem cells. Overexpression of miR-16 or inhibition of Wip1 suppresses the self-renewal and growth of mouse mammary tumor stem cells and sensitizes MCF-7 human breast cancer cells to the chemotherapeutic drug doxorubicin. Together, our results suggest an important role of miR-16 in the regulation of Wip1 phosphatase in the DNA damage response and mammary tumorigenesis. Cancer Res; 70(18); 7176–86. ©2010 AACR.
Fechner's Aesthetics Revisited
Authors: Norman J. Farley , Beers Amanda , Phillips Flip 
Published: July 2010

AbstractGustav Fechner is widely respected as a founding father of experimental psychology and psychophysics but fewer know of his interests and work in empirical aesthetics. In the later 1800s, toward the end of his career, Fechner performed experiments to empirically evaluate the beauty of rectangles, hypothesizing that the preferred shape would closely match that of the so-called 'golden rectangle'. His findings confirmed his suspicions, but in the intervening decades there has been significant evidence pointing away from that finding. Regardless of the results of this one study, Fechner ushered in the notion of using a metric to evaluate beauty in a psychophysical way. In this paper, we recreate the experiment using more naturalistic stimuli. We evaluate subjects' preferences against models that use various types of object complexity as metrics. Our findings that subjects prefer either very simple or very complex objects runs contrary to the hypothesized results, but are systematic none the less. We conclude that there are likely to be useful measures of aesthetic preference but they are likely to be complicated by the difficulty in defining some of their constituent parts.
Peer Telephone Counseling for Adults With Type 2 Diabetes Mellitus
Authors: Plotnikoff Ronald C. , Johnson Steven T. , Luchak Mila , Pollock Cathy , Holt Nicholas L. , Leahy Annabel , Liebreich Tanis , Sigal Ronald J. , Boulé Normand G. 
Published: July 2010

Purpose The purpose of this case study was to determine the feasibility of peer-led telephone counseling for people with type 2 diabetes mellitus related to physical activity (PA) and to establish preliminary efficacy of peer-led telephone counseling for eliciting recommended changes in PA-related cognitions and behaviors for adults with type 2 diabetes mellitus. Methods A total of 8 adults (5 males and 3 females, aged 59.5 (6.5) years) with type 2 diabetes mellitus completed quantitative self-report measures of aerobic-based PA, resistance training (RT), along with metrics from social cognitive theory (SCT) before and after a 12-week intervention. Qualitative data from weekly peer-led telephone sessions were collected by a peer counselor and subsequently organized into themes and analyzed using a mixed-methods, collective case-study approach. Results PA behaviors remained relatively constant over the 12-week intervention. Self-efficacy for RT improved ( z = -2.03; P = .04). From the peer counselor’s perspective, identifiable inhibitors to PA, which included low self-efficacy and disease condition limitations, were successfully translated into enablers/motivators. Perceived health benefits were frequently reported by the peer counselor as motivators for the participants over the study period. Participants believed peer counseling by telephone influenced their decision to continue to participate in PA. Conclusion Theory-based, peer-led telephone counseling shows some promise for increasing receptiveness to PA, but had little effect on improving behavior for most participants. Further studies will be necessary to determine the effectiveness and the sustainability of this approach.
Bevacizumab-associated hyperlipoproteinemia type IIb in a patient with advanced invasive-ductal breast cancer
Authors: Joerger M , Riesen WF , Thürlimann B 
Published: July 2010

Aim: We report a case of bevacizumab-associated hyperlipoproteinemia in a patient with advanced breast cancer. Case summary: A 57-year-old woman with advanced invasive-ductal breast cancer was administered bevacizumab from March 2008 to February 2009. Pretreatment laboratory showed borderline hypercholesterolemia (5.1 mmol/L, 197 mg/dL) and normal triglycerides (1.3 mmol/L, 115 mg/dL). Three months on treatment with bevacizumab, both serum cholesterol (11.9 mmol/L, 460 mg/dL) and triglycerides (7.4 mmol/L, 655 mg/dL) increased substantially, and remained well above the normal range for a period of bevacizumab treatment. From March 2008 to August 2008, the patient also received anticancer treatment with liposomal doxorubicin that was stopped early due to hand-foot syndrome. No concurrent hyperlipidemic drugs have been taken by the patient at the time of bevacizumab treatment. In February 2009, bevacizumab was stopped and the patient went on to receive paclitaxel for hepatic tumor progression. By December 2009, both serum triglycerides (1.3 mmol/L, 115 mg/dL) and cholesterol (3.2 mmol/L, 123 mg/dL) had normalized. Discussion: This is the first published case of bevacizumab-associated hyperlipoproteinemia. By applying the Naranjo ADR probability scales, at least a possible relationship between hyperlipoproteinemia type IIb and bevacizumab in this patient is supported by the data (Naranjo score 4). No hyperlipidemic drugs were given concurrently with bevacizumab, and the serum cholesterol and triglycerides decreased quickly after bevacizumab was discontinued. Conclusions: This study describes a case of bevacizumab-associated hyperlipidemia. Patients receiving bevacizumab should have their cholesterol and triglycerides checked for potential worsening.
ATP secreted by endothelial cells blocks CX3CL1-elicited natural killer cell chemotaxis and cytotoxicity via P2Y11 receptor activation
Authors: Gorini Stefania , Callegari Giulia , Romagnoli Giulia , Mammi Caterina , Mavilio Domenico , Rosano Giuseppe , Fini Massimo , Di Virgilio Francesco , Gulinelli Sara , Falzoni Simonetta , Cavani Andrea , Ferrari Davide , la Sala Andrea 
Published: July 2010

AbstractEndothelial cells (ECs) represent a major source of actively secreted adenosine triphosphate (ATP). Natural killer (NK) cells can mediate vascular injury in several pathologic conditions, including cytomegalovirus infection and vascular leak syndrome. We studied NK-cell expression of P2 receptors and the role of these nucleotide receptors in the regulation of endothelial-NK cell cross-talk. NK cells from healthy subjects expressed P2Y1,2,4,6,11,12,13,14 and P2X1,4,5,6,7 receptors. NK cells stimulated with ATP, but not uridine triphosphate, increased intracellular Ca2+ and chemokinesis. Moreover, ATP, but not uridine triphosphate, inhibited NK chemotaxis in response to CX3CL1, whereas chemotaxis to CXCL12 was increased. CX3CL1 elicited killing of human umbilical vein ECs and human coronary artery ECs by NK cells. However, in the presence of ATP, CX3CL1 failed to stimulate killing of ECs. Such inhibitory effect was lost on exogenous addition of the ATP-hydrolyzing enzyme apyrase or by pharmacologic inhibition of the P2Y11R, and correlated with increased intracellular cyclic adenosine monophosphate concentrations induced by ATP or other P2Y11R agonists, including NAD+. Extracellular ATP regulates NK-cell cytotoxicity via P2Y11R activation, protecting ECs from CX3CL1-elicited NK cell–mediated killing. These findings point out the P2Y11R as a potential target for pharmacologic intervention aimed at reducing NK-mediated vascular injury.
The LKB1/AMPK signaling pathway has tumor suppressor activity in acute myeloid leukemia through the repression of mTOR-dependent oncogenic mRNA translation
Authors: Green Alexa S. , Chapuis Nicolas , Trovati Maciel Thiago , Willems Lise , Lambert Mireille , Arnoult Christophe , Boyer Olivier , Bardet Valerie , Park Sophie , Foretz Marc , Viollet Benoit , Ifrah Norbert , Dreyfus François , Hermine Olivier , Cruz Moura Ivan , Lacombe Catherine , Mayeux Patrick , Bouscary Didier , Tamburini Jerome 
Published: July 2010

AbstractFinding an effective treatment for acute myeloid leukemia (AML) remains a challenge, and all cellular processes that are deregulated in AML cells should be considered in the design of targeted therapies. We show in our current study that the LKB1/AMPK/TSC tumor suppressor axis is functional in AML and can be activated by the biguanide molecule metformin, resulting in a specific inhibition of mammalian target of rapamycin (mTOR) catalytic activity. This induces a multisite dephosphorylation of the key translation regulator, 4E-BP1, which markedly inhibits the initiation step of mRNA translation. Consequently, metformin reduces the recruitment of mRNA molecules encoding oncogenic proteins to the polysomes, resulting in a strong antileukemic activity against primary AML cells while sparing normal hematopoiesis ex vivo and significantly reducing the growth of AML cells in nude mice. The induction of the LKB1/AMPK tumor-suppressor pathway thus represents a promising new strategy for AML therapy.
Overexpression of hTERT increases stem-like properties and decreases spontaneous differentiation in human mesenchymal stem cell lines
Authors: Tsai Chih-Chien , Chen Chun-Li , Liu Hwa-Chung , Lee Yi-Ting , Wang Hsei-Wei , Hou Lein-Tuan , Hung Shih-Chieh 
Published: July 2010

Abstract
To overcome loss of stem-like properties and spontaneous differentiation those hinder the expansion and application of human mesenchymal stem cells (hMSCs), we have clonally isolated permanent and stable human MSC lines by ectopic overexpression of primary cell cultures of hMSCs with HPV 16 E6E7 and human telomerase reverse transcriptase (hTERT) genes. These cells were found to have a differentiation potential far beyond the ordinary hMSCs. They expressed trophoectoderm and germline specific markers upon differentiation with BMP4 and retinoic acid, respectively. Furthermore, they displayed higher osteogenic and neural differentiation efficiency than primary hMSCs or hMSCs expressed HPV16 E6E7 alone with a decrease in methylation level as proven by a global CpG island methylation profile analysis. Notably, the demethylated CpG islands were highly associated with development and differentiation associated genes. Principal component analysis further pointed out the expression profile of the cells converged toward embryonic stem cells. These data demonstrate these cells not only are a useful tool for the studies of cell differentiation both for the mesenchymal and neurogenic lineages, but also provide a valuable source of cells for cell therapy studies in animal models of skeletal and neurological disorders.