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Biomedical subjects

F Chen

Publications and source records attributed to F Chen.

At least 271 records · Page 15Linked to original sources
PubMed1999

Acellular collagen matrix as a possible "off the shelf" biomaterial for urethral repair.

OBJECTIVES: To determine whether a naturally derived collagen-based tissue substitute developed for urethral reconstruction would be suitable for urethral repair in an animal model. Several urethral conditions often require nongenital tissues for reconstruction, such as skin grafts or mucosal grafts from the bladder or buccal regions. However, the use of these tissues for urethroplasty may be associated with additional procedures for graft retrieval, prolonged hospitalization, and morbidity. METHODS: A ventral urethral defect was created in 10 male rabbits. The acellular collagen matrix, obtained and processed from porcine bladder submucosa, was trimmed and used to replace the urethral defect in an onlay fashion. Serial urethrography was performed pre- and postoperatively at 0.5, 1, 2, 3, and 6 months. The animals were sacrificed 0.5, 1, 2, 3, and 6 months after surgery. The retrieved implants were analyzed grossly, histologically, and with immunocytochemistry. RESULTS: All animals survived until being sacrificed without any noticeable voiding dysfunction. Serial urethrograms confirmed the maintenance of a wide urethral caliber without any signs of strictures. Gross examination at retrieval showed normally appearing tissue without any evidence of fibrosis. Histologically, the implanted matrices contained host cell infiltration and generous angiogenesis by 2 weeks after surgery. The presence of a confluent transitional cell layer was confirmed by immunocytochemical analyses using pancytokeratin antibodies. Anti-alpha actin antibodies demonstrated the migration of unorganized muscle fiber bundles 2 months after implantation and organized muscle bundles 6 months after implantation. CONCLUSIONS: The acellular collagen matrix appears to be a useful material for urethral repair in the rabbit. The matrix can be processed easily, has good characteristics for tissue handling and urethral function, and has the advantage of being an "off the shelf" material.

Animals↗
PubMed1999

Defective expression of the SHP-1 phosphatase in polycythemia vera.

The SHP-1 phosphatase associates with the receptors for erythropoietin, stem cell factor, and interleukin-3, and negatively regulates the mitogenic signals generated during engagement by their respective ligands. The erythroid progenitors of patients with polycythemia vera are hypersensitive to the mitogenic effects of these growth factors despite the fact that the numbers and binding affinities for their receptors are not increased. To determine whether post-receptor signaling defects may account for growth factor-hypersensitivity in polycythemia vera, we determined the expression of SHP-1 in highly purified erythroid progenitors from polycythemia vera patients. Our data demonstrate that in approximately 60% of the patients, expression of SHP-1 in the colony forming unit-erythroid population is diminished. The decreased expression of the protein may result from a transcriptional defect, as suggested by the diminished SHP-1 mRNA expression in the erythroid progenitors of these patients. Studies to determine the level of maturation of polycythemia vera and normal cells indicated that there was no difference between the two at early colony forming unit-erythroid stage of differentiation although polycythemia vera cells showed retarded differentiation kinetics at late colony forming unit-erythroid stage of differentiation. Furthermore, SHP-1 expression in normal colony forming unit-erythroid demonstrated downregulation of mRNA and protein levels during terminal differentiation, suggesting that its function is required for growth control during the early stages of erythropoiesis. These results indicate an important role for SHP-1 in the regulation of normal human erythroid progenitors and suggest that defective expression of the protein may contribute to the pathogenesis of polycythemia vera.

Cell Differentiation↗
PubMed1999

MR imaging of the liver and spleen: a comparison of the effects on signal intensity of two superparamagnetic iron oxide agents.

We compared the effects of two superparamagnetic iron oxide (SPIO) contrast agents, ferumoxides and SHU-555A, in MR imaging of the liver and spleen. Thirty-six patients with known malignant lesions of the liver underwent T2W turbo spin-echo (TSE) and T1WGRE FLASH opposed-phase imaging before and after SPIO injection on a 1.0 T MR system. Post-ferumoxides images were obtained in 18 patients 90 min after infusion of 15 micrommol Fe/kg of the agent. In 18 other patients SHU-555A was administered as a rapid bolus at a dose of 7.0-12.9 micrommol Fe/kg. T1WGRE FLASH images were obtained immediately, 30 s and 480 s and T2WTSE images 10 min after injection. Signal intensity of the liver, spleen, and malignant liver lesions before and after SPIO was measured with operator-defined regions of interest. The effects of ferumoxides and SHU-555A were measured as the percentage signal intensity change (PSIC) and in the malignant liver lesions additionally as changes in lesion-to-liver contrast-to-noise ratio (deltaDCNR). On T2W TSE images, there was no significant difference between the two agents in signal loss of liver parenchyma (p > 0.05). The signal loss in the spleen produced by ferumoxides was greater than with SHU-555A (p < 0.05). Both SPIO agents produced a significant increase in the CNR of malignant liver lesions. Delta CNR was slightly greater with ferumoxides than with SHU-555A (p < 0.05). On T1WGRE FLASH images, a slight decrease of liver SI induced by both agents was found on late post-SPIO images. No significant difference of liver PSIC between the two SPIO agents was noted on T1W images. The SI of spleen was significantly increased with both agents on T1W images and no difference in PSIC of spleen was noted (p > 0.05). The T1 and T2 effects produced by ferumoxides and SHU-555A were comparable in the liver although ferumoxides produced a stronger T2 effect in the spleen.

Contrast Media↗
PubMed1999

A biomechanical study of Tang's multiple locking techniques for flexor tendon repair.

This study was designed to biomechanically compare Tang's multiple looped locking techniques with various suture techniques for flexor tendon repair in the hand. Fifty flexor digitorum profondus tendons taken from pig toes were used as models; The tendons were transected in the middle part of zone 2 defined as the area beneath bifurcation of the flexor digitorum superficialis tendons, and were repaired by five different suture methods: (1) modified Kessler, (2) Tsuge's suture, (3) double Kessler, (4) modified Kessler plus Tsuge, and (5) Tang's suture. The repaired tendons were placed in an Instron tensile testing machine to determine the tensile properties of the repair. 2 mm gap formation force and ultimate tensile strength were measured during the test. Maximal work to failure were calculated according to area under the load-displacement curve of the test. 2 mm gap formation force was 21.5 N for the Kessler, 20.6 N for the Tsuge, 31.6 N for double Kessler, 30.9 N for the Kessler plus Tsuge and 41.4 N for the Tang. Ultimate tensile strength was 23.5 N for the Kessler, 22.9 N for the Tsuge, 34.5 N for the Kessler plus Tsuge and 45.6 N for the Tang. Statistically, Tang's suture had the greatest gap formation force, ultimate strength and energy for failure among the five techniques (p < 0.01 or p < 0.001). Gap formation force, ultimate strength and energy to failure for double Kessler or the Kessler plus Tsuge were significantly greater than those for the Kessler or the Tsuge (p < 0.05 or < 0.01). The tendons repaired by Tang's method tolerated a significantly higher tensile load (133 to 198% of the other techniques) than the other methods. Among the methods tested, Tang's multiple looped locking suture provides sufficient gap resistance and tensile strength that may be able to withstand early active mobilization after primary flexor tendon repair.

Analysis of Variance↗
PubMed1999

Lbx2, a novel murine homeobox gene related to the Drosophila ladybird genes is expressed in the developing urogenital system, eye and brain.

We describe the cloning, expression pattern, and genomic organization of Lbx2, a murine homologue of the Drosophila and mammalian ladybird genes. Lbx2 includes a homeodomain motif most closely related to those of Lbx1 and the Drosophila ladybird proteins. Lbx2 transcripts are first detected at E10.5 when they are located in the gonadal component of the urogenital ridge. Expression of Lbx2 dramatically increases by E11.5 in the urogenital ridges, and in the cranial surface ectoderm. At later stages, Lbx2 transcripts are expressed in the brain and organs derived from the urogenital ridge, including the gonadal tubercle, kidneys, and adrenal glands. From E14.5 to birth, Lbx2 expression is evident in the developing retinal neuroepithelium and the vibrissa.

Amino Acid Sequence↗
PubMed1999

RAG2:GFP knockin mice reveal novel aspects of RAG2 expression in primary and peripheral lymphoid tissues.

We generated mice in which a functional RAG2:GFP fusion gene is knocked in to the endogenous RAG2 locus. In bone marrow and thymus, RAG2:GFP expression occurs in appropriate stages of developing B and T cells as well as in immature bone marrow IgM+ B cells. RAG2:GFP also is expressed in IgD+ B cells following cross-linking of IgM on immature IgM+ IgD+ B cells generated in vitro. RAG2:GFP expression is undetectable in most immature splenic B cells; however, in young RAG2:GFP mice, there are substantial numbers of splenic RAG2:GFP+ cells that mostly resemble pre-B cells. The latter population decreases in size with age but reappears following immunization of older RAG2:GFP mice. We discuss the implications of these findings for current models of receptor assembly and diversification.

Animals↗
PubMed1999

Hydrolysis kinetics of astaxanthin esters and stability of astaxanthin of Haematococcus pluvialis during saponification.

The reaction kinetics for the hydrolysis of astaxanthin esters and the degradation of astaxanthin during saponification of the pigment extract from the microalga Haematococcus pluvialis were investigated. Different concentrations of sodium hydroxide in methanol were used for the saponification under nitrogen in darkness at ambient temperature (22 degrees C) followed by the analysis of astaxanthins and other carotenoids using an HPLC method. The concentration of methanolic NaOH solution was important for promoting the hydrolysis of astaxanthin esters and minimizing the degradation of astaxanthin during saponification. With a higher concentration of methanolic NaOH solution, the reaction rate of hydrolysis was high, but the degradation of astaxanthin occurred significantly. The rate constants of the hydrolysis reaction (first order) of astaxanthin esters and the degradation reaction (zero-order) of astaxanthin were directly proportional to the concentration of sodium hydroxide in the saponified solution. Although the concentration of sodium hydroxide in the saponified solution was 0.018 M, complete hydrolysis of astaxanthin esters was achieved in 6 h for different concentrations (10-100 mg/L) of pigment extracts. Results also indicated that a higher temperature should be avoided to minimize the degradation of astaxanthin. In addition, during saponification, no loss of lutein, beta-carotene, and canthaxanthin was found.

Chromatography, High Pressure Liquid↗
PubMed1999

Degradation of ginsenosides in American ginseng (Panax quinquefolium) extracts during microwave and conventional heating.

The degradation of ginsenosides in American ginseng (Panax quinquefolium) extracts during microwave and water (oil) bath heating (conventional heating) was investigated. Both the 50% ethanol-water extracts and the aqueous extracts were boiled in a modified laboratory microwave oven and in a water (or oil) bath, respectively. The neutral ginsenosides (Rb(1), Rc, Rd, and Re) and malonyl ginsenosides (m-Rb(1), m-Rc, and m-Rd) were determined by reverse-phase high-performance liquid chromatography. The results showed that the degradation of ginsenosides in 50% ethanol-water extracts was a first-order reaction. The malonyl ginsenosides were much less stable than the corresponding neutral ginsenosides, with the rate constant value of the malonyl ginsenosides being 3-60 times that of the neutral ginsenosides. At the same temperature, the effect of microwave heating on the degradation of ginsenosides was the same as that of conventional heating.

Cooking↗
PubMed1999

Simultaneous quantification of ginsenosides in American ginseng (Panax quinquefolium) root powder by visible/near-infrared reflectance spectroscopy.

Near-infrared reflectance spectroscopy (NIRS) was examined as a possible alternative to high-performance liquid chromatography (HPLC) for the analysis of ginsenosides from American ginseng (Panax quinquefolium) root powder (n = 26). NIR spectra were collected over 400-2500 nm. For each sample and individual ginsenoside quantified by HPLC, spectral data were regressed against the chemical data to develop prediction equations. The spectral prediction equations produced high correlation coefficient (1-VR) values and low standard errors of cross validation (SECV) values for the determination of individual and total ginsenosides. The contents of individual ginsenosides, Rb(1), Rb(2), Rc, Rd, Re, Rg(1), Ro, m-Rb(1), m-Rb(2), m-Rc, m-Rd, and total ginsenosides (X +/- SECV) were (1.29+/-0.18)%, (0.273+/-0.096)%, (0.298+/-0.052)%, (0.091+/-0.027)%, (1. 015+/-0.114)%, (0.116+/-0.018)%, (0.25+/-0.040)%, (0.776+/-0.116)%, (0.197+/-0.074)%, (0.239+/-0.083)%, (0.143+/-0.042)%, and (4.393+/-0.283)%, respectively. The (1-VR) values of cross validation were 0.877, 0.872, 0.955, 0.834, 0.899, 0.919, 0.325, 0.849, 0.902, 0.877, 0.871, and 0.963, respectively. Results indicated that the NIRS method could be used for the analysis of the major ginsenosides, Rb(1), Re, and m-Rb(1), as well as the total ginsenosides in American ginseng.

Calibration↗
PubMed1999

Isomerization of trans-astaxanthin to cis-isomers in organic solvents.

The isomerization of trans-astaxanthin to cis-isomers in organic solvents was investigated. trans-Astaxanthin was dissolved in dimethyl sulfoxide, dichloromethane, chloroform, acetone, methanol, acetonitrile, and a mixture of dichloromethane and methanol (25:75) respectively, and heated at 35 degrees C followed by analyzing cis- and trans-astaxanthins in the solutions using HPLC. The isomerization rates of trans-astaxanthin were dependent on the solvent, and the following order was found: dichloromethane > chloroform > the mixture of dichloromethane and methanol (25:75) > methanol > acetonitrile > acetone > dimethyl sulfoxide. In different solvents, the relative contents of 9-cis- and 13-cis-astaxanthins formed during isomerization were different. In all solvents, 13-cis-isomer was the main cis-isomer from trans-astaxanthin. trans-Astaxanthin dissolved in dichloromethane or chloroform was very readily isomerized to cis-isomers, especially for dichloromethane, in which a maximum isomerization percentage was found and an equilibrium practically was reached after an appropriate time interval. Results also indicated that a higher temperature could promote markedly the isomerization of trans-astaxanthin.

Kinetics↗
PubMed1999

The role of hydroxyl radical as a messenger in the activation of nuclear transcription factor NF-kappaB.

Although it is generally believed that reactive oxygen species activate NF-kappaB, a primary oxidative stress-responsive transcription factor, it is unclear which one among these species causes NF-kappaB activation. Our hypothesis is that hydroxyl radical (*OH) functions as a messenger for the activation of NF-kappaB. Jurkat cells, macrophages and JB6 cells were used to test this hypothesis. Cr(VI), silica and ZnO were used as sources of *OH radicals. None of these *OH generating systems involves exogenous H2O2. Cr(VI) expressed enhanced activity in induction of NF-kappaB in Jurkat cells. This activation of NF-kappaB was decreased by a metal chelator, diethylene triaminepentaacetic acid or a H2O2 scavenger, catalase, but was increased by superoxide dismutase. Mn(II), which reacts with Cr(IV) to inhibit this metal ion-mediated *OH generation, decreased the NF-kappaB activation. Sodium formate, an *OH radical scavenger, also inhibited the NF-kappaB activation. Electron spin resonance measurements show that Cr(VI) was reduced by Jurket cells to Cr(IV) and Cr(V). During the reduction process, molecular oxygen was reduced to O2 and then to H2O2, which reacted with Cr(IV) and Cr(V) to generate *OH radical. The *OH generation correlated with the Cr(VI)-induced NF-kappaB activation. Similarly, silica caused NF-kappaB activation in macrophages via the *OH radical-mediated reaction. This radical was generated via metal mediated reaction from H2O2, which was generated by the reduction of molecular oxygen via O2- as an intermediate during the silica-stimulated 'respirable burst'. Silica particles did not cause *OH generation either in Jurket or in JB6 cells and thus did not cause any observable NF-kappaB activation in these cells. ZnO induced NF-kappaB activation in JB6 cells through the generation of *OH resulting from light irradiation of ZnO which was measured by electron spin resonance. The results thus show that *OH radical functions as a messenger for NF-kappaB activation. Antioxidants, which scavenge *OH radical or its precursors, inhibit NF-kappaB activation. Metal chelators, which make metal ions incapable of generating *OH from H2O2, inhibit activation of this transcription factor.

Animals↗
PubMed1999

Antioxidant properties of aspirin: characterization of the ability of aspirin to inhibit silica-induced lipid peroxidation, DNA damage, NF-kappaB activation, and TNF-alpha production.

Electron spin resonance (ESR) was used to investigate the reaction of aspirin toward reactive oxygen species, such as hydroxyl radicals (*OH), superoxide radicals (O2-) and H2O2. The Fenton reaction (Fe(II) + H2O2 ---> FE(III) + *OH + OR) was used as a source of *OH radicals. The results show that aspirin is an efficient *OH radical scavenger with a reaction rate constant of k = 3.6 x 10(10) M(-1) sec(-1), which is faster than several well established antioxidants, such as ascorbate, glutathione and cysteine. However, aspirin is not a good scavenger for O2- or H2O2. Through its antioxidant property, aspirin exhibited a protective effect against silica-induced lipid peroxidation and DNA strand breakage. Aspirin also inhibited the activation of nuclear transcription factor-kappaB induced by silica, lipopolysaccharide or the transition metal, Fe(II), as demonstrated by electrophoretic mobility shift assay. The results show that aspirin functions as an antioxidant via its ability to scavenge *OH radicals. This antioxidant property may explain some of its various physiological and pharmacological actions.

Animals↗
PubMed1999

Dependence of NF-kappaB activation and free radical generation on silica-induced TNF-alpha production in macrophages.

Tumor necrosis factor alpha (TNFalpha) plays an important role in the pathogenesis of silicosis and other chronic inflammatory lung diseases. The present study investigates the role nuclear transcription factor kappaB (NF-kappaB) and oxygen free radicals in silica-induced TNFalpha production in primary alveolar macrophages and RAW 264.7 cells. Using electrophoretic mobility shift assay (EMSA) and enzyme-linked immunoadsorbent assay (ELISA), we have demonstrated that silica can induce NF-kappaB activation and TNFalpha expression in a dose-dependent manner. Transient transfection assays with a plasmid construct containing NF-kappaB binding sites linked to a reporter gene further show that silica is able to induce the transcriptional activation of NF-kappaB-dependent gene. Inhibition of NF-kappaB activation by SN50, a specific NF-kappaB blocker, abolishes silica-induced TNFalpha production. Pretreatment of the cells with catalase (H2O2 scavenger) or deferoxamine (*OH scavenger) effectively inhibits NF-kappaB and TNFalpha activation, whereas superoxide dismutase (O2 scavenger) has an opposite effect. These results indicate that silica-mediated free radical generation and NF-kappaB activation play important roles in silica-induced TNFalpha gene expression.

Animals↗
PubMed1999

Presenilin mutations associated with Alzheimer disease cause defective intracellular trafficking of beta-catenin, a component of the presenilin protein complex.

The presenilin proteins are components of high-molecular-weight protein complexes in the endoplasmic reticulum and Golgi apparatus that also contain beta-catenin. We report here that presenilin mutations associated with familial Alzheimer disease (but not the non-pathogenic Glu318Gly polymorphism) alter the intracellular trafficking of beta-catenin after activation of the Wnt/beta-catenin signal transduction pathway. As with their effect on betaAPP processing, the effect of PS1 mutations on trafficking of beta-catenin arises from a dominant 'gain of aberrant function' activity. These results indicate that mistrafficking of selected presenilin ligands is a candidate mechanism for the genesis of Alzheimer disease associated with presenilin mutations, and that dysfunction in the presenilin-beta-catenin protein complexes is central to this process.

Alzheimer Disease↗
PubMed1999

Kinetic models for astaxanthin production by high cell density mixotrophic culture of the microalga Haematococcus pluvialis.

High cell density cultivation of Haematococcus pluvialis for astaxanthin production was carried out in batch and fed-batch modes in 3.7-L bioreactors with stepwise increased light intensity control mode. A high cell density of 2.65 g x L(-1) (batch culture) or 2.74 g x L(-1) (fed-batch culture) was obtained, and total astaxanthin production in the fed-batch culture (64.36 mg x L(-1)) was about 20.5% higher than in the batch culture (53.43 mg x L(-1)). An unstructured kinetic model to describe the microalga culture system including cell growth, astaxanthin formation, as well as sodium acetate consumption was proposed. Good agreement was found between the model predictions and experimental data. The models demonstrated that the optimal light intensity for mixotrophic growth of H. pluvialis in batch or fed-batch cultures in a 3.7-L bioreactor was 90-360 micromol x m(-2) x s(-1), and that the stepwise increased light intensity mode could be replaced by a constant light intensity mode.

Animals↗
PubMed1999

Dynamics and stability analysis of the growth and astaxanthin production system of Haematococcus pluvialis.

This paper investigated high cell density cultivation of Haematococcus pluvialis for astaxanthin production in 3.7-L bioreactors. A biomass concentration of 2.74 g L-1and an astaxanthin yield of 64.4 mg L-1 were obtained. Based on the experimental results, a new and simple dynamic model is proposed, differing from Monod kinetics, to describe cell growth, product formation and substrate consumption. Good agreement was found between the model predictions and experimental data. The model revealed that there was cell growth inhibition on product formation and product feedback compensation for substrate consumption, but no substrate inhibition or product inhibition of cell growth. Stability analysis demonstrated that no multiplicity of steady states was observed; the unique positive steady state was locally asymptotically stable; and the effect of dilution rate on steady states was greater than that of the initial substrate concentration.

Journal Article↗
PubMed1999

Specific regulation of fos family transcription factors in thymocytes at two developmental checkpoints.

A central question in T cell development is what makes cortical thymocytes respond to stimulation in a qualitatively different way than any other thymocyte subset. Part of the answer is that AP-1 function changes drastically at two stages of T cell development. It undergoes striking down-regulation as thymocytes differentiate from immature, CD4(-)CD8(-) double-negative (DN) TCR- thymocytes to CD4(+)CD8(+) double-positive (DP) TCRlo cortical cells, and then returns in the cells that mature to TCRhigh, CD4(+)CD8(-) or CD4(-)CD8(+) single-positive (SP) thymocytes. At all three stages, the jun family mRNAs can be induced similarly. However, we demonstrate that DP cortical thymocytes are specifically impaired in c-fos and fosB mRNA induction, even when stimuli are used that optimize survival of the cells and a form of in vitro maturation. fra-2 expression is induction independent but much lower in DP cells than in the other subsets. Overall Fos family protein induction accordingly is severely decreased in DP cells. Defective c-Fos and FosB expression in cortical thymocytes is functionally significant, because antibody supershift experiments show that in activated immature and mature thymocytes, most detectable AP-1 DNA-binding complexes do contain c-Fos or FosB. Thus, defective c-Fos and FosB expression in cortical thymocytes qualitatively alters any AP-1 complexes they might express. The cortical thymocytes are not deficient in mRNA expression for any of the constitutive transcription factors that are known to be needed to drive c-Fos or FosB expression, so it is possible that the activity of these factors is developmentally regulated through a post-transcriptional mechanism.

Animals↗