bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Spaceflight on Ability of Monocytes To Respond to Endotoxins of Gram-Negative Bacteria
Authors: Kaur Indreshpal , Simons Elizabeth R. , Kapadia Asha S. , Ott C. Mark , Pierson Duane L. 
Published: September 2008

ABSTRACT
Astronauts live and work in relatively crowded, confined environments on the Space Shuttle and the International Space Station. They experience a unique set of stressors that contribute to a diminishment of many immune responses. This study investigated the ability of the shuttle crew members' monocytes to respond to gram-negative endotoxin that they could encounter during infections. Blood specimens were collected from 20 crew members and 15 control subjects 10 days before launch, 3 to 4 h after landing, and 15 days after landing and from crew members during their annual medical examination at 6 to 12 months after landing. When challenged with gram-negative endotoxin, the crew member's monocytes collected at all three time points produced lower levels of interleukin-6 (IL-6) and IL-1β and higher levels of IL-1ra and IL-8 compared to those of control subjects. Cytokines were assessed by measuring the number of cells positive for intracellular cytokines. These values returned to normal 6 to 12 months after landing, except for IL-1ra, which was still higher (five- to sixfold) than in controls. This phenomenon was accompanied by an increased expression of Toll-like receptor 4 and decreased expression of CD14 on the crew members' monocytes at all time points. There were also increased levels of the lipopolysaccharide binding protein in the plasma of the crew members 3 to 4 h and 15 days after landing. This study shows that spaceflight-associated factors (in-flight and preflight) modulate the response of monocytes to gram-negative endotoxins.
Evaluation of a Multianalyte Profiling Assay and an Enzyme-Linked Immunosorbent Assay for Serological Examination of Epstein-Barr Virus-Specific Antibody Responses in Diagnosis of Nasopharyngeal Carcinoma
Authors: Gu Ai-Di , Mo Hao-Yuan , Xie Yan-Bo , Peng Rou-Jun , Bei Jin-Xin , Peng Juan , Li Miao-Yan , Chen Li-Zhen , Feng Qi-Sheng , Jia Wei-Hua , Zeng Yi-Xin 
Published: September 2008

ABSTRACT

Assessment of antibody responses to Epstein-Barr virus (EBV) antigens has been used to assist in nasopharyngeal carcinoma (NPC) diagnosis by several methods. In this study, we evaluated an in-house Luminex multianalyte profiling (xMAP) technology and commercial enzyme-linked immunosorbent assay (ELISA) kits for serological examination of EBV-specific antibody responses in 135 NPC patients and 130 healthy controls. Four EBV biomarkers were measured: immunoglobulin A (IgA) against viral capsid antigen (VCA), EBV nuclear antigen 1 (EBNA1), diffused early antigen (EA-D), and IgG against EA-D. The sensitivities and specificities of the four markers ranged between 71.5 and 90% for xMAP assays and 80 and 92% for ELISA. Logistic regression analysis revealed that the combined markers in the xMAP assay had overall sensitivity and specificity values of 82% and 92%, respectively. The correlation coefficient (
r
) values for the xMAP assay and ELISA were lowest for IgA-VCA (0.468) and highest for IgA-EBNA1 (0.846); for IgA-EA-D and IgG-EA-D, the
r
values were 0.719 and 0.798, respectively. The concordances of the two methods for NPC discrimination were good (79 to 88%). Our results suggest that both the xMAP assay and ELISA are satisfactory for EBV antibody evaluation when multiple antigens are included.
Hyperproliferation of B Cells Specific for a Weakly Immunogenic PorA in a Meningococcal Vaccine Model
Authors: Luijkx Thomas A. , van Gaans-van den Brink Jacqueline A. M. , van Dijken Harry H. , van den Dobbelsteen Germie P. J. M. , van Els Cécile A. C. M. 
Published: September 2008

ABSTRACTHighly homologous meningococcal porin A (PorA) proteins induce protective humoral immunity againstNeisseria meningitidisgroup B infection but with large and consistent differences in the levels of serum bactericidal activity achieved. We investigated whether a poor PorA-specific serological outcome is associated with a limited size of the specific B-cell subpopulation involved. The numbers of PorA-specific splenic plasma cells, bone marrow (BM) plasma cells, and splenic memory B cells were compared between mice that received priming and boosting with the weakly immunogenic PorA (P1.7-2,4) protein and those that received priming and boosting with the highly immunogenic PorA (P1.5-1,2-2) protein. Immunoglobulin G (IgG) titers (except at day 42), bactericidal activity, and the avidity of IgG produced against P1.7-2,4 were significantly lower at all time points after priming and boosting than against P1.5-1,2-2. These differences, however, were not associated with a lack of P1.7-2,4-specific plasma cells. Instead, priming with both of the PorAs resulted in the initial expansion of comparable numbers of splenic and BM plasma cells. Moreover, P1.7-2,4-specific BM plasma cells, but not P1.5-1,2-2-specific plasma cells, expanded significantly further after boosting. Likewise, after a relative delay during the priming phase, the splenic P1.7-2,4-specific memory B cells largely outnumbered those specific for P1.5-1,2-2, upon boosting. These trends were observed with different vaccine formulations of the porins. Our results show for the first time that B-cell subpopulations involved in a successfully maturated antibody response against a clinically relevant vaccine antigen are maintained at smaller population sizes than those associated with poor affinity maturation. This bears consequences for the interpretation of immunological memory data in clinical vaccine trials.
Root Canal Microbiota of Teeth with Chronic Apical Periodontitis
Authors: Rôças I. N. , Siqueira J. F. 
Published: September 2008

ABSTRACT

Samples from infected root canals of 43 teeth with chronic apical periodontitis were analyzed for the presence and relative levels of 83 oral bacterial species and/or phylotypes using a reverse-capture checkerboard hybridization assay. Associations between the most frequently detected taxa were also recorded. The most prevalent taxa were
Olsenella uli
(74%),
Eikenella corrodens
(63%),
Porphyromonas endodontalis
(56%),
Peptostreptococcus anaerobius
(54%), and
Bacteroidetes
oral clone X083 (51%). When prevalence was considered only for bacteria present at levels >10
5
,
Bacteroidetes
clone X083 was the most frequently isolated bacterium (37%), followed by
Parvimonas micra
(28%),
E. corrodens
(23%), and
Tannerella forsythia
(19%). The number of target taxa per canal was directly proportional to the size of the apical periodontitis lesion, with lesions >10 mm in diameter harboring a mean number of approximately 20 taxa. Several positive associations for the most prevalent taxa were disclosed for the first time and may have important ecological and pathogenic implications. In addition to strengthening the association of several cultivable named species with chronic apical periodontitis, the present findings using a large-scale analysis allowed the inclusion of some newly named species and as-yet-uncultivated phylotypes in the set of candidate pathogens associated with this disease.
Phenotypic and Genotypic Characterization of Verotoxin-ProducingEscherichia coliO103:H2 Isolates from Cattle and Humans
Authors: Karama Musafiri , Johnson Roger P. , Holtslander Robert , Gyles Carlton L. 
Published: September 2008

ABSTRACTCharacterization of important non-O157 verotoxin-producingEscherichia coli(VTEC) has lagged considerably behind that of O157:H7 strains. This study characterized 91 VTEC O103:H2 strains from bovine and human sources and of North American and European origins by virulence or putative virulence genes, pulsed-field gel electrophoresis (PFGE) patterns, plasmid profiles, antimicrobial resistance, and colicin production. All strains were positive forvt1andeae-ε; 97% were positive forehxA; and all were negative forhlyA. Two strains carriedvt2. There were 66 PFGE patterns grouped in six clusters, and there were 25 different plasmid profiles. Plasmid-encodedkatPandetpgenes were significantly more frequent in European than in North American human strains. The distribution of selected phenotypes was as follows: enterohemorrhagicE. coli(EHEC) hemolysin, 95%; colicin production, 38%; antimicrobial resistance, 58%. All the strains were negative for the alpha-hemolytic phenotype. In conclusion, the VTEC O103:H2 strains were diverse, as shown by PFGE, plasmid profiles, virulence markers, and antimicrobial resistance patterns, and all strains showed an EHEC hemolytic phenotype instead of the alpha-hemolytic phenotype that has been shown previously.
Fatal Outcome of Hepatitis A Virus (HAV) Infection in a Traveler with Incomplete HAV Vaccination and Evidence of Rift Valley Fever Virus Infection
Authors: Oltmann Anke , Kämper Stephanie , Staeck Oliver , Schmidt-Chanasit Jonas , Günther Stephan , Berg Thomas , Frank Christina , Krüger Detlev H. , Hofmann Jörg 
Published: September 2008

ABSTRACT
Hepatitis A virus (HAV) infection is rarely fatal except in patients with chronic liver disease. In the case reported here, an elderly women died of HAV infection 12 years after incomplete HAV vaccination. The possible role of a concordant Rift Valley fever virus infection acquired in Kenya is discussed.
Escherichia hermannii
as the Sole Isolate from a Patient with Purulent Conjunctivitis
Authors: Poulou Aggeliki , Dimitroulia Evangelia , Markou Fani , Tsakris Athanassios 
Published: September 2008

ABSTRACT

Escherichia hermannii
was isolated in pure culture from a patient with acute purulent conjunctivitis after a minor ocular injury. This is the first report of
E. hermannii
isolated as the sole pathogen from an infected site without prior antibiotic exposure, confirming the pathogenic potential of the microorganism.
Lentivirus Vector Can Be Readministered to Nasal Epithelia without Blocking Immune Responses
Authors: Sinn Patrick L. , Arias Ariadna C. , Brogden Kim A. , McCray Paul B. 
Published: September 2008

ABSTRACT
For many envisioned applications of lentivirus vectors as tools in respiratory biology and therapeutic gene delivery, the efficiency of gene transfer must be improved. We previously demonstrated stable, persistent (>11 months) in vivo expression following a single application of a feline immunodeficiency virus (FIV)-based lentivirus vector (GP64-FIV) to murine nasal epithelia. Here we investigate the efficacy of repeated administration of lentivirus vectors to the airways. Using quantitative bioluminescent imaging, we found that consecutive daily dosing achieved a linear increase in gene expression and greatly increased the number of epithelial cells targeted. Surprisingly, reporter gene expression also increased additively following each of seven doses of FIV delivered over consecutive weeks (1 dose/week), without the development of systemic or local neutralizing antibodies. This approach enhanced expression of both reporter and therapeutic transgenes. Transduction efficiency achieved following a single dose of FIV expressing mouse erythropoietin was insufficient to increase hematocrit, whereas seven consecutive daily doses significantly increased hematocrit. These unexpected results contrast strikingly with findings reported for adenovirus vectors. Prolonged gene expression has been observed in vivo following a single dose of virus vector; however, depending on the application, repeated administration of vector may be necessary to achieve stable, therapeutic gene expression.
Hepatitis C Virus Infection Induces Apoptosis through a Bax-Triggered, Mitochondrion-Mediated, Caspase 3-Dependent Pathway
Authors: Deng Lin , Adachi Tetsuya , Kitayama Kikumi , Bungyoku Yasuaki , Kitazawa Sohei , Ishido Satoshi , Shoji Ikuo , Hotta Hak 
Published: September 2008

ABSTRACT

We previously reported that cells harboring the hepatitis C virus (HCV) RNA replicon as well as those expressing HCV NS3/4A exhibited increased sensitivity to suboptimal doses of apoptotic stimuli to undergo mitochondrion-mediated apoptosis (Y. Nomura-Takigawa, et al., J. Gen. Virol. 87:1935-1945, 2006). Little is known, however, about whether or not HCV infection induces apoptosis of the virus-infected cells. In this study, by using the chimeric J6/JFH1 strain of HCV genotype 2a, we demonstrated that HCV infection induced cell death in Huh7.5 cells. The cell death was associated with activation of caspase 3, nuclear translocation of activated caspase 3, and cleavage of DNA repair enzyme poly(ADP-ribose) polymerase, which is known to be an important substrate for activated caspase 3. These results suggest that HCV-induced cell death is, in fact, apoptosis. Moreover, HCV infection activated Bax, a proapoptotic member of the Bcl-2 family, as revealed by its conformational change and its increased accumulation on mitochondrial membranes. Concomitantly, HCV infection induced disruption of mitochondrial transmembrane potential, followed by mitochondrial swelling and release of cytochrome
c
from mitochondria. HCV infection also caused oxidative stress via increased production of mitochondrial superoxide. On the other hand, HCV infection did not mediate increased expression of glucose-regulated protein 78 (GRP78) or GRP94, which are known as endoplasmic reticulum (ER) stress-induced proteins; this result suggests that ER stress is not primarily involved in HCV-induced apoptosis in our experimental system. Taken together, our present results suggest that HCV infection induces apoptosis of the host cell through a Bax-triggered, mitochondrion-mediated, caspase 3-dependent pathway(s).
Duck Hepatitis B Virus Requires Cholesterol for Endosomal Escape during Virus Entry
Authors: Funk Anneke , Mhamdi Mouna , Hohenberg Heinz , Heeren Jörg , Reimer Rudolph , Lambert Carsten , Prange Reinhild , Sirma Hüseyin 
Published: September 2008

ABSTRACT
The identity and functionality of biological membranes are determined by cooperative interaction between their lipid and protein constituents. Cholesterol is an important structural lipid that modulates fluidity of biological membranes favoring the formation of detergent-resistant microdomains. In the present study, we evaluated the functional role of cholesterol and lipid rafts for entry of hepatitis B viruses into hepatocytes. We show that the duck hepatitis B virus (DHBV) attaches predominantly to detergent-soluble domains on the plasma membrane. Cholesterol depletion from host membranes and thus disruption of rafts does not affect DHBV infection. In contrast, depletion of cholesterol from the envelope of both DHBV and human HBV strongly reduces virus infectivity. Cholesterol depletion increases the density of viral particles and leads to changes in the ultrastructural appearance of the virus envelope. However, the dual topology of the viral envelope protein L is not significantly impaired. Infectivity and density of viral particles are partially restored upon cholesterol replenishment. Binding and entry of cholesterol-deficient DHBV into hepatocytes are not significantly impaired, in contrast to their release from endosomes. We therefore conclude that viral but not host cholesterol is required for endosomal escape of DHBV.
Mutations at Alternative 5′ Splice Sites of M1 mRNA Negatively Affect Influenza A Virus Viability and Growth Rate
Authors: Chiang Chiayn , Chen Guang-Wu , Shih Shin-Ru 
Published: September 2008

ABSTRACT
Different amino acid sequences of influenza virus proteins contribute to different viral phenotypes. However, the diversity of the sequences and its impact on noncoding regions or splice sites have not been intensively studied. This study focuses on the sequences at alternative 5′ splice sites on M1 mRNA. Six different mutations at the splice sites were introduced, and viral growth characteristics for those mutants generated by reverse genetics with 12 plasmids were examined, for which G12C (the G-to-C mutation at the first nucleotide of the intron for the mRNA3 5′ splice site), C51G (at the 3′ end of the exon of the M2 mRNA 5′ splice site), and G146C (for the first nucleotide of the intron for mRNA4) are lethal mutations. On the other hand, mutants with the mutation G11C (at the 3′ end of exon of the mRNA3 5′ splice site), G52C (for the first nucleotide of the intron for M2 mRNA), or G145A (at the 3′ end of the exon of mRNA4) were rescued, although they had significantly attenuated growth rates. Notably, these mutations did not change any amino acids in M1 or M2 proteins. The levels of precursor (M1 mRNA) and spliced products (M2 mRNA, mRNA3, and mRNA4) from the recombinant mutant virus-infected cells were further analyzed. The production levels of mRNA3 in cells infected with G11C, G52C, and G145A mutant viruses were reduced in comparison with that in wild-type recombinant virus-infected ones. More M2 mRNA was produced in G11C mutant virus-infected cells than in wild-type-virus-infected cells, and there was little M2 mRNA and none at all in G145A and G52C mutant virus-infected ones, respectively. Results obtained here suggest that introducing these mutations into the alternative 5′ splice sites disturbed M1 mRNA splicing, which may attenuate viral growth rates.
Measles Virus-Induced Block of Transendothelial Migration of T Lymphocytes and Infection-Mediated Virus Spread across Endothelial Cell Barriers
Authors: Dittmar Sandra , Harms Harry , Runkler Nicole , Maisner Andrea , Kim Kwang Sik , Schneider-Schaulies Jürgen 
Published: September 2008

ABSTRACTIn order to analyze whether measles virus (MV) is transported via transmigrating leukocytes across endothelial barriers or whether virus spreads via infection of endothelial cells and basolateral release, we investigated the migratory behavior of infected human primary T lymphocytes across polarized cell layers of human brain microvascular endothelial cells. We found that the capacity of lymphocytes to migrate through filter pores was only slightly affected by wild-type MV infection, whereas their capacity to migrate through endothelial barriers was drastically reduced. MV infection stimulated the expression and activation of the leukocyte integrins LFA-1 and VLA-4, mediating a strong adherence to the surface of endothelial cells. Furthermore, the formation of engulfing membrane protrusions by endothelial cells, so-called transmigratory cups, was induced, but transmigration was impaired. As a consequence of this close cell-cell contact, MV infection was transmitted from lymphocytes to the endothelium. MV envelope proteins were expressed on the apical and basolateral surfaces of infected polarized endothelial cells, and virus was released from both sides. Wild-type MV infection did not induce the formation of syncytia, suggesting virus spread from cell to cell via cell processes and contacts. Our data indicate that transendothelial migration of infected T cells is strongly inhibited, whereas virus can cross endothelial barriers by productive infection of the endothelium and subsequent bipolar virus release.
Transactivation of the Hepatitis B Virus Core Promoter by the Nuclear Receptor FXRα
Authors: Ramière Christophe , Scholtès Caroline , Diaz Olivier , Icard Vinca , Perrin-Cocon Laure , Trabaud Mary-Anne , Lotteau Vincent , André Patrice 
Published: September 2008

ABSTRACT

Hepatitis B virus (HBV) core promoter activity is positively and negatively regulated by nuclear receptors, a superfamily of ligand-activated transcription factors, via
cis
-acting sequences located in the viral genome. In this study, we investigated the role of farnesoid X receptor alpha (FXRα) in modulating transcription from the HBV core promoter. FXRα is a liver-enriched nuclear receptor activated by bile acids recognizing hormone response elements by forming heterodimers with retinoid X receptor alpha (RXRα). Electrophoretic mobility shift assays demonstrated that FXRα-RXRα heterodimers can bind two motifs on the HBV enhancer II and core promoter regions, presenting high homology to the consensus (AGGTCA) inverted repeat FXRα response elements. In transient transfection of the human hepatoma cell line Huh-7, bile acids enhanced the activity of a luciferase reporter containing the HBV enhancer II and core promoter sequences through FXRα. Moreover, using a greater-than-genome-length HBV construct, we showed that FXRα also increased synthesis of the viral pregenomic RNA and DNA replication intermediates. The data strongly suggest that FXRα is another member of the nuclear receptor superfamily implicated in the regulation of HBV core promoter activity and that bile acids could play an important role in the natural history of HBV infection.
Identification of Monomorphic and Divergent Haplotypes in the 2006-2007 Norovirus GII/4 Epidemic Population by Genomewide Tracing of Evolutionary History
Authors: Motomura Kazushi , Oka Tomoichiro , Yokoyama Masaru , Nakamura Hiromi , Mori Hiromi , Ode Hirotaka , Hansman Grant S. , Katayama Kazuhiko , Kanda Tadahito , Tanaka Tomoyuki , Takeda Naokazu , Sato Hironori 
Published: September 2008

ABSTRACTOur norovirus (NoV) surveillance group reported a >4-fold increase in NoV infection in Japan during the winter of 2006-2007 compared to the previous winter. Because the increase was not linked to changes in the surveillance system, we suspected the emergence of new NoV GII/4 epidemic variants. To obtain information on viral changes, we conducted full-length genomic analysis. Stool specimens from 55 acute gastroenteritis patients of various ages were collected at 11 sites in Japan between May 2006 and January 2007. Direct sequencing of long PCR products revealed 37 GII/4 genome sequences. Phylogenetic study of viral genome and partial sequences showed that the two new GII/4 variants in Europe, termed 2006a and 2006b, initially coexisted as minorities in early 2006 in Japan and that 2006b alone had dominated over the resident GII/4 variants during 2006. A combination of phylogenetic and entropy analyses revealed for the first time the unique amino acid substitutions in all eight proteins of the new epidemic strains. These data and computer-assisted structural study of the NoV capsid protein are compatible with a model of antigenic drift with tuning of the structure and functions of multiple proteins for the global outgrowth of new GII/4 variants. The availability of comprehensive information on genome sequences and unique protein changes of the recent global epidemic variants will allow studies of diagnostic assays, molecular epidemiology, molecular biology, and adaptive changes of NoV in nature.