bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunophenotyping of lymphocytes in liver tissue of patients with chronic liver diseases by flow cytometry
Authors: Li Xiuming , Jeffers Lennox J. , Reddy Rajender K. , de Medina Maria , Silva Marcelo , Villanueva Steven , Klimas Nancy G. , Esquenazi Violet , Schiff Eugene R. 
Published: March 2007

Immunological factors are important in the pathogenesis of a spectrum of hepatobiliary diseases. To characterize the nature of specific immunological responses in liver disease, we determined lymphocyte changes in liver tissue and in blood using flow cytometry. A total of 113 liver biopsy specimens was collected from patients with the following diseases: 19 chronic hepatitis B; 39 chronic non-A, non-B hepatitis; 27 alcoholic liver disease; 10 hepatic malignancy; 8 autoimmune hepatitis; 6 fatty liver and 4 primary biliary cirrhosis. The lymphocytes were isolated from the liver biopsy specimens by mechanical and enzymatic methods. The lymphocyte yield was 7,901 ± 575 cells/mg of liver tissue. The viability of lymphocytes was 97.7% ± 0.3%. Lymphocytes were stained with four pairs of two-color mixed fluorescein—conjugated monoclonal antibodies, including T4-T8 (CD4/CD8), T11-B1 (CD2-CD20), NKH1-T8 (CD56-CD8), IL-2R1-T11 (CD25-CD2), and the ratios were determined by an Epics Profile flow cytometer. Immunophenotyping of lymphocytes in whole blood samples was simultaneously analyzed.
Variability in lymphocyte yield and different patterns of lymphocyte subsets were found in the liver biopsy specimens. The yields of lymphocytes from patients with chronic non-A, non-B and autoimmune hepatitis were highest, and the lowest yield was from patients with fatty liver. Patients with primary biliary cirrhosis, fatty liver and hepatic malignancy had relatively high ratios of CD4/CD8, CD56/CD8 and CD25/CD2; whereas patients with chronic hepatitis B, autoimmune hepatitis and non-A, non-B hepatitis had lower ratios of CD4/CD8, CD56/CD8 and CD25/CD2. No difference in lymphocyte ratios between the patients with cirrhotic and noncirrhotic alcoholic liver disease was found. The ratio of CD2/CD20 decreased, and the ratios of CD56/CD8 and CD25/CD2 increased in patients with chronic non-A, non-B hepatitis after 6 mo of interferon treatment, whereas no significant changes occurred in subsets in patients with chronic hepatitis B. The patterns of lymphocyte subsets in blood samples did not correlate with those found in the corresponding liver samples.
These results demonstrate the feasibility of immunophenotyping lymphocyte subpopulations in small liver biopsy specimens using a novel approach. Such methodology is needed to establish the immunological mechanisms in liver damage and the effects of therapy. (HEPATOLOGY 1991;14:121-127.)
Anodized titanium and stainless steel in contact with CFRP: An electrochemical approach considering galvanic corrosion
Authors: Mueller Yves , Tognini Roger , Mayer Joerg , Virtanen Sannakaisa 
Published: March 2007

AbstractThe combination of different materials in an implant gives the opportunity to better fulfill the requirements that are needed to improve the healing process. However, using different materials increases the risk of galvanic coupling corrosion. In this study, coupling effects of gold‐anodized titanium, stainless steel for biomedical applications, carbon fiber reinforced polyetheretherketone (CFRP), and CFRP containing tantalum fibers are investigated electrochemically and by long‐term immersion experiments in simulated body fluid (SBF). Potentiodynamic polarization experiments (i/E curves) and electrochemical impedance spectroscopy (EIS) of the separated materials showed a passive behavior of the metallic samples. Anodized titanium showed no corrosion attacks, whereas stainless steel is highly susceptibility for localized corrosion. On the other side, an active dissolution behavior of both of the CFRPs in the given environment could be determined, leading to delaminating of the carbon fibers from the matrix. Long‐term immersion experiments were carried out using a set‐up especially developed to simulate coupling conditions of a point contact fixator system (PC‐Fix) in a biological environment. Electrochemical data were acquired in situ during the whole immersion time. The results of the immersion experiments correlate with the findings of the electrochemical investigation. Localized corrosion attacks were found on stainless steel, whereas anodized titanium showed no corrosion attacks. No significant differences between the two CFRP types could be found. Galvanic coupling corrosion in combination with crevice conditions and possible corrosion mechanisms are discussed. © 2007 Wiley Periodicals, Inc. JBiomed Mater Res, 2007
Surface engineering of titanium thin films with silk fibroin via layer‐by‐layer technique and its effects on osteoblast growth behavior
Authors: Cai Kaiyong , Hu Yan , Jandt Klaus D. 
Published: March 2007

AbstractThe objective of the present study was to surface modify the titanium thin films to improve its biocompatibility. A layer‐by‐layer (LBL) self‐assembly technique, based on the electrostatic interactions mediated adsorption of chitosan (Chi) and silk fibroin (SF), was used leading to the formation of multilayers on the titanium thin film surfaces. The surface chemistry and wettability of LBL films were investigated by X‐ray photoelectron spectroscopy (XPS), water contact angle measurement, and atomic force microscopy, respectively. XPS and contact angle measurement results indicated that a full SF/Chi pair film was formed after the deposition layers of PEI/(SF/Chi)2 on the titanium film surfaces. The topographies of multilayered films were directly related to the corresponding outmost layer components. The build‐up of such SF/Chi pair films on titanium films may in turn affect the biocompatibility of the modified titanium films. Therefore, an in vitro investigation was performed to confirm this hypothesis. Cell proliferation, cell viability, DNA synthesis as well as differentiation function (alkaline phosphatase) of osteoblasts on LBL‐modified titanium films and control samples were investigated, respectively. Osteoblasts cultured on modified titanium films was found to be higher proliferation tendency than that on control (p < 0.05). Cell viability, alkaline phosphatase as well as DNA synthesis measurement indicated that osteoblasts on LBL‐modified films were greater (p < 0.05 or p < 0.01) than the control, respectively. These results suggest that surface engineering of titanium was successfully achieved via LBL deposition of Chi/SF pairs, and enhanced its cell biocompatibility. The approach presented in the study may be exploited as an efficient alternative for surface engineering of titanium‐based implants. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
The interaction between hydrolytic and oxidative pathways in macrophage‐mediated polyurethane degradation
Authors: McBane Joanne E. , Santerre J. Paul , Labow Rosalind S. 
Published: March 2007

AbstractAlthough relatively resistant to oxidation, polycarbonate‐based polyurethanes (PCNUs) are degraded by monocyte‐derived macrophages (MDM) by a co‐mediated mechanism involving both hydrolytic and oxidative pathways. Since a previous study showed that PCNU pretreatment with H2O2 modulated degradation by esterases, human MDM were used to further elucidate this dual pathway mechanism of degradation for 14C‐radiolabeled PCNUs (synthesized with 1,6‐hexane diisocyanate:polycarbonatediol: butanediol with different stoichiometry (HDI431 and HDI321) or another diisocyanate 4,4′‐methylene bisphenyl diisocyanate (MDI321)). Scanning electron microscopy of PCNU slips pretreated with 20% H2O2 showed that HDI431 had visible holes with more radiolabel release than from the other PCNUs. When MDM were seeded on H2O2‐treated PCNUs, degradation of HDI321 and MDI321, but not HDI431 was decreased. Esterase activity was inhibited in MDM on all surfaces except MDI321, whereas inhibition of acid phosphatase occurred on all surfaces. The material surface itself, induced H2O2 release from live MDM, with more H2O2 elicited by phorbol myristate acetate treated MDM when cultured on HDI431 but not the other materials. H2O2 pretreatment affected cell function by chemically altering the material surface and MDM‐mediated degradation, known to be dependent on surface chemistry. The findings highlight that both oxidative and hydrolytic mechanisms need to be understood in order to tailor material chemistry to produce desired cell responses for in vivo applications. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Novel low temperature setting nanocrystalline calcium phosphate cements for bone repair: Osteoblast cellular response and gene expression studies
Authors: Sethuraman Swaminathan , Nair Lakshmi S. , El‐Amin Saadiq , Nguyen My‐Tien N. , Greish Yaser E. , Bender Jared D. , Brown Paul W. , Allcock Harry R. , Laurencin Cato T. 
Published: March 2007

AbstractLow temperature setting calcium phosphate cements (CPC) formed from reactive calcium phosphate precursors are receiving great attention in the fields of orthopaedics and tissue engineering. The purpose of this study was to evaluate the mechanical properties and osteocompatibility of a novel calcium deficient hydroxyapatite (CDSHA) with a Ca/P ratio of 1.6 developed in our laboratories and compare it to a previously developed calcium deficient hydroxyapatite (CDHA) with a Ca/P ratio of 1.5. The results demonstrated that the calcium‐deficient hydroxyapatites (HA) formed from the CPCs were similar to biological HA at physiological temperature and the elastic moduli of CDHA and CDSHA were found to be 174.42 ± 20.41 MPa (p < 0.05) and 115.86 ± 24.8 MPa (p < 0.05), respectively. The surface morphologies of the two calcium deficient HA's formed were identical with a micro/nano porous structure as evidenced from SEM. The cellular proliferation on CDHA, and CDSHA, was comparable to the control, tissue culture polystyrene (TCPS) (p < 0.05). Alkaline phosphatase activity was significantly elevated on CDHA and CDSHA matrices at early time points when compared with the control (TCPS) (p < 0.05). Osteoblast cells gene expression on CDHA, and CDSHA showed type I collagen, alkaline phosphatase, osteocalcin, and osteopontin activity at both 7 and 14 days of culture. Thus, novel calcium‐deficient HAs, CDHA, and CDSHA formed at low temperature are promising candidates for orthopaedic applications based on their ability to promote osteoblast cell adhesion and gene expression in vitro. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Integrin‐linked kinase production prevents anoikis in human mesenchymal stem cells
Authors: Benoit Danielle S.W. , Tripodi Margaret C. , Blanchette James O. , Langer Steve J. , Leinwand Leslie A. , Anseth Kristi S. 
Published: March 2007

AbstractHuman mesenchymal stem cells (hMSCs) were infected with an adenovirus expressing integrin‐linked kinase (ILK) to understand the role of cell‐ECM signal transduction cascades in suppressing anoikis. Survivability of ILK‐infected hMSCs encapsulated in poly(ethylene glycol) (PEG) hydrogels, an anoikis‐inducing environment, was sustained at 90% over 7 weeks, and survival was attributed to increased protein kinase B (PKB/Akt) activation. hMSCs encapsulated in RGD‐modified hydrogels induced an upregulation in ILK production, PKB/Akt activation, and subsequent survival to the same extent of ILK‐infected, encapsulated hMSCs. As negative controls, encapsulated hMSCs were infected with cyclization recombinase (a protein not associated with cell survival)‐expressing virus, and uninfected hMSCs exhibited very little ILK production, PKB/Akt activation, and survival (∼55% after 7 weeks). As a measure of cell–matrix interactions, vinculin was also quantified for the encapsulated hMSCs and found to be 30‐fold greater for cells encapsulated in RGD‐modified hydrogels and fivefold greater for ILK‐infected hMSCs than controls, indicating that cell–material interactions are inducing the cell survivability of hMSCs encapsulated in RGD‐modified hydrogels. In sum, ILK infection can support cell survival in the absence of matrix interactions and enable fundamental studies of three‐dimensional cell function in response to extrinsic signals, independently of matrix–ligand interactions. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Disparity between ratios of diameters and blood flows in central pulmonary arteries in postoperative congenital heart disease using MRI
Authors: Ordovás Karen G. , Tan Christopher , Reddy Gautham P. , Weber Oliver M. , Lu Ying , Higgins Charles B. 
Published: March 2007

AbstractPurposeTo compare the relative severity of stenoses of right or left pulmonary arteries with differences in flow to each lung after repair of congenital heart disease (CHD).Materials and MethodsA total of 15 patients with postoperative congenital heart disease underwent MRI to evaluate branch pulmonary artery stenoses. Spin‐echo images and MR angiography were used to assess morphology, and velocity‐encoded cine (VEC) MRI was used to measure flow in the right and left pulmonary arteries. The ratios of the narrowest diameters of the right to left pulmonary arteries (R/L size) and right to left pulmonary arterial flow (R/L flow) were compared using Spearman's correlation. F test was used to assess the significance of the regression coefficients.ResultsR/L size ratio varied from 0.50 to 2.66, while the R/L flow ratio varied from 0.36 to 12.02. There was an exponential relationship between R/L size and R/L flow, with r2 = 0.78 and P = 0.001. However, severity of morphologic stenoses was not clinically useful for predicting flow reduction. Prediction residuals ranged from −136% to 54% of the true R/L flow.ConclusionAnatomical evaluation of the pulmonary arteries does not predict accurately differential blood flow in patients with pulmonary stenoses. Therefore, blood flow measurements are essential when considering the need for further surgical or interventional procedures. J. Magn. Reson. Imaging 2007. © 2007 Wiley‐Liss, Inc.
What causes diminished corticomedullary differentiation in renal insufficiency?
Authors: Lee Vivian S. , Kaur Manmeen , Bokacheva Louisa , Chen Qun , Rusinek Henry , Thakur Ravi , Moses Daniel , Nazzaro Carol , Kramer Elissa L. 
Published: March 2007

AbstractPurposeTo investigate whether the loss of corticomedullary differentiation (CMD) on T1‐weighted MR images due to renal insufficiency can be attributed to changes in T1 values of the cortex, medulla, or both.Materials and MethodsStudy subjects included 10 patients (serum creatinine range 0.6–3.0 mg/dL) referred for suspected renovascular disease who underwent 99mTc‐diethylene triamine pentaacetic acid (DTPA) renography to determine single kidney glomerular filtration rate (SKGFR) and same‐day MRI, which included T1 measurements and unenhanced T1‐weighted gradient echo imaging. Corticomedullary differentiation on T1‐weighted images was assessed qualitatively and quantitatively.ResultsSKGFR values ranged from 3.5 to 89.4 mL/minute based on radionuclide studies. T1 relaxation times of the medulla exceeded those of renal cortex by 147.9 ± 176.0 msec (mean ± standard deviation [SD]). Regression analysis showed a negative correlation between cortex T1 and SKGFR (r = −0.5; P = 0.03), whereas there was no significant correlation between medullary T1 and SKGFR. The difference between medullary and cortical T1s correlated significantly with SKGFR (r = 0.58; P < 0.01). In all five kidneys with a corticomedullary contrast‐to‐noise ratio (CNR) <5.0 on T1‐weighted images, SKGFR was less than 20 mL/minute.ConclusionIn our subject population, loss of CMD with decreasing SKGFR can be attributed primarily to an increased T1 relaxation time of the cortex. Medullary T1 values vary but do not appear to correlate with degree of renal insufficiency. J. Magn. Reson. Imaging 2007. © 2007 Wiley‐Liss, Inc.
Case report: Role of hepatitis E virus in the etiology of community‐acquired non‐A, non‐B hepatitis in greece
Authors: Tassopoulos Nicolaos C. , Krawczynski Krzysztof , Hatzakis Angelos , Katsoulidou Antigoni , Delladetsima Ioanna , Koutelou Maria G. , Trichopoulos Dimitrios 
Published: March 2007

AbstractThe aim of this study was to determine the frequency of hepatitis E virus (HEV) infection in a population of Greek adults with community‐acquired (sporadic) non‐A, non‐B hepatitis found to be seronegative for antibodies to hepatitis C virus (anti‐HCV). All patients admitted to the Liver Unit of Western Attica General Hospital and diagnosed as having acute community‐acquired non‐A, non‐B hepatitis between February, 1986, and May, 1990, were enrolled in follow up studies (n = 66). Nineteen patients with HCV infection and 11 patients with acute non‐A, non‐B, non‐C hepatitis that progressed to chronicity were excluded. Convalescent sera were tested for antibody to HEV (anti‐HEV) by a fluorescent antibody blocking assay in 33 of 36 eligible patients. One of the 33 (3%) patients was found to be positive for anti‐HEV. Anti‐HEV testing of all 20 available serum specimens from this patient showed evidence of anti‐HEV seroconversion at the fourth week after the onset of hepatitis. The patient had not travelled abroad or within Greece or had not had apparent contact with people from foreign countries for the previous 3 months. These data show that HEV infection is not a major cause of community‐acquired non‐A, non‐B hepatitis in Greece. However, the reported case of HEV hepatitis suggests that HEV may retain a low endemicity in Greece. More extensive seroprevalence studies are needed for an accurate estimation of the extent of HEV infection in the southeastern European countries. © 1994 Wiiey‐Liss, Inc.
Etiological role of hepatitis E virus in sporadic fulminant hepatitis
Authors: Nanda Santosh K. , Yalcinkaya Kezban , Panigrahi Aswini K. , Acharya Subrat K. , Jameel Shahid , Panda Subrat K. 
Published: March 2007

AbstractNon‐A, non‐B hepatitis viruses have been implicated as the etiological agent(s) in up to 60% of patients with fulminant hepatitis. These agents are reported to induce a higher mortality than other causes of fulminant hepatitis. Hepatitis E virus (HEV) and hepatitis C virus (HCV) at present constitute the major identifiable non‐A, non‐B hepatitis agents. Of these, HEV has been established as the sole cause of epidemic hepatitis in Afro‐Asian countries, and fulminant hepatitis has been recorded during such epidemics. However, in sporadic cases, the etiological role of HEV in fulminant hepatitis has remained uncertain. The role of HCV in acute liver disease and fulminant hepatitis remains unclear. The present study was undertaken to investigate the association of HEV and HCV in patients with fulminant hepatitis by direct detection of the viral genome using reverse transcription‐polymerase chain reaction (RT‐PCR). Serum samples from 50 sero‐logically identified non‐A, non‐B fulminant hepatitis cases negative for cryptic hepatitis B virus (HBV) infection examined via PCR were tested for HEV and HCV RNA using RT‐PCR. For HEV primers from the nonstructural region (ORF‐1) were used, and for HCV primers from the highly conserved 5′ untranslated regions were used. The products were analysed using agarose gel electrophoresis and confirmed by hybridisation with radiolabelled internal oligonucleotide probes. HEV was detected in 31 (62%) of the 50 fulminant non‐A, non‐B hepatitis cases. In 18 (36%) cases, HCV RNA was detected. In 11 (22%) of the HCV cases, the HEV genome was also amplified. In 20 (40%) cases, HEV was detected alone. Twelve (24%) patients were negative for all viral hepatitis markers. This study establishes HEV as one of the major agents associated with sporadic fulminant hepatitis in a geographical region where epidemics of hepatitis caused by HEV are frequent. © 1994 Wiley‐Liss, inc.
Seroprevalence studies using a recombinant norwalk virus protein enzyme immunoassay
Authors: Parker S. P. , Cubitt W. D. , Jiang X. J. , Estes M. K. 
Published: March 2007

AbstractA recombinant Norwalk virus (NV) protein enzyme immunoassay was used to study the age of acquisition of NV IgG in various populations. In London, England, there was little evidence of infection during the first 2 years of life. However, the prevalence of NV IgG rose steadily throughout the period that children attend school, reaching a peak of 70% in the group aged 11–16 years. High levels of maternal antibody were detected in infants aged <3 months. Comparison of the acquisition of antibodies to three strains of human calicivirus in Japanese children in northern Japan indicated that although the majority had experienced infection with strains Japan and UK1 by the age of 12 years, only 22% possessed antibodies to NV. In Australian aborigines NV infection occurs early in life; by the age of 6 years over 90% of children were seropositive. © 1994 Wiley‐Liss, Inc.
Presence of hepatitis B and C viral genomes in US blood donors as detected by polymerase chain reaction amplification
Authors: Liang T. Jake , Bodenheimer Henry C. , Yankee Ronald , Brown Nancy V. , Chang Kenneth , Huang Jiakang , Wands Jack R. 
Published: March 2007

AbstractHepatitis C virus (HCV) represents a major cause of posttransfusion hepatitis worldwide. Post‐transfusion hepatitis associated with hepatitis B virus (HBV) continues to occur. HBsAg‐negative donor sera from the Rhode Island Blood Center between 1987 and 1988 were screened using more sensitive techniques to assess the prevalence of low level HBV infection. Group I consists of 866 healthy blood donors without HBV sero‐logic markers, group II consists of 377 donors with ALT elevations (>45 IU/L), group II consists of 148 donors positive for anti‐HBc, and group IV consists of eight donors positive for both surrogate markers. A sensitive monoclonal immuno‐radiometric assay (M‐IRMA) was employed for detection of HBsAg‐associated epitopes (detection limit of 20 pg/ml) in serum. A subset of sera were analyzed for the presence of HBV DNA using the method of anti‐HBs capture of HBV related virions in serum followed by polymerase chain reaction (PCR) amplification. Using these techniques, 0.8% and 1.7% of donors were positive for HBsAg and HBV DNA respectively in group I. In contrast, 0.9% and 9.5% in group II and 0.7% and 18.1% in group III were positive, respectively. There were eight donors with both ALT elevation and anti‐HBc; and four (50%) of these were positive for HBV DNA. In the group with anti‐HBc, the majority (80%) of donors with HBV DNA had either no or low (signal to noise ratio < 10) anti‐HBs titer. Using anti‐HCV testing and reverse transcription‐PCR for detection of HCV genomes, we detected evidence of HCV infection in nine of the 49 donors with low level HBV DNA.