bluuebunny/crossref_metadata_2025_split huggingface dataset:
Symplectomorphism groups and embeddings of balls into rational ruled 4-manifolds
Authors: Pinsonnault Martin 
Published: March 2008

AbstractLet Mμ0 denote S2×S2 endowed with a split symplectic form $\mu \sigma \oplus \sigma $ normalized so that μ≥1 and σ(S2)=1. Given a symplectic embedding $\iota :B_{c}\hookrightarrow M^0_{\mu }$ of the standard ball of capacity c∈(0,1) into Mμ0, consider the corresponding symplectic blow-up $\widetilde {M}^0_{\mu ,c}$. In this paper, we study the homotopy type of the symplectomorphism group ${\mathrm {Symp}}(\widetilde {M}^0_{\mu ,c})$ and that of the space $\Im {\mathrm {Emb}}(B_{c},M^0_{\mu })$ of unparametrized symplectic embeddings of Bc into Mμ0. Writing ℓ for the largest integer strictly smaller than μ, and λ∈(0,1] for the difference μ−ℓ, we show that the symplectomorphism group of a blow-up of ‘small’ capacity c<λ is homotopically equivalent to the stabilizer of a point in Symp(Mμ0), while that of a blow-up of ‘large’ capacity c≥λ is homotopically equivalent to the stabilizer of a point in the symplectomorphism group of a non-trivial bundle $\mathbb {C}P^2\#\,\overline {\mathbb {C}P^2}$ obtained by blowing down $\widetilde {M}^0_{\mu ,c}$. It follows that, for c<λ, the space $\Im {\mathrm {Emb}}(B_{c},M^0_{\mu })$ is homotopy equivalent to S2 ×S2, while, for c≥λ, it is not homotopy equivalent to any finite CW-complex. A similar result holds for symplectic ruled manifolds diffeomorphic to $\mathbb {C}P^2\#\,\overline {\mathbb {C}P^2}$. By contrast, we show that the embedding spaces $\Im {\mathrm {Emb}}(B_{c},\mathbb {C}P^{2})$ and $\Im {\mathrm {Emb}}(B_{c_{1}}\sqcup B_{c_{2}},\mathbb {C}P^{2})$, if non-empty, are always homotopy equivalent to the spaces of ordered configurations $F(\mathbb {C}P^{2},1)\simeq \mathbb {C}P^{2}$ and $F(\mathbb {C}P^{2},2)$. Our method relies on the theory of pseudo-holomorphic curves in 4 -manifolds, on the computation of Gromov invariants in rational 4 -manifolds, and on the inflation technique of Lalonde and McDuff.
Enhanced Protection against Bovine Tuberculosis after Coadministration ofMycobacterium bovisBCG with a Mycobacterial Protein Vaccine-Adjuvant Combination but Not after Coadministration of Adjuvant Alone
Authors: Wedlock D. Neil , Denis Michel , Painter Gavin F. , Ainge Gary D. , Vordermeier H. Martin , Hewinson R. Glyn , Buddle Bryce M. 
Published: March 2008

ABSTRACTCurrent efforts are aimed at optimizing the protective efficacy ofMycobacterium bovisBCG by the use of vaccine combinations. We have recently demonstrated that the protection afforded by BCG alone is enhanced by vaccinating cattle with a combination of vaccines comprising BCG and a protein tuberculosis vaccine, namely, culture filtrate proteins (CFPs) fromM. bovisplus an adjuvant. In the current study, three different adjuvant systems were compared. The CFP was formulated with a depot adjuvant, dimethyldioctadecyl ammonium bromide (DDA), together with one of three different immunostimulants: monophosphoryl lipid A (MPL), a synthetic mycobacterial phosphatidylinositol mannoside-2 (PIM2), and a synthetic lipopeptide (Pam3Cys-SKKKK [Pam3CSK4]). Groups of cattle (n= 10/group) were vaccinated with BCG-CFP-DDA-PIM2, BCG-CFP-DDA-MPL, or BCG-CFP-DDA-Pam3CSK4. Two additional groups (n= 10) were vaccinated with BCG alone or BCG-adjuvant (DDA-MPL), and a control group was left unvaccinated. Protection was assessed by challenging the cattle intratracheally withM. bovis. Groups of cattle vaccinated with BCG-CFP-DDA-PIM2, BCG-CFP-DDA-MPL, BCG-CFP-DDA-Pam3CSK4, and BCG alone showed significant reductions in three, three, five, and three pathological and microbiological disease parameters, respectively, compared to the results for the nonvaccinated group. Vaccination with the combination of BCG and the DDA-MPL adjuvant alone abrogated the protection conferred by BCG alone. The profiling of cytokine gene expression following vaccination, prior to challenge, did not illuminate significant differences which could explain the latter result. Vaccination of cattle with a combination of BCG and protein tuberculosis vaccine enhances protection against tuberculosis.
Specificity of Subcapsular Antibody Responses in Ethiopian Patients following Disease Caused by Serogroup A Meningococci
Authors: Norheim Gunnstein , Aseffa Abraham , Yassin Mohammed Ahmed , Mengistu Getahun , Kassu Afework , Fikremariam Dereje , Tamire Wegene , Merid Yared , Høiby E. Arne , Caugant Dominique A. , Fritzsønn Elisabeth , Tangen Torill , Melak Berhanu , Berhanu Degu , Harboe Morten , Kolberg Jan , Rosenqvist Einar 
Published: March 2008

ABSTRACTDissecting the specificities of human antibody responses following disease caused by serogroup A meningococci may be important for the development of improved vaccines. We performed a study of Ethiopian patients during outbreaks in 2002 and 2003. Sera were obtained from 71 patients with meningitis caused by bacteria of sequence type 7, as confirmed by PCR or culture, and from 113 Ethiopian controls. Antibody specificities were analyzed by immunoblotting (IB) against outer membrane antigen extracts of a reference strain and of the patients' own isolates and by enzyme-linked immunosorbent assay for immunoglobulin G (IgG) levels against lipooligosaccharide (LOS) L11 and the proteins NadA and NspA. IB revealed that the main antigens targeted were the proteins PorA, PorB, RmpM, and Opa/OpcA, as well as LOS. MenA disease induced significant increases in IgG against LOS L11 and NadA. The IgG levels against LOS remained elevated following disease, whereas the IgG anti-NadA levels returned to acute-phase levels in the late convalescent phase. Among adults, the anti-LOS IgG levels were similar in acute-phase patient sera as in control sera, whereas anti-NadA IgG levels were significantly higher in acute-phase sera than in controls. The IgG antibody levels against LOS and NadA correlated moderately but significantly with serum bactericidal activity against MenA strains. Future studies on immune response during MenA disease should take into account the high levels of anti-MenA polysaccharide IgG commonly found in the population and seek to clarify the role of antibodies against subcapsular antigens in protection against MenA disease.
LiveMycobacterium aviumsubsp.paratuberculosisand a Killed-Bacterium Vaccine Induce Distinct Subcutaneous Granulomas, with Unique Cellular and Cytokine Profiles
Authors: Lei Liying , Plattner Brandon L. , Hostetter Jesse M. 
Published: March 2008

ABSTRACTType II (lepromatous) granulomas are characterized by a lack of organization, with large numbers of macrophages heavily burdened with bacilli and disorganized lymphocyte infiltrations. Type II granulomas are a characteristic feature of the enteric lesions that develop during clinicalMycobacterium aviumsubsp.paratuberculosisinfection in the bovine. Considering the poor organization and function of these granulomas, it is our hypothesis that dendritic cell (DC) function within the granuloma is impaired during initial infection. In order to test our hypothesis, we used a subcutaneousM. aviumsubsp.paratuberculosisinfection model to examine early DC function withinM. aviumsubsp.paratuberculosis-induced granulomas. In this model, we first characterized the morphology, cellular composition, and cytokine profiles of subcutaneous granulomas that develop 7 days after subcutaneous inoculation with either vaccine or liveM. aviumsubsp.paratuberculosis. Second, we isolated CD11c+cells from within granulomas and measured their maturation status and ability to induce T-cell responses. Our results demonstrate thatM. aviumsubsp.paratuberculosisor vaccine administration resulted in the formation of distinct granulomas with unique cellular and cytokine profiles. These distinct profiles corresponded to significant differences in the phenotypes and functional responses of DCs from within the granulomas. Specifically, the DCs from theM. aviumsubsp.paratuberculosis-induced granulomas had lower levels of expression of costimulatory and chemokine receptors, suggesting limited maturation. This DC phenotype was associated with weaker induction of T-cell proliferation. Taken together, these findings suggest thatM. aviumsubsp.paratuberculosisinfection in vivo influences DC function, which may shape the developing granuloma and initial local protection.
Evaluation of 16S rRNA Gene-Based PCR Assays for Genus-Level Identification of
Helicobacter
Species
Authors: Moyaert H. , Pasmans F. , Ducatelle R. , Haesebrouck F. , Baele M. 
Published: March 2008

ABSTRACT

The inclusivity, exclusivity, and detection limit of six 16S rRNA gene-based
Helicobacter
genus-specific PCR assays were examined. Five out of six assays were 100% inclusive, but the tests varied considerably in their exclusivity (9.1 to 95.5%). The clinical detection limit varied between 10
3
and 1 viable bacterial cell per reaction mixture.
Comparison of Neo-Sensitabs Tablet Diffusion Assay with CLSI Broth Microdilution M38-A and Disk Diffusion Methods for Testing Susceptibility of Filamentous Fungi with Amphotericin B, Caspofungin, Itraconazole, Posaconazole, and Voriconazole
Authors: Espinel-Ingroff A. , Canton E. 
Published: March 2008

ABSTRACT

We compared the Neo-Sensitabs tablet assay to both reference M38-A broth microdilution and disk diffusion methods for testing the susceptibility of 183 filamentous isolates to amphotericin B, caspofungin, itraconazole, posaconazole, and voriconazole. Neo-Sensitabs and disk assay inhibition zone diameters, in millimeters, were obtained on nonsupplemented Mueller-Hinton agar at 16 to 48 h. The reproducibility of zone diameters (i.e., the percentage of replicate zone diameters that were within 2 standard deviations of the means), their correlation with either MICs or minimum effective concentrations (for caspofungin only), and the categorical agreement were similar between tablet and disk assays (93 to 100% [
R
, >0.70] and 79 to 96%, respectively) with four of the five agents. The exceptions were the results for posaconazole tablets (
R
, 0.686; disk, 0.757; 84% categorical agreement for tablet and 96% for disk). These data suggest the potential value of the Neo-Sensitabs assay for testing 5-μg caspofungin and 1-μg voriconazole posaconazole tablets against all mold isolates, 8-μg itraconazole and 5-μg tablets against all mold isolates except zygomycetes, and 10-μg amphotericin B tablets against zygomycete isolates only.
Novel Wide-Range Quantitative Nested Real-Time PCR Assay for
Mycobacterium tuberculosis
DNA: Clinical Application for Diagnosis of Tuberculous Meningitis
Authors: Takahashi Teruyuki , Tamura Masato , Asami Yukihiro , Kitamura Eiko , Saito Kosuke , Suzuki Tsukasa , Takahashi Sachiko Nonaka , Matsumoto Koichi , Sawada Shigemasa , Yokoyama Eise , Takasu Toshiaki 
Published: March 2008

ABSTRACT

Although the “gold standard” for diagnosis of tuberculous meningitis (TBM) is bacterial isolation of
Mycobacterium tuberculosis
, there are still several complex issues. Recently, we developed an internally controlled novel wide-range quantitative nested real-time PCR (WR-QNRT-PCR) assay for
M. tuberculosis
DNA in order to rapidly diagnose TBM. For use as an internal control calibrator to measure the copy number of
M. tuberculosis
DNA, an original new-mutation plasmid (NM-plasmid) was developed. Due to the development of the NM-plasmid, the WR-QNRT-PCR assay demonstrated statistically significant accuracy over a wide detection range (1 to 10
5
copies). In clinical applications, the WR-QNRT-PCR assay revealed sufficiently high sensitivity (95.8%) and specificity (100%) for 24 clinically suspected TBM patients. In conditional logistic regression analysis, a copy number of
M. tuberculosis
DNA (per 1 ml of cerebrospinal fluid) of >8,000 was an independent risk factor for poor prognosis for TBM (i.e., death) (odds ratio, 16.142; 95% confidence interval, 1.191 to 218.79;
P
value, 0.0365). In addition, the copy numbers demonstrated by analysis of variance statistically significant alterations (
P
< 0.01) during the clinical treatment course for 10 suspected TBM patients. In simple regression analysis, the significant correlation (
R
2
= 0.597;
P
< 0.0001) was demonstrated between copy number and clinical stage of TBM. We consider the WR-QNRT-PCR assay to be a useful and advanced assay technique for assessing the clinical treatment course of TBM.
Role of Nonstructural Protein NS2A in Flavivirus Assembly
Authors: Leung Jason Y. , Pijlman Gorben P. , Kondratieva Natasha , Hyde Jennifer , Mackenzie Jason M. , Khromykh Alexander A. 
Published: March 2008

ABSTRACT
Flavivirus nonstructural (NS) proteins are involved in RNA replication and modulation of the host antiviral response; however, evidence is mounting that some NS proteins also have essential roles in virus assembly. Kunjin virus (KUN) NS2A is a small, hydrophobic, transmembrane protein that is part of the replication complex and inhibits interferon induction. Previously, we have shown that an isoleucine (I)-to-asparagine (N) substitution at position 59 of the NS2A protein blocked the production of secreted virus particles in cells electroporated with viral RNA carrying this mutation. We now show that prolonged incubation of mutant KUN NS2A-I59N replicon RNA, in an inducible BHK-derived packaging cell line (expressing KUN structural proteins C, prM, and E), generated escape mutants that rescued the secretion of infectious virus-like particles. Sequencing identified three groups of revertants that included (i) reversions to wild-type, hydrophobic Ile, (ii) pseudorevertants to more hydrophobic residues (Ser, Thr, and Tyr) at codon 59, and (iii) pseudorevertants retaining Asn at NS2A codon 59 but containing a compensatory mutation (Thr-to-Pro) at NS2A codon 149. Engineering hydrophobic residues at NS2A position 59 or the compensatory T149P mutation into NS2A-I59N replicon RNA restored the assembly of secreted virus-like particles in packaging cells. T149P mutation also rescued virus production when introduced into the full-length KUN RNA containing an NS2A-I59N mutation. Immunofluorescence and electron microscopy analyses of NS2A-I59N replicon-expressing cells showed a distinct lack of virus-induced membranes normally present in cells expressing wild-type replicon RNA. The compensatory mutation NS2A-T149P restored the induction of membrane structures to a level similar to those observed during wild-type replication. The results further confirm the role of NS2A in virus assembly, demonstrate the importance of hydrophobic residues at codon 59 in this process, implicate the involvement of NS2A in the biogenesis of virus-induced membranes, and suggest a vital role for the virus-induced membranes in virus assembly.
Role for the L1-52/55K Protein in the Serotype Specificity of Adenovirus DNA Packaging
Authors: Wohl Beverly P. , Hearing Patrick 
Published: March 2008

ABSTRACT

The packaging of adenovirus (Ad) DNA into virions is dependent upon
cis
-acting sequences and
trans
-acting proteins. We studied the involvement of Ad packaging proteins in the serotype specificity of packaging. Both Ad5 and Ad17 IVa2 and L4-22K proteins complemented the growth of Ad5 IVa2 and L4-22K mutant viruses, respectively. In contrast, the Ad5 L1-52/55K protein complemented an Ad5 L1-52/55K mutant virus, but the Ad17 L1-52/55K protein did not. The analysis of chimeric proteins demonstrated that the N-terminal half of the Ad5 L1-52/55K protein mediated this function. Finally, we demonstrate that the L4-33K and L4-22K proteins have distinct functions during infection.
Systemic and Brain Macrophage Infections in Relation to the Development of Simian Immunodeficiency Virus Encephalitis
Authors: Bissel Stephanie J. , Wang Guoji , Bonneh-Barkay Dafna , Starkey Adam , Trichel Anita M. , Murphey-Corb Michael , Wiley Clayton A. 
Published: March 2008

ABSTRACTThe brains of individuals with lentiviral-associated encephalitis contain an abundance of infected and activated macrophages. It has been hypothesized that encephalitis develops when increased numbers of infected monocytes traffic into the central nervous system (CNS) during the end stages of immunosuppression. The relationships between the infection of brain and systemic macrophages and circulating monocytes and the development of lentiviral encephalitis are unknown. We longitudinally examined the extent of monocyte/macrophage infection in blood and lymph nodes of pigtailed macaques that did or did not develop simian immunodeficiency virus encephalitis (SIVE). Compared to levels in macaques that did not develop SIVE, more ex vivo virus production was detected from monocyte-derived macrophages and nonadherent peripheral blood mononuclear cells (PBMCs) from macaques that did develop SIVE. Prior to death, there was an increase in the number of circulating PBMCs following a rise in cerebrospinal fluid viral load in macaques that did develop SIVE but not in nonencephalitic macaques. At necropsy, macaques with SIVE had more infected macrophages in peripheral organs, with the exception of lymph nodes. T cells and NK cells with cytotoxic potential were more abundant in brains with encephalitis; however, T-cell and NK-cell infiltration in SIVE and human immunodeficiency virus encephalitis was more modest than that observed in classical acute herpes simplex virus encephalitis. These findings support the hypothesis that inherent differences in host systemic and CNS monocyte/macrophage viral production are associated with the development of encephalitis.
Dimerization of the Human Papillomavirus Type 16 E2 N Terminus Results in DNA Looping within the Upstream Regulatory Region
Authors: Hernandez-Ramon Elena E. , Burns Julie E. , Zhang Wenke , Walker Hannah F. , Allen Stephanie , Antson Alfred A. , Maitland Norman J. 
Published: March 2008

ABSTRACT
Papillomavirus E2 proteins play a central role in regulating viral gene expression and replication. DNA-binding activity is associated with the C-terminal domain of E2, which forms a stable dimer, while the N-terminal domain is responsible for E2's replication and transactivation functions. The crystal structure of the latter domain revealed a second dimerization interface on E2 which may be responsible for DNA loop formation in the regulatory region of the human papillomavirus (HPV) genome. We investigated the biological significance of the N-terminal dimerization by introducing single amino acid substitutions into the dimerization interface. As expected, these substitutions did not influence the C-terminal dimerization and DNA-binding functions of E2. However, the mutations led to reduced transactivation of a synthetic E2-responsive reporter gene, while HPV DNA replication was unaffected. The effect of the mutations on DNA looping was visualized by atomic force microscopy. While wild-type E2 was able to generate DNA loops, all three mutant E2 proteins were defective in this ability. Our results suggest that N-terminal dimerization plays a role in E2-mediated transactivation, probably via DNA looping, a common mechanism for remote regulation of gene transcription.
Live Visualization of Herpes Simplex Virus Type 1 Compartment Dynamics
Authors: de Oliveira Anna Paula , Glauser Daniel L. , Laimbacher Andrea S. , Strasser Regina , Schraner Elisabeth M. , Wild Peter , Ziegler Urs , Breakefield Xandra O. , Ackermann Mathias , Fraefel Cornel 
Published: March 2008

ABSTRACT
We have constructed a recombinant herpes simplex virus type 1 (HSV-1) that simultaneously encodes selected structural proteins from all three virion compartments—capsid, tegument, and envelope—fused with autofluorescent proteins. This triple-fluorescent recombinant, rHSV-RYC, was replication competent, albeit with delayed kinetics, incorporated the fusion proteins into all three virion compartments, and was comparable to wild-type HSV-1 at the ultrastructural level. The VP26 capsid fusion protein (monomeric red fluorescent protein [mRFP]-VP26) was first observed throughout the nucleus and later accumulated in viral replication compartments. In the course of infection, mRFP-VP26 formed small foci in the periphery of the replication compartments that expanded and coalesced over time into much larger foci. The envelope glycoprotein H (gH) fusion protein (enhanced yellow fluorescent protein [EYFP]-gH) was first observed accumulating in a vesicular pattern in the cytoplasm and was then incorporated primarily into the nuclear membrane. The VP16 tegument fusion protein (VP16-enhanced cyan fluorescent protein [ECFP]) was first observed in a diffuse nuclear pattern and then accumulated in viral replication compartments. In addition, it also formed small foci in the periphery of the replication compartments which, however, did not colocalize with the small mRFP-VP26 foci. Later, VP16-ECFP was redistributed out of the nucleus into the cytoplasm, where it accumulated in vesicular foci and in perinuclear clusters reminiscent of the Golgi apparatus. Late in infection, mRFP-VP26, EYFP-gH, and VP16-ECFP were found colocalizing in dots at the plasma membrane, possibly representing mature progeny virus. In summary, this study provides new insights into the dynamics of compartmentalization and interaction among capsid, tegument, and envelope proteins. Similar strategies can also be applied to assess other dynamic events in the virus life cycle, such as entry and trafficking.
Transcriptome Analysis of Infection of the Archaeon
Sulfolobus solfataricus
with
Sulfolobus
Turreted Icosahedral Virus
Authors: Ortmann Alice C. , Brumfield Susan K. , Walther Jasper , McInnerney Kathleen , Brouns Stan J. J. , van de Werken Harmen J. G. , Bothner Brian , Douglas Trevor , van de Oost John , Young Mark J. 
Published: March 2008

ABSTRACT

Microarray analysis of infection by
Sulfolobus t
urreted
i
cosahedral
v
irus (STIV) revealed insights into the timing and extent of virus transcription, as well as differential regulation of host genes. Using a microarray containing genes from both the host and the virus, the infection cycle of STIV was studied. Following infection of
Sulfolobus solfataricus
strain 2-2-12 with STIV, transcription of virus genes was first detected at 8 h postinfection (p.i.), with a peak at 24 h p.i. Lysis of cells was first detected at 32 h p.i. There was little temporal control of the transcription of virus genes, although the three open reading frames on the noncoding strand were transcribed later in the infection process. During the infection, 177 host genes were determined to be differentially expressed, with 124 genes up-regulated and 53 genes down-regulated. The up-regulated genes were dominated by genes associated with DNA replication and repair and those of unknown function, while the down-regulated genes, mostly detected at 32 h p.i., were associated with energy production and metabolism. Examination of infected cells by transmission electron microscopy revealed alterations in cell ultrastructure consistent with the microarray analysis. The observed patterns of transcription suggest that up-regulated genes are likely used by the virus to reprogram the cell for virus replication, while the down-regulated genes reflect the imminent lysis of the cells.
Transmission of Simian Immunodeficiency Virus Carrying Multiple Cytotoxic T-Lymphocyte Escape Mutations with Diminished Replicative Ability Can Result in AIDS Progression in Rhesus Macaques
Authors: Seki Sayuri , Kawada Miki , Takeda Akiko , Igarashi Hiroko , Sata Tetsutaro , Matano Tetsuro 
Published: March 2008

ABSTRACT

Cytotoxic T-lymphocyte (CTL) responses frequently select for immunodeficiency virus mutations that result in escape from CTL recognition with viral fitness costs. The replication in vivo of such viruses carrying not single but multiple escape mutations in the absence of the CTL pressure has remained undetermined. Here, we have examined the replication of simian immunodeficiency virus (SIV) with five
gag
mutations selected in a macaque possessing the major histocompatibility complex haplotype
90
-
120
-
Ia
after its transmission into
90
-
120
-
Ia
-negative macaques. Our results showed that even such a “crippled” SIV infection can result in persistent viral replication, multiple reversions, and AIDS progression.