bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of pericardial disease by magnetic resonance and computed tomography
Authors: Axel Leon 
Published: May 2004

AbstractPericardial disease and its consequences can be well shown with magnetic resonance imaging (MRI) and computed tomography (CT). Here I review the normal and pathologic anatomy and physiology of the pericardium, approaches to MRI and CT imaging of the pericardium, and some specific considerations in common conditions affecting the pericardium. J. Magn. Reson. Imaging 2004;19:816–826. © 2004 Wiley‐Liss, Inc.
Magnetic resonance and computed tomographic evaluation of congenital heart disease
Authors: Boxt Lawrence M. 
Published: May 2004

AbstractMagnetic resonance imaging (MRI) and contrast‐enhanced computed tomography (CT) provide noninvasive visualization of morphologic changes in pediatric and adult patients with congenital heart disease, as well as the functional changes caused by the underlying morphologic abnormalities. Clinical experience with MRI is richer than that with fast CT, but CT appears to provide accurate and high‐quality imagery for diagnosis. The two modalities may be complementary. That is, intracardiac anatomy is so well depicted by MRI, and CT provides exquisite images of the great vessels. Furthermore, in adult patients, MR and CT are helpful in demonstrating and quantitating physiologic changes superimposed by acquired cardiovascular disease on the underlying congenital malformations. Using MRI, spin echo acquisitions provide the image data for evaluation of morphologic changes, and gradient reversal techniques add functional and flow data to complement morphologic changes. Contrast‐enhanced electrocardiographic (ECG)‐gated multidetector and electron beam CT examination provide morphologic information and may be used as a data set for off‐line functional quantitation. J. Magn. Reson. Imaging 2004;19:827–847. © 2004 Wiley‐Liss, Inc.
Magnetic resonance and computed tomography imaging of arrhythmogenic right ventricular dysplasia
Authors: Tandri Harikrishna , Bomma Chandra , Calkins Hugh , Bluemke David A. 
Published: May 2004

AbstractArrhythmogenic right ventricular dysplasia (ARVD) is a familial cardiomyopathy that causes fibro‐fatty replacement of the right ventricle (RV), leading to sudden death due to ventricular arrhythmias. The disease is an important cause of sudden death in individuals younger than 35 years of age. Structural and functional abnormalities of the RV constitute an important diagnostic criterion for the disease. Diagnosis of ARVD is often a challenge as conventional imaging modalities have significant limitations to visualize the RV. Recently, magnetic resonance imaging (MRI) and computed tomographic (CT) imaging have emerged as robust clinical tools for evaluation of myocardial pathology. In addition to providing morphologic and functional information, both imaging modalities have the ability to demonstrate intramyocardial fat, which is the pathological hallmark in ARVD. This article discusses the current status and role of MRI and CT imaging in the diagnosis of ARVD. J. Magn. Reson. Imaging 2004;19:848–858. © 2004 Wiley‐Liss, Inc.
MR imaging assessment of cardiac function
Authors: Pujadas Sandra , Reddy Gautham P. , Weber Oliver , Lee Jennifer J. , Higgins Charles B. 
Published: May 2004

AbstractMagnetic resonance (MR) imaging is an accurate and reproducible technique for assessment of ventricular function. Although echocardiography is the mainstay for evaluation of cardiac function, dobutamine stress MR imaging has been shown to be as safe as echocardiography for patients with coronary artery disease and more accurate in patients with suboptimal echocardiographic image quality. This article reviews MR imaging techniques, methods of pharmacologic stress, and clinical applications for assessment of cardiac function, primarily left ventricular function. J. Magn. Reson. Imaging 2004;19:789–799. © 2004 Wiley‐Liss, Inc.
Isolation and molecular identification of echovirus 13 isolated from patients of aseptic meningitis in Korea, 2002
Authors: Cheon Doo‐Sung , Lee Jiwon , Lee Kangbum , Lee Sunhwa , Park Kwisung , Ahn Jungbae , Jee Youngmee , Yoon Jaedeuk , Cho Haewol 
Published: May 2004

AbstractDuring 2002, several epidemics of aseptic meningitis were attributed to echovirus 13 in Korea. The causative agents of these outbreaks were isolated and identified using rhabdosarcoma cells, HEp‐2 and Buffalo green monkey kidney cells, and a neutralization test using monospecific antiserum. Fifty‐four echovirus 13 isolates were isolated from patients with aseptic meningitis in the provinces, Seoul, Kyonggi, Gwangju, Jeonju, Busan, and Ulsan. Symptoms associated with aseptic meningitis infection in patients included the occurrence of headaches and mild fever. Molecular characterization of echovirus 13 samples was achieved by sequence and phylogenetic analyses on partial VP1 sequences from 20 Korean isolates and 10 foreign isolates listed in Genbank. Minor variation was observed among the Korean isolates, which formed a unique cluster with isolates of German and Japanese origin. The marked similarities between isolates could be attributed to a relatively recent arrival of the virus in Korea. This is the first such investigation of aseptic meningitis caused by echovirus 13 on the Korean peninsula. J. Med. Virol. 73:439–442, 2004. © 2004 Wiley‐Liss, Inc.
SARS coronavirus induces apoptosis in Vero E6 Cells
Authors: Yan Huimin , Xiao Gengfu , Zhang Jiamin , Hu Yuanyang , Yuan Fang , Cole David K. , Zheng Congyi , Gao George F. 
Published: May 2004

AbstractSevere acute respiratory syndrome (SARS) is an emerging infectious disease. Its etiological agent has been convincingly identified as a new member of family Coronaviridae (SARS‐CoV). It causes serious damage to the respiratory system yet the mechanism is not clear. Infection‐induced apoptosis or necrosis is suspected but no direct evidence for this yet exists. To date, Vero E6 cells are the only cell line that could be used to replicate the virus with obvious CPE (cytopathic effect) in vitro. It is known for some viruses (including members of family Coronaviridae) that CPE can be caused either by virus‐induced apoptosis (active death) or cell necrosis (passive death). In this study, we examined the apoptosis in the SARS‐CoV infected Vero E6 cells. Indeed, the results do show that the CPE was induced by apoptosis rather than necrosis, shown by typical DNA fragmentation, through the existence of apoptotic bodies and swollen mitochondria. This observation has some implications for the SARS‐CoV pathogenicity: SARS‐CoV does induce apoptosis in cell cultures and might have the same effect in vivo, responsible for the severe damage of the respiratory system. J. Med. Virol. 73:323–331, 2004. © 2004 Wiley‐Liss, Inc.
The life cycle of SARS coronavirus in Vero E6 cells
Authors: Qinfen Zhang , Jinming Cui , Xiaojun Huang , Huanying Zheng , Jicheng Huang , Ling Fang , Kunpeng Li , Jingqiang Zhang 
Published: May 2004

AbstractThe aim of the study was to establish the life cycle of severe acute respiratory syndrome‐associated coronavirus (SARS CoV) in host cells and determine the pathogenesis of SARS. Vero E6 cells (African green monkey kidney cells) were inoculated with SARS coronavirus for 3, 7, 24, 48, and 72 hr, respectively, and were observed under electron microscope. It was found that the SARS coronavirus entered the cells through membrane fusion instead of endocytosis, and then the nucleocapsids assembled in the RER and matured by budding into the smooth vesicles, which were derived from the Golgi apparatus. The smooth vesicles fused with the cell membrane, and the mature particles were released. A special phenomenon was that some virus‐like particles appeared in the nucleus. We propose a scheme of the life cycle of SARS coronavirus and discuss the mechanism of its replication in Vero E6 cells. J. Med. Virol. 73:332–337, 2004. © 2004 Wiley‐Liss, Inc.
Evaluation of antibody responses against SARS coronaviral nucleocapsid or spike proteins by immunoblotting or ELISA
Authors: Huang Li‐Rung , Chiu Chi‐Ming , Yeh Shiou‐Hwei , Huang Wen‐Hung , Hsueh Po‐Ren , Yang Wen‐Zieh , Yang Jyh‐Yuan , Su Ih‐Jen , Chang Shan‐Chwen , Chen Pei‐Jer 
Published: May 2004

AbstractSevere acute respiratory syndrome (SARS)‐CoV is a newly emerging virus that causes SARS with high mortality rate in infected people. To study the humoral responses against SARS‐CoV, we evaluated nucleocapsid (N) and spike (S) proteins‐specific antibodies in patients' sera by Western blotting and enzyme‐linked immunosorbent assay (ELISA). Recombinant N and S proteins of SARS‐CoV were purified from transformed E. coli. Serum specimens from 40 SARS‐CoV‐infected patients in the convalescent phase were analyzed by Western blotting using the purified antigens. Serial serum specimens from 12 RT‐PCR‐confirmed SARS patients were assayed by ELISA using the recombinant N protein as coated antigen. By Western blotting, 97.5% of the SARS patients were positive for N protein‐specific antibodies whereas only 47.5% of the samples were positive for S protein‐specific antibodies. Using N protein‐based ELISA, 10 out of the 12 patients were positive for N protein‐specific antibodies and 6 of them showed seroconversion at mean of 16 days after onset of fever. Immunoblotting was useful for detecting the humoral immune response after SARS‐CoV infection. Antibodies against SARS‐CoV N protein appear at the early stage of infection, therefore, N protein‐based ELISA could serve as a simple, sensitive, and specific test for diagnosing SARS‐CoV infection. J. Med. Virol. 73:338–346, 2004. © 2004 Wiley‐Liss, Inc.
Failure and success of HIV tests for the prevention of HIV‐1 transmission by blood and tissue donations
Authors: Najioullah Fatiha , Barlet Valérie , Renaudier Philippe , Guitton Cathy , Crova Philippe , Guérin Jean‐Claude , Peyramond Dominique , Trabaud Marie‐Anne , Coudurier Nicole , Tardy Jean‐Claude , André Patrice 
Published: May 2004

AbstractFrench blood banks recently implemented nucleic acid testing (NAT) of all blood donations to reduce the risk of HIV transmission during the pre‐seroconversion period. For tissue donation, HIV infection screening relies on HIV p24 antigen and anti‐HIV1 and 2 antibody detection. In this report, two related cases of infectious donations are described from a cornea donor during the preseroconversion window who was infected by an HIV antibody and NAT negative blood donor. After investigation, the blood donor was found to be herself in the preseroconversion window. Two months after donation, she was found to be HIV positive. The residual risk of HIV infectious blood donations since NAT has been introduced is estimated to be lower than one out of 2.5 millions. Individual NAT instead of minipool testing would not increase significantly the blood transfusion safety. In contrast, introduction of NAT should be considered to increase tissue donation safety as soon as such screening will be possible technically. J. Med. Virol. 73:347–349, 2004. © 2004 Wiley‐Liss, Inc.
Long‐term suppression of plasma viremia with highly active antiretroviral therapy despite virus evolution and very limited selection of drug‐resistant genotypes
Authors: Pariente Nonia , Pernas María , Rosa Rafael de la , Gómez‐Mariano Gema , Fernández Guerau , Rubio Amalia , López Mariola , Benito José Miguel , López‐Galíndez Cecilio , Leal Manuel , Domingo Esteban , Martinez Miguel Angel , Mas Antonio 
Published: May 2004

AbstractHIV‐1 evolution and the possible emergence of mutations associated with resistance to antiretroviral inhibitors have been evaluated in a cohort of sixty‐three patients successfully treated with highly active antiretroviral therapy (HAART). The patients under effective HAART were recruited in three different hospitals in Spain, and none of them had been treated (naïve) before entering this study. HIV‐1 RNA levels, CD4+, and CD8+ T‐cell counts were determined, and nucleotide sequences of proviral regions encoding protease and reverse transcriptase (RT) were obtained for longitudinal blood samples spanning a mean follow‐up period of 88 weeks. Phylogenetic reconstructions and calculations of genetic distances among the different sequences of each patient were performed. All except one of the patients under study showed an early and sustained decrease in plasma HIV‐1 RNA to levels that were below 200 copies/ml. The plasma viral decline paralleled a significant increase in the CD4+ T‐lymphocyte counts. Amino acid sequence analyses revealed the occurrence of mutations associated with antiretroviral resistance in nine patients (14.3%) during HAART treatment, that in some cases could be attributed to excess G to A transitions. In six of the nine patients, the mutations conferred resistance to inhibitors administered in the treatment regime, although the mutations did not result in treatment failure. Sequence comparisons revealed viral evolution during the period of treatment in 47.5% of the patients. The results indicate successful suppression of HIV‐1 under HAART for extended time periods, indistinguishable for patients in which evidence of virus evolution could or could not be documented. J. Med. Virol. 73:350–361, 2004. © 2004 Wiley‐Liss, Inc.
Downregulation of CXCR5 in CD27− B cells of HIV‐1 infected patients
Authors: Chong Yong , Nabeshima Shigeki , Furusyo Norihiro , Murata Masayuki , Yamaji Kouzaburo , Hayashi Jun 
Published: May 2004

AbstractThe CD27− (naive) B cells of HIV‐1 infected patients have been shown to be increased in frequency and to be activated, as indicated by high CD38 expression on the cell surface. CXCR5, a B cell chemokine receptor, is expressed on circulating CD27− (naive) B cells and plays a pivotal role in peripheral B cell development. To investigate the effect of HIV‐1 infection on the expression of this chemokine receptor on naive B cells, the expression level of CXCR5 on CD27− B cells was examined in 19 drug‐naive HIV‐1 infected patients, 27 HAART‐treated patients, and 20 controls. CXCR5 expression on CD27− B cells was significantly lower in drug‐naive patients than in HAART‐treated patients and controls (P < 0.01). CD27− B cells with high CD38 expression exhibited low CXCR5 expression. The CXCR5 expression level on CD27− B cells recovered to within the normal range after effective antiretroviral therapy. These findings suggested that HIV‐1 infection induces a remarkable phenotypic alteration of naive B cells and that the activated naive B cells found in HIV‐1 infection downregulate CXCR5 on their surface. Impaired homing of naive B cells may contribute to HIV‐1 induced immunological deficiencies. J. Med. Virol. 73:362–367, 2004. © 2004 Wiley‐Liss, Inc.
Genetic analysis of hepatitis A virus isolates from Brazil
Authors: de Paula Vanessa S. , Lu Ling , Niel Christian , Gaspar Ana M.C. , Robertson Betty H. 
Published: May 2004

AbstractA limited number of hepatitis A virus (HAV) isolates from South America have been characterised at the genomic level. IgM anti‐HAV positive serum samples collected from patients with hepatitis A living in the five geographical regions of Brazil (North, Northeast, Central, South, and Southeast) were used to obtain HAV isolates and determine their genetic relatedness. Of the 232 case isolates, sequence data were obtained from the VP1/2A junction region of the HAV genome. All isolates were classified in genotype I; 231 belonged to subgenotype IA, and one to subgenotype IB. HAV isolates from four States formed distinct clusters of highly related sequences. However, isolates from other states did not cluster and the sequences from those states were intermingled with sequences found in the other states. The amino acid sequences of all but two isolates showed a Leu → Ile substitution at position 42 in the 2A protein. This substitution appeared to be a characteristic geographic fingerprint of HAV sequences within Brazil. J. Med. Virol. 73:378–383, 2004. © 2004 Wiley‐Liss, Inc.
Immunoglobulin GM and KM genotypes in hepatitis C virus infection
Authors: Vejbaesya Sasijit , Tanwandee Taweesak , Pandey Janardan P. 
Published: May 2004

AbstractHepatitis C virus (HCV) is a major health problem, affecting over 170 million people worldwide. HCV causes a wide spectrum of liver disease, varying from persistent to asymptomatic infection. To evaluate the role of immunoglobulin (Ig) GM and KM genes in HCV infection, 191 HCV‐infected Thai subjects were studied. These included 43 individuals with transient HCV infection and 148 individuals with persistent chronic HCV infection. The controls consisted of 134 healthy individuals. Several GM and KM alleles were determined by polymerase chain reaction‐based methods. The frequency of G1M(f) homozygotes was lower (52.4% vs. 64.2%, P = 0.03) and the frequency of G1M(z) homozygotes was higher (10.5% vs. 3.7%, P = 0.02) in patients than the respective frequencies in controls. These results suggest that GM genotypes make a significant contribution to the risk of acquiring HCV infection. J. Med. Virol. 73:384–386, 2004. © 2004 Wiley‐Liss, Inc.
Evaluation of a total hepatitis C virus (HCV) core antigen assay for the detection of antigenaemia in anti‐HCV positive individuals
Authors: Valcavi Pierpaolo , Medici Maria Cristina , Casula Francesca , Arcangeletti Maria Cristina , De Conto Flora , Pinardi Federica , Calderaro Adriana , Chezzi Carlo , Dettori Giuseppe 
Published: May 2004

AbstractA new, sensitive enzyme immunoassay has been developed for detecting and quantifying total hepatitis C virus (HCV) core antigen in anti‐HCV positive or negative sera (“trak‐C™”, Ortho Clinical Diagnostics, Raritan, NJ). The purpose of this study was to evaluate the performance of trak‐C as an additional laboratory diagnostic marker of viraemia. The performance was compared to HCV‐RNA detection in the “screening” of sera from a large heterogeneous population of hospitalised patients and outpatients. Six hundred and eighteen anti‐HCV negative sera, 405 anti‐HCV positive/HCV‐RNA negative sera, 604 anti‐HCV positive/HCV‐RNA positive sera and 67 anti‐HCV negative sera containing antigens or antibodies potentially interfering with the performance of the assay were analysed. Supplemental HCV antibody testing was performed using a commercial strip immunoblot assay. HCV‐RNA was investigated using a qualitative commercial assay. A quantitative commercial RT‐PCR was used for the analysis of selected samples. Sensitivity and specificity values were 94.7 and 100%, respectively. The latter was also confirmed when anti‐HCV negative samples containing potentially interfering antigens/antibodies were examined. Sensitivity below 100% was probably due to an antigenaemia below the detection limit of trak‐C. Besides, because 65.6% of HCV‐RNA positive/trak‐C negative samples presented specific antibodies against all four RIBA antigens, the hypothesis was raised that, in some cases, the dissociation step efficiency could be sub‐optimal. In conclusion, trak‐C seems suitable for identifying HCV infection on large based populations. It is a rapid to perform, reliable and specific assay that can be adapted to any laboratory setting. J. Med. Virol. 73:397–403, 2004. © 2004 Wiley‐Liss, Inc.
Genetic analysis of crimean‐congo hemorrhagic fever virus in Iran
Authors: Chinikar Sadegh , Persson Stine‐Mari , Johansson Marie , Bladh Linda , Goya Mehdi , Houshmand Badakhshan , Mirazimi Ali , Plyusnin Alexander , Lundkvist Åke , Nilsson Mikael 
Published: May 2004

AbstractCrimean‐Congo hemorrhagic fever (CCHF) is a potentially fatal disease caused by a tick‐borne virus in the family Bunyavridae. The disease occurs in parts of Africa, Asia, Middle East, and Eastern Europe. During recent years, an increasing number of human CCHF cases have been diagnosed in Iran, but very little information is available on the prevalence and genetic diversity of CCHFV in Iran. In the present study, CCHF virus (CCHFV) isolates from nine Iranian patients infected during 2002 were examined genetically. Nucleotide sequencing of the S‐ and M‐segments, encoding the nucleocapsid protein (NP) and the glycoproteins, respectively, revealed that the different isolates were related closely to each other with nucleotide sequence identities exceeding 98% for both S‐ and M‐segments. Phylogenetic analysis of partial S‐segment nucleotide sequences showed that the viruses clustered along with strains from Pakistan and Madagascar in one distinct lineage. Phylogenetic analysis also demonstrated that the Iranian isolates examined in this study and the previously published CCHFV strain ArTeh193‐3 clustered into different genetic groups, indicating that at least two genetic lineages of CCHFV could be co‐circulating in Iran. J. Med. Virol. 73:404–411, 2004. © 2004 Wiley‐Liss, Inc.
Lymphocyte activation and hepatic cellular infiltration in immunocompetent mice infected by dengue virus
Authors: Chen Hsuen‐Chin , Lai Show‐Yun , Sung Jui‐Min , Lee Shu‐Hwae , Lin Yu‐Chin , Wang Wei‐Kung , Chen Yee‐Chun , Kao Chuan‐Liang , King Chwan‐Chuen , Wu‐Hsieh Betty A. 
Published: May 2004

AbstractActivation and expansion of dengue virus‐specific T cells and abnormal liver functions in dengue patients have been documented. However, it remains to be determined whether T cells are involved in the pathogenic mechanism of dengue virus infection. In this study, immunocompetent C57BL/6 mice were employed to study dengue virus‐induced T cell activation. Mice were inoculated with 108 PFU dengue virus serotype 2 strain 16681 by the intravenous route. Dengue viral core RNA was detected by RT‐PCR in mouse serum, liver, spleen, and brain at different time points after infection. Splenic T cells were activated as evidenced by their expression of CD69 and O‐glycosylated CD43 at as early as day 3 after infection. Splenic T cell expression of O‐glycosylated CD43 and IFN‐γ production coordinately peaked at day 5. Coincided with the peak of splenic T cell activation was hepatic lymphocyte infiltration and elevation of liver enzymes. Flow cytometric analysis revealed the infiltrating CD8+ T cell to CD4+ T cell ratio was 5/3. After a second inoculation of dengue virus, hepatic T cell infiltration and liver enzyme levels increased sharply. The infiltrating hepatic CD8+ T cell to CD4+ T cell ratio increased to 5.8/1. A strong correlation was found between T cell activation and hepatic cellular infiltration in immunocompetent mice infected with dengue virus. The kinetics of liver enzyme elevation also correlated with that of T cell activation. These data suggest a relationship between T cell infiltration and elevation of liver enzymes. J. Med. Virol. 73:419–431, 2004. © 2004 Wiley‐Liss, Inc.