bluuebunny/crossref_metadata_2025_split huggingface dataset:
New Enzyme-Linked Immunosorbent Assay for Detection of Antibodies against Hepatitis Delta Virus Using a Hepatitis Delta Antigen Derived from a Taiwanese Clone and Comparison to the Abbott Radioimmunoassay
Authors: Kuo Yung-Bin , Chao Mei , Lee Yi-Hsuan , Yeh Chau-Ting , Chan Err-Cheng 
Published: March 2012

ABSTRACTAn anti-hepatitis delta (HD) enzyme-linked immunosorbent assay (ELISA) using a specific recombinant hepatitis delta antigen derived from a local dominant hepatitis delta virus (hepatitis D virus; HDV) strain in Taiwan has been established. The detection efficiency of this assay was comparable to that of the commercially available Abbott anti-HD radioimmunoassay (RIA) and could be useful in routine laboratory diagnoses of HDV infection.
Molecular Fingerprinting of Mycobacterium abscessus Strains in a Cohort of Pediatric Cystic Fibrosis Patients
Authors: Harris Kathryn A. , Kenna Dervla T. D. , Blauwendraat Cornelis , Hartley John C. , Turton Jane F. , Aurora Paul , Dixon Garth L. J. 
Published: March 2012

ABSTRACT

Forty-one
Mycobacterium abscessus
complex isolates from 17 pediatric cystic fibrosis (CF) patients were typed using a novel variable-number tandem repeat (VNTR) scheme and an automated repetitive-PCR (rep-PCR) system. Both VNTR and rep-PCR typing methods differentiate between members of the
M. abscessus
complex. The isolates from individual patients are indistinguishable, and the data strongly suggest that individual CF patients are persistently infected with one strain and also suggests that different CF patients can harbor the same strain.
A New and Frequent Human T-Cell Leukemia Virus Indeterminate Western Blot Pattern: Epidemiological Determinants and PCR Results in Central African Inhabitants
Authors: Filippone Claudia , Bassot Sylviane , Betsem Edouard , Tortevoye Patricia , Guillotte Micheline , Mercereau-Puijalon Odile , Plancoulaine Sabine , Calattini Sara , Gessain Antoine 
Published: March 2012

ABSTRACT
Human T-cell leukemia virus (HTLV) indeterminate Western blot (WB) serological patterns are frequently observed in plasma/serum from persons living in intertropical areas. In the framework of ongoing projects on HTLV-1/2 and related viruses in Central Africa, we systematically analyzed plasma from villagers living in South Cameroon by WB. The group included 1,968 individuals (mean age, 44 years; age range, 5 to 90 years; 978 women/990 men), both Bantus (1,165) and Pygmies (803). Plasma samples were tested by WB analysis (MPD HTLV Blot 2.4) and interpreted according to the manufacturer's instructions. Only clear bands were considered in the analysis. Among the 1,968 plasma samples, 38 (1.93%) were HTLV-1, 13 (0.66%) were HTLV-2, and 6 (0.3%) were HTLV WB seropositive. Furthermore, 1,292 (65.65%) samples were WB sero-indeterminate, including 104 (5.28%) with an HTLV-1 Gag-indeterminate pattern (HGIP) and 68 (3.45%) with a peculiar yet unreported pattern exhibiting mostly a strong shifted GD21 and a p28. The other 619 (31.45%) samples were either WB negative or exhibited other patterns, mostly with unique p19 or p24 bands. DNA, extracted from peripheral blood buffy coat, was subjected to PCR using several primer pairs known to detect HTLV-1/2/3/4. Most DNAs from HTLV-1- and HTLV-seropositive individuals were PCR positive. In contrast, all the others, from persons with HTLV-2, HGIP, new WB, and other indeterminate patterns, were PCR negative. Epidemiological determinant analysis of the persons with this new peculiar WB pattern revealed that seroprevalence was independent from age, sex, or ethnicity, thus resembling the indeterminate profile HGIP rather than HTLV-1. Moreover, this new pattern persists over time.
Adaptation of a Genotype 3 Hepatitis E Virus to Efficient Growth in Cell Culture Depends on an Inserted Human Gene Segment Acquired by Recombination
Authors: Shukla P. , Nguyen H. T. , Faulk K. , Mather K. , Torian U. , Engle R. E. , Emerson S. U. 
Published: March 2012

ABSTRACT
An infectious cDNA clone of a genotype 3 strain of hepatitis E virus adapted to growth in HepG2/C3A human hepatoma cells was constructed. This virus was unusual in that the hypervariable region of the adapted virus contained a 171-nucleotide insertion that encoded 58 amino acids of human S17 ribosomal protein. Analyses of virus from six serial passages indicated that genomes with this insert, although initially rare, were selected during the first passage, suggesting it conferred a significant growth advantage. RNA transcripts from this cDNA and the viruses encoded by them were infectious for cells of both human and swine origin, the major host species for this zoonotic virus. Mutagenesis studies demonstrated that the S17 insert was a major factor in cell culture adaptation. Introduction of 54 synonymous mutations into the insert had no detectable effect, thus implicating protein, rather than RNA, as the important component. Truncation of the insert by 50% decreased the levels of successful transfection by ∼3-fold. Substitution of the S17 sequence by a different ribosomal protein sequence or by GTPase-activating protein sequence resulted in a partial enhancement of transfection levels, whereas substitution with 58 amino acids of green fluorescent protein had no effect. Therefore, both the sequence length and the amino acid composition of the insert were important. The S17 sequence did not affect transfection of human hepatoma cells when inserted into the hypervariable region of a genotype 1 strain, but this chimeric genome acquired a dramatic ability to replicate in hamster cells.
Attenuated Influenza Virus Construct with Enhanced Hemagglutinin Protein Expression
Authors: Maamary Jad , Pica Natalie , Belicha-Villanueva Alan , Chou Yi-ying , Krammer Florian , Gao Qinshan , García-Sastre Adolfo , Palese Peter 
Published: March 2012

ABSTRACT
Influenza A viruses encoding an altered viral NS1 protein have emerged as promising live attenuated vaccine platforms. A carboxy-terminal truncation in the NS1 protein compromises its interferon antagonism activity, making these viruses attenuated in the host yet still able to induce protection from challenge with wild-type viruses. However, specific viral protein expression by NS1-truncated viruses is known to be decreased in infected cells. In this report, we show that recombinant H5N1 and H1N1 influenza viruses encoding a truncated NS1 protein expressed lower levels of hemagglutinin (HA) protein in infected cells than did wild-type viruses. This reduction in HA protein expression correlated with a reduction in HA mRNA levels in infected cells. NS1 truncation affected the expression of HA protein but not that of the nucleoprotein (NP). This segment specificity was mapped to the terminal sequences of their specific viral RNAs. Since the HA protein is the major immunogenic component in influenza virus vaccines, we sought to restore its expression levels in NS1-truncated viruses in order to improve their vaccine efficacy. For this purpose, we generated an NS1-truncated recombinant influenza A/Puerto Rico/8/34 (rPR8) virus carrying the G3A C8U “superpromoter” mutations in the HA genomic RNA segment. This strategy retained the attenuation properties of the recombinant virus but enhanced the expression level of HA protein in infected cells. Finally, mice immunized with rPR8 viruses encoding a truncated NS1 protein and carrying the G3A C8U mutations in the HA segment demonstrated enhanced protection from wild-type virus challenge over that for mice vaccinated with an rPR8 virus encoding the truncated NS1 protein alone.
Shelterin Dysfunction and p16
INK4a
-Mediated Growth Inhibition in HIV-1-Specific CD8 T Cells
Authors: Lichterfeld Mathias , Cung Thai , Seiss Katherine , Rosenberg Eric S. , Pereyra Florencia , Yu Xu G. 
Published: March 2012

ABSTRACT

HIV-1-specific cytotoxic T cell responses are expanded during advanced HIV-1 infection but seem unable to effectively protect the host against disease progression. These cells are able to produce gamma interferon and remain metabolically active but have defective proliferative activities, shortened telomeric DNA, and other signs of accelerated aging. To investigate the molecular mechanisms underlying the premature senescence of HIV-1-specific T cells, we focused here on the expression and function of a group of six nucleoproteins that are responsible for protecting and maintaining the structural integrity of telomeric DNA and are commonly referred to as “shelterin.” We show that in progressive HIV-1 infection, the two major shelterin components TRF2 and TPP1 are selectively reduced in HIV-1-specific CD8 T cells, but not in T cells recognizing alternative viral species. This coincided with increased recruitment of 53BP1, a prominent DNA damage response factor, to telomeric DNA sites and was associated with elevated expression of the tumor suppressor p16
INK4a
, which causes cellular growth inhibition in response to structural DNA damage. Notably, defective shelterin function and upregulation of p16
INK4a
remained unaffected by experimental blockade of PD-1, indicating a possibly irreversible structural defect in HIV-1-specific CD8 T cells in progressors that cannot be overcome by manipulation of inhibitory cell-signaling pathways. These data suggest that shelterin dysfunction and ensuing upregulation of the tumor suppressor p16
INK4a
promote accelerated aging of HIV-1-specific T cells during progressive HIV-1 infection.
Vaccinia Virus A6 Is Essential for Virion Membrane Biogenesis and Localization of Virion Membrane Proteins to Sites of Virion Assembly
Authors: Meng Xiangzhi , Embry Addie , Rose Lloyd , Yan Bo , Xu Chungui , Xiang Yan 
Published: March 2012

ABSTRACT

Poxvirus acquires its primary envelope through a process that is distinct from those of other enveloped viruses. The molecular mechanism of this process is poorly understood, but several poxvirus proteins essential for the process have been identified in studies of vaccinia virus (VACV), the prototypical poxvirus. Previously, we identified VACV A6 as an essential factor for virion morphogenesis by studying a temperature-sensitive mutant with a lesion in A6. Here, we further studied A6 by constructing and characterizing an inducible virus (iA6) that could more stringently repress A6 expression. When A6 expression was induced by the inducer isopropyl-β-
d
-thiogalactoside (IPTG), iA6 replicated normally, and membrane proteins of mature virions (MVs) predominantly localized in viral factories where virions were assembled. However, when A6 expression was repressed, electron microscopy of infected cells showed the accumulation of large viroplasm inclusions containing virion core proteins but no viral membranes. Immunofluorescence and cell fractionation studies showed that the major MV membrane proteins A13, A14, D8, and H3 did not localize to viral factories but instead accumulated in the secretory compartments, including the endoplasmic reticulum. Overall, our results show that A6 is an additional VACV protein that participates in an early step of virion membrane biogenesis. Furthermore, A6 is required for MV membrane protein localization to sites of virion assembly, suggesting that MV membrane proteins or precursors of MV membranes are trafficked to sites of virion assembly through an active, virus-mediated process that requires A6.
TNPO3 Is Required for HIV-1 Replication after Nuclear Import but prior to Integration and Binds the HIV-1 Core
Authors: Valle-Casuso Jose Carlos , Di Nunzio Francesca , Yang Yang , Reszka Natalia , Lienlaf Maritza , Arhel Nathalie , Perez Patricio , Brass Abraham L. , Diaz-Griffero Felipe 
Published: March 2012

ABSTRACT
TNPO3 is a nuclear importer required for HIV-1 infection. Here, we show that depletion of TNPO3 leads to an HIV-1 block after nuclear import but prior to integration. To investigate the mechanistic requirement of TNPO3 in HIV-1 infection, we tested the binding of TNPO3 to the HIV-1 core and found that TNPO3 binds to the HIV-1 core. Overall, this work suggests that TNPO3 interacts with the incoming HIV-1 core in the cytoplasm to assist a process that is important for HIV-1 infection after nuclear import.
Structure of the Fab-Labeled “Breathing” State of Native Poliovirus
Authors: Lin Jun , Lee Lily Y. , Roivainen Merja , Filman David J. , Hogle James M. , Belnap David M. 
Published: March 2012

ABSTRACT
At 37°C, the structure of poliovirus is dynamic, and internal polypeptides VP4 and N terminus of VP1 (residues 1 to 53) externalize reversibly. An Fab fragment of a monospecific antibody, which binds to residues 39 to 55 of VP1, was utilized to locate the N termini of VP1 in native (160S) particles in this “breathing” state. Fab and virus were mixed and imaged via cryogenic electron microscopy. The resulting reconstruction showed the capsid expands similarly to the irreversibly altered cell entry intermediate (135S) particle, but the N terminus of VP1 is located near the 2-fold axes, instead of the “propeller tip” as in 135S particles.
Mouse Prion Protein (PrP) Segment 100 to 104 Regulates Conversion of PrP
C
to PrP
Sc
in Prion-Infected Neuroblastoma Cells
Authors: Hara Hideyuki , Okemoto-Nakamura Yuko , Shinkai-Ouchi Fumiko , Hanada Kentaro , Yamakawa Yoshio , Hagiwara Ken'ichi 
Published: March 2012

ABSTRACT

Prion diseases are characterized by the replicative propagation of disease-associated forms of prion protein (PrP
Sc
; PrP refers to prion protein). The propagation is believed to proceed via two steps; the initial binding of the normal form of PrP (PrP
C
) to PrP
Sc
and the subsequent conversion of PrP
C
to PrP
Sc
. We have explored the two-step model in prion-infected mouse neuroblastoma (ScN2a) cells by focusing on the mouse PrP (MoPrP) segment 92-GGTHNQWNKPSKPKTN-107, which is within a region previously suggested to be part of the binding interface or shown to differ in its accessibility to anti-PrP antibodies between PrP
C
and PrP
Sc
. Exchanging the MoPrP segment with the corresponding chicken PrP segment (106-GGSYHNQKPWKPPKTN-121) revealed the necessity of MoPrP residues 99 to 104 for the chimeras to achieve the PrP
Sc
state, while segment 95 to 98 was replaceable with the chicken sequence. An alanine substitution at position 100, 102, 103, or 104 of MoPrP gave rise to nonconvertible mutants that associated with MoPrP
Sc
and interfered with the conversion of endogenous MoPrP
C
. The interference was not evoked by a chimera (designated MCM2) in which MoPrP segment 95 to 104 was changed to the chicken sequence, though MCM2 associated with MoPrP
Sc
. Incubation of the cells with a synthetic peptide composed of MoPrP residues 93 to 107 or alanine-substituted cognates did not inhibit the conversion, whereas an anti-P8 antibody recognizing the above sequence in PrP
C
reduced the accumulation of PrP
Sc
after 10 days of incubation of the cells. These results suggest the segment 100 to 104 of MoPrP
C
plays a key role in conversion after binding to MoPrP
Sc
.
Bacteriophages ϕMR299-2 and ϕNH-4 Can Eliminate Pseudomonas aeruginosa in the Murine Lung and on Cystic Fibrosis Lung Airway Cells
Authors: Alemayehu Debebe , Casey Pat G. , McAuliffe Olivia , Guinane Caitriona M. , Martin James G. , Shanahan Fergus , Coffey Aidan , Ross R. Paul , Hill Colin 
Published: March 2012

ABSTRACT

Pseudomonas aeruginosa
is a common cause of infection in the lungs of patients with cystic fibrosis (CF). In addition, biofilm formation and antibiotic resistance of
Pseudomonas
are major problems that can complicate antibiotic therapy. We evaluated the efficacy of using bacteriophages to kill the pathogen in both biofilms and in the murine lung. We isolated and characterized two phages from a local wastewater treatment plant, a myovirus (ϕNH-4) and a podovirus (ϕMR299-2). Both phages were active against clinical isolates of
P. aeruginosa
. Together, the two phages killed all 9 clinical isolate strains tested, including both mucoid and nonmucoid strains. An equal mixture of the two phages was effective in killing
P. aeruginosa
NH57388A (mucoid) and
P. aeruginosa
MR299 (nonmucoid) strains when growing as a biofilm on a cystic fibrosis bronchial epithelial CFBE41o- cell line. Phage titers increased almost 100-fold over a 24-h period, confirming replication of the phage. Furthermore, the phage mix was also effective in killing the pathogen in murine lungs containing 1 × 10
7
to 2 × 10
7
P. aeruginosa
.
Pseudomonas
was effectively cleared (reduced by a magnitude of at least 3 to 4 log units) from murine lungs in 6 h. Our study demonstrates the efficacy of these two phages in killing clinical
Pseudomonas
isolates in the murine lung or as a biofilm on a pulmonary cell line and supports the growing interest in using phage therapy for the control and treatment of multidrug-resistant
Pseudomonas
lung infections in CF patients.

IMPORTANCE
Given the rise in antibiotic resistance, nonantibiotic therapies are required for the treatment of infection. This is particularly true for the treatment of
Pseudomonas
infection in patients with cystic fibrosis. We have identified two bacterial viruses (bacteriophages) that can kill
Pseudomonas
growing on human lung cells and in an animal model of lung infection. The use of bacteriophages is particularly appropriate because the killing agent can replicate on the target cell, generating fresh copies of the bacteriophage. Thus, in the presence of a target, the killing agent multiplies. By using two bacteriophages we can reduce the risk of resistant colonies developing at the site of infection. Bacteriophage therapy is an exciting field, and this study represents an important demonstration of efficacy in validated infection models.
Decreased length of stay after addition of healthcare provider in emergency department triage: a comparison between computer-simulated and real-world interventions
Authors: Day Theodore Eugene , Al-Roubaie Abdul Rahim , Goldlust Eric Jonathan 
Published: March 2012

Objective(1) To determine the effects of adding a provider in triage on average length of stay (LOS) and proportion of patients with >6 h LOS. (2) To assess the accuracy of computer simulation in predicting the magnitude of such effects on these metrics.MethodsA group-level quasi-experimental trial comparing the St. Louis Veterans Affairs Medical Center emergency department (1) before intervention, (2) after institution of provider in triage, and discrete event simulation (DES) models of similar (3) ‘before’ and (4) ‘after’ conditions. The outcome measures were daily mean LOS and percentage of patients with LOS >6 h.ResultsThe DES-modelled intervention predicted a decrease in the %6-hour LOS from 19.0% to 13.1%, and a drop in the daily mean LOS from 249 to 200 min (p<0.0001). Following (actual) intervention, the number of patients with LOS >6 h decreased from 19.9% to 14.3% (p<0.0001), with the daily mean LOS decreasing from 247 to 210 min (p<0.0001).ConclusionPhysician and mid-level provider coverage at triage significantly reduced emergency department LOS in this setting. DES accurately predicted the magnitude of this effect. These results suggest further work in the generalisability of triage providers and in the utility of DES for predicting quantitative effects of process changes.
Analysis of genetic diversity inElytrigia repensgermplasm using intersimple sequence repeat (ISSR) markers
Authors: Meng Lin , Zhang Xiaoyan , Mao Peichun , Tian Xiaoxia 
Published: March 2012

The genetic diversity among 30 accessions of Elytrigia repens (L.) Nevski was analyzed using 100 intersimple sequence repeat (ISSR) primers, 12 of which generated distinct amplification products. Out of the 132 repeatable bands detected, 100 bands were polymorphic. The percentage of polymorphic bands was 70.66%, with a mean of 8.33 percentage of polymorphic bands per primer. The ISSR-based genetic similarity coefficients among the 30 accessions ranged from 0.509 to 0.873, revealing high genetic diversity. The 30 E. repens accessions were divided into eight groups based on an unweighted pair-group method with arithmetic mean cluster analysis and a principal components analysis. We found that genetic distance is correlated with geographical distance among the 30 E. repens accessions studied (r = 0.812, p < 0.05) using Mantel’s test. Our results confirm the potential value of genetic diversity preservation for future breeding programs.
CLASSIFICATION AND PATHOLOGICAL REALIZATIONS OF TRANSCONDUCTANCE AMPLIFIERS
Authors: SOLIMAN AHMED M. 
Published: March 2012

Classification of transconductance amplifiers (TA) based on the number of input ports and output ports is given. A systematic generation method of TA based on using nullator, norator elements, and pathological mirror elements is used to provide pathological realizations of different types of TA. Four pathological realizations of the single input balanced output TA each using two grounded G are given. Four pathological realizations of the differential input single output TA each using two grounded G are given. Six pathological realizations of the differential input balanced output TA known as BOTA are given. Three pathological realizations for each of the two types of the differential input double output TA are also given. Finally, four alternative ideally equivalent realizations of the BOTA using two current conveyors (CCII) or two inverting current conveyors (ICCII) are generated from the pathological realizations.
HAUSDORFF MEASURE OF CARTESIAN PRODUCT OF THE TERNARY CANTOR SET
Authors: DENG JUAN , RAO HUI , WEN ZHI-YING 
Published: March 2012

Computing the Hausdorff measure of C × C, where C is the classical ternary Cantor set, is a long standing difficult problem. It is well-known that for a self-similar set, calculating the Hausdorff measure is equivalent to determining its optimal sets. This paper studies optimal sets of C × C: their diameters, measures, symmetries and the shapes. For this purpose, we introduce several devices: the repulsive principle, a bipartite graph G and a W-function. We show that the diameter of the optimal set B is between 1.2993 and 1.3082. Two symmetry properties of B are proved. Finally, we show that the shape of B is very close to a disk. We conjecture that an optimal set might be a disk.
Vanilloid Receptor-1 Regulates Neurogenic Inflammation in Colon and Protects Mice from Colon Cancer
Authors: Vinuesa Amaya G. , Sancho Rocío , García-Limones Carmen , Behrens Axel , ten Dijke Peter , Calzado Marco A. , Muñoz Eduardo 
Published: March 2012

Abstract
Neuroinflammation driven by the vanilloid-type ion channel receptor transient receptor potential vanilloid type 1 (TRPV-1) is suspected to play a role in the pathophysiology of inflammatory bowel disease. Because inflammatory bowel disease is known to elevate the risk of colon cancer, we examined postulated roles for TRPV-1–driven neuroinflammation in promoting colitis-associated and spontaneous colon cancer development. Using a well-established model of colitis-associated cancer (CAC), we found that mice genetically deficient in TRPV-1 showed a higher incidence and number of tumors in the distal colon. In like manner, genetic deficiency of TRPV-1 in the APCMin/+ model of spontaneous colon cancer accentuated the number of colonic adenomas formed. Mechanistic analyses in the CAC model revealed an increased infiltration of inflammatory cells into the tumors along with elevated expression of interleukin (IL)-6 and IL-11 and activation of the STAT3 and NF-κB signaling pathways. Notably, TPRV-1–deficient mice exhibited a defect in expression of the anti-inflammatory neuropeptides, vasoactive intestinal peptide (VIP), and pituitary adenylate cyclase–activating peptide (PACAP) which contributed to the generation of a local proinflammatory environment. Together, our findings argue that by limiting neuroinflammatory processes, TRPV-1 exerts a protective role that restricts the initiation and progression of colon cancer. Cancer Res; 72(7); 1705–16. ©2012 AACR.