bluuebunny/crossref_metadata_2025_split huggingface dataset:
Real-Time PCR Assay for Rapid Detection and Analysis of PfCRT Haplotypes of Chloroquine-Resistant
Plasmodium falciparum
Isolates from India
Authors: Keen Jessica , Farcas Gabriella A. , Zhong Kathleen , Yohanna Seychelle , Dunne Michael W. , Kain Kevin C. 
Published: July 2007

ABSTRACT

Chloroquine-resistant
Plasmodium falciparum
(CRPF) malaria isolates in Southeast Asia and sub-Saharan Africa share the same
Plasmodium falciparum
chloroquine resistance transporter (PfCRT) haplotype (CVIET; amino acids 72 to 76). It is believed that CRPF malaria emerged in Southeast Asia and spread to sub-Saharan Africa via the Indian subcontinent. Based on this assumption, we hypothesized that CRPF isolates in India should possess the same drug resistance haplotype (PfCRT haplotype CVIET) as
P. falciparum
isolates in Southeast Asia and Africa and that the prevalence of CRPF may be higher and more widespread in India than appreciated. To test this postulate, we utilized a standardized real-time PCR assay to assess the prevalence and distribution of PfCRT haplotypes in
P. falciparum
isolates (
n
= 406) collected from Western, Central, and Eastern states in India and compared them to isolates from South America and Africa. Based on the proportion of isolates possessing the molecular marker K76T, the prevalence of chloroquine resistance was high in all five regions of India studied (91%), as well as in Uganda (98%) and Suriname (100%). All isolates from Suriname contained the chloroquine-resistant SVMNT haplotype typical of South American isolates, and 98% of isolates from Uganda possessed the chloroquine-resistant CVIET haplotype characteristic of Southeast Asian/African strains. However, of 246
P. falciparum
isolates from across India that contained the molecular marker for chloroquine resistance, 81% contained the SVMNT haplotype. In conclusion, the prevalence of CRPF malaria was high in geographically dispersed regions of India, and the primary haplotype observed, SVMNT, did not support a presumed geographic spread from contiguous Southeast Asia.
Community-Acquired Lung Abscess Caused by
Legionella micdadei
in a Myeloma Patient Receiving Thalidomide Treatment
Authors: Girard Louis P. , Gregson Daniel B. 
Published: July 2007

ABSTRACT

Legionella infection causes 2 to 14% of community-acquired pneumonia (CAP).
Legionella micdadei
constitutes <1% of these infections. We describe a case of cavitary
L. micdadei
CAP in a myeloma patient receiving thalidomide treatment. The importance of considering pneumonia and problems in diagnosing pneumonia caused by
L. micdadei
in this patient population are reviewed.
Defect of Human Immunodeficiency Virus Type 2 Gag Assembly in
Saccharomyces cerevisiae
Authors: Morikawa Yuko , Goto Toshiyuki , Yasuoka Daisuke , Momose Fumitaka , Matano Tetsuro 
Published: July 2007

ABSTRACT

We have previously shown that the expression of human immunodeficiency virus type 1 (HIV-1) Gag protein in
Saccharomyces cerevisiae
spheroplasts produces Gag virus-like particles (VLPs) at the plasma membrane, indicating that yeast has all the host factors necessary for HIV-1 Gag assembly. Here we expand the study by using diverse primate lentiviral Gags and show that yeast does not support the production of HIV-2 or simian immunodeficiency virus SIVmac Gag VLPs but allows the production of SIVagm and SIVmnd Gag VLPs. Particle budding was observed at the surfaces of cells expressing SIVagm and SIVmnd Gags, but cells expressing HIV-2 and SIVmac Gags showed only membrane-ruffling structures, although they were accompanied with electron-dense submembrane layers, suggesting arrest at an early stage of particle budding. Comparison of HIV-1 and HIV-2 Gag expression revealed broadly equivalent levels of intracellular Gag expression and Gag N-terminal myristoylation in yeast. Both Gags showed the same membrane-binding ability and were incorporated into lipid raft fractions at a physiological concentration of salt. HIV-2 Gag, however, failed to form a high-order multimer and easily dissociated from the membrane, phenomena which were not observed in higher eukaryotic cells. A series of chimeric Gags between HIV-1 and HIV-2 and Gag mutants with amino acid substitutions revealed that a defined region in helix 2 of HIV-2 MA (located on the membrane-binding surface of MA) affects higher-order Gag assembly and particle production in yeast. Together, these data suggest that yeast may lack a host factor(s) for HIV-2 and SIVmac Gag assembly.
Evidence of Intragenic Recombination in G1 Rotavirus VP7 Genes
Authors: Phan Tung Gia , Okitsu Shoko , Maneekarn Niwat , Ushijima Hiroshi 
Published: July 2007

ABSTRACT
The G1 rotavirus is the most widespread genotype causing acute gastroenteritis in children. In an attempt to investigate the occurrence of intragenic recombination, 131 complete coding region sequences of VP7 genes of the G1 rotaviruses in GenBank were examined. Three hitherto-unreported intragenic recombinant rotaviruses were identified. It was noteworthy that two different types (interlineage and intersublineage) of intragenic recombination in rotaviruses were also found. This is the first report to demonstrate the existence of intragenic recombinations between interlineage and intersublineage in G1 rotaviruses.
Replication of Poliovirus Requires Binding of the Poly(rC) Binding Protein to the Cloverleaf as Well as to the Adjacent C-Rich Spacer Sequence between the Cloverleaf and the Internal Ribosomal Entry Site
Authors: Toyoda Hidemi , Franco David , Fujita Kentaro , Paul Aniko V. , Wimmer Eckard 
Published: July 2007

ABSTRACT

The 5′ nontranslated region of poliovirus RNA contains two highly structured regions, the cloverleaf (CL) and the internal ribosomal entry site (IRES). A cellular protein, the poly(rC) binding protein (PCBP), has been reported to interact with the CL either alone or in combination with viral protein 3CD
pro
. The formation of the ternary complex is essential for RNA replication and, hence, viral proliferation. PCBP also interacts with stem-loop IV of the IRES, an event critical for the initiation of cap-independent translation. Until recently, no special function was assigned to a spacer region (nucleotides [nt] 89 to 123) located between the CL and the IRES. However, on the basis of our discovery that this region strongly affects the neurovirulent phenotype of poliovirus, we have embarked upon genetic and biochemical analyses of the spacer region, focusing on two clusters of C residues (C
93-95
and C
98-100
) that are highly conserved among entero- and rhinoviruses. Replacement of all six C residues with A residues had no effect on translation in vitro but abolished RNA replication, leading to a lethal growth phenotype of the virus in HeLa cells. Mutation of the first group of C residues (C
93-95
) resulted in slower viral growth, whereas the C
98-100
A change had no significant effect on viability. Genetic analyses of the C-rich region by extensive mutagenesis and analyses of revertants revealed that two consecutive C residues (C
94-95
) were sufficient to promote normal growth of the virus. However, there was a distinct position effect of the preferred C residues. A 142-nt-long 5′-terminal RNA fragment including the CL and spacer sequences efficiently bound PCBP, whereas no PCBP binding was observed with the CL (nt 1 to 88) alone. Binding of PCBP to the 142-nt fragment was completely ablated after the two C clusters in the spacer were mutated to A clusters. In contrast, the same mutations had no effect on the binding of 3CD
pro
to the 142-nt RNA fragment. Stepwise replacement of the C residues with A residues resulted in impaired replication that covaried with weaker binding of PCBP in vitro. We conclude that PCBP has little, if any, binding affinity for the CL itself (nt 1 to 88) but requires additional nucleotides downstream of the CL for its function as an essential cofactor in poliovirus RNA replication. These data reveal a new essential function of the spacer between the CL and the IRES in poliovirus proliferation.
Enhanced Phosphorylation of Transcription Factor Sp1 in Response to Herpes Simplex Virus Type 1 Infection Is Dependent on the Ataxia Telangiectasia-Mutated Protein
Authors: Iwahori Satoko , Shirata Noriko , Kawaguchi Yasushi , Weller Sandra K. , Sato Yoshitaka , Kudoh Ayumi , Nakayama Sanae , Isomura Hiroki , Tsurumi Tatsuya 
Published: July 2007

ABSTRACT
The ataxia telangiectasia-mutated (ATM) protein, a member of the related phosphatidylinositol 3-like kinase family encoded by a gene responsible for the human genetic disorder ataxia telangiectasia, regulates cellular responses to DNA damage and viral infection. It has been previously reported that herpes simplex virus type 1 (HSV-1) infection induces activation of protein kinase activity of ATM and hyperphosphorylation of transcription factor, Sp1. We show that ATM is intimately involved in Sp1 hyperphosphorylation during HSV-1 infection rather than individual HSV-1-encoded protein kinases. In ATM-deficient cells or cells silenced for ATM expression by short hairpin RNA targeting, hyperphosphorylation of Sp1 was prevented even as HSV-1 infection progressed. Mutational analysis of putative ATM phosphorylation sites on Sp1 and immunoblot analysis with phosphopeptide-specific Sp1 antibodies clarified that at least Ser-56 and Ser-101 residues on Sp1 became phosphorylated upon HSV-1 infection. Serine-to-alanine mutations at both sites on Sp1 considerably abolished hyperphosphorylation of Sp1 upon infection. Although ATM phosphorylated Ser-101 but not Ser-56 on Sp1 in vitro, phosphorylation of Sp1 at both sites was not detected at all upon infection in ATM-deficient cells, suggesting that cellular kinase(s) activated by ATM could be involved in phosphorylation at Ser-56. Upon viral infection, Sp1-dependent transcription in ATM expression-silenced cells was almost the same as that in ATM-intact cells, suggesting that ATM-dependent phosphorylation of Sp1 might hardly affect its transcriptional activity during the HSV-1 infection. ATM-dependent Sp1 phosphorylation appears to be a global response to various DNA damage stress including viral DNA replication.
Maturation-Dependent Human Immunodeficiency Virus Type 1 Particle Fusion Requires a Carboxyl-Terminal Region of the gp41 Cytoplasmic Tail
Authors: Jiang Jiyang , Aiken Christopher 
Published: July 2007

ABSTRACT
Lentiviruses, including human immunodeficiency virus type 1 (HIV-1), typically encode fusion glycoproteins with long cytoplasmic tails (CTs). We previously reported that immature HIV-1 particles are inhibited for fusion with target cells by a mechanism requiring the 152-amino-acid CT of gp41. The gp41 CT was also shown to mediate the detergent-resistant association of the HIV-1 envelope glycoprotein complex with immature HIV-1 particles, indicating that the gp41 CT forms a stable complex with Gag in immature virions. In the present study, we analyzed the effects of progressive truncations and point mutations in the gp41 CT on the fusion of mature and immature HIV-1 particles with target cells. We also determined the effects of these mutations on the detergent-resistant association of gp41 with immature HIV-1 particles. Removal of the C-terminal 28 amino acids relieved the dependence of HIV-1 fusion on maturation. However, a mutant Env protein lacking this region remained associated with immature HIV-1 particles treated with nonionic detergent. Further mutational analysis of the C-terminal region of gp41 revealed two specific sequences required for maturation-dependent HIV-1 fusion. Collectively, our results demonstrate that the extreme C terminus of gp41 plays a key role in coupling HIV-1 fusion competence to virion maturation. They further indicate that the stable association of gp41 with Gag in immature virions is not sufficient for inhibition of immature HIV-1 particle fusion.
Human T-Cell Leukemia Virus Type 1 (HTLV-1) p12IDown-Modulates ICAM-1 and -2 and Reduces Adherence of Natural Killer Cells, Thereby Protecting HTLV-1-Infected Primary CD4+T Cells from Autologous Natural Killer Cell-Mediated Cytotoxicity despite the Reduction of Major Histocompatibility Complex Class I Molecules on Infected Cells
Authors: Banerjee Prabal , Feuer Gerold , Barker Edward 
Published: July 2007

ABSTRACTAlthough natural killer (NK) cell-mediated control of viral infections is well documented, very little is known about the ability of NK cells to restrain human T-cell leukemia virus type 1 (HTLV-1) infection. In the current study we show that NK cells are unable to kill HTLV-1-infected primary CD4+T cells. Exposure of NK cells to interleukin-2 (IL-2) resulted in only a marginal increase in their ability to kill HTLV-1-infected primary CD4+T cells. This inability of NK cells to kill HTLV-1-infected CD4+T cells occurred despite the down-modulation of major histocompatibility complex (MHC) class I molecules, one of the ligands for the major NK cell inhibitory receptor, by HTLV-1 p12Ion CD4+T cells. One reason for this diminished ability of NK cells to kill HTLV-1-infected cells was the decreased ability of NK cells to adhere to HTLV-1-infected cells because of HTLV-1 p12I-mediated down-modulation of intercellular adhesion molecule 1 (ICAM-1) and ICAM-2. We also found that HTLV-1-infected CD4+T cells did not express ligands for NK cell activating receptors, NCR and NKG2D, although they did express ligands for NK cell coactivating receptors, NTB-A and 2B4. Thus, despite HTLV-1-mediated down-modulation of MHC-I molecules, HTLV-1-infected primary CD4+T cells avoids NK cell destruction by modulating ICAM expression and shunning the expression of ligands for activating receptors.
Kaposi's Sarcoma-Associated Herpesvirus ORF57 Protein Enhances mRNA Accumulation Independently of Effects on Nuclear RNA Export
Authors: Nekorchuk Michael , Han Zhao , Hsieh Ting-Ting , Swaminathan Sankar 
Published: July 2007

ABSTRACT
The ORF57 protein expressed by Kaposi's sarcoma-associated herpesvirus (KSHV) during lytic replication is essential for KSHV virion production. ORF57 enhances gene expression by increasing accumulation of target gene mRNAs. ORF57 interacts with the cellular export factor REF and with RNA, suggesting that it may provide target mRNAs with access to REF, which mediates nuclear RNA export by binding to TAP/NXF1. A mutational analysis of ORF57 was performed to study the role of REF binding, RNA interaction, and multimerization in ORF57 function. ORF57 was shown to directly bind RNA. The ability to bind REF did not correlate with ORF57 function in enhancing mRNA accumulation. ORF57 enhanced the nuclear levels of mRNA and PAN, a nuclear KSHV RNA, and the activity of various ORF57 mutants on the levels of mRNA paralleled their ability to enhance nuclear PAN accumulation, suggesting that ORF57 may also act on messenger RNAs by export-independent effects on RNA stability. Finally, an ORF57 mutant lacking a region homologous to a nucleolar localization signal in herpesvirus saimiri was constructed. This mutant retained function, demonstrating that, unlike the ORF57 homolog in herpesvirus saimiri, nucleolar trafficking is not required for ORF57 function in enhancing mRNA accumulation.
Probing the Interaction between Feline Immunodeficiency Virus and CD134 by Using the Novel Monoclonal Antibody 7D6 and the CD134 (O×40) Ligand
Authors: Willett Brian J. , McMonagle Elizabeth L. , Logan Nicola , Spiller O. Brad , Schneider Pascal , Hosie Margaret J. 
Published: July 2007

ABSTRACTThe feline immunodeficiency virus (FIV) targets activated CD4-positive helper T cells preferentially, inducing an AIDS-like immunodeficiency in its natural host species, the domestic cat. The primary receptor for FIV is CD134, a member of the tumor necrosis factor receptor superfamily, and all primary viral strains tested to date use CD134 for infection. We examined the expression of CD134 in the cat using a novel anti-feline CD134 monoclonal antibody (MAb), 7D6, and showed that as in rats and humans, CD134 expression is restricted tightly to CD4+, and not CD8+, T cells, consistent with the selective targeting of these cells by FIV. However, FIV is also macrophage tropic, and in chronic infection the viral tropism broadens to include B cells and CD8+T cells. Using 7D6, we revealed CD134 expression on a B220-positive (B-cell) population and on cultured macrophages but not peripheral blood monocytes. Moreover, macrophage CD134 expression and FIV infection were enhanced by activation in response to bacterial lipopolysaccharide. Consistent with CD134 expression on human and murine T cells, feline CD134 was abundant on mitogen-stimulated CD4+T cells, with weaker expression on CD8+T cells, concordant with the expansion of FIV into CD8+T cells with progression of the infection. The interaction between FIV and CD134 was probed using MAb 7D6 and soluble CD134 ligand (CD134L), revealing strain-specific differences in sensitivity to both 7D6 and CD134L. Infection with isolates such as PPR and B2542 was inhibited well by both 7D6 and CD134L, suggesting a lower affinity of interaction. In contrast, GL8, CPG, and NCSU were relatively refractory to inhibition by both 7D6 and CD134L and, accordingly, may have a higher-affinity interaction with CD134, permitting infection of cells where CD134 levels are limiting.
Effects of acute prednisolone administration on exercise endurance and metabolism
Authors: Arlettaz A , Collomp K , Portier H , Lecoq A-M , Rieth N , Le Panse B , De Ceaurriz J 
Published: July 2007

Objective:To examine whether acute glucocorticoid (GC) intake alters performance and selected hormonal and metabolic variables during submaximal exercise.Methods:In total, 14 recreational male athletes completed two cycling trials at 70–75% maximum O2uptake starting 3 h after an ingestion of either a lactose placebo or oral GC (20 mg of prednisolone) and continuing until exhaustion, according to a double-blind randomised protocol. Blood samples were collected at rest, after 10, 20, 30 minutes, and at exhaustion and recovery for measurement of growth hormone (GH), adrenocorticotropic hormone (ACTH), dehydroepiandrosterone (DHEA), prolactin, insulin, blood glucose, lactate and interleukin (IL)-6 determination.Results:Cycling duration was not significantly changed after GC or placebo administration (55.9 (5.2)v48.8 (2.9) minutes, respectively). A decrease in ACTH and DHEA (p<0.01) was observed with GC during all of the experiments and in IL-6 after exhaustion (p<0.05). No change in basal, exercise or recovery GH, prolactin, insulin or lactate was found between the two treatments but blood glucose was significantly higher with GC (p<0.05) at any time point.Conclusion:From these data, acute systemic GC administration does seem to alter some metabolic markers but did not influence performance during submaximal exercise.
Urinary isotopic analysis in the UK Armed Forces: no evidence of depleted uranium absorption in combat and other personnel in Iraq
Authors: Bland D , Rona R , Coggon David , Anderson J , Greenberg N , Hull L , Wessely S 
Published: July 2007

Objectives:To assess the distribution and risk factors of depleted uranium uptake in military personnel who had taken part in the invasion of Iraq in 2003.Methods:Sector field inductively coupled plasma-mass spectrometry (SF-ICP-MS) was used to determine the uranium concentration and238U/235U isotopic ratio in spot urine samples. The authors collected urine samples from four groups identified a priori as having different potential for exposure to depleted uranium. These groups were: combat personnel (n = 199); non-combat personnel (n = 96); medical personnel (n = 22); and “clean-up” personnel (n = 24) who had been involved in the maintenance, repair or clearance of potentially contaminated vehicles in Iraq. A short questionnaire was used to ascertain individual experience of circumstances in which depleted uranium exposure might have occurred.Results:There was no statistically significant difference in the238U/235U ratio between groups. Mean ratios by group varied from 138.0 (95% CI 137.3 to 138.7) for clean-up personnel to 138.2 (95% CI 138.0 to 138.5) for combat personnel, and were close to the ratio of 137.9 for natural uranium. The two highest individual ratios (146.9 and 147.7) were retested using more accurate, multiple collector inductively coupled plasma-mass spectrometry (MC-ICP-MS) and found to be within measurement of error of that for natural uranium. There were no significant differences in isotope ratio between participants according to self-reported circumstances of potential depleted uranium exposure.Conclusions:Based on measurements using a SF-ICP-MS apparatus, this study provides reassurance following concern for potential widespread depleted uranium uptake in the UK military. The rare occurrence of elevated ratios may reflect the limits of accuracy of the SF-ICP-MS apparatus and not a real increase from the natural proportions of the isotopes. Any uptake of depleted uranium among participants in this study sample would be very unlikely to have any implications for health.
TWO CASES OF ENDOSCOPIC MANAGEMENT OF CARPAL TUNNEL SYNDROME IN MACRODACTYLY PATIENTS
Authors: Yoshida A. , Okutsu I. , Hamanaka I. , Morimoto S. 
Published: July 2007

Some cases of carpal tunnel syndrome in macrodactyly patients have been reported. We performed endoscopic carpal canal release on two unilateral macrodactyly patients suffering from bilateral carpal tunnel syndrome. We measured carpal canal pressure before performing endoscopic surgery using the Universal Subcutaneous Endoscope system to confirm median nerve compression. We diagnosed median nerve compression in each patient due to the high preoperative carpal canal pressure. Carpal canal pressure immediately decreased to within normal range following release of both the flexor retinaculum and the distal holdfast fibres of the flexor retinaculum.One patient recovered to within normal in terms of sensory disturbances and abductor pollicis brevis muscle strength. The other patient showed improvement in terms of sensory disturbance, however, muscle power did not recover because this patient had suffered from carpal tunnel syndrome for ten years.Endoscopic carpal canal release and decompression surgery was effective for carpal tunnel syndrome in both macrodactyly patients.
Impact of Different Sampling Strategies on Score Results of the Nine Equivalents of Nursing Manpower Use Score (NEMS)
Authors: Junger A. , Klasen J. , Brenck F. , Röhrig R. , Hempelmann G. , Hartmann B. 
Published: July 2007

Summary

Objective:
Prospective observational study to assess the impact of two differentsampling strategies on the score results of the NEMS, used widely to estimate the amount of nursing workload in an ICU.

Methods:
NEMS scores of all patients admitted to the surgical ICU over a one-year period were automatically calculated twice a day with a patient data management system for each patient day on ICU using two differentsampling strategies (NEMSindividual: 24-hour intervals starting from the time of admission; NEMS8a.m.: 24-hour intervals starting at 8 a.m.).

Results:
NEMSindividual and NEMS8a.m. were collected on 3236 patient days; 687 patients were involved. Significantly lower scores were found for the NEMS8a.m. (25.0 ± 8.7) compared to the NEMSindividual (26.1 ± 8.9, p <0.01); the interclass correlation coefficient (ICC) was good but not excellent: 0.78. The inter-rater correlation between the two NEMS scores was high or very high (κ = 0.6-1.0) for six out of nine variables of the NEMS.

Conclusions:
Different sampling strategies produce different score values, especiallydueto the end of stay. This has to betaken into accountwhen using the NEMS in quality assurance projects and multi-center studies.