bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of hemodialysis schedules and membranes on hepatocyte growth factor and hepatitis C virus RNA levels
Authors: Barril Guillermina , Bartolomé Javier , Sanz Paloma , Buoncristiani Emmanuela , Traver Juan Antonio , Selgas Rafael , Buoncristiani Umberto , Castillo Inmaculada , Quiroga Juan Antonio , Carreño Vicente 
Published: March 2010

AbstractHemodialysis induces production of the hepatocyte growth factor (HGF) and decrease of serum hepatitis C virus (HCV) RNA in patients with HCV infection, but it is not known if the hemodialysis schedule or type of membrane affect both the HGF production and HCV viremia. The effects on both parameters of alternate‐day intermittent hemodialysis and short‐daily hemodialysis and high and low flux membranes were investigated in 41 patients treated by hemodialysis. Sixteen (39%) patients were anti‐HCV positive and 11 (69%) had HCV RNA. Twenty‐six patients were on alternate‐day intermittent and 15 on short‐daily hemodialysis. High flux membranes were used for 29 patients and low flux membranes for 12 patients. A decrease in HCV RNA was observed at the end of hemodialysis (8.6 × 105 ± 1.1 × 106 IU/ml vs. 4.4 × 105 ± 7.3 × 105 IU/ml, P = 0.003). The proportion of HCV RNA decrease was similar in patients dialyzed with both schedules and with both types of membranes. The HGF levels increased from 2,605.9 ± 1,428.7 to >8,000 pg/ml at 15 min. At the end of the session, the HGF levels decreased to 5,106.7 ± 2,533.9 pg/ml. The HGF levels at the start of the next session were similar to those at baseline (2,680.0 ± 1,209.3 pg/ml). The increase and dynamics of the HGF levels were similar in patient's hemodialyzed with both schedules and with both types of membranes. These results suggest that changes in HCV RNA and HGF levels during hemodialysis are not influenced by the schedule or type of membrane used. J. Med. Virol. 82: 763–767, 2010. © 2010 Wiley‐Liss, Inc.
Detection of human polyomavirus proteins, T‐antigen and agnoprotein, in human tumor tissue arrays
Authors: Del Valle Luis , Khalili Kamel 
Published: March 2010

AbstractExpression of the human polyomavirus JCV genome in several experimental animals induces a variety of neural origin tumors. The viral proteins, T‐antigen and Agnoprotein, contribute to the oncogenesis of JCV by associating with several tumor suppressor proteins and dysregulating signaling pathways, which results in uncontrolled cell proliferation. In addition, T‐antigen and Agnoprotein have been associated with DNA damage and interfering with DNA repair mechanisms. In this study, we have utilized commercially available tissue arrays of human tumors of various origins and demonstrated the expression of both T‐antigen and Agnoprotein in some, but not all, tumors of neural and non‐neural origin. Most notably, more than 40% of human glioblastomas and greater than 30% of colon adenocarcinomas express viral proteins. The detection of viral transforming proteins, T‐antigen and Agnoprotein in the absence of viral capsid proteins suggests a role for JCV in the development and/or progression of human tumors. These results invite further large‐scale investigation on the role of polyomaviruses, particularly JCV in the pathogenesis of human cancer. J. Med. Virol. 82: 806–811, 2010. © 2010 Wiley‐Liss, Inc.
Pegylated interferon monotherapy of chronic hepatitis C in dialysis patients: Meta‐analysis of clinical trials
Authors: Fabrizi Fabrizio , Dixit Vivek , Messa Piergiorgio , Martin Paul 
Published: March 2010

AbstractThe efficacy and safety of pegylated interferon monotherapy in patients with chronic renal failure and chronic hepatitis C remains unclear, although a number of small clinical trials have been published addressing this issue. A systematic review of the literature with a meta‐analysis of clinical trials was performed in order to assess efficacy and safety of initial pegylated interferon monotherapy in chronic renal failure patients with chronic hepatitis C. The primary outcome was sustained virological response (as a measure of efficacy); the secondary outcome was drop‐out rate (as a measure of tolerability). The random effects model of Der Simonian and Laird was used, with heterogeneity and sensitivity analyses. Sixteen clinical trials (254 unique patients) were identified, five (31%) being controlled studies; the majority (15/16 = 94%) regarded patients on long‐term dialysis. The summary estimate for sustained virological response and drop‐out rate was 33% [95% Confidence Intervals (95%CI) 24–43] and 23% (95%CI, 14–33), respectively. The most frequent side‐effects requiring interruption of treatment were haematological (18%) and gastrointestinal (14%). In the group of controlled clinical trials, the summary estimate for sustained viral response and drop‐out rate was 38% (95% CI, 18–59), and 15% (95% CI, 3–26), respectively. The studies were heterogeneous with regard to sustained virological response and drop‐out rate. Pegylated IFN does not provide an added benefit in terms of virological response in comparison with standard IFN monotherapy. Tolerance to pegylated‐IFN monotherapy was unsatisfactory. Prospective trials are in progress to assess the optimal antiviral therapy for chronic hepatitis C in dialysis patients. J. Med. Virol. © 2010 Wiley‐Liss, Inc. J. Med. Virol. 82: 768–775, 2010. © 2010 Wiley‐Liss, Inc.
Sequence analysis of the VP7 gene of human rotaviruses G2 and G4 isolated in Japan, China, Thailand, and Vietnam during 2001–2003
Authors: Trinh Quang Duy , Pham Ngan Thi Kim , Nguyen Tuan Anh , Phan Tung Gia , Yan Hainian , Hoang Le Phuc , Khamrin Pattara , Maneekarn Niwat , Li Yan , Okitsu Shoko , Mizuguchi Masashi , Ushijima Hiroshi 
Published: March 2010

AbstractSequence and phylogenetic analyses of the rotavirus VP7 gene were performed on 52 human G2 and G4 strains isolated in Japan, China, Thailand, and Vietnam during 2001–2003. All genotype G2 strains included in the study clustered into lineage II of the phylogenetic tree, together with the majority of global G2 strains detected since 1995. The amino acid substitution at position 96 from aspartic acid to asparagine was noted among the emerging or re‐emerging G2 rotavirus strains in Japan, Thailand, and Vietnam during 2002–2003. Genotype G4 strains detected in Vietnam grouped into lineage Ia of the phylogenetic tree, whereas Japanese G4 strains clustered in lineage Ic which included emerging G4 strains from Argentina, Italy, Paraguay, and Uruguay. It is noteworthy that an insertion of asparagine was found at position 76 in all the Japanese strains and that its presence might be involved in the emergence of G4 rotavirus in Japan during 2002–2003. J. Med. Virol. 82: 878–885, 2010. © 2010 Wiley‐Liss, Inc.
The entire core protein of HCV JFH1 is required for efficient formation of infectious JFH1 pseudoparticles
Authors: Shukla Priyanka , Faulk Kristina N. , Emerson Suzanne U. 
Published: March 2010

AbstractThe vast majority of hepatitis C virus (HCV) strains cannot be grown in cell culture. Therefore, tests for neutralizing antibodies have relied heavily on retrovirus pseudoparticles displaying the envelope glycoproteins of HCV on their surface (HCVpp). Unfortunately, the envelope proteins of some strains, especially of JFH1, did not efficiently form functional HCVpp. We have manipulated the length and composition of the HCV core gene in the HCVpp expression vectors for three strains of HCV in an attempt to obtain more efficient production of pseudoparticles. The results demonstrated that the truncated core region included in the HCV expression plasmids of the classic pseudoparticle system was optimal for formation of strain H77pp, suboptimal for strain J6pp, and insufficient for strain JFH1pp. Efficiency of JFH1pp formation increased 20‐fold when the truncated core gene was replaced with the entire core gene. The full core from J6 and HK had modest effect on the production of infectious J6 and HKpp. The data suggested that pairs of HCV glycoproteins differ inherently in their ability to associate into functional heterodimers and that the core protein, provided in cis as the beginning of the polyprotein product, can in some cases facilitate this process, possibly by increasing the rate of proper folding of the glycoproteins. J. Med. Virol. 82: 783–790, 2010. Published 2010 Wiley‐Liss, Inc.
Determination of the geographical origin of unidentified cadavers based on geographical differences in genotype of varicella–zoster virus
Authors: Inoue Hiroyuki , Motani‐Saitoh Hisako , Sakurada Koichi , Ikegaya Hiroshi , Yajima Daisuke , Hayakawa Mutsumi , Sato Yayoi , Otsuka Katsura , Kobayashi Kazuhiro , Nagasawa Sayaka , Iwase Hirotaro 
Published: March 2010

AbstractA new method was developed for determining the geographical origin of unidentified cadavers by examining the genome of varicella–zoster virus (VZV), which resides latently throughout life in most individuals and the genotypes which show distinct geographical distribution. VZV DNA samples extracted from the trigeminal ganglia of 62 cadavers (59 from Japan, and 1 each from the United Kingdom, Mongolia, and Pakistan) submitted for medico‐legal autopsy were examined. Sequencing was performed on a 358‐bp region in the open reading frame (ORF) 22 containing four single nucleotide polymorphisms (SNPs) and a 419‐bp region in ORF 62 containing 2 SNPs in the VZV genome. Using these SNP markers, the VZV genome was classified into the nine genotypes described previously. Phylogenetic tree analysis was also undertaken for the sequenced regions and for the 22 existing VZV strains described previously. In addition, 21 samples were subcloned for detection of co‐infection. The VZV genome was classified successfully into nine genotypes using four SNPs in ORF 22 and two SNPs in ORF 62 as markers. Among Japanese cadavers, 57 carried genotype J, 1 carried genotype M1, and 1 carried genotype M2. The British and the Mongolian cadavers carried genotype E1 and the Pakistani cadaver carried M1. Phylogenetic tree analysis showed that VZV strains can be classified into different genotypes with high bootstrap values. None of the subcloned samples showed evidence of co‐infection. These results suggest that valuable additional information for determining the geographical origin of unidentified cadavers can be provided by examining the VZV genome. J. Med. Virol. 82: 903–998, 2010. © 2010 Wiley‐Liss, Inc.
The route of inoculation determines the tissue tropism of modified vaccinia tiantan expressing the spike glycoprotein of SARS‐CoV in mice
Authors: Liu Huan , Yu Wenbo , Tang Xian , Wang Haibo , Ouyang Wenjie , Zhou Jingying , Chen Zhiwei 
Published: March 2010

AbstractThe live replication‐competent modified vaccinia virus Tiantan (MVTT) is an attractive vaccine vector, yet little is known about its tissue tropism and pathology in vivo. Recently, we demonstrated that a recombinant MVTT expressing the spike glycoprotein of SARS‐CoV (namely MVTT‐S) is superior to the non‐replicating modified vaccinia Ankara (MVA‐S) for inducing high level of neutralizing antibodies through mucosal vaccination. In this study, we further determined the tissue tropism and safety of MVTT‐S after the vaccine was administrated through various routes including: intramuscular (i.m.), intranasal (i.n.), and intravaginal (i.vag.) inoculations, respectively. Using real‐time PCR, nested PCR, immunohistochemistry and in situ hybridization assays, we found that MVTT‐S was able to produce a transient infection in all cases within 48 hr post‐inoculation, yet the major site of viral replication in various tissues or organs was dependent on the route of viral administration. We demonstrated that i.m. injection of MVTT‐S primarily targeted draining inguinal lymph nodes, whereas mucosal inoculation had broader range of tissue infections. i.n. inoculation involved infections in lungs, kidneys, spleens and cervix lymph nodes while i.vag. administration targeted uteruses, ovaries, kidneys and spleens. Critically, the infection did not cause severe pathogenic consequences in infected tissues, which was consistent to the attenuated phenotype of MVTT‐S. Our findings have implications for the optimization of vaccination route and for studies on the correlation between the magnitude of immune responses and the extent of tissue involvement in vivo. J. Med. Virol. 82: 727–734, 2010. © 2010 Wiley‐Liss, Inc.
Impact of highly active antiretroviral therapy on hepatitis C virus protease quasispecies diversity in HIV co‐infected patients
Authors: Winters Mark A. , Chary Aarthi , Eison Robert , Asmuth David , Holodniy Mark 
Published: March 2010

AbstractMany hepatitis C virus (HCV)‐infected patients are also infected with HIV, and undergo antiretroviral (ARV) treatment for their human immunodeficiency virus (HIV) infection. Due to changes in HIV burden and immunologic status, HIV ARV treatment may have indirect effects on the HCV population, which could impact the effectiveness of subsequent HCV protease inhibitor (PI) treatment. The genetic variability of the protease‐encoding HCV NS3 gene was evaluated in 10 co‐infected patients initiating ARVs (both before and after ARV initiation), and compared to the genetic variability in 10 patients on stable ARV therapy. After RT‐PCR of plasma‐derived HCV RNA, a mean of 20 clones per patient time‐point were sequenced and analyzed for changes in the HCV quasispecies population. No significant differences in sequence diversity or complexity at the nucleic acid or amino acid levels were seen at baseline between groups or between the two time points in either group. HCV protease diversity in the pre‐ and post‐ARV treatment samples was not significantly different than samples from patients on stable ARV therapy. There was no significant development of amino acid substitutions known to confer HCV PI resistance in either group. Initiation of ARV for HIV infection does not significantly alter the genetic diversity or complexity of the HCV NS3 gene or result in increased number of HCV PI‐associated amino acid changes. These results suggest ARV treatment for HIV would not affect the efficacy of HCV PI treatment. J. Med. Virol. 82: 791–798, 2010. © 2010 Wiley‐Liss, Inc.
Comparison of the technical and clinical performance of the Elecsys® HBsAg II assay with the Architect®, AxSym®, and Advia® Centaur HBsAg screening assays
Authors: Louisirirotchanakul S. , Khupulsup K. , Akraekthalin S. , Chan K.P. , Saw S. , Aw T.C. , Cho D.‐H. , Shin M.‐G. , Lim J. 
Published: March 2010

AbstractSouth East Asia has some of the highest prevalence rates of hepatitis B virus (HBV) infection (≥8%) in the world, and the emergence of hepatitis B surface antigen (HBsAg) mutant strains is a growing problem. Assays with the highest levels of sensitivity, including mutant detection, should be used for routine HBsAg screening. In this large multicenter study, the clinical and technical performance of the fully automated Elecsys HBsAg II assay was compared with the Architect, AxSYM, and Advia Centaur HBsAg assays for HBsAg screening. Nine laboratories (three each from Thailand, Korea, and Singapore) compared the Elecsys HBsAg II assay with their routine HBsAg screening assay against a range of stored and routine clinical samples, including recombinant mutants. The Elecsys HBsAg II assay demonstrated equivalent sensitivity and specificity to the Architect HBsAg assay. However, the Elecsys HBsAg II assay recognized a native mutant sample (L94S, L97V, L98V, T123A) that the Architect HBsAg assay failed to detect. The AxSYM and Advia Centaur HBsAg assays appeared less sensitive for the detection of early HBV infection and also failed to detect some of the recombinant mutant strains. There was almost complete agreement between the Elecsys HBsAg II assay and comparator assays with respect to routine serum samples. The results of this study demonstrate that the Elecsys HBsAg II assay is a highly sensitive and specific screening assay for HBsAg and detects reliably the most important and clinically relevant HBV mutants and genotypes. It is suitable for routine HBsAg screening in Asia. J. Med. Virol. 82: 755–762, 2010. © 2010 Wiley‐Liss, Inc.
Mechanism of HIV‐1‐TAT induction of interleukin‐1β from human monocytes: Involvement of the phospholipase C/protein kinase C signaling cascade
Authors: Yang Yongbo , Wu Jianguo , Lu Yuanan 
Published: March 2010

AbstractHuman immunodeficiency virus TAT plays an important role in the disregulation of cytokine production associated with the neurological disorders that follow HIV infection. IL‐1β is one of the important inflammatory cytokines secreted by immune‐activated monocytes/macrophages. Previous reports have shown that extracellular TAT stimulates IL‐1β expression in monocytes/macrophages. However, little is known about the mechanisms and possible TAT‐responsive elements within the IL‐1β promoter. The present study shows that TAT increases the production of IL‐1β in human monocytes; PLC‐PKC pathway‐dependent phosphorylation of p44/42 and JNK MAP kinases participates partially in IL‐1β induction by TAT; specific C/EBP and NF‐κB transcription factor binding elements within the IL‐1β promoter are involved in TAT regulation of IL‐1β production. This study identifies a signaling mechanism for HIV‐1‐induced IL‐1β production in human monocytes that may be involved in the neuropathogenesis of HIV‐associated dementia. J. Med. Virol. 82: 735–746, 2010. © 2010 Wiley‐Liss, Inc.
Norovirus GII‐4 2006b variant circulating in patients with acute gastroenteritis in Thailand during a 2006–2007 study
Authors: Kittigul Leera , Pombubpa Kannika , Taweekate Yuthana , Diraphat Pornphan , Sujirarat Dusit , Khamrin Pattara , Ushijima Hiroshi 
Published: March 2010

AbstractNoroviruses (NoVs) are recognized as a significant cause of acute gastroenteritis in children and adults. A 14‐month study, from January 2006 to February 2007, was undertaken in a hospital in Thailand to determine the prevalence and genetic characterization of NoVs in patients of all ages with acute gastroenteritis. Based on reverse transcription‐nested polymerase chain reaction (RT‐nested PCR), NoVs were detected in 122 of 273 (44.7%) collected stool samples. Of the 122 NoV‐positive samples, 28 (23%) belonged to GI, 79 (64.8%) belonged to GII, and 15 (12.2%) were mixed infections of GI and GII strains. Three NoV GI‐positive and 42 NoV GII‐positive samples were characterized successfully by DNA sequencing of the RT‐nested PCR products and phylogenetic analysis. For NoV GI, two genotypes were identified: GI‐2 (one sample) and GI‐6 (two samples). NoV GII could be classified further into five distinct genotypes: GII‐2 (1 sample), GII‐3 (3 samples), GII‐4 (14 samples), GII‐6 (3 samples), and GII‐17 (2 samples), and one unclassified genotype (19 samples). All NoV GII‐4 strains showed 88–98% nucleotide identity with NoV GII‐4 2006b variants reported worldwide. Among genotypes of NoV characterized, one co‐infected stool sample exhibited NoVs GI‐6 and GII‐4 2006b. This study suggests that there is an important role of NoVs as etiologic agents in patients with acute gastroenteritis. The predominant circulating genotype of NoV infections is GII‐4 2006b variant. J. Med. Virol. 82: 854–860, 2010. © 2010 Wiley‐Liss, Inc.
B2 attenuates polyglutamine‐expanded androgen receptor toxicity in cell and fly models of spinal and bulbar muscular atrophy
Authors: Palazzolo Isabella , Nedelsky Natalia B. , Askew Caitlin E. , Harmison George G. , Kasantsev Aleksey G. , Taylor J. Paul , Fischbeck Kenneth H. , Pennuto Maria 
Published: March 2010

AbstractExpanded polyglutamine tracts cause neurodegeneration through a toxic gain‐of‐function mechanism. Generation of inclusions is a common feature of polyglutamine diseases and other protein misfolding disorders. Inclusion formation is likely to be a defensive response of the cell to the presence of unfolded protein. Recently, the compound B2 has been shown to increase inclusion formation and decrease toxicity of polyglutamine‐expanded huntingtin in cultured cells. We explored the effect of B2 on spinal and bulbar muscular atrophy (SBMA). SBMA is caused by expansion of polyglutamine in the androgen receptor (AR) and is characterized by the loss of motor neurons in the brainstem and spinal cord. We found that B2 increases the deposition of mutant AR into nuclear inclusions, without altering the ligand‐induced aggregation, expression, or subcellular distribution of the mutant protein. The effect of B2 on inclusions was associated with a decrease in AR transactivation function. We show that B2 reduces mutant AR toxicity in cell and fly models of SBMA, further supporting the idea that accumulation of polyglutamine‐expanded protein into inclusions is protective. Our findings suggest B2 as a novel approach to therapy for SBMA. © 2010 Wiley‐Liss, Inc.
Low levels of mutant ubiquitin are degraded by the proteasome in vivo
Authors: van Tijn Paula , Verhage Marian C. , Hobo Barbara , van Leeuwen Fred W. , Fischer David F. 
Published: March 2010

AbstractThe ubiquitin‐proteasome system fulfills a pivotal role in regulating intracellular protein turnover. Impairment of this system is implicated in the pathogenesis of neurodegenerative diseases characterized by ubiquitin‐ containing proteinaceous deposits. UBB+1, a mutant ubiquitin, is one of the proteins accumulating in the neuropathological hallmarks of tauopathies, including Alzheimer's disease, and polyglutamine diseases. In vitro, UBB+1 properties shift from a proteasomal ubiquitin‐fusion degradation substrate at low expression levels to a proteasome inhibitor at high expression levels. Here we report on a novel transgenic mouse line (line 6663) expressing low levels of neuronal UBB+1. In these mice, UBB+1 protein is scarcely detectable in the neuronal cell population. Accumulation of UBB+1 commences only after intracranial infusion of the proteasome inhibitors lactacystin or MG262, showing that, at these low expression levels, the UBB+1 protein is a substrate for proteasomal degradation in vivo. In addition, accumulation of the protein serves as a reporter for proteasome inhibition. These findings strengthen our proposition that, in healthy brain, UBB+1 is continuously degraded and disease‐related UBB+1 accumulation serves as an endogenous marker for proteasomal dysfunction. This novel transgenic line can give more insight into the intrinsic properties of UBB+1 and its role in neurodegenerative disease. © 2010 Wiley‐Liss, Inc.
Effect of thermal adaptation on seasonal outdoor thermal comfort
Authors: Lin Tzu‐Ping , de Dear Richard , Hwang Ruey‐Lung 
Published: March 2010

AbstractThermal perceptions and preferences of individuals outdoors cannot be entirely explained by the energy balance of the human body. They are also affected by psychological and behavioural factors or the so‐called thermal adaptation. To examine the effect of thermal adaptation on seasonal outdoor thermal comfort, 1644 interviews with concurrent micrometeorological measurements were conducted outdoors in central Taiwan. Results indicate a deviation of 1.3 °C standard effective temperature (SET*) in neutral temperatures between hot and cool seasons, and a deviation of 1.8 °C SET* in preferred temperature between hot and cool seasons. Additionally, although subjects' temperature and sunshine preferences were highly correlated with SET*, they diverged between seasons for identical SET* exposures in the two seasons. Analysis reveals that people's thermal perceptions were strongly related to the air temperature (Ta) and mean radiant temperature (Tmrt), but not significant to air speed and air humidity. These results demonstrate that thermal adaptation markedly influences seasonal outdoor thermal comfort, knowledge of which may be useful in the planning and design of outdoor environments in hot–humid regions. Copyright © 2010 Royal Meteorological Society