PubMed Health⌕ Search

Biomedical subjects

Tao Chen

Publications and source records attributed to Tao Chen.

At least 91 records · Page 5Linked to original sources
PubMed2005

[Experimental study of using acellular dermal dermis instead of donor sclera in orbital implantation].

OBJECTIVE: To evaluate the histocompatibility of homologous acellular dermal matrix as a wrapping material for a hydroxyapatite orbital implant and compare the speed of fibrovascular ingrowth in hydroxyapatite orbital implant wrapped with homologous acellular dermal matrix and homologous sclera respectively. METHODS: Twenty four New Zealand rabbits were divided into two groups randomly. One group is implanted with hydroxyapatite orbital implant wrapped with homologous acellular dermal matrix behind the globe, the other group with homologous sclera. The observation included immunological reaction of the globe postoperation. Biopsies of implanted material were taken on weeks 1, 4, 8 and 12 postoperation for histopathological and electron microscope examination. RESULTS: Histological examination showed the homologous acellular dermal matrix has no immunological and inflammatory reaction after implanted in orbit. But the speed of fibrovascular ingrowth is a little slower than that of homologous sclera. CONCLUSIONS: The homologous acellular dermal matrix has the better histocompatibility as an encapsulating biomaterial, it can be a new material instead of homologous sclera.

Animals↗
PubMed2005

[Clinical value of ultrasound guided transperineal prostate biopsy in detecting prostate cancer].

OBJECTIVE: To report our experience of ultrasound guided transperineal 6-core prostate biopsy (UG6CPB) in the diagnosis of prostate cancer (PCa). METHODS: In a prospective study, we performed UG6CPB in 104 suspected PCa patients with tPSA more than 4 microg/L and analysed the positive rate and complications of the diagnostic approach. RESULTS: PCa was detected in 24 of the 104 patients (23%), with low grade Gleason 2 to 4 in 3 cases (12.5%), intermediate grade Gleason 5 to 7 in 15 (62.5%) and high grade Gleason 8 to 10 in the remaining 6 (25%). Complications included temporary hematuria in 5 patients (4.8%), mild postbiopsy perineal discomfort in 5 (4.8%) and fever in 4 (3.8%). TPSA > or =10 microg/L, fPSA > or = 2 microg/L, fPSA/tPSA < 0.16, PSAD > or = 0.2 and prostate volume < 40 ml were the significant influencing factors of biopsy positive rate (P < 0.05). CONCLUSION: UG6CPB is an exact and a safe way of detecting PCa.

Biopsy, Needle↗
PubMed2004

The DNA methylation events in normal and cloned rabbit embryos.

To study the DNA methylation events in normal and cloned rabbit embryos, we investigated the methylation status of a satellite sequence and the promoter region of a single-copy gene using bisulfite-sequencing technology. During normal rabbit embryo development, both sequences maintained hypermethylation status until the 8- to 16-cell stage when progressive demethylation took place. In cloned embryos, the single-copy gene promoter sequence was rapidly demethylated and precociously de novo methylated, while the satellite sequence maintained the donor-type methylation status in all examined stages. Our results indicate that unique sequences as well as satellite sequences may have aberrant methylation patterns in cloned embryos.

Animals↗
PubMed2004

Differential mutagenicity of riddelliine in liver endothelial and parenchymal cells of transgenic big blue rats.

Riddelliine is a naturally occurring pyrrolizidine alkaloid that induces liver hemangiosarcomas in rats and mice. We previously reported higher levels of DNA adducts in liver endothelial cells than in liver parenchymal cells of riddelliine-treated mice and rats [Cancer Lett. 193 (2003) 119], suggesting that the tumor specificity is due to higher levels of DNA damage in the cells that form hemangosarcomas. In the present study, we evaluated the cell-specificity of riddelliine mutagenicity in rat liver. Female transgenic Big Blue rats were treated by gavage with 0.3 mg riddelliine per kg body weight, 5 days a week for 12 weeks. One day after the last treatment, the rats were sacrificed and liver parenchymal and endothelial cell fractions were isolated and purified. DNA was extracted from the cell fractions and used to assay for mutant frequency (MF) in the cII transgene. While there was no difference in the cII MFs of liver parenchymal cells in control and riddelliine-treated rats, the cII MF of liver endothelial cells from treated rats was significantly greater than the cII MF of endothelial cells from control rats. Molecular analysis of the mutants in liver endothelial cells indicated that G:C-->T:A transversion, a mutation that is characteristically induced by riddelliine, accounted for only 9% of all mutations in control rats, but made up 17% of mutations in treated rats. In contrast, G:C-->A:T transition, the major mutation in control rats where it made up 54% of all mutations, was reduced to 40% of mutations in riddelliine-treated rats. These results suggest that the relatively high mutagenicity of riddelliine in rat liver endothelial cells may be partially responsible for the tumorigenic specificity of this agent.

Animals↗
PubMed2004

Evidence for serine/threonine and histidine kinase activity in the tobacco ethylene receptor protein NTHK2.

Ethylene plays important roles in plant growth, development, and stress responses. Two ethylene receptors, ETR1 from Arabidopsis and NTHK1 from tobacco (Nicotiana tabacum), have been found to have His kinase (HK) activity and Ser/Thr kinase activity, respectively, although both show similarity to bacterial two-component HK. Here, we report the characterization of another ethylene receptor homolog gene, NTHK2, from tobacco. This gene also encodes a HK-like protein and is induced by dehydration and CaCl(2) but not significantly affected by NaCl and abscisic acid treatments. The biochemical properties of the yeast (Schizosaccharomyces pombe)-expressed NTHK2 domains were further characterized. We found that NTHK2 possessed Ser/Thr kinase activity in the presence of Mn(2+) and had HK activity in the presence of Ca(2+). Several lines of evidence supported this conclusion, including hydrolytic stability, phosphoamino acid analysis, mutation, deletion, and substrate analysis. These properties have implications in elucidation of the complexity of the ethylene signal transduction pathway and understanding of ethylene functions in plants.

Abscisic Acid↗
PubMed2004

Time course of cII gene mutant manifestation in the liver, spleen, and bone marrow of N-ethyl-N-nitrosourea-treated Big Blue transgenic mice.

The time between treatment and the appearance of mutants (mutant manifestation time) is a critical variable for in vivo transgenic mutation assays. There are, however, limited data describing the optimal sampling time for detecting mutations in various tissues of mutagen-treated animals. In this study, we investigated the time course of cII gene mutant induction in the liver, spleen, and bone marrow of Big Blue transgenic mice treated with N-ethyl-N-nitrosourea (ENU). Six-month-old female mice were treated with a single dose (120 mg/kg) of ENU, and the animals were sacrificed, and the cII mutant frequencies (MFs) were determined at 1, 3, 7, 15, 30, and 120 days after the treatment. The MFs in the liver cII gene of ENU-treated mice increased with time after the treatment, while the MFs for concurrent controls remained constant. The liver cII MFs in ENU-treated mice were significantly increased at day 30 and 120 (p < 0.01), with the largest increase at day 120. The spleen cII MFs in ENU-treated mice were increased significantly at day 7 and later (p < 0.01), and reached a plateau at day 30. In the bone marrow, the cII MFs in ENU-treated mice were increased significantly at all sampling times (p < 0.01), with the maximum MF at day 3. These results confirm that the time after treatment required to reach the maximum MF is tissue specific, with the approximate time for the maximum ENU-induced cII MF response being: bone marrow, 3 days; spleen, 14-30 days; and liver, more than 30 days.

Alkylating Agents↗
PubMed2004

Genotoxicity of malachite green and leucomalachite green in female Big Blue B6C3F1 mice.

Malachite green, a triphenylmethane dye used in aquaculture as an antifungal agent, is rapidly reduced in vivo to leucomalachite green. Previous studies in which female B6C3F1 mice were fed malachite green produced relatively high levels of liver DNA adducts after 28 days, but no significant induction of liver tumors was detected in a 2-year feeding study. Comparable experiments conducted with leucomalachite green resulted in relatively low levels of liver DNA adducts but a dose-responsive induction of liver tumors. In the present study, we fed transgenic female Big Blue B6C3F1 mice with 450 ppm malachite green and 204 and 408 ppm leucomalachite green (the high doses used in the tumor bioassays) and evaluated genotoxicity after 4 and 16 weeks of treatment. Neither malachite green nor leucomalachite green increased the peripheral blood micronucleus frequency or Hprt lymphocyte mutant frequency at either time point; however, the 16-week treatment with 408 ppm leucomalachite green did increase the liver cII mutant frequency. Similar increases in liver cII mutant frequency were not seen in the mice treated for 16 weeks with malachite green or in female Big Blue rats treated with a comparable dose of leucomalachite green for 16 weeks in a previous study [Mutat. Res. 547 (2004) 5]. These results indicate that leucomalachite green is an in vivo mutagen in transgenic female mouse liver and that the mutagenicities of malachite green and leucomalachite green correlate with their tumorigenicities in mice and rats. The lack of increased micronucleus frequencies and lymphocyte Hprt mutants in female mice treated with leucomalachite green suggests that its genotoxicity is targeted to the tissue at risk for tumor induction.

Analysis of Variance↗
PubMed2004

N-ethyl-N-nitrosourea (ENU) increased brain mutations in prenatal and neonatal mice but not in the adults.

The incidence of childhood cancer is increasing. One of the most common cancers for children under 15 years of age, gliomas for example, has been reported to have increased in incidence over the last 20 years by approximately 40%. The rising trend of childhood cancer in brain may be associated with environmental exposure to genotoxins and susceptibility to mutation in early development. To investigate age-dependent mutagenic sensitivity of brain tissue to genotoxins, the Big Blue mouse model was utilized in this study. Groups of five male mice were treated with a single dose of 120 mg/kg ENU transplacentally at three days before birth (prenatal), eight days (neonate) or eighteen weeks (adult) after birth. The animals were sacrificed six weeks after the treatment. The mutant frequencies and types of mutations in the brain cII gene from ENU-treated and concurrent control mice were determined. A significant increase in mutant frequencies over control was found in the prenatal and neonatal groups whereas there was no significant difference between the adult group and its control. Molecular analysis of the mutants also indicated that the mutational spectra from the ENU-treated mice were age-dependent. The percentage of A:T --> T:A transversion, the typical type of mutation induced by ENU, was inversely related to the treatment age, whereas G:C --> A:T transition was the main type of mutation in the adult group, the same as the control. These results demonstrate a differential mutagenic effect of ENU on the mouse brain depending on the stages of development and suggest an enhanced susceptibility of brain cancer hazard for perinatal exposure to genotoxicants.

Aging↗
PubMed2004

Endomorphin 1- and endomorphin 2-like immunoreactive neurons in the hypothalamus send axons to the parabrachial nucleus in the rat.

Endomorphin 1 (EM1) and endomorphin 2 (EM2) are the endogenous peptides with high affinity and selectivity for the mu-opioid receptor (MOR). We examined whether or not EM1- and EM2-expressing hypothalamic neurons might send their axons to the parabrachial nucleus (PBN), where many MOR-expressing neurons have been observed. Immunofluorescence histochemistry was combined with fluorescent retrograde tract-tracing method. In the rats injected with Fluoro-Gold (FG) into the PBN, some of EM1- and EM2-immunoreactive hypothalamic neurons were labeled retrogradely with FG. The majority of the EM1/FG and EM2/FG double-labeled neurons were distributed in the dorsomedial hypothalamus nucleus, centromedial hypothalamic region, and arcuate nucleus; a few of them were also seen in the periventricular hypothalamic nucleus and posterior hypothalamic nucleus. Endomorphins released from PBN-projecting hypothalamic neurons may modulate the gustatory, autonomic and nociceptive functions through MOR-expressing PBN neurons.

Animals↗
PubMed2004

Blastocysts produced by nuclear transfer between chicken blastodermal cells and rabbit oocytes.

Interspecies nuclear transfer (INT) has been used as an invaluable tool for studying nucleus-cytoplasm interactions; and it may also be a method for rescuing endangered species whose oocytes are difficult to obtain. In the present study, we investigated interaction of the chicken genome with the rabbit oocyte cytoplasm. When chicken blastodermal cells were transferred into the perivitelline space of rabbit oocytes, 79.3% of the couplets were fused and 9.7% of the fused embryos developed to the blastocyst stage. Both M199 and SOF medium were used for culturing chicken-rabbit cloned embryos; embryo development was arrested at the 8-cell stage obtained in SOF medium, while the rates of morulae and blastocysts were 12.1 and 9.7%, respectively, in M199 medium. Polymerase chain reaction (PCR) amplification of nuclear DNA and karyotype analyses confirmed that genetic material of morulae and blastocysts was derived from the chicken donor cells. Analysis mitochondrial constitution of the chicken-rabbit cloned embryos found that mitochondria, from both donor cells and enucleated oocytes, co-existed. Our results suggest that: (1) chicken genome can coordinate with rabbit oocyte cytoplasm in early embryo development; (2) there may be an 8- to 16-cell stage block for the chicken-rabbit cloned embryos when cultured in vitro; (3) mitochondrial DNA from the chicken donor cells was not eliminated until the blastocyst stage in the chicken-rabbit cloned embryos; (4) factors existing in ooplasm for somatic nucleus reprogramming may be highly conservative.

Animals↗
PubMed2004

Preparation and characterization of polyclonal antibodies against VLDL receptor.

The polyclonal antibodies against VLDL receptor were prepared and identified. Rabbits were immunized with polypeptide fragment of VLDL receptor as antigen. The collected blood serum of the immunized rabbits was analyzed and identified by using ELISA and Western Blot. The results showed that the rabbit against mouse and human VLDL receptor antibodies were obtained with high titer and could recognize the natural VLDL receptors through Western blot. The prepared polyclonal antibodies against VLDL receptor provide a new tool to study the protein of VLDL receptor.

Animals↗
PubMed2004

Study on the distribution of active centers in novel low Ti-loading MgCl2-supported Ziegler-Natta catalyst.

Novel MgCl2-supported Ziegler-Natta (Z-N) catalysts prepared using a new one-pot ball milling method can effectively control the amounts of Ti-loading in the catalysts. Complex GPC data on polypropylene synthesized by these novel catalysts were analyzed using the method of fitting the molecular weight distribution (MWD) curves with a multiple Flory-Schulz function. It was found that multiple active centers exist in these novel catalysts. Detailed study of the effects of the Ti-loadings in the catalysts on the distribution of the active centers showed that the Ti-loadings in the novel MgCl2-supported Z-N catalysts might affect the proportion of each type of active centers; and might be the main factor responsible for the effect of the Ti-loadings on the microstructure, the molecular weight and molecular weight distribution width of the resultant polymer, the catalytic activity and polymerization kinetics.

Catalysis↗
PubMed2004

Lesion detectability of a gamma camera based coincidence system with FDG in patients with malignant tumors: a comparison with dedicated positron emission tomography.

OBJECTIVE: The aim of this study was to investigate the lesion detectability of a gamma camera based coincidence detector system (c-PET system) in comparison to the dedicated PET system (d-PET system), and thereby clarify the feasibility of the clinical application of this system and also describe any factors influencing the lesion detectability of the c-PET system. METHODS: We examined 74 patients including 19 with malignant lymphoma, 16 with lung cancer, 9 with primary malignant bone tumor, 7 with esophageal cancer, 6 with malignant melanoma, 3 with hepatocellular carcinoma, 3 with primary unknown cancer, 2 with breast cancer, 2 with colon cancer, and 7 with others. d-PET images were obtained using ECAT EXACT HR+ at 60 min, followed by c-PET imaging using ECAM at 120 min after the injection of 185 MBq of FDG. Each image was reconstructed without any attenuation correction. In the image interpretation, the whole body was classified into 16 regions (5 superficial regions and 11 deep regions). The FDG accumulation of the lesions was evaluated by visual grading based on the consensus of three nuclear medicine physicians, and the findings were classified into three grades; (++), (+), and (-). The lesions were also classified into 3 groups according to their size: large group (> or =2 cm), middle group (1 < or = <2 cm) and small group (<1 cm). RESULTS: In 627 regions, the abnormal FDG uptake was detected in 109 regions by the d-PET system. Out of 109 regions, the c-PET system could detect the lesions in 91 regions and was false positive in 1 region. Therefore, the sensitivity, specificity, and accuracy of the c-PET system were 83.5%, 99.8% and 97.0%, respectively. Lesion detectability of the small group (54.5%) was significantly lower than that of the large group (97.9%) (p < 0.001) and that of the middle group (93.1%) (p < 0.001); however, the difference in lesion detectability between the large and middle groups was not significant. Neither the degree of FDG accumulation nor the location of the lesion markedly influenced the lesion detectability of the c-PET system. However, when we focused on the large and middle size lesions, the detectability of deep lesions tended to be lower than that of superficial lesions. CONCLUSION: In conclusion, the lesion detectability of the c-PET system was inferior to that of the d-PET system, especially in the case of small lesions. Further examination is required to assess the clinical usefulness of the c-PET system.

Adolescent↗
PubMed2004

Mutations induced by the carcinogenic pyrrolizidine alkaloid riddelliine in the liver cII gene of transgenic big blue rats.

Riddelliine is a naturally occurring pyrrolizidine alkaloid that forms a number of different mononucleotide and dinucleotide adducts in DNA. It is a rodent carcinogen and a potential human hazard via food contamination. To examine the mutagenicity of riddelliine, groups of six female transgenic Big Blue rats were gavaged with 0.1, 0.3, and 1.0 mg riddelliine per kg body weight. The middle and high doses resulted in liver tumors in a previous carcinogenesis bioassay. The animals were treated 5 days a week for 12 weeks and sacrificed 1 day after the last treatment. The liver DNA was isolated for analysis of the mutant frequency (MF) in the transgenic cII gene, and the types of mutations were characterized by sequencing the mutants. A significant dose-dependent increase in MF was found, increasing from 30 x 10(-)(6) in the control animals to 47, 55, and 103 x 10(-)(6) in the low, middle, and high dose groups, respectively. Molecular analysis of the mutants indicated that there was a statistically significant difference between the mutational spectra from the riddelliine-treated and the control rats. A G:C --> T:A transversion (35%) was the major type of mutation in rats treated with riddelliine, whereas a G:C --> A:T transition (55%) was the predominant mutation in the controls. In addition, mutations from the riddelliine-treated rats included an unusually high frequency (8%) of tandem base substitutions of GG --> TT and GG --> AT. These results indicate that riddelliine is a genotoxic carcinogen in rat liver and that the types of mutations induced by riddelliine are consistent with riddelliine adducts involving G:C base pairs.

Animals↗
PubMed2004

Distal cationic poly(ethylene glycol) lipid conjugates in large unilamellar vesicles prepared by extrusion enhance liposomal cellular uptake.

Cationic poly(ethylene glycol)-lipid conjugates (CPLs), a class of lipid designed to enhance the interaction of liposomes with cells, possess the following architectural features: 1) a hydrophobic lipid anchor of distearoylphosphatidylethanolamine (DSPE); 2) a hydrophilic spacer of poly(ethylene glycol); and 3) a cationic head group prepared with 0, 1, 3, or 7 lysine residues located at the distal end of the PEG chain, giving rise to CPL possessing 1, 2, 4, or 8 positive charges, respectively (CPL1 to CPL8). Previously we have described the synthesis of CPL, have characterized the postinsertion of CPL into PEG-containing LUVs and SPLP (stabilized plasmid-lipid particles), have shown significant increases in the binding of CPL-LUV to cells, and have observed dramatically enhanced transfection (up to a million-fold) of cells with CPL-SPLP in the presence of calcium [Chen et al. (2000) Bioconjugate Chem. 11, 433-437; Fenske et al. (2001) Biochim. Biophys. Acta 1512, 259-272; Palmer et al. (2003) Biochim. Biophys. Acta 1611, 204-216]. In the present study, we examine a variety of CPL properties (such as polarity and CMC) and characterize CPL-vesicular systems formed by extrusion and examine their interaction with cells. While CPL polarity was observed to increase dramatically with increasing charge number, CMC values were all found to be low, in the range of other PEGylated lipids, and exhibited only a small increase, going from CPL1 (1.3 microM) to CPL8 (2 microM). The CPLs were almost quantitatively incorporated into large unilamellar vesicles (LUVs) prepared by the extrusion method and were evenly distributed across the lipid bilayer. Lower levels of incorporation were obtained when CPLs were incubated with preformed liposomes (DSPC/Chol, 55:45) at 60 degrees C. The binding of CPL-LUVs to BHK cells in vitro was found to be dependent on the distal charge density of the CPL rather than total surface charge. Liposomes possessing CPL4 or CPL8 were observed to bind efficiently to cell surfaces and enhance cellular uptake in BHK cells (as observed with both lipid and aqueous content markers), whereas those possessing CPL1 or CPL2 exhibited little or no binding. These results suggest new directions for the design of liposomal systems capable of in vivo delivery of both conventional and genetic (plasmid and antisense) drugs.

Animals↗
PubMed2004

Group I metabotropic receptor antagonism blocks depletion of calcium stores and reduces potentiated capacitative calcium entry in strain-injured neurons and astrocytes.

Antagonism of the group I metabotropic receptor subtype 1 (mGluR1) with (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA) has been shown to reduce deficits after in vivo or in vitro traumatic brain injury. We have previously demonstrated that AIDA prevents elevation of astrocyte IP3 subsequent to injury-induced activation of mGluRs and phospholipase C. Since IP3 can cause release of intracellular Ca2+ stores we tested the hypothesis that pre- or post-injury treatment with AIDA can affect (1) the depletion of Ca2+ stores which occurs soon after strain injury of cultured neurons and astrocytes and (2) the delayed potentiation of capacitative calcium entry in strain-injured neurons. Astrocyte or neuronal plus glial cultures were grown on Silastic membranes that were subjected to a 50-msec pulse of compressed gas, which caused membrane displacement and biaxial strain (stretch) injury of the adhering cells. Cells were treated 10 min before or immediately after injury with 100 microM AIDA and the intracellular free Ca2+ ([Ca2+]i) response to thapsigargin, which inhibits the ability of the stores to sequester Ca2+, was measured at 15 min or 3 h after injury. AIDA pre- or post-injury treatment prevented the depletion of intracellular calcium stores at 15 min post-injury in astrocytes and neurons and reduced the potentiated neuronal capacitative calcium influx 3 h after injury. Since Ca2+ and Ca2+ stores influence many factors, including neuronal excitability, plasticity, protein synthesis, and neuronal-glial interactions, prevention of Ca2+ store depletion and subsequent exaggerated capacitative calcium entry may be an important subcellular mechanism by which antagonism of mGluR1 receptors exert an injury-reducing effect. More globally, the results further emphasize the importance of altered signaling and calcium regulatory mechanisms in the immediate and delayed sequelae of traumatic brain injury.

Animals↗
PubMed2004

S100B protein is released by in vitro trauma and reduces delayed neuronal injury.

S100B protein in brain is produced primarily by astrocytes, has been used as a marker for brain injury and has also been shown to be neurotrophic and neuroprotective. Using a well characterized in vitro model of brain cell trauma, we examined the potential role of exogenous S100B in preventing delayed neuronal injury. Neuronal plus glial cultures were grown on a deformable Silastic membrane and then subjected to strain (stretch) injury produced by a 50 ms displacement of the membrane. We have previously shown that this injury causes an immediate, but transient, nuclear uptake of the fluorescent dye propidium iodide by astrocytes and a 24-48 h delayed uptake by neurons. Strain injury caused immediate release of S100-beta with further release by 24 and 48 h. Adding 10 or 100 nm S100B to injured cultures at 15 s, 6 h or 24 h after injury reduced delayed neuronal injury measured at 48 h. Exogenous S100B was present in the cultures through 48 h. These studies directly demonstrate the release and neuroprotective role of S100B after traumatic injury and that, unlike most receptor antagonists used for the treatment of trauma, S100B is neuroprotective when given at later, more therapeutically relevant time points.

Animals↗