bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bisphosphonate and vitamin D supplementation for osteoporosis
Authors: Bender DA 
Published: February 2012

Ralston SH, Binkley N, Boonen S, Kiel DP, Reginster JY, Roux C, Chen L, Rosenberg E, Santora A.Randomized trial of alendronate plus vitamin D3 versus standard care in osteoporotic postmenopausal women with vitamin D insufficiency.Calcif Tissue Int 2011; 88: 485–94.
Prevalence and predictors of complementary and alternative medicine use in African‐Americans with acquired immune deficiency syndrome
Authors: Owen‐Smith Ashli , McCarty Frances , Hankerson‐Dyson Dana , DiClemente Ralph 
Published: February 2012

AbstractThe use of CAM among human immunodeficiency virus (HIV)‐positive individuals is becoming increasingly widespread. Unfortunately, some CAM therapies may jeopardise the efficacy of conventional HIV medication, making it critical to understand CAM use among this population. The objective of this study was to investigate the prevalence and predictors of CAM use in a theory‐driven, multidimensional manner. African‐American individuals who had received a diagnosis of acquired immune deficiency syndrome (AIDS) were recruited. The computer‐administered survey asked questions about participants' CAM use and various psychosocial and socio‐demographic characteristics. Participants' most recent CD4+ cell counts and HIV RNA levels were abstracted from medical records. Linear regression analyses, adjusted for potential confounders, were conducted to assess the independent contribution of various factors in explaining frequency of CAM use. A total of 182 subjects participated in the survey. Results indicate that most (94%) participants used at least one type of CAM therapy. The majority of participants (79.7%) used CAM therapies as a complement (rather than an alternative) to their HIV medications though half had not discussed these therapies with their healthcare providers. Female gender, high yearly income, high health literacy and high HIV RNA levels were associated with a greater frequency of CAM use, while stronger emotional well‐being was associated with a lower frequency of CAM use. The implications of these findings are discussed and suggestions for future research are provided.
Detection of Taenia solium Taeniasis Coproantigen Is an Early Indicator of Treatment Failure for Taeniasis
Authors: Bustos Javier A. , Rodriguez Silvia , Jimenez Juan A. , Moyano Luz M. , Castillo Yesenia , Ayvar Viterbo , Allan James C. , Craig Philip S. , Gonzalez Armando E. , Gilman Robert H. , Tsang Victor C. W. , Garcia Hector H. 
Published: February 2012

ABSTRACTTaenia soliumcauses taeniasis and cysticercosis, a zoonotic complex associated with a significant burden of epilepsy in most countries. Reliable diagnosis and efficacious treatment of taeniasis are needed for disease control. Currently, cure can be confirmed only after a period of at least 1 month, by negative stool microscopy. This study assessed the performance of detection by a coproantigen enzyme-linked immunosorbent assay (CoAg-ELISA) for the early evaluation of the efficacy of antiparasitic treatment of humanT. soliumtaeniasis. We followed 69 tapeworm carriers who received niclosamide as standard treatment. Stool samples were collected on days 1, 3, 7, 15, 30, and 90 after treatment and were processed by microscopy and CoAg-ELISA. The efficacy of niclosamide was 77.9% (53/68). Thirteen patients received a second course of treatment and completed the follow-up. CoAg-ELISA was therefore evaluated for a total of 81 cases (68 treatments, 13 retreatments). In successful treatments (n= 64), the proportion of patients who became negative by CoAg-ELISA was 62.5% after 3 days, 89.1% after 7 days, 96.9% after 15 days, and 100% after 30 days. In treatment failures (n= 17), the CoAg-ELISA result was positive for 70.6% of patients after 3 days, 94.1% after 7 days, and 100% after 15 and 30 days. Only 2 of 17 samples in cases of treatment failure became positive by microscopy by day 30. The presence of one scolex, but not multiple scolices, in posttreatment stools was strongly associated with cure (odds ratio [OR], 52.5;P< 0.001). CoAg-ELISA is useful for the assessment of treatment failure in taeniasis. Early assessment at day 15 would detect treatment failure before patients become infective.
Ganciclovir-Resistant Cytomegalovirus (CMV) Retinitis in a Patient with Wild-Type CMV in Her Plasma
Authors: Moss Hart B. , Chavala Sai , Say Emil , Miller Melissa B. 
Published: February 2012

ABSTRACT
A patient with systemic cytomegalovirus (CMV), including chorioretinitis, received localized and systemic ganciclovir, systemic cidofovir analog, and localized foscarnet. Mutations conferring ganciclovir and cidofovir resistance were detected in CMV from the aqueous fluid but not in CMV from plasma. Quantifying CMV from aqueous fluid was valuable for monitoring the clinical response and predicting resistance.
Colonization with Vancomycin-Intermediate Staphylococcus aureus Strains Containing the
vanA
Resistance Gene in a Tertiary-Care Center in North India
Authors: Banerjee Tuhina , Anupurba Shampa 
Published: February 2012

ABSTRACT

A nasal carriage survey for methicillin-resistant
Staphylococcus aureus
(MRSA) in an intensive care unit detected four strains of MRSA with reduced susceptibility to vancomycin. The
vanA
gene was found in two of these vancomycin-intermediate
Staphylococcus aureus
(VISA) strains. The absence of selective vancomycin pressure might have resulted in reduced expression of the resistant gene.
Human Papillomavirus Load Measured by Linear Array Correlates with Quantitative PCR in Cervical Cytology Specimens
Authors: Wentzensen Nicolas , Gravitt Patti E. , Long Rodney , Schiffman Mark , Dunn S. Terence , Carreon J. Daniel , Allen Richard A. , Gunja Munira , Zuna Rosemary E. , Sherman Mark E. , Gold Michael A. , Walker Joan L. , Wang Sophia S. 
Published: February 2012

ABSTRACT

Carcinogenic human papillomavirus (HPV) infections are necessary causes of most anogenital cancers. Viral load has been proposed as a marker for progression to cancer precursors but has been confirmed only for HPV16. Challenges in studying viral load are related to the lack of validated assays for a large number of genotypes. We compared viral load measured by Linear Array (LA) HPV genotyping with the gold standard, quantitative PCR (Q-PCR). LA genotyping and Q-PCR were performed in 143 cytology specimens from women referred to colposcopy. LA signal strength was measured by densitometry. Correlation coefficients and receiver operating characteristic (ROC) analyses were used to evaluate analytical and clinical performance. We observed a moderate to strong correlation between the two quantitative viral load measurements, ranging from an
R
value of 0.61 for HPV31 to an
R
value of 0.86 for HPV52. We also observed agreement between visual LA signal strength evaluation and Q-PCR. Both quantifications agreed on the disease stages with highest viral load, which varied by type (cervical intraepithelial neoplasia grade 2 [CIN2] for HPV52, CIN3 for HPV16 and HPV33, and cancer for HPV18 and HPV31). The area under the curve (AUC) for HPV16 Q-PCR at the CIN3 cutoff was 0.72 (
P
= 0.004), and the AUC for HPV18 LA at the CIN2 cutoff was 0.78 (
P
= 0.04). Quantification of LA signals correlates with the current gold standard for viral load, Q-PCR. Analyses of viral load need to address multiple infections and type attribution to evaluate whether viral load has clinical value beyond the established HPV16 finding. Our findings support conducting comprehensive studies of viral load and cervical cancer precursors using quantitative LA genotyping data.
Brain Abscess Caused by Enterococcus faecalis following a Dental Procedure in a Patient with Hereditary Hemorrhagic Telangiectasia
Authors: Mylona Eleni , Vadala Chariklia , Papastamopoulos Vasilios , Skoutelis Athanasios 
Published: February 2012

ABSTRACT

Hereditary hemorrhagic telangiectasia (HHT) is a disease characterized by arteriovenous malformations (AVMs). Brain abscess is a complication of HHT with AVMs. Literature provides evidence that
Enterococcus faecalis
can cause endodontic infections. We present the case of an HHT patient who developed brain abscess due to
E. faecalis
after a dental procedure.
Invasive Serogroup B Neisseria meningitidis in Québec, Canada, 2003 to 2010: Persistence of the ST-269 Clone Since It First Emerged in 2003
Authors: Zhou Jianwei , Lefebvre Brigitte , Deng Saul , Gilca Rodica , Deceuninck Genevieve , Law Dennis K. S. , De Wals Philippe , Tsang Raymond S. W. 
Published: February 2012

ABSTRACT

In the era after the introduction of the meningococcal serogroup C conjugate vaccine, from 1 January 2003 to 31 December 2010, serogroup B meningococci were the major cause of invasive meningococcal disease in the province of Québec, Canada, being responsible for 72% of all meningococcal disease cases. Of the 334 invasive serogroup B
Neisseria meningitidis
strains analyzed, 53.9% belonged to the ST-269 clonal complex (CC). Since it first emerged in 2003, the percentage of invasive serogroup B isolates that belonged to the ST-269 CC had increased from 35% in 2003 to 76% in 2010. Among the 180 meningococci in the ST-269 CC, 91.7% belonged to a single ST (ST-269). The most common PorA genotypes identified in the ST-269 CC were (i) VR1 19-1, VR2 15-11, VR3 36 (84%) and (ii) VR1 18-7, VR2 9, VR3 35-1 (9%). Cases of invasive disease due to the ST-269 CC were commonly found in those aged 11 to 19 years (30.5%) and 20 to 40 years (25.5%). Meningococci of the ST-269 CC were uncommon in other Canadian provinces. In contrast to the ST-269 CC, invasive serogroup B meningococci that belonged to the ST-41/44 CC were much more diverse genetically. However, one ST (ST-571), which is uncommon in the United States, accounted for 35% of all cases due to this CC. The current finding suggests that the ST-269 clone may indeed represent an emerging hypervirulent clone of meningococci.
Effect of γ34.5 Deletions on Oncolytic Herpes Simplex Virus Activity in Brain Tumors
Authors: Kanai Ryuichi , Zaupa Cecile , Sgubin Donatella , Antoszczyk Slawomir J. , Martuza Robert L. , Wakimoto Hiroaki , Rabkin Samuel D. 
Published: February 2012

ABSTRACT

The ICP34.5 protein of herpes simplex virus (HSV) is involved in many aspects of viral pathogenesis; promoting neurovirulence, inhibiting interferon-induced shutoff of protein synthesis, interacting with PCNA and TBK1, inhibiting dendritic cell (DC) maturation, and binding to Beclin 1 to interfere with autophagy. Because of its key role in neuropathogenicity, the γ34.5 gene is deleted in all oncolytic HSVs (oHSVs) currently in clinical trial for treating malignant gliomas. Unfortunately, deletion of γ34.5 attenuates virus replication in cancer cells, especially human glioblastoma stem cells (GSCs). To develop new oHSVs for use in the brain and that replicate in GSCs, we explored the effect of deleting the γ34.5 Beclin 1 binding domain (BBD). To ensure cancer selectivity and safety, we inactivated the ICP6 gene (UL39, large subunit of ribonucleotide reductase), constructing ICP6 mutants with different γ34.5 genotypes: Δ68HR-6, intact γ34.5; Δ68H-6, γ34.5 BBD deleted; and 1716-6, γ34.5 deleted. Multimutated Δ68H-6 exhibited minimal neuropathogenicity in HSV-1-susceptible mice, as opposed to Δ68H and Δ68HR-6. It replicated well in human glioma cell lines and GSCs, effectively killing cells
in vitro
and prolonging survival of mice bearing orthotopic brain tumors. In contrast, 1716 and 1716-6 barely replicated in GSCs. Infection of glioma cells with Δ68H-6 and 1716-6 induced autophagy and increased phosphorylation of eIF2α, while inhibition of autophagy, by Beclin 1 short hairpin RNA (shRNA) knockdown or pharmacological inhibition, had no effect on virus replication or phosphorylated eIF2α (p-eIF2α) levels. Thus, Δ68H-6 represents a new oHSV vector that is safe and effective against a variety of brain tumor models.
Herpes B Virus Utilizes Human Nectin-1 but Not HVEM or PILRα for Cell-Cell Fusion and Virus Entry
Authors: Fan Qing , Amen Melanie , Harden Mallory , Severini Alberto , Griffiths Anthony , Longnecker Richard 
Published: February 2012

ABSTRACT
To investigate the requirements of herpesvirus entry and fusion, the four homologous glycoproteins necessary for herpes simplex virus (HSV) fusion were cloned from herpes B virus (BV) (or macacine herpesvirus 1, previously known as cercopithecine herpesvirus 1) and cercopithecine herpesvirus 2 (CeHV-2), both related simian simplexviruses belonging to the alphaherpesvirus subfamily. Western blots and cell-based enzyme-linked immunosorbent assay (ELISA) showed that glycoproteins gB, gD, and gH/gL were expressed in whole-cell lysates and on the cell surface. Cell-cell fusion assays indicated that nectin-1, an HSV-1 gD receptor, mediated fusion of cells expressing glycoproteins from both BV and CeHV-2. However, herpesvirus entry mediator (HVEM), another HSV-1 gD receptor, did not facilitate BV- and CeHV-2-induced cell-cell fusion. Paired immunoglobulin-like type 2 receptor alpha (PILRα), an HSV-1 gB fusion receptor, did not mediate fusion of cells expressing glycoproteins from either simian virus. Productive infection with BV was possible only with nectin-1-expressing cells, indicating that nectin-1 mediated entry while HVEM and PILRα did not function as entry receptors. These results indicate that these alphaherpesviruses have differing preferences for entry receptors. The usage of the HSV-1 gD receptor nectin-1 may explain interspecies transfer of the viruses, and altered receptor usage may result in altered virulence, tropism, or pathogenesis in the new host. A heterotypic cell fusion assay resulting in productive fusion may provide insight into interactions that occur to trigger fusion. These findings may be of therapeutic significance for control of deadly BV infections.
Opposing Effects of Bacitracin on Human Papillomavirus Type 16 Infection: Enhancement of Binding and Entry and Inhibition of Endosomal Penetration
Authors: Campos Samuel K. , Chapman Janice A. , Deymier Martin J. , Bronnimann Matthew P. , Ozbun Michelle A. 
Published: February 2012

ABSTRACT
Cell invasion by human papillomavirus type 16 (HPV16) is a complex process relying on multiple host cell factors. Here we describe an investigation into the role of cellular protein disulfide isomerases (PDIs) by studying the effects of the commonly used PDI inhibitor bacitracin on HPV16 infection. Bacitracin caused an unusual time-dependent opposing effect on viral infection. Enhanced cellular binding and entry were observed at early times of infection, while inhibition was observed at later times postentry. Bacitracin was rapidly taken up by host cells and colocalized with HPV16 at late times of infection. Bacitracin had no deleterious effect on HPV16 entry, capsid disassembly, exposure of L1/L2 epitopes, or lysosomal trafficking but caused a stark inhibition of L2/viral DNA (vDNA) endosomal penetration and accumulation at nuclear PML bodies. γ-Secretase has recently been implicated in the endosomal penetration of L2/vDNA, but bacitracin had no effect on γ-secretase activity, indicating that blockage of this step occurs through a γ-secretase-independent mechanism. Transient treatment with the reductant β-mercaptoethanol (β-ME) was able to partially rescue the virus from bacitracin, suggesting the involvement of a cellular reductase activity in HPV16 infection. Small interfering RNA (siRNA) knockdown of cellular PDI and the related PDI family members ERp57 and ERp72 reveals a potential role for PDI and ERp72 in HPV infection.
Spike Protein VP8* of Human Rotavirus Recognizes Histo-Blood Group Antigens in a Type-Specific Manner
Authors: Huang Pengwei , Xia Ming , Tan Ming , Zhong Weiming , Wei Chao , Wang Leyi , Morrow Ardythe , Jiang Xi 
Published: February 2012

ABSTRACT

Rotaviruses (RVs), an important cause of severe diarrhea in children, have been found to recognize sialic acid as receptors for host cell attachment. While a few animal RVs (of P[1], P[2], P[3], and P[7]) are sialidase sensitive, human RVs and the majority of animal RVs are sialidase insensitive. In this study, we demonstrated that the surface spike protein VP8* of the major P genotypes of human RVs interacts with the secretor histo-blood group antigens (HBGAs). Strains of the P[4] and P[8] genotypes shared reactivity with the common antigens of Lewis b (Le
b
) and H type 1, while strains of the P[6] genotype bound the H type 1 antigen only. The bindings between recombinant VP8* and human saliva, milk, or synthetic HBGA oligosaccharides were demonstrated, which was confirmed by blockade of the bindings by monoclonal antibodies (MAbs) specific to Le
b
and/or H type 1. In addition, specific binding activities were observed when triple-layered particles of a P[8] (Wa) RV were tested. Our results suggest that the spike protein VP8* of RVs is involved in the recognition of human HBGAs that may function as ligands or receptors for RV attachment to host cells.
C7L Family of Poxvirus Host Range Genes Inhibits Antiviral Activities Induced by Type I Interferons and Interferon Regulatory Factor 1
Authors: Meng Xiangzhi , Schoggins John , Rose Lloyd , Cao Jingxin , Ploss Alexander , Rice Charles M. , Xiang Yan 
Published: February 2012

ABSTRACT

Vaccinia virus (VACV) K1L and C7L function equivalently in many mammalian cells to support VACV replication and antagonize antiviral activities induced by type I interferons (IFNs). While K1L is limited to orthopoxviruses, genes that are homologous to C7L are found in diverse mammalian poxviruses. In this study, we showed that the C7L homologues from sheeppox virus and swinepox virus could rescue the replication defect of a VACV mutant deleted of both K1L and C7L (vK1L
−
C7L
−
). Interestingly, the sheeppox virus C7L homologue could rescue the replication of vK1L
−
C7L
−
in human HeLa cells but not in murine 3T3 and LA-4 cells, in contrast to all other C7L homologues. Replacing amino acids 134 and 135 of the sheeppox virus C7L homologue, however, made it functional in the two murine cell lines, suggesting that these two residues are critical for antagonizing a putative host restriction factor which has some subtle sequence variation in human and murine cells. Furthermore, the C7L family of host range genes from diverse mammalian poxviruses were all capable of antagonizing type I IFN-induced antiviral activities against VACV. Screening of a library of more than 350 IFN-stimulated genes (ISGs) identified interferon-regulated factor 1 (IRF1) as an inhibitor of vK1L
−
C7L
−
but not wild-type VACV. Expression of either K1L or C7L, however, rendered vK1L
−
C7L
−
resistant to IRF1-induced antiviral activities. Altogether, our data show that K1L and C7L antagonize IRF1-induced antiviral activities and that the host modulation function of C7L is evolutionally conserved in all poxviruses that can readily replicate in tissue-cultured mammalian cells.
Genetic Evidence of a Long-Range RNA-RNA Interaction between the Genomic 5′ Untranslated Region and the Nonstructural Protein 1 Coding Region in Murine and Bovine Coronaviruses
Authors: Guan Bo-Jhih , Su Yu-Pin , Wu Hung-Yi , Brian David A. 
Published: February 2012

ABSTRACT

Higher-order RNA structures in the 5′ untranslated regions (UTRs) of the mouse hepatitis coronavirus (MHV) and bovine coronavirus (BCoV), separate species in the betacoronavirus genus, appear to be largely conserved despite an ∼36% nucleotide sequence divergence. In a previous study, each of three 5′-end-proximal
cis
-acting stem-loop domains in the BCoV genome, I/II, III, and IV, yielded near-wild-type (wt) MHV phenotypes when used by reverse genetics to replace its counterpart in the MHV genome. Replacement with the BCoV 32-nucleotide (nt) inter-stem-loop fourth domain between stem-loops III and IV, however, required blind cell passaging for virus recovery. Here, we describe suppressor mutations within the transplanted BCoV 32-nt domain that along with appearance of potential base pairings identify an RNA-RNA interaction between this domain and a 32-nt region ∼200 nt downstream within the nonstructural protein 1 (Nsp1)-coding region. Mfold and phylogenetic covariation patterns among similarly grouped betacoronaviruses support this interaction, as does cotransplantation of the BCoV 5′ UTR and its downstream base-pairing domain. Interestingly, cotransplantation of the BCoV 5′ UTR and BCoV Nsp1 coding region directly yielded an MHV wt-like phenotype, which demonstrates a cognate interaction between these two BCoV regions, which in the MHV genome act in a fully interspecies-compliant manner. Surprisingly, the 30-nt inter-stem-loop domain in the MHV genome can be deleted and viral progeny, although debilitated, are still produced. These results together identify a previously undescribed long-range RNA-RNA interaction between the 5′ UTR and Nsp1 coding region in MHV-like and BCoV-like betacoronaviruses that is
cis
acting for viral fitness but is not absolutely required for viral replication in cell culture.
The Human Cytomegalovirus-Specific
UL1
Gene Encodes a Late-Phase Glycoprotein Incorporated in the Virion Envelope
Authors: Shikhagaie Medya , Mercé-Maldonado Eva , Isern Elena , Muntasell Aura , Albà M. Mar , López-Botet Miguel , Hengel Hartmut , Angulo Ana 
Published: February 2012

ABSTRACT

We have investigated the previously uncharacterized human cytomegalovirus (HCMV)
UL1
open reading frame (ORF), a member of the rapidly evolving HCMV RL11 family.
UL1
is HCMV specific; the absence of
UL1
in chimpanzee cytomegalovirus (CCMV) and sequence analysis studies suggest that
UL1
may have originated by the duplication of an ancestor gene from the
RL11-TRL
cluster (
TRL11
,
TRL12
, and
TRL13
). Sequence similarity searches against human immunoglobulin (Ig)-containing proteins revealed that HCMV pUL1 shows significant similarity to the cellular carcinoembryonic antigen-related (CEA) protein family N-terminal Ig domain, which is responsible for CEA ligand recognition. Northern blot analysis revealed that
UL1
is transcribed during the late phase of the viral replication cycle in both fibroblast-adapted and endotheliotropic strains of HCMV. We characterized the protein encoded by hemagglutinin (HA)-tagged UL1 in the AD169-derived HB5 background. UL1 is expressed as a 224-amino-acid type I transmembrane glycoprotein which becomes detectable at 48 h postinfection. In infected human fibroblasts, pUL1 colocalized at the cytoplasmic site of virion assembly and secondary envelopment together with TGN-46, a marker for the
trans
-Golgi network, and viral structural proteins, including the envelope glycoprotein gB and the tegument phosphoprotein pp28. Furthermore, analyses of highly purified AD169 UL1-HA epitope-tagged virions revealed that pUL1 is a novel constituent of the HCMV envelope. Importantly, the deletion of
UL1
in HCMV TB40/E resulted in reduced growth in a cell type-specific manner, suggesting that pUL1 may be implicated in regulating HCMV cell tropism.