bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oral Immunization with Recombinant Mycobacterium smegmatis Expressing the Outer Membrane Protein 26-Kilodalton Antigen Confers Prophylactic Protection against Helicobacter pylori Infection
Authors: Lü Lin , Zeng Han-qing , Wang Pi-long , Shen Wei , Xiang Ting-xiu , Mei Zhe-chuan 
Published: September 2011

ABSTRACT

Helicobacter pylori
infection is prevalent worldwide and results in chronic gastritis, which may lead to gastric mucosa-associated lymphoid tissue lymphoma and gastric cancer. We have previously reported that oral immunization with recombinant
Mycobacterium smegmatis
expressing the
H. pylori
outer membrane protein 26-kilodalton (Omp26) antigen affords therapeutic protection against
H. pylori
infection in mice. In the present study, we investigated the prophylactic effects of this vaccine candidate on
H. pylori
challenge in mice. We found that oral immunization with recombinant
Mycobacterium
Omp26 significantly reduced
H. pylori
colonization in the stomach compared to inoculation with wild-type
M. smegmatis
in control mice. Six of the recombinant
Mycobacterium
-immunized mice (60%) were completely protected from
H. pylori
infection. The severity of
H. pylori
-associated chronic gastritis assessed histologically was significantly milder in mice vaccinated with recombinant
Mycobacterium
than in control animals. Mice immunized with recombinant
Mycobacterium
showed enhanced antigen-specific lymphocyte proliferation and antibody responses. Moreover, immunization with recombinant
Mycobacterium
resulted in an increased expression of interleukin-2 and gamma interferon in the stomach and spleen, as determined by reverse transcription-PCR analysis. Our results collectively suggest that vaccination with recombinant
Mycobacterium
Omp26 confers prophylactic protection against
H. pylori
infection. The inhibition of
H. pylori
colonization is associated with the induction of antigen-specific humoral and cell-mediated immune responses.
Role of Interleukin-23 (IL-23) Receptor Signaling for IL-17 Responses in Human Lyme Disease
Authors: Oosting Marije , ter Hofstede Hadewych , van de Veerdonk Frank L. , Sturm Patrick , Kullberg Bart-Jan , van der Meer Jos W. M. , Netea Mihai G. , Joosten Leo A. B. 
Published: September 2011

ABSTRACTInterleukin-23 (IL-23) is known to play a crucial role in the development and maintenance of T helper 17 cells. It has been previously demonstrated that IL-17 is involved in experimental Lyme arthritis, caused byBorrelia burgdorferibacteria. However, the precise role of the IL-23 receptor (IL-23R) for theB. burgdorferi-induced IL-17 responses or human Lyme disease has not yet been elucidated. IL-23R single nucleotide polymorphism (SNP) rs11209026 was genotyped using the TaqMan assay. Functional studies were performed using peripheral blood mononuclear cells, and cytokines were measured using enzyme-linked immunosorbent assay (ELISA). Dose-dependent production of IL-23 and IL-17 byB. burgdorfericould be observed. Interestingly, when IL-23 bioactivity was inhibited by a specific antibody against IL-23p19, IL-17 production was significantly downregulated. In contrast, production of gamma interferon (IFN-γ) was not affected after the blockade of IL-23 activity. Moreover, individuals bearing a single nucleotide polymorphism in the IL-23R gene (Arg381Gln) produced significantly less IL-17 afterB. burgdorferistimulation compared with that of the individuals bearing the wild type. Despite lower IL-17 production, the IL-23R gene polymorphism did not influence the development of chronic Lyme disease in a cohort of patients with Lyme disease. This study demonstrates that IL-23R signaling is needed forB. burgdorferi-induced IL-17 productionin vitroand that an IL-23R gene SNP leads to impaired IL-17 production. However, the IL-23R gene polymorphism is not crucial for the pathogenesis of chronic Lyme.
New Technologies in Clinical Microbiology
Authors: Wolk Donna M. , Dunne W. Michael 
Published: September 2011

ABSTRACT
Rapid identification of microorganisms in the clinical microbiology laboratory can be of great value for selection of optimal patient management strategies for infections caused by bacteria, viruses, fungi, mycobacteria, and parasites. Rapid identification of microorganisms in clinical samples enables expedient de-escalation from broad-spectrum agents to targeted antimicrobial therapy. The switch to tailored therapy minimizes risks of antibiotics, namely, disruption of normal flora, toxic side effects, and selective pressure. There is a critical need for new technologies in clinical microbiology, particularly for bloodstream infections, in which associated mortality is among the highest of all infections. Just as importantly, there is a need for the clinical laboratory community to embrace the practices of evidence-based interventional laboratory medicine and collaborate in translational research projects to establish the clinical utility, cost benefit, and impact of new technologies.
Molecular Typing and Virulence Analysis of Serotype K1 Klebsiella pneumoniae Strains Isolated from Liver Abscess Patients and Stool Samples from Noninfectious Subjects in Hong Kong, Singapore, and Taiwan
Authors: Siu L. Kristopher , Fung Chang-Phone , Chang Feng-Yee , Lee Nelson , Yeh Kuo-Ming , Koh Tse Hsien , Ip Margaret 
Published: September 2011

ABSTRACT

Serotype K1
Klebsiella pneumoniae
with multilocus sequence type 23 (ST23) has been strongly associated with liver abscess in Taiwan. Few data regarding the strain types and virulence of this serotype from other Asian countries are available. Serotype K1
K. pneumoniae
strains isolated from liver abscess and stool samples from subjects hospitalized in Hong Kong, Singapore, and Taiwan hospitals were examined. Forty-seven serotype K1 isolates were identified: 26 from liver abscess samples and 21 from stool samples. MLST revealed 7 sequence types: 85.1% (40 of 47 isolates) belonged to ST23, 1 isolate belonged to ST163 (a single-locus variant of ST23), and 2 isolates were ST249 (a 3-locus variant of ST23). New STs, namely, ST367, ST425, and ST426, were allocated to 3 of 4 isolates from stool samples. The virulence of these strains was determined by neutrophil phagocytosis and mouse infection models. Except for two ST23 isolates, all
Klebsiella pneumoniae
isolates were resistant to phagocytosis. Resistance to serum killing varied in isolates of ST23, while all non-ST23 strains were susceptible to serum killing except one with ST249 from a liver abscess. All hypervirulent isolates with a 50% lethal dose of <10
2
CFU were from ST23, were resistant to phagocytosis and serum killing, and also carried both virulence-associated genes,
rmpA
and aerobactin. Multilocus sequence typing genotype 23 was the most prevalent sequence type among serotype K1
K. pneumoniae
isolates from both liver abscess and stool samples in the Asia Pacific region. Serotype K1
K. pneumoniae
isolates with capsule expression leading to phagocytic resistance and with the aerobactin gene were associated with hypervirulence.
Histone H3 Interacts and Colocalizes with the Nuclear Shuttle Protein and the Movement Protein of a Geminivirus
Authors: Zhou Yanchen , Rojas Maria R. , Park Mi-Ri , Seo Young-Su , Lucas William J. , Gilbertson Robert L. 
Published: September 2011

ABSTRACT

Geminiviruses are plant-infecting viruses with small circular single-stranded DNA genomes. These viruses utilize nuclear shuttle proteins (NSPs) and movement proteins (MPs) for trafficking of infectious DNA through the nuclear pore complex and plasmodesmata, respectively. Here, a biochemical approach was used to identify host factors interacting with the NSP and MP of the geminivirus
Bean dwarf mosaic virus
(BDMV). Based on these studies, we identified and characterized a host nucleoprotein, histone H3, which interacts with both the NSP and MP. The specific nature of the interaction of histone H3 with these viral proteins was established by gel overlay and
in vitro
and
in vivo
coimmunoprecipitation (co-IP) assays. The NSP and MP interaction domains were mapped to the N-terminal region of histone H3. These experiments also revealed a direct interaction between the BDMV NSP and MP, as well as interactions between histone H3 and the capsid proteins of various geminiviruses. Transient-expression assays revealed the colocalization of histone H3 and NSP in the nucleus and nucleolus and of histone H3 and MP in the cell periphery and plasmodesmata. Finally, using
in vivo
co-IP assays with a Myc-tagged histone H3, a complex composed of histone H3, NSP, MP, and viral DNA was recovered. Taken together, these findings implicate the host factor histone H3 in the process by which an infectious geminiviral DNA complex forms within the nucleus for export to the cell periphery and cell-to-cell movement through plasmodesmata.
Crystal Structure of Swine Major Histocompatibility Complex Class I SLA-1*0401 and Identification of 2009 Pandemic Swine-Origin Influenza A H1N1 Virus Cytotoxic T Lymphocyte Epitope Peptides
Authors: Zhang Nianzhi , Qi Jianxun , Feng Sijia , Gao Feng , Liu Jun , Pan Xiaocheng , Chen Rong , Li Qirun , Chen Zhaosan , Li Xiaoying , Xia Chun , Gao George F. 
Published: September 2011

ABSTRACTThe presentation of viral epitopes to cytotoxic T lymphocytes (CTLs) by swine leukocyte antigen class I (SLA I) is crucial for swine immunity. To illustrate the structural basis of swine CTL epitope presentation, the first SLA crystal structures, SLA-1*0401, complexed with peptides derived from either 2009 pandemic H1N1 (pH1N1) swine-origin influenza A virus (S-OIVNW9; NSDTVGWSW) or Ebola virus (EbolaAY9; ATAAATEAY) were determined in this study. The overall peptide–SLA-1*0401 structures resemble, as expected, the general conformations of other structure-solved peptide major histocompatibility complexes (pMHC). The major distinction of SLA-1*0401 is that Arg156has a “one-ballot veto” function in peptide binding, due to its flexible side chain. S-OIVNW9and EbolaAY9bind SLA-1*0401 with similar conformations but employ different water molecules to stabilize their binding. The side chain of P7 residues in both peptides is exposed, indicating that the epitopes are “featured” peptides presented by this SLA. Further analyses showed that SLA-1*0401 and human leukocyte antigen (HLA) class I HLA-A*0101 can present the same peptides, but in different conformations, demonstrating cross-species epitope presentation. CTL epitope peptides derived from 2009 pandemic S-OIV were screened and evaluated by thein vitrorefolding method. Three peptides were identified as potential cross-species influenza virus (IV) CTL epitopes. The binding motif of SLA-1*0401 was proposed, and thermostabilities of key peptide–SLA-1*0401 complexes were analyzed by circular dichroism spectra. Our results not only provide the structural basis of peptide presentation by SLA I but also identify some IV CTL epitope peptides. These results will benefit both vaccine development and swine organ-based xenotransplantation.
Detection and Characterization of a Distinct Bornavirus Lineage from Healthy Canada Geese (Branta canadensis)
Authors: Payne Susan , Covaleda Lina , Jianhua Guo , Swafford Seth , Baroch John , Ferro Pamela J. , Lupiani Blanca , Heatley Jill , Tizard Ian 
Published: September 2011

ABSTRACT

Avian bornaviruses (ABV), identified in 2008, infect captive parrots and macaws worldwide. The natural reservoirs of these viruses are unknown. Reverse transcription-PCR (RT-PCR) was used to screen oropharyngeal/cloacal swab and brain samples from wild Canada geese (
Branta canadensis
) for ABV. Approximately 2.9% of swab samples were positive for bornavirus sequences. Fifty-two percent of brain samples from 2 urban flocks also tested positive, and brain isolates were cultured in duck embryo fibroblasts. Phylogenetic analyses placed goose isolates in an independent cluster, and more notably, important regulatory sequences present in Borna disease virus but lacking in psittacine ABVs were present in goose isolates.
2009 Pandemic H1N1 Influenza Virus Causes Disease and Upregulation of Genes Related to Inflammatory and Immune Responses, Cell Death, and Lipid Metabolism in Pigs
Authors: Ma Wenjun , Belisle Sarah E. , Mosier Derek , Li Xi , Stigger-Rosser Evelyn , Liu Qinfang , Qiao Chuanling , Elder Jake , Webby Richard , Katze Michael G. , Richt Juergen A. 
Published: September 2011

ABSTRACT
There exists limited information about whether adaptation is needed for cross-species transmission of the 2009 pandemic H1N1 influenza virus (pH1N1). Here, we compare the pathogenesis of two pH1N1 viruses, one derived from a human patient (A/CA/04/09 [CA09]) and the other from swine (A/swine/Alberta/25/2009 [Alb09]), with that of the 1918-like classical swine influenza virus (A/swine/Iowa/1930 [IA30]) in the pig model. Both pH1N1 isolates induced clinical symptoms such as coughing, sneezing, decreased activity, fever, and labored breathing in challenged pigs, but IA30 virus did not cause any clinical symptoms except fever. Although both the pH1N1 viruses and the IA30 virus caused lung lesions, the pH1N1 viruses were shed from the nasal cavities of challenged pigs whereas the IA30 virus was not. Global gene expression analysis indicated that transcriptional responses of the viruses were distinct. pH1N1-infected pigs had an upregulation of genes related to inflammatory and immune responses at day 3 postinfection that was not seen in the IA30 infection, and expression levels of genes related to cell death and lipid metabolism at day 5 postinfection were markedly different from those of IA30 infection. These results indicate that both pH1N1 isolates are more virulent due in part to differences in the host transcriptional response during acute infection. Our study also indicates that pH1N1 does not need prior adaptation to infect pigs, has a high potential to be maintained in naïve swine populations, and might reassort with currently circulating swine influenza viruses.
Intragenic and Extragenic Suppression of a Mutation in Herpes Simplex Virus 1 UL34 That Affects both Nuclear Envelope Targeting and Membrane Budding
Authors: Roller Richard J. , Haugo Alison C. , Kopping Nora J. 
Published: September 2011

ABSTRACT
Late in infection herpesviruses move DNA-filled capsids from the nucleus to the cytoplasm by enveloping DNA-containing capsids at the inner nuclear membrane (INM) and deenveloping them at the outer nuclear membrane. This process requires two conserved herpesvirus proteins, pUL31 and pUL34. Interaction between pUL34 and pUL31 is essential for targeting both proteins to the nuclear envelope (NE), and sequences that mediate the targeting interaction have been mapped in both proteins. Here, we show that a mutation in the INM-targeting domain of pUL34 fails to support production of infectious virus or plaque formation. The mutation results in multiple defects, including impaired interaction between pUL34 and pUL31, poor NE targeting of pUL34, and misregulated, capsid-independent budding of the NE. The mutant defects in virus production, plaque formation, and pUL31 interaction can be suppressed by other mutations in the INM-targeting domain of pUL31 and by additional mutations in the pUL34 coding sequence.
Citalopram for major depressive disorder in adults: a systematic review and meta-analysis of published placebo-controlled trials
Authors: Apler Alex 
Published: September 2011

ObjectiveTo assess the effectiveness of citalopram for major depressive disorder (MDD) in adults, in a systematic review of all published, randomised, double-blind studies comparing it with a placebo.Data sourcesCochrane Central Register of Controlled Trials, Medline, PsychINFO and Embase.Study selectionRandomised, double-blind, placebo-controlled studies of citalopram in adults with MDD were included. Studies with medically ill or treatment resistant subjects were excluded, as were studies of relapse prevention. Remission of MDD was defined as a primary outcome, and response or change from baseline scores were defined as secondary.Data extractionRemission, response and symptom improvement scores on the Hamilton Depression Scale, Montgomery–Asberg Depression Rating Scale and Clinical Global Impressions-Severity scales were extracted. A random-effects meta-analysis was carried out on the response rates and symptom improvement scores. Included studies were examined for the presence of bias and small study effects.ResultsEight studies (n=2025) met the inclusion criteria. Two studies provided data on remission, but only one of these showed a significant difference between citalopram and placebo (RR=1.59, 95% CI 1.10 to 2.31). Meta-analysis of response rates in five studies (n=1010) revealed significant superiority of citalopram (RR=1.42, 95% CI 1.17 to 1.73). Meta-analysis of change from baseline scores in five studies (n=1541) gave a standardised mean difference (Hedges' g) of −0.27 (95% CI −0.38 to to −0.16), showing a reduction in MDD symptoms to be significant for citalopram relative to placebo. There was no evidence of any significant small study effects. The overall quality of reporting was poor, with insufficient information on the methodology or outcomes. Seven studies received industry sponsorship.ConclusionsData concerning remission rates for citalopram, relative to placebo, are inconclusive. Response rates and symptom reduction scores in citalopram-treated patients with MDD are significantly better relative to placebo treatment, according to a meta-analysis of published reports. Evaluation of unpublished data is necessary to assess more definitively the effectiveness of citalopram for MDD.
Assessment of proliferation markers in metastatic melanoma in sentinel lymph nodes
Authors: Joannou-Coetzee André , Villena Noranette , Powell Barry W E M , Cook Martin G 
Published: September 2011

AimSome views on sentinel nodes for melanoma seem to cast doubt on the relevance of micrometastases in the sentinel nodes of patients with melanoma, suggesting that small metastases or isolated tumour cells can be ignored. Tumour dormancy has been proposed for their postulated lack of progression. The implication of the argument seems to be that minute metastases are inactive and therefore non-threatening, whereas larger ones are proliferative and therefore have aggressive potential.Methods54 sentinel lymph nodes were studied with histologically identified micrometastatic melanoma using the protocol accepted by the European Organisation for Research and Treatment of Cancer melanoma group. These were studied with respect to metastasis size and by use of immunohistochemical markers of proliferation (MIB-1) and dormancy (p16).ResultsThe authors have demonstrated no correlation between the size of metastases and their proliferative activity. Very small metastases may not show proliferative activity, but this may be a reflection of the small number of assessable cells rather than a genuine reflection of the tumoural characteristics. Furthermore, the minute size of some of these metastases resulted in no residual tumour being present in adjacent sections. Where further sections did show more tumour, these small metastases were invariably p16 negative, suggesting dormancy was not the explanation for the lack of measurable proliferation. Occasionally, larger metastases, clearly not clinically insignificant, showed no proliferative activity presumably, considering their size, a transient phenomenon.ConclusionThese findings suggest that variable phases in proliferation occur in metastases, and no conclusion of clinical insignificance can be made on the basis of small size.
Pseudoinvasion of benign squamous epithelium following cervical biopsy: a pseudoneoplastic phenomenon mimicking invasive squamous carcinoma
Authors: Boyle David P , McCluggage W Glenn 
Published: September 2011

AimsTo describe an unusual and hitherto unreported pseudoneoplastic phenomenon that is characterised by the entrapment of benign squamous epithelium following cervical loop excision or punch biopsy and that may mimic invasive squamous carcinoma.Methods and ResultsThe authors report six cases in patients aged 25–45 years in whom benign squamous epithelium is incorporated within the cervical stroma as a result of the healing process following prior loop excision (four cases) or punch biopsy (two cases). The entrapped nests of squamous epithelium typically have a hypereosinophilic appearance and are associated with a granulation tissue-like and inflammatory stromal response and sometimes with retraction artefact mimicking lymphovascular permeation.ConclusionsThe overall morphological appearances, especially in the context of a prior or current diagnosis of cervical intraepithelial neoplasia, may result in misdiagnosis as invasive squamous carcinoma. Pathologists should be aware of this pseudoneoplastic artefact so that an erroneous diagnosis of malignancy is not made.
Human Cytomegalovirus US28 Found in Glioblastoma Promotes an Invasive and Angiogenic Phenotype
Authors: Soroceanu Liliana , Matlaf Lisa , Bezrookove Vladimir , Harkins Loui , Martinez Roxanne , Greene Mary , Soteropoulos Patricia , Cobbs Charles S. 
Published: September 2011

Abstract
Human cytomegalovirus (HCMV) infections are seen often in glioblastoma multiforme (GBM) tumors, but whether the virus contributes to GBM pathogenesis is unclear. In this study, we explored an oncogenic role for the G-protein–coupled receptor-like protein US28 encoded by HCMV that we found to be expressed widely in human GBMs. Immunohistochemical and reverse transcriptase PCR approaches established that US28 was expressed in approximately 60% of human GBM tissues and primary cultures examined. In either uninfected GBM cells or neural progenitor cells, thought to be the GBM precursor cells, HCMV infection or US28 overexpression was sufficient to promote secretion of biologically active VEGF and to activate multiple cellular kinases that promote glioma growth and invasion, including phosphorylated STAT3 (p-STAT3) and endothelial nitric oxide synthase (e-NOS). Consistent with these findings, US28 overexpression increased primary GBM cell invasion in Matrigel. Notably, this invasive phenotype was further enhanced by exposure to CCL5/RANTES, a US28 ligand, associated with poor patient outcome in GBM. Conversely, RNA interference–mediated knockdown of US28 in human glioma cells persistently infected with HCMV led to an inhibition in VEGF expression and glioma cell invasion in response to CCL5 stimulation. Analysis of clinical GBM specimens further revealed that US28 colocalized in situ with several markers of angiogenesis and inflammation, including VEGF, p-STAT3, COX2, and e-NOS. Taken together, our results indicate that US28 expression from HCMV contributes to GBM pathogenesis by inducing an invasive, angiogenic phenotype. In addition, these findings argue that US28–CCL5 paracrine signaling may contribute to glioma progression and suggest that targeting US28 may provide therapeutic benefits in GBM treatment. Cancer Res; 71(21); 6643–53. ©2011 AACR.