bluuebunny/crossref_metadata_2025 huggingface dataset:
Thyroxine-binding globulin, hyperthyroxinemia and hepatocellular carcinoma
Authors: Gumucio Jorge J. , Kew Michael C.
Published: March 2007

To determine serum thyroxine-binding globulin (TBG) levels, we used radioimmunoassay, and compared the results obtained with other tests in 231 patients with chronic hepatitis B virus infection to evaluate its clinical implications. All of these patients were hepatitis B surface antigen (HBsAg)-positive. Among them, 38 patients had hepatocellular carcinoma (HCC), 18 had chronic persistent hepatitis, 70 had chronic lobular or active hepatitis (grouped as CAH), 31 had active cirrhosis (AC), 25 had inactive cirrhosis, 20 had decompensated cirrhosis, and 29 were “healthy” HBsAg carriers. Twenty-seven patients with acute hepatitis, 12 with cancer metastasis to the liver, and 81 normal adults served as disease or normal controls. The results showed that serum TBG level increased significantly in patients with CAH, AC, or HCC. Serum TBG did not correlate with albumin or bilirubin level, but correlated with alanine aminotransferase (ALT) positively in patients with CAH (p < 0.001) and negatively in patients with HCC (p < 0.01) (slope difference p < 0.05). Serial determination of serum TBG and ALT also showed parallel changes in 15 patients with CAH, but not in nine patients with HCC. In contrast, the fall and rise of serum TBG levels in patients with HCC coincided with tumor resection and recurrence. The data suggest that serum TBG elevation in patients with hepatitis activity is the result of hepatocellular damage, whereas that in patients with HCC is due to increased synthesis. Whether serum TBG elevation without concomitant rise of ALT could be used as a marker of HCC awaits further study.
Increased tumor necrosis factor-α receptor number in chronic hepatitis B virus infection
Authors: Lau Johnson Y. N. , Sheron Nick , Nouri-Aria Kayhan T. , Alexander Graeme J. M. , Williams Roger
Published: March 2007

Production of the antiviral cytokine, tumor necrosis factor-α is increased in chronic hepatitis B virus infection, and clinical studies of tumor necrosis factor-α have indicated a proviral effect at higher doses. To determine whether this might be related to abnormal cell surface tumor necrosis factor-α receptor expression, binding characteristics of cell surface tumor necrosis factor-α receptor on peripheral blood mononuclear cells in chronic hepatitis B virus carriers were studied using radioiodinated recombinant tumor necrosis factor-α. The specific binding curves generated were analyzed according to the method of Scatchard to determine cell surface receptor numbers and dissociation constants.

A single class of cell surface tumor necrosis factor-α receptor was demonstrated on peripheral blood mononuclear cells and mononuclear subsets. The median number (range) of cell surface tumor necrosis factor-α receptors on peripheral blood mononuclear cells from controls (n = 11), chronic hepatitis B virus patients seropositive for hepatitis B virus DNA (n = 8) and seronegative for hepatitis B virus DNA (n = 8) were 2,329 (range = 1,538 to 3,133), 3,375 (range = 2,300 to 6,718) (p < 0.01) and 3,113 (range = 2,229 to 5,246) (p < 0.05) sites/cell, respectively. They all had similar dissociation constants of 8.4 × 10−10 mol/L (range = 4.1 to 16.9), respectively. Further dissection of the peripheral blood mononuclear cells showed that this increase in cell surface receptor number was confined to the monocyte fraction (p < 0.01). Plasma tumor necrosis factor-α levels in five patients with increased monocyte cell surface tumor necrosis factor-α receptor numbers were also elevated. No correlation between cell surface tumor necrosis factor-α receptor number and serum AST, HBsAg, hepatitis B virus DNA or liver histology was observed.

These data indicate that cell surface tumor necrosis factor-α receptor number is increased in monocytes but normal in lymphocytes and support previous observations that monocytes are activated in chronic hepatitis B virus infection. (HEPATOLOGY 1991;14:44-50.)
The significance of antibody to hepatitis C virus in patients with chronic hepatitis B
Authors: Fong Tse-Ling , Di Bisceglie Adrian M. , Waggoner Jeanne G. , Banks Steven M. , Hoofnagle Jay H.
Published: March 2007

We assessed the prevalence and clinical significance of antibodies to hepatitis C virus among a cohort of 148 patients with chronic hepatitis B virus infection. Sixteen patients (11%) had anti-hepatitis C virus detectable by enzyme-linked immunoassay. The results from eight of these patients were positive by recombinant immunoblot assay. The results of recombinant immunoblot assay testing were not consistent; therefore the analysis of the patients’ data was based on anti-hepatitis C virus enzyme-linked immunoassay results. Patients with chronic hepatitis B with anti-hepatitis C virus were more likely to be cirrhotic (44% vs. 21%) and to have decompensated liver disease (24% vs. 6%). Hepatitis B virus replication appeared to be suppressed in patients with both infections as measured by hepatitis B virus—associated DNA polymerase activity (mean = 2,055 vs. 2,555 cpm). Human immunodeficiency virus infection was more common in the anti-hepatitis C virus positive group (36% vs. 11%). Thus hepatitis C virus appears to suppress hepatitis B virus replication and to cause more severe liver disease in patients with chronic hepatitis B infection. (HEPATOLOGY 1991;14:64-67.)
Visualization of the interaction of native and modified lipoproteins with parenchymal, endothelial and Kupffer cells from human liver
Authors: Kleinherenbrink-Stins Monique F. , van de Boom Hans J. , Schouten Donald , Roholl Paul J. M. , van der Heyde Niels M. , Brouwer Adriaan , Berkel Theo J. C. V. , Knook Dick L.
Published: March 2007

The interaction of low density lipoprotein, acetylated low density lipoprotein and apolipoprotein E—free high density lipoprotein with parenchymal, endothelial and Kupffer cells of human liver was visualized. For this purpose, the fluorescent phospholipid analog 1,1′-dioctadecyl-3,3,3′,3′-tetramethyl indocarbocyanine perchlorate was used to label the lipoproteins. The involvement of both parenchymal and nonparenchymal cells in the uptake of 1,1′-dioctadecyl-3,3,3′,3′-tetramethyl indocarbocyanine perchlorate—labeled low density lipoprotein and acetylated low density lipoprotein was studied using in vitro perfusion of human liver tissue blocks. In addition, primary hepatocyte cultures were used to visualize the interaction with 1,1′-dioctadecyl-3,3,3′,3′-tetramethyl indocarbocyanine perchlorate-labeled apolipoprotein E—free high density lipoprotein and (modified) low density lipoprotein.

1,1′-dioctadecyl-3,3,3′,3′-tetramethyl indocarbocyanine perchlorate-low density lipoprotein showed a time-dependent and concentration-dependent interaction with both hepatocytes and Kupffer cells, although the intensity of the interaction with parenchymal cells varied strongly among the liver donors. Uptake of 1,1′-dioctadecyl-3,3,3′,3′-tetramethyl indocarbocyanine perchlorate-low density lipoprotein by both cell types was strongly inhibited by the presence of excess unlabeled low density lipoprotein in the (perfusion) medium. Methylation and hydroxyac-etaldehyde treatment of low density lipoprotein prevented the uptake of low density lipoprotein. This indicated that the uptake of low density lipoprotein by Kupffer and parenchymal cells was mediated by the low density lipoprotein receptor.

1,1′-dioctadecyl-3,3,3′,3′-tetramethyl indocarbocyanine perchlorate-acetylated low density lipoprotein was mainly taken up in situ by liver endothelial cells and by a minor population of Kupffer cells. Polyinosinic acid, a known inhibitor of the scavenger receptor, prevented the uptake by liver endothelial cells. Therefore human liver endothelial cells express active scavenger receptors on their surface.

Apolipoprotein E—free 1,1′-dioctadecyl-3,3,3′,3′-tetramethyl indocarbocyanine perchlorate-high density lipoprotein was found to be associated with the membrane of cultured liver parenchymal cells but was not taken up intracellularly, indicating a cholesterol exchange process occurring extracellularly at the plasma membrane. The cellular localization of lipoprotein receptors and uptake of the various classes of lipoproteins are comparable with the situation in rats. (HEPATOLOGY 1991;13:79-90.)
Aztreonam vs. cefotaxime in the treatment of gram-negative spontaneous peritonitis in cirrhotic patients
Authors: Ariza Javier , Xiol Xavier , Esteve Maria , Bañeres Fernando Fernández , Liñares Josefina , Alonso Teresa , Gudiol Francisco
Published: March 2007

Aztreonam and cefotaxime were compared in 44 cirrhotic patients who had 52 episodes of gramnegative spontaneous peritonitis. Patients were randomized into two therapeutic groups of similar characteristics. Group A (28 episodes) received 0.5 gm of aztreonam every 8 hr, and group B (24 episodes) received 1 gm of cefotaxime every 6 hr, for a planned 14-day period. Peak and trough serum and ascitic fluid levels of both antibiotics were several times higher than the minimum inhibitory concentrations of causative microorganisms. Eleven patients (21%) died within the first 48 hr after beginning therapy, which included seven in the aztreonam group and four in the cefotaxime group. In the remaining patients, signs and symptoms of infection were promptly controlled, and ascitic fluid cultures became negative after 48 hr in all cases, except in one patient from the aztreonam group, who was a clinical failure. Two patients from the aztreonam group and one from the cefotaxime group relapsed after treatment. The overall mortality rate was 50%, which was lower than classically reported: 12 patients (43%) died in the aztreonam group, and 14 (58%) died in the cefotaxime group (p = 0.265, NS). Hepatorenal syndrome and digestive tract hemorrhage were the most frequent causes of death occurring after the first 48 hr of treatment. Streptococcal superinfections developed in three patients (14.2%) in the aztreonam group. We conclude that both antibiotics at the low doses used in this study are similarly well tolerated and effective in controlling this infection. Because the use of aztreonam as the initial empirical treatment requires a concomitant antibiotic against gram-positive infections and the possibility of streptococcal superinfections, cefotaxime seems to be a more advantageous therapeutic alternative for this patient population. (HEPATOLOGY1991;14:91-98.)
Expression of androgen receptor mRNA in human hepatocellular carcinomas and hepatoma cell lines
Authors: Nakagama Hitoshi , Gunji Toshiaki , Ohnishi Shin , Kaneko Takashi , Ishikawa Takashi , Makino Reiko , Hayashi Kenshi , Shiga Junji , Takaku Fumimaro , Imawari Michio
Published: March 2007

The expression of androgen receptor messenger RNA in hepatocellular carcinomas and hepatoma cell lines was studied using Northern-blot analysis and the complementary DNA—polymerase chain reaction method. Androgen receptor messenger RNAs were detected (although in low levels) in both hepatocellular carcinoma tissues and noncancerous tissues of the liver in all eight cases we studied, except for the tumor sample of one case. None of the hepatoma cell lines studied, however, expressed detectable levels of androgen receptor messenger RNA except for the SKHEP-1 hepatoma cell line. (HEPATOLOGY 1991;14:99-102.)
Perfluorochemical emulsions decrease Kupffer cell phagocytosis
Authors: Bottalico Lori A. , Betensky Hannah T. , Min Young B. , Weinstock Shelley B.
Published: March 2007

One drawback to using perfluorochemical emulsions as blood substitutes is that perfluorochemical particles are cleared from the blood by the reticuloendothelial system, primarily liver and spleen. We measured the impact of two perfluorochemical emulsions on clearance of colloidal carbon (< 1 μm) and 51Cr-sheep red blood cells (about 8 μm) by the reticuloendothelial system in vivo and in the isolated perfused liver. Male rats were injected with 2 ml/100 gm body wt of Fluosol-DA or Oxypherol-ET for 4 consecutive days. Carbon (1 ml/100 gm body wt) or sheep red blood cells (0.05 ml of 5% vol/vol/100 gm body wt) were then injected intravenously (in vivo) or added to perfusate. Samples were taken at several time points for 1 hr. In the isolated perfused liver, carbon clearance was depressed by 25% 1 day after treatment. Rates returned to control levels by 12 days in Fluosol-DA—treated rats but remained depressed by 67% in Oxypherol-ET—treated rats. Sheep red blood cell (8 μm) clearance was two to five times slower than carbon clearance and depressed by 40% in livers from Fluosol-DA rats 1 day and 12 days after treatment. Added serum did not improve phagocytosis. In vivo carbon clearance remained normal in Fluosol-DA—treated rats but decreased by 74% in Oxypherol-ET—treated rats 1 day after treatment, returning to normal by 12 days. Clearance rates were similar in control rats in vivo and in the perfused liver. We conclude that the isolated perfused liver is a good model to measure liver clearance function. Although low doses of perfluorochemical emulsions may depress Kupffer cell phagocytosis, general reticuloendothelial system function is not significantly compromised. (HEPATOLOGY 1991;14:169-174.)
Purification of hepatocyte couplets by centrifugal elutriation
Authors: Wilton Joanne C. , Williams Delyth E. , Strain Alastair J. , Parslow Rosemary A. , Chipman Kevin J. , Coleman Roger
Published: March 2007

An initial preparation of rat hepatocytes containing approximately 30% couplets was enriched by centrifugal elutriation. Of the couplets loaded onto the elutriator, 87% were eluted at medium flow rates of 60 to 80 ml/min at a rotor speed of 1,100 rpm; cells eluted in this range maintained a viability of more than 95%. Peak fractions were enriched in couplets to 84.5% ± 2.5%. After elutriation, couplets retained the ability to secrete fluorescent cholephiles into sealed canalicular vacuoles. The preparation can now be used in hepatobiliary and hepatotoxicity studies not possible with preparations in which they are minor components. (HEPATOLOGY 1991;14:180-183.)
Hyperglycemia-induced cholestasis in the isolated perfused rat liver
Authors: Marin Jose J. G. , Bravo Pilar , Barriocanal Fernando Perez , El-Mir Mohamad Y. , Villanueva Gloria R.
Published: March 2007

In a previous report we showed that cholestasis in diabetic rats is due in part to hyperglycemia. To gain information about the mechanism responsible for this phenomenon, bile flow was studied in isolated perfused rat livers. The perfusion media were modified erythrocyte-free Krebs-Henseleit solutions. Under these experimental conditions, no cholestasis was observed in isolated rat livers obtained from rats treated with streptozotocin (6 mg/100 gm body wt) 6 days before the experiments. We then proceeded to use normal animals. The composition of the perfusion media was modified to maintain the osmolality even after increasing D-glucose concentrations from 0 to 35 mmol/L. Bile flow was not affected with doses up to 15 mmol/L D-glucose. Beyond a threshold value for plasma D-glucose concentrations between 15 and 20 mmol/L, cholestasis was observed. Using D-glucose analogs such as L-glucose and 3-O-methyl-D-glucose, bile flow was also reduced (by 0.54 and 0.53 μl/min/gm liver, respectively). Isosmotic sucrose-containing perfusion media were also observed to impair bile flow (by 0.66 μl/min/gm liver). However, i-erythritol and D-mannitol failed to inhibit bile formation. The study of bile/plasma concentration ratios determined using tracer amounts of radioactive sugars indicated that this value was much lower for cholestatic sucrose (0.11) and L-glucose (0.31) than for noncholestatic i-erythritol (0.99) and D-mannitol (0.98). Cholestasis was partly reversed after induction by 35 mmol/L D-glucose if perfusion media were replaced by sugar-free ones, but also by media containing 25 mmol/L D-glucose. Insulin given during the perfusion with sugar-free media was observed to have no effect on bile flow. However, this hormone induced a significant increase in bile flow when cholestasis had previously been induced by hyperglycemia. This was not due to changes in plasma D-glucose concentrations. Insulin was also observed to reduce the cholestasis induced by 3-O-methyl-D-glucose but not by L-glucose. This suggests a process in which D-glucose transport rather than metabolism is involved. Biliary D-glucose output was very low up to a threshold value for plasma D-glucose concentration similar to those observed in hyperglycemia-induced cholestasis. Beyond this, it increased proportionally to plasma D-glucose concentrations. Insulin had no effect on biliary D-glucose output in livers perfused with sugar-free media, but a stimulation of this process was observed when the hormone was administered to livers perfused with cholestatic concentrations of D-glucose. The addition of phloridzin greatly increased (threefold) insulin-induced D-glucose output into bile, but it abolished insulin-induced reduction of cholestasis. In summary, these results confirm that hyperosmolality is not mandatory for hyperglycemia-induced cholestasis and that insulin deficiency may play a direct role in the cholestasis observed in diabetes. (HEPATOLOGY 1991;14:184-191.)
Evaluation of laser spallation as a technique for measurement of cell adhesion strength
Authors: Hagerman Elizabeth , Shim Jaewoo , Gupta Vijay , Wu Ben
Published: March 2007

Cell adhesion to material surfaces is one of the fundamental phenomena of cellular response to implanted devices. Controlling the strength, dynamics, and mechanics of cell adhesion offer opportunities for designing novel biomaterials for tissue engineering and biotechnology. Many techniques have been developed for the purpose of quantifying various types of cell–biomaterial interaction. One method to evaluate cell affinity for a biomaterial is to measure the stress required to remove adherent cells from the material. This study investigates the possibility of using laser spallation, a technique previously developed for measuring the tensile strength of thin film interfaces, for evaluation of initial cell attachment strength. MC3T3‐E1 preosteoblasts were cultured on fibronectin‐coated polystyrene, a surface known to engage cells in receptor mediated adhesion, and untreated polystyrene, which elicit nonspecific adhesion mechanisms during early stages of cell attachment. The laser spallation technique effectively detached cells from polymer substrates and also distinguished relative cell adhesion strengths to surfaces with known differences in cell binding affinities. Scanning electron micrographs determined that cell detachment resulting from laser spallation left a cleaner surface than jet impingement, possibly suggesting a more complete detachment mechanism. Absolute values of adhesion strengths determined by laser spallation were significantly higher than those found using jet impingement, a previously reported hydrodynamic technique. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Mechanism of degradation of AgCL coating on biopotential sensors
Authors: Shih Chun‐Che , Shih Chun‐Ming , Chou Kuang‐Yi , Lin Shing‐Jong , Su Yea‐Yang , Gerhardt Rosario A.
Published: March 2007

AgCl coated Ag foil has been widely used as the biopotential sensor to diagnose problems of the human heart. Evidence shows that quality of AgCl on the electrode could experience degradation during the process of long‐term monitoring for irregular activities of the heart. To study the degradation of AgCl/Ag electrode, new and used electrodes were collected. Electrochemical tests such as open‐circuit potential (OCP), cathodic stripping, electrochemical impedance spectroscopy (EIS), scanning electron microscopy (SEM), and X‐ray mapping of elemental distribution were applied to understand the electrochemical properties of the sensors during the progress of degradation. Results revealed that OCP values shift from positive potential of new sensor to negative potential of used sensor (OCPnew: +30 mV; OCPused: −300 mV, p < 0.05) and a significant difference in impedance (Impedancenew: 3000 Ω; Impedanceused: 1 MΩ, p < 0.05). Ratio of the average AgCl thickness on good and bad eletrocardiographic (ECG or EKG) electrodes is 4.83 (p < 0.05). Simulated degradation by exposing the biosensor to deaerated sweat solution and by cathodic stripping of AgCl proposed that the degradation occurs by cathodic reduction of AgCl due to the presence of hydrogen ions in the low pH value of human sweat under deaerated condition. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Rapid aqueous photo‐polymerization route to polymer and polymer‐composite hydrogel 3D inverted colloidal crystal scaffolds
Authors: Liu Yuanfang , Wang Shaopeng , Krouse Justin , Kotov Nicholas A. , Eghtedari Mohammad , Vargas Gracie , Motamedi Massoud
Published: March 2007

Successful regeneration of biological tissues in vitro requires the utilization of three‐dimensional (3D) scaffolds that provide a near natural microenvironment for progenitor cells to grow, interact, replicate, and differentiate to form target tissues. In this work, a rapid aqueous photo‐polymerization route was developed toward the fabrication of a variety of polymer hydrogel 3D inverted colloidal crystal (ICC) scaffolds having different physical and chemical properties. To demonstrate the versatility of this technique, a variety of polymer hydrogel ICC scaffolds were prepared, including (1) polyacrylamide (pAAM) scaffolds, (2) poly(2‐hydroxyethyl methacrylate) (pHEMA) scaffolds, (3) poly(2‐hydroxyethyl acrylate) (pHEA) scaffolds, and composite scaffolds including (4) pAAM‐pHEMA scaffolds, (5) pHEMA‐pMAETAC [poly(2‐methacryloyloxy) trimethyl ammonium] scaffolds, and (6) pHEA‐pMEATAC scaffolds. Templates for scaffolds incorporated both uniform sized (104 μm diameter) and nonuniform sized (100 ± 20 μm diameter) closely packed noncrosslinked poly(methyl methacrylate) beads. Human bone marrow stromal HS‐5 cells were cultured on the six different types of scaffolds to demonstrate biocompatibility. Experimental results show that cells can remain viable in these scaffolds for at least 5 weeks. Of the six scaffolds, maximal cell adhesion and proliferation are obtained on the positively charged composite hydrogel pHEMA‐pMEATAC and pHEA‐pMAETAC scaffolds. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Incidental magnetization transfer effects in multislice brain MRI at 3.0T
Authors: Chang Yongmin , Bae Sung Jin , Lee Young Ju , Hwang Moon Jung , Lee Sang Heun , Lee Jongmin , Lee Sang Kwon , Woo Seongku
Published: March 2007

Purpose

To evaluate the effect of incidental magnetization transfer (iMT) in multislice brain imaging at 3.0T.

Materials and Methods

The contribution of iMT to multislice brain MRI was evaluated at 3.0T. In 10 normal subjects we obtained multislice fast spin‐echo (FSE) MR images using a 16‐echo pulse train without an off‐resonance MT pulse at 3.0T and 1.5T. We quantified the extent of iMT by calculating the iMT ratio (iMTR).

Results

We found that the iMT contrast (iMTC) has a greater effect at 3.0T. As the number of slices increased in multislice FSE imaging, the difference between two field strengths became larger. Compared to WM structures, however, the difference in iMT effect between 1.5T and 3.0T was smaller in the case of GM structures.

Conclusion

The iMTC has a greater effect at 3.0T. The strength of the iMT is different for different tissue types and also varies according to the number of slices used. J. Magn. Reson. Imaging 2007. © 2007 Wiley‐Liss, Inc.
Propagation of JC virus in human neuroblastoma cell line IMR‐32
Authors: Akatani Kaoru , Imai Mayumi , Kimura Michio , Nagashima Kazuo , Ikegami Nobuko
Published: March 2007

JC virus (JCV), the causative agent of a human demyelinating disease, progressive multifocal leukoencephalopathy, has a very narrow host range. Cells permissive for infection by JCV have been essentially limited to primary human fetal glial cells, which are difficult to obtain and maintain. In pilot studies, it was found that JCV can multiply in an established cell line of human neuroblastoma. JCV strains Mad‐1 and Tokyo‐1 were inoculated, respectively, into two cell lines, IMR‐32 (neuroblastoma) and A‐172 (glioblastoma). Viral infection with cytopathic effect was observed only in IMR‐32 cells, and the most efficient viral proliferation was obtained in cells cultured in medium containing 2% fetal calf serum (FCS). Both Mad‐1 and Tokyo‐1 strains propagated well, with the former being more efficient than the latter. Viral replication was confirmed by immunofluorescence, electron microscopy, and a hemagglutination assay. Sodium dodecyl sulfate (SDS)‐polyacrylamide gel electrophore‐sis and Western blot analysis of the purified virus revealed the characteristic JCV protein profile. Thus, IMR‐32 cells have been found to be permissive for JCV, which should provide a useful system for further studies of virus proliferation and viral tissue tropism. © 1994 Wiley‐Liss, Inc.
Locations of antibody binding sites within conserved regions of the hepatitis C virus core protein
Authors: Sällberg Matti , Pumpen Pauls , Zhang Zhu‐Xu , Lundholm Peter , Gusars Indulis , Rudén Ulla , Wahren Britta , Magnius Lars O.
Published: March 2007

The binding sites for human antibodies recognising antigenic domains within the hepatitis C virus (HCV) core protein were analyzed using synthetic peptides. Omission peptide analogues where a pair of residues was sequentially omitted were produced corresponding to the regions 1–18, 11–28, 21–38, 51–68, and 101–118. The N‐terminal part of HCV core was found to contain three distinct antibody binding sites, which includes the previously reported one at residues 9–16. The other two were located at residues 19–26 and residues 29–34. Within the region 51–68 two overlapping sites were found, the first at residues 51–60 and the second at residues 59–68. Within the region 101–118, residues 107–114 were identified as the binding site, which contains two residues differing between genotypes I/II and III/VI. Thus the HCV core protein contains at least six distinct linear antibody binding sites, located at regions highly conserved between the genotypes of HCV. The human recognition of these regions show a variation with respect to the amino‐ and carboxy‐terminal extension of each individual binding site. These findings will have implications for the prediction of the structure of the HCV core protein, since these antibody binding sequences are likely to be more or less accessible from the exterior of either, or both, of the native HCV core and its precursor polyprotein. © 1994 Wiley‐Liss, Inc.
Identification of adenoviruses in faeces from patients with diarrhoea at the hospitals for sick children, London, 1989–1992
Authors: Noel J. , Mansoor A. , Thaker U. , Herrmann J. , Perron‐Henry D. , Cubitt W. D.
Published: March 2007

Faecal samples from 137 patients that had been shown to contain adenoviruses by electron microscopy were identified in a series of enzyme immunoassays (EIA) using a single monoclonal antibody (Mab) to adenovirus 40 and four different Mabs to adenovirus 41. Adenoviruses were partially characterised by restriction enzyme analysis (REA) of DNA extracts using Smal. Samples were also run in a commercial EIA (Adenovirus IDEIA; Dako, Ltd.) which detects group antigen. The majority (84%) of adenoviruses were subgenus F: adenovirus type 41, 87 (64%) and adenovirus type 40, 28 (20.4%). Subgenus A viruses were identified in ten, (7%) patients, eight were type 31, and two type 12. The adeno IDEIA test was sensitive and specific, detecting 127 of 131 positives and giving no false‐positive results with other enteric viruses. Use of monoclonal‐based ElAs showed significant differences depending on which adeno 41 Mab was used, although the restriction patterns obtained using Smal appeared to be identical for 66 of 69 samples that produced recognisable bands. The Mab that performed best, M 4.3.1, was raised against strains obtained from children in England and detected 83 of 84 (99%) of the adenovirus 41 samples tested. In contrast Mab JH/41 raised against the prototype strain of adenovirus 41 (Tak) detected only 69 of 87 (79%). © 1994 Wiley‐Liss, Inc.
Studies of the pathogenesis of wild‐type virus and six temperature‐sensitive mutants of mouse cytomegalovirus
Authors: Furrarah A. M. , Sweet C.
Published: March 2007

A comparison of six temperature‐sensitive (ts) mutants with the parental wild‐type (wt) virus showed that, when 1‐week‐old BALB/c mice were inoculated intraperitoneally with 300 pfu of mouse passaged virus, the viruses could be broadly categorized into two groups. Two viruses (wt and tsm6) were lethal at this dose (10 and 2 LD50 respectively); animals died within 4–6 days of inoculation and the virus became generalized infecting heart, lung, liver, spleen, kidney, and salivary glands to high titre (>4.3 log10 pfu/ g). In contrast, for viruses (tsm1,tsm3, and tsm4) not lethal at this dose (300 pfu = 0.1 to 0.25 LD50), viral replication was poor (<3.4 log10 pfu/g) except in the salivary glands (5.6 to 7.5 log10 pfu/g). Mutant tsm5 failed to replicate in any tissue while mutant tsm2, lethal at this dose (300 pfu = 1 LD50), produced levels of virus similar to those found with tsm1, tsm3, and tsm4. Comparison of all viruses at sub‐lethal doses (0.1 to 0.25 LD50) did show minor differences in their replication in heart, and in levels of virus and duration of infection in kidney and salivary glands. More marked differences were evident between the viruses in their ability to be reactivated from the latent state during immunosuppression. Wild‐type virus was most easily reactivated in that 67% of animals exhibited virus in salivary glands, heart, lung, spleen, and kidney. Mutants tsm1, tsm2, tsm3 and tsm6 could be reactivated but from fewer animals (33%, 33%, 18%, and 38% respectively) and fewer tissues. Mutants tsm4 and tsm5 could not be reactivated. Differences in the ability of the viruses to replicate in the lungs and to cause penumonitis in intranasally‐inoculated immunosuppressed mice were also seen. Although immunosuppression was necessary for the induction of severe pneumonitis, differences in severity of pneumonitis resulted from differences in the ability of the mutants to replicate in the lung in vivo. These different mutants should prove useful for examining the viral and host factors involved in CMV‐induced pneumonitis, and for examining mechanisms involved in latency and reactivation. © 1994 Wiley‐Liss, Inc.
Antibodies to hepatitis E virus among chinese patients with acute hepatitis in Taiwan
Authors: Tsai Jung‐Fa , Jeng Jen‐Eing , Chang Wen‐Yu , Lin Zu‐Yau , Tsai Juei‐Hsiung
Published: March 2007

The prevalence of antibodies to hepatitis E virus (anti‐HEV) was investigated in patients with acute hepatitis, and correlated with the clinical features. Sera from 110 patients with acute hepatitis and 60 healthy controls were tested for anti‐HEV, antibody to hepatitis C virus (anti‐HCV), and hepatitis B surface antigen (HBsAg). There were significant differences in the prevalence of anti‐HEV, anti‐HCV, and HBsAg between patients and controls (21.8% vs. 0%, 16.3% vs. 1.6% and 58.1% vs. 18.0%, respectively). Anti‐HEV was detected in 6 (25.0%) of 24 patients with anti‐HCV, 6 (9.3%) of 64 patients with HBsAg, and another 6 (22.2%) of 27 patients with acute hepatitis non‐A, non‐B, non‐C. Anti‐HEV was found in 15 men and three women, whose ages ranged from 34 to 75 (median, 57) years old. The median age of patients with anti‐HEV was older than that in patients without this antibody (57 vs. 38 years; P = 0.001). The prevalence of anti‐HEV in patients with anti‐HCV alone (35.2%) was higher than that (11.1%) in patients with HBsAg alone (P = 0.03). Compared to patients without anti‐HEV, HEV‐infected patients had a higher frequency of travel to a foreign country (P = 0.0001), had a lower HBsAg rate (P = 0.019), and had higher serum alkaline phosphatase levels (P = 0.04) and gamma‐glutamyl transpeptidase levels (P = 0.01). In conclusion, HEV infection occurs in 22.2% of patients with acute hepatitis non‐A, non‐B, non‐C. HEV superinfection may occur in patients with chronic hepatitis B or C virus infection. © 1994 Wiley‐Liss, Inc.
Antibody response to E6, E7, and L1 proteins of human papillomavirus 16 in an Italian population
Authors: Di Lonardo A. , Campo M. S. , Venuti A. , Marcante M. L.
Published: March 2007

The serological response to human papillomavirus type 16 (HPV16) E6, E7, and L1 proteins was investigated in Italian patients with cervical cancer, cervical intraepithelial neoplasia (CIN), flat cervical warts, condylomas, and in healthy individuals. Bacterially expressed β‐galactosidase fusion proteins were purified and used as antigen in Western blot assays. The HPV16 DNA status was also determined in most of the women. The incidence of antibody response to E6 and E7 proteins was higher in cervical cancer than in CIN patients. No variation of antibody titre against E6 was observed in the cervical cancer patients, while one patient in an advanced stage of disease displayed very high levels of E7 antibodies. High seroprevalence to both E6 and L1 was observed in patients with genital condylomas, but this may be due to cross‐reactivity between HPV6 or 11 antibodies and the experimental HPV16 antigens. Antibodies to L1 were detected in control women, suggesting that HPV infection is widespread. The data obtained in this study are in agreement with previous findings in Other countries. © 1994 Wiley‐Liss, Inc.
Cervical cytomegalovirus infection in prostitutes and in women attending a sexually transmitted disease clinic
Authors: Shen Chen‐Yang , Chang Shu‐Fen , Lin Hwa‐Jen , Ho Hon‐Nan , Yeh Te‐Shien , Yang Show‐Lin , Huang Eng‐Shang , Wu Cheng‐Wen
Published: March 2007

This study aimed to determine the frequency of, and to define factors associated with, cervical shedding of Cytomegalovirus (CMV) in highly sexually active women (licensed prostitutes) and in women attending a sexually transmitted disease (STD) clinic. Cervical specimens obtained from 195 licensed prostitutes and 187 STD patients aged 17‐50 years were compared for the presence of cervical CMV with specimens from 70 women of the same ages attending a gynecologic clinic. Cervical CMV was identified by the presence of a CMV specific immediate‐early gene sequence amplified by the polymerase chain reaction. Cervical CMV prevalences of 38.9% and 34.8% were found for licensed prostitutes and STD patients, respectively. These rates were significantly higher than the 24.3% cervical CMV prevalence for women attending the gynecologic clinic. The data suggest that frequent sexual contact with many sexual partners is responsible for the high frequency of cervical CMV observed in licensed prostitutes. The interaction between CMV and urogenital bacterial infections is a plausible explanation for the high cervical CMV prevalence in STD patients. © 1994 Wiley‐Liss, Inc.
Hepatitis E—An important cause of imported non‐A, non‐B hepatitis among migrant workers in Qatar
Authors: Shidrawi Ray G. , Skidmore Susan J. , Coleman Jonathan C. , Dayton Ralph , Murray‐Lyon Iain M.
Published: March 2007

In 1985, Glynn et al. [Journal of Medical Virology 17:371–375] reported on epidemic viral hepatitis in Qatar and concluded that 72% (91/126) had acute enteric ally transmitted non‐A, non‐B viral hepatitis (ET‐NANBH). Most of the patients (98%) presented within 8 weeks of arrival in Qatar and were migrant workers from the Indian subcontinent. The data was reanalyzeda for evidence of infection with hepatitis E virus (HEV). Seventy‐eight of 91 (86%) of stored sera were still suitable for analysis since collection in 1981. A newly described enzyme immunoassay (EIA) for both IgG and IgM anti‐HEV was used (Abbott Laboratories, Delkenheim, Germany); 59/78 (76%) were positive for either or both assays. All but two were from the Indian subcontinent. The data suggest that HEV was the major cause of ET‐NANBH in Qatar in 1981, particularly among newly arrived migrant workers from the Indian subcontinent. © 1994 Wiley‐Liss, Inc.
Immunoglobulin M and A antibodies to hepatitis C core antigen in chronic hepatitis C virus infection
Authors: Lau George K. K. , Lesniewski Richard , Johnson Rhonda G. , Davis Gary L. , Lau Johnson Y. N.
Published: March 2007

To determine the prevalence and clinical significance of IgM and IgA antibody to hepatitis C virus (HCV) core antigen in chronic HCV infection, sera from 47 patients were tested for immunoglobulin class M (IgM) and immunoglobulin A (IgA) antibody to HCV core antigen by solid‐phase enzyme‐linked immunoassay using a re‐combinant core protein (aa1‐‐150). Results were correlated with the clinical, biochemical and histological parameters, serum HCV RNA levels (determined by branched DNA signal amplification assay), and subsequent clinical response to in‐terferon‐α therapy. IgM anti‐HCV core was detected in 11 patients (23.4 percent). There was no correlation between the presence of IgM anti‐HCV core and the clinical features (sex, age, mode of acquisition), biochemical parameters (serum ALT, AST, alkaline phosphatase, and albumin level), autoimmune markers [serum globulin levels, anti‐nuclear antibody (+ at < 1:80 in 7/47 patients)], serum HCV RNA levels, subsequent response to interferon‐α therapy, and the histological features. Immunoglobulin A anti‐HCV core was not detected in any of the patients. The presence of IgM ant‐HCV core in a proportion of patients with chronic HCV infection indicates that the presence of serum IgM anti‐HCV core may not be unique to acute HCV infection. © 1994 Wiley‐Liss, Inc.
Case report: Psychosis associated with hepatitis B
Authors: Weber H. C. , Schoeman J. F. , Nowitz A. , Becker M. L. B.
Published: March 2007

An acute disintegrative disorder in a child with acute hepatitis B virus (HBV) infection is described. Both hepatitis B surface antigen (HBsAg) and HBV‐DNA were detected in cere‐brospinal fluid (CSF) by means of enzyme‐linked immunosorbent assay (ELISA) and the poly‐merase chain reaction (PCR) technique respectively. A markedly elevated level of CSF adeny‐late kinase (AK), which normalised as the patient recovered spontaneously, suggested an organic brain disorder. Demonstration of intra‐blood‐brain barrier production of IgG supported the possibility of local infection by HBV within the central nervous system. © 1994 Wiley‐Liss, inc.
Atypical strain of hepatitis E virus (HEV) from North India
Authors: Chauhan Ashok , Dilawari J. B. , Kaur Upjeet , Ganguly N. K. , Bushnurmath S. , Chawla Y. K.
Published: March 2007

Hepatitis E virus (HEV) infection was detected during an epidemic in North India. Virus particles present in the stool of an acutely ill patient (YAM‐67) was transmitted intravenously into rhesus monkeys (M. mulata) and orally to a human volunteer. Virus‐like particles (VLPs) of 32–34 nm were detected in the bile of monkeys and in the stools of the human volunteer by means of solid phase immune electron microscopy (SPIEM) with acute homologous and heterologous sera. The VLPs were confirmed to be HEV by a reverse transcription polymerase chain reaction (RT‐PCR). Virus‐like particles from human volunteer stools were passaged further into rhesus monkeys. A bimodal rise in aminotransferase levels were observed in the animals, and liver histopa‐thology indicated mild to severe form of hepatitis. Further, SPIEM and RT‐PCR analysis in monkey bile revealed presence of virus from 15 to 45 days post‐inoculation. Rechallenge of the animals 6 months after recovery with the same viral inoculum failed to produce abnormal liver function tests indicating the presence of protective immunity during this period. The VLPs in the stool from the patient (YAM‐67) with epidemic hepatitis were found to retain infectivity even after several cycles of freeze‐thawing and exposure at 37°C for 2 days. Moreover, these VLPs from the patient, human volunteer, and monkeys did not react with an anti‐HEV chimpanzee serum from NIH, Bethesda, MD. These findings indicate that this North India isolate of HEV is an atypical strain of HEV. The present study further validates that the rhesus monkey is a suitable experimental model for HEV. © 1994 Wiley‐Liss, Inc.
Elevated rubella antibodies in patients with chronic liver disease
Authors: Kalvenes May Britt , Flø Reinhardt , Kalland Karl‐Henning , Haukenes Gunnar
Published: March 2007

Patients with autoimmune chronic active hepatitis (AICAH) and certain other chronic liver disorders often have very high titres of haemagglutination ‐inhibition (HI) antibodies to rubella virus. In this study it is shown, using floatation centrifugation, that the high rubella HI reactivity is not caused by nonspecific lipoprotein inhibitors but rather by antibodies specific for the rubella haemagglutinin (E1 glycoprotein). After sucrose density gradient ultracentrifugation of sera the major HI reactivity was recovered in the IgG containing fractions. The IgG antibody fraction was strongly reactive by an indirect enzyme‐linked immunosorbent assay (ELISA). Higher prevalence and titres of rubella antibodies were also demonstrated by the complement fixation (CF) test using a haemagglutinin‐free antigen, and by an indirect haemagglutination (IHA) test (Rubacell) using a cell‐associated antigen which is distinct from the antigens used in the HI and CF tests. This high rubella antibody response is therefore demonstrated using three distinct antigen‐antibody systems. By means of absorption experiments and radioimmunoprecipitation assays the coating antigen used in the IHA test was shown to reside in the E2 glycoprotein. The cause of this enhanced antibody response to rubella virus structural proteins remains elusive. © 1994 Wiley‐Liss, Inc.
Hepatitis C virus antibody prevalence among human immunodeficiency virus‐1‐infected individuals: Analysis with different test systems
Authors: Nübling Claudius Micha , Von Wangenheim Gudrun , Staszewski Schlomo , Löwer Johannes
Published: March 2007

Sera of 383 human immunodeficiency virus (HIV)‐l‐infected individuals from Frankfurt (Main)/Germany were assayed by two hepatitis C virus (HCV) screening tests (Abbott second generation, Ortho second generation). This population showed a prevalence for reactivity with both tests of 20.8% (80/383). Examination of all reactive sera (91/383) by a supplemental assay (Chiron RIBA 2) gave for 46 sera a positive, for 33 sera an indeterminate, and for 12 sera a negative result. Further analysis focussed on these RIBA 2‐indeterminate and ‐negative samples. Analysis of the sera using an in‐house Western blot with three different Escherichia coli‐expressed HCV proteins revealed that none of the RIBA 2‐nega‐tive, but 24 of the 33 RIBA 2‐indeterminate sera, including 3 of 4 c33c (NSS)‐reactive samples, were reactive with a recombinant core protein. Twenty‐one of 22 c22‐3 (core) indeterminates stained the core antigen in the in‐house Western blot and 3 of them in addition a NS5 moiety. HCV‐polymerase chain reaction (PCR) was positive for 14 of the 24 RIBA 2 ‐indeterminate sera, but for none of the RIBA 2‐negative or Western blot nonreactive samples. Discrepant results between the two screening tests could not be explained by differences in the antigen compositions (i.e., a NS3‐NS4 moiety of 111 amino acids present in the Ortho enzyme‐linked immunosor‐bent assay (ELISA), not present in the Abbott or RIBA 2 assays). © 1994 Wiley‐Liss, Inc.
Evidence for superantigen activity of the bel 3 protein of the human foamy virus
Authors: Weissenberger Jakob , Altmann Annette , Meuer Stefan , Flügel Rolf M.
Published: March 2007

The human foamy virus is a complex retrovirus that codes for several regulatory bel genes in addition to the conventional gag, pol, and env genes. The bel 3 gene is located in the 3′part of the viral genome comparable to that of the superantigen of the mouse mammary tumor virus. Superantigens bound to major histocompatibility complex (MHC) class II molecules have been shown to stimulate T cells in a Vp‐specific manner. The recombinant Bel 3 protein purified to near homogeneity was assayed in vitro to determine whether or not it functions as a superantigen that stimulates human T lymphocytes expressing particular Vβ T cell receptor (TCP) chains. Therefore, an analysis including all known human Vβ elements was performed. The expression of different Vβ chains of the TCR was analyzed by reverse transcription of the Vp RNAs and subsequent amplification of the corresponding Vβ cDNA elements by polymerase chain reaction in unstimulated, phytohemaggluttinin (PHA)‐ and Bel 3‐stimulated human T lymphocytes. In addition, eight monoclonal antibodies directed against particular Vβ family members were used to determine any change in the expression of the remaining known Vβ elements upon treatment with PHA and Bel 3. The comparative Vp‐specific transcriptional analysis revealed that the in vitro expression of the Vβ18 chain was specifically and strongly expanded in Bel 3‐stimulated human T cells, a property characteristic for a superantigen. © 1994 Wiley‐Liss, Inc.
Genotype distribution of hepatitis C virus infection in Taiwan
Authors: Wu Jau‐Shin , Lee Han‐Fang , Hsiau Hui‐Ling , Lu Hsiu‐Ying , Chou Wen‐Hsiang , Lu Chih‐Feng , Chen Hour‐Young , Lee Fong‐Nien , Chen Pei‐Yuan , Tarn Kim‐Man
Published: March 2007

To investigate the prevalence of genotype distribution of hepatitis C virus (HCV) infection in Taiwan, genotypes were identified in 122 (36 anti‐HCV‐positive blood donors, 44 anti‐HCV‐positive aborigines, 28 hemodialysis patients, and 14 patients with chronic liver diseases) of 280 subjects, using polymerase chain reaction by Okamoto's type‐specific primer method. Type II was the dominant (66.7%) type among anti‐HCV‐positive blood donors, followed by type III and type IV with the same percentages (16.7%), while none of type I was detected. The prevalence of genotype distribution were 75.0%, 81.1%, and 64.3% for type 11,4.6%, 17.9%, and 21.4% for type III, 13.6%, 0%, and 7.1% for type IV, for the aborigines, hemodialysis, and chronic liver diseases groups, respectively. Four subjects revealed mixed infections by two different genotypes: two cases of II and III; and each one case of II and IV, and III and IV. Diverse genotype distributions in two hemodialysis groups disclose the existence of obvious regional differences even within a region. The results reveal the highest prevalence of type II as in Japan. However, there is a higher prevalence rate of type IV than in Japan. © 1994 Wiley‐Liss, inc.
Immune responses of blood donors to peptides of various lengths and those with genotypic sequence variations corresponding to the N‐terminal portion of the core protein of hepatitis C virus
Authors: Sato Atsushi , Sho Yukihiko , Nakamura Haruji , Kunitomo Tetsunosuke , Arima Terukatsu
Published: March 2007

Immune reactivities of blood donor sera with the peptides of various lengths (24, 30, 40 and 50 mer) and those with genotypic sequence variations in the N‐terminal portion of the core protein of hepatitis C virus (HCV) were compared by enzyme‐linked immunosorbent assays. It was found that a 40‐mer oligopeptide (amino acids 2–41) was recognized more frequently than other peptides even in serum samples that did not react with the C22‐3 (core) by the recombinant immunoblot assay (RIBA‐II). On the other hand, a 30‐mer peptide (amino acids 1–30) had good correlation with viremia as confirmed by the polymerase chain reaction (PCR). In addition, four individuals showed the obvious differences in the immune responses to 30‐mer oligopep‐tides representing the 4 genotypic variations. As a result, some samples that were PCR‐positive but nonreactive by a commercial assay were found to react with short synthetic peptides in the N‐terminal portion of the core protein. © 1994 Wiley‐Liss, Inc.