[The expression and biological effects of stem cell factor and its receptor in nervous system].
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Animals↗
Biomedical subjects
L Y Li
Publications and source records attributed to L Y Li.
[Pathological changes and host tissue reaction in alveolar echinococcosis].
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Adult↗
[Clinical study on relationship of CD62p, CD63 and TSP to the qi-stagnation induced blood-stasis syndrome and qi-deficiency induced blood-stasis syndrome in aged patients].
OBJECTIVE: To observe the relationship of platelet activation to the Qi-stagnation induced blood-stasis (QSBS) or Qi-deficiency induced blood-stasis (QDBS) syndrome. METHODS: Expressions of platelet activating molecules, including alpha-granule membrane glycoprotein (CD62p), lysosomal integral membrane protein (CD63) and thrombospondin (TSP), in patients with QSBS and QDBS were determined quantitatively with flow-cytometry and specific monoclonal antibody against activated platelet. And platelet aggregation was tested simultaneously. RESULTS: CD62p, CD63 and TSP expressions in Blood-Stasis patients, both QSBS and QDBS, were higher than those in the normal control significantly (all P < 0.01); all the three expressions were higher in QSBS group than those in QDBS group (all P < 0.01), Positive correlation was shown between CD62p and CD63 (r = 0.740, P < 0.01), CD62p and TSP (r = 0.744, P < 0.01), TSP and CD63 (r = 0.635, P < 0.01), and between CD62p and ADP induced platelet aggregation (r = 0.715, P < 0.01). CONCLUSION: Platelet activation was involved in the pathogenesis and development of Blood-Stasis Syndrome, especially closely related with the QSBS Syndrome.
Aged↗
[Comprehensive utilization and development of traditional Tibetan medicine in China].
OBJECTIVE: To deal with the further investigation field by discussing the status and present problem of traditional Tibetan medicine. METHOD: Previous relevant investigations and literatures were summed up in the field. The present situation of traditional Tibetan medicine in China was analysed. RESULT: The textual research, basic medicinal property, exploration of developable medicinal resource and protection of endangered medicinal species etc. were elaborated and the key problem of further investigation in 21st century was expounded. CONCLUSION: The textual research, basic medicinal property, exploration of develoable medicinal resources, especially monographic study on protection of major endangered medicinal resources should be intensified. Domestication and cultivation, and exploration of good-quality medicinal resources, quality evaluation and exploitation of effectual prescriptions are the focal field in the study of traditional Tibetan medicine.
Conservation of Natural Resources↗
[Effect of Rg2 on hemodynamics of hemorrhagic shock and its antioxidation in dogs].
OBJECTIVE: To investigate the protective effect of Rg2 on hemodynamics of hemorrhagic shock and its antioxidant properties. METHOD: Twenty mongrel dogs were randomly divided into Rg2 group, Shen Mai group and control group. The hemorrhagic shock model was built in all dogs by artery bleeding and mean arterial blood pressure was kept < 5.33 kPa for 4.5 hours. Rg2 0.5-1.0 mg.kg-1 and Shen Mai 100 mg.kg-1 were intravenously administered after hemorrhagic shock appeared. RESULT: Rg2 significantly enhanced blood pressure, LVSP and +/- dp/dtmax on hemorrhagic shock dogs who had lost compensation ability. Rg2 0.5-1.0 mg.kg-1 could reduce serum MDA, increase superoxide dismutase activity and prolong survival rate of dogs after shock. All these data have statistically significant when compared to control group (P < 0.05, P < 0.01, P < 0.001). CONCLUSION: These results suggest that Rg2 is more potent and effective than Shen Mai in improving hemodynamic state and activiting SOD on hemorrhagic shock dogs.
Animals↗
[Evaluation of positron emission tomography in diagnosing and staging of lung cancer].
OBJECTIVE: To evaluate positron emission tomography (PET) in diagnosing and staging of lung cancer. METHODS: One hundred and forty-seven patients (93 with lung cancer, 15 with lung metastatic tumors, 39 with benign lesions) were involved in the study. 163 whole body examinations (twice in 12 cases and 3 times in 2 cases) were performed after injection of 18F-fluro-deoxy-glucose (18FDG) with a Siemens ECAT EXACT HR + PET system. The results of PET were compared with pathological diagnoses (112 cases), clinical follow-up (35 cases), CT (68 malignant and 30 benign cases), and other imaging diagnoses. RESULTS: For the 147 cases with lung lesions, the sensitivity, specificity, and accuracy of FDG PET in differentiating the malignant from the benign were 97.2%, 89.7%, and 94.6% respectively. For the 93 lung cancer cases, more lesions were detected by PET in 58 (62.4%) cases, and changed staging in 36 (38.7%). In the 98 cases examinations, PET positive findings were consistent with CT in 39 (39.8%) cases; PET detected more lesions than CT in 29 (29.6%) cases; the lesions detected by CT were negative or with low uptake in the PET images in 30 (30.6%) cases, and they were finally proved as benign by follow-up. However, CT provided better detailed anatomical structures of the lesions than PET, and image fusion should give more information about the lesions. CONCLUSIONS: FDG PET had advantages in diagnosing and staging of lung cancer by providing metabolic information of the lesions. Comparison and fusion of PET with CT will give much help to clinical diagnosis.
Fluorodeoxyglucose F18↗
[Relationship between hot spot mutation in hepatitis B virus basic core promotor and HBeAg status].
OBJECTIVE: This paper was to study the influence of hot spot mutation in hepatitis B virus (HBV) basic core promotor (BCP) (nt1762 and nt1764) on HBeAg status of asymptomatic HBV carriers. METHODS: Mismatched PCR was used to amplify the fragment of HBVBCP and the fragments were analysed by restrict enzyme assay. Ninety cases of HBV infection were tested for hot spot mutations in HBVBCP. RESULTS: Twenty-six (43.3%) of 60 asymptomatic HBV carriers with HBeAg negative were found to have hot spot mutations in HBVBCP, among which 20 cases were accompanied by the mutation of nt 1896 in HBV Pre-C region. Hot-spot mutation in HBVBCP, however, occurred only in 3(10%) of 30 asymptomatic HBV carriers with HBeAg positive. For further investigation the HBVBCP hot spot mutations in asymptomatic HBV carriers without mutation of HBV Pre-C region were studied. Six(31.6%) of 19 asymptomatic HBV carriers with HBeAg negative were found to have hot spot mutation in HBVBCP. Two(7.1%) of 28 asymptomatic HBV carriers with HBeAg positive had hot spot mutations in HBVBCP, and there was a statistically significant difference between two groups. CONCLUSIONS: Hot spot mutations in HBVBCP is common in the HBV carriers with HBeAg negative and usually accompanies with nt1896 mutation of HBV Pre-C region. It is possible that Hot spot mutation in HBVBCP is a new reason of HBeAg negative HBV infection.
Adult↗
Expression of the Epstein-Barr virus BHRF1 gene, a homologue of Bcl-2, in nasopharyngeal carcinoma tissue.
Epstein-Barr virus (EBV) infection is associated closely with the pathogenesis of nasopharyngeal carcinoma (NPC). The EBV gene product, BHRF1, has been demonstrated in vitro and is structurally and functionally similar to the oncogene bcl-2, that is able to protect cells from programmed cell death. To determine whether the BHRF1 gene is expressed in vivo, BHRF1 mRNA or protein were sought in tissues from NPC and non-NPC patients. BHRF1 transcripts were specifically detected in the NPC tumours (32 out of 44, 72.7%) rather than the non-NPC tissues (0 out of 25) by reverse transcription, polymerase chain reaction and Southern hybridization. Other EBV genes, such as the lytic gene BZLF1 and latent genes EBNA1 and LMP2A, were also investigated. BZLF1 transcripts also were found specifically in NPC tumours (33 out of 44, 75%). EBNA1 was expressed in 79.5% of NPC, and 28% of non- NPC, tissues and LMP2A was expressed in 70.5% of NPC, and 88% of non-NPC, tissues. BHRF1 protein was detected by immunohistochemistry in 4 metastatic NPC, of 36 NPC tissue sections available. The BHRF1 protein was distributed in both the nucleus and cytoplasm of the neoplastic epithelial cells. IgG antibody against the BHRF1 protein was detected in 6 of 17 (35. 3%) NPC plasma, but the protein and IgG were both absent from the non-NPC controls. BHRF1 DNA sequences were determined for 11 NPC and 3 non-NPC samples. No sequence was specific for the EBV isolates from NPC tissue. Amino acids 79 and 88 always appeared in the same form, however, for every tested isolate and both were valine or leucine. This particular characteristic was not present in the B95-8 strain or in the corresponding regions of homologues, Bcl-2 and Bcl-XL, and was regarded as unique to Oriental EBV strains.
Amino Acids↗
Cloning and functional expression of a synthetic gene encoding huwentoxin-I, a neurotoxin from the Chinese bird spider (Selenocosmia huwena).
Cloning and functional expression of a synthetic gene encoding huwentoxin-I, a neurotoxin from the Chinese bird spider Selenocosmia huwena. A gene encoding huwentoxin-I, a peptide neurotoxin consisted of 33 amino acid residues from the venom of the Chinese bird spider Selenocosmia huwena, was designed, synthesized and expressed in Escherichia coli as a hybrid protein fused with glutathione S-transferase at the N-terminal. The fusion protein was purified by GSH-Sepharose 4B affinity column chromatography and cleaved by thrombin to release the toxin peptide. The amino acid sequence of the recombinant toxin was consistent with the designed one by sequence determination and MALDI-TOF mass analysis, suggesting that the recombinant huwentoxin-I produced the same expression product as the native one. After reduction and renaturation, the biological activity of the recombinant toxin was identical with that of the native huwentoxin-I by electrophysiological method.
Amino Acid Sequence↗
Expression and function of angiopoietin-1 in breast cancer.
Angiopoietin-1 (Ang1) has been shown to act as an angiogenic promoter in embryonic angiogenesis by promoting vascular branching, pericyte recruitment and endothelial survival. We have investigated the role of Ang1 in tumour neovascularization under clinical conditions and in animal models. The expression of Ang1 in clinical breast cancer specimens was analysed by using laser-capture microdissection and reverse transcriptase-linked polymerase chain reaction (RT-PCR) on RNA isolated from the samples. Despite the expression of Ang1 in many human breast cancer cell lines, the gene was expressed in only three of 21 breast cancer clinical specimens, even though its receptor, Tie2, is abundant in the vasculature of all of these tumours. Ang1 was then overexpressed in a human breast cancer cell line (MCF-7) on its own and in conjunction with FGF1, an angiogenic factor shown to be able to increase the tumorigenicity of MCF-7 cells. High concentrations of Ang1 were produced in the conditioned media of the transfected cells (range 156-820 ng ml(-1)). However, in contrast to its physiological role as promoter of angiogenesis, overexpression of Ang1 did not enhance tumour growth, but instead caused up to a 3-fold retardation of tumour growth (P = 0.003).
Angiopoietin-1↗
Oral delivery of HIV-protease inhibitors.
Strategies for optimizing the oral delivery of HIV-protease inhibitors draw from drug discovery efforts in molecular design, drug development tools in dosage formulation, and dosage regimen considerations in clinical medicine. This review outlines the evolution of these strategies for drugs that have been approved for human use, drug candidates still in development, and molecules that are no longer in development but from which valuable delivery information was obtained. Molecular design for obtaining desirable pharmacokinetics following oral administration primarily involved maximizing aqueous solubility and minimizing first-pass metabolism. Optimization of molecular design for oral drug delivery purposes is tempered by additional considerations for drug potency, toxicity, potential for interactions, and development of viral resistance. Strategies for improving oral bioavailability through dosage formulation use information from the effects of coadministered meals on drug plasma levels. Patient adherence to dosage regimens remains a major issue in assuring effective oral drug treatment and in preventing the development of resistance. Progress has been made in clinical studies where improved oral bioavailability and reductions in drug plasma level variability have been achieved with appropriate dosage regimen adjustment.
Administration, Oral↗
Adult-onset "infant" botulism: an unusual cause of weakness in the intensive care unit.
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Adult↗
Inhibition of angiogenesis and breast cancer xenograft tumor growth by VEGI, a novel cytokine of the TNF superfamily.
Recently, we reported a novel protein of the tumor necrosis factor (TNF) superfamily, named vascular endothelial cell growth inhibitor (VEGI), which is expressed predominantly in endothelial cells. When a secreted form of this new protein was overexpressed in mouse colon cancer cells, the growth of tumors formed by these cells in black mice was inhibited. We now report that recombinant VEGI inhibits the proliferation of endothelial cells but not that of other types of cells examined. The protein also inhibits formation of capillary-like structures by endothelial cells in collagen gels, and the growth of capillaries into collagen gels placed on the chick chorioallantoic membrane. The anticancer potential of VEGI was examined in a breast cancer xenograft tumor model in which the cancer cells were co-injected with Chinese hamster ovary cells overexpressing a secreted form of the protein. The co-injection resulted in potent inhibition of xenograft tumor growth. Our findings are consistent with the view that VEGI is an endothelial cell-specific negative regulator of angiogenesis.
Animals↗
Science, medicine, and the future. Antivascular therapy: a new approach to cancer treatment.
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Angiostatins↗
Pretreatment with intravenous FGF-13 reduces infarct volume and ameliorates neurological deficits following focal cerebral ischemia in rats.
Fibroblast growth factor-13 (FGF-13), novel member of FGF family has recently been molecularly cloned as a result of high throughput sequencing of a ovarian cancer cell, hippocampal, and kidney cDNA libraries. The human gene encodes for a protein with a molecular weight of 22 kDa that is most homologous to FGF-8 (70% similarity). In the current study, we tested the effects of intravenously administered FGF-13 in a model of permanent focal cerebral ischemia in Sprague-Dawley rats. FGF-13 or the vehicle was administered systematically via the tail vein 30 min prior, and 30 min and 24 h after the occlusion of the left middle cerebral artery (MCAo). Animals were weighed and evaluated behaviorally prior to and at 24 and 48 h after MCAo. The volume of cerebral infarct and swelling were determined using an image analysis system (BioQuant) and cresyl violet stained sequential sections from the forebrain region. Histopathology was evaluated to compare the therapeutic effects. We found a 63% reduction in infarct volume in FGF-13- vs. vehicle-treated animals (infarct volume was 21.9+/-3.8% in vehicle- and 8.1+/-1.6% in FGF-13-treated rats, p=0.0016) and a moderate inhibition of brain swelling by FGF-13. The reduction in infarct volume and brain swelling were associated with improvement of clinical deficits in FGF-13 treated animals (p<0.001). Histopathological examination determined that nervous tissue was better preserved in FGF-13 treated rats than those of controls. These data show that pretreatment with intravenous FGF-13 reduces infarct size and ameliorates neurological deficits following permanent focal cerebral ischemia in rats.
Animals↗
Offspring born from chimeras reconstructed from parthenogenetic and in vitro fertilized bovine embryos.
Chimeric embryos were produced by aggregation of parthenogenetic (Japanese Red breed) and in vitro fertilized (Holstein breed) bovine embryos at the Yamaguchi Research Station in Japan and by aggregation of parthenogenetic (Red Angus breed) and in vitro fertilized (Holstein breed) embryos at the St. Gabriel Research Station in Louisiana. After embryo reconstruction, live offspring were produced at each station from transplanting these embryos. The objective of this joint study was to evaluate the developmental capacity of reconstructed parthenogenetic and in vitro fertilized bovine embryos. In experiment I, chimeric embryos were constructed: by aggregation of four 8-cell (demi-embryo) parthenogenetic and four 8-cell stage (demi-embryo) IVF-derived blastomeres (method 1) and by aggregation of a whole parthenogenetic embryo (8-cell stage) and a whole IVF-derived embryo (8-cell stage) (method 2). Similarly in experiment II, chimeric embryos were constructed by aggregating IVF-derived blastomeres with parthenogenetic blastomeres. In this experiment, three categories of chimeric embryos with different parthenogenetic IVF-derived blastomere ratios (2:6; 4:4, and 6:2) were constructed from 8-cell stage bovine embryos. In experiment III, chimeric embryos composed of four 8-cell parthenogenetic and two 4-cell IVF-derived blastomeres or eight 16-cell parthenogenetic and four 8-cell IVF-derived blastomeres were constructed. Parthenogenetic demi-embryos were aggregated with sexed (male) IVF demi-embryos to produce chimeric blastocysts (experiment IV). In the blastocyst stage, hatching and hatched embryos were karyotyped. In experiment V, chimeric embryos that developed to blastocysts (zona-free) were cryopreserved in ethylene glycol (EG) plus trehalose (T) with different concentrations of polyvinylpyrrolidone (PVP; 5%, 7.5%, and 10%). In experiment I, the aggregation rate of the reconstructed demi-embryos cultured in vitro without agar embedding was significantly lower than with agar embedding (53% for 0% agar, 93% for 1% agar, and 95% for 1.2% agar, respectively). The aggregation was also lower when the aggregation resulted from a whole parthenogenetic and IVF-derived embryos cultured without agar than when cultured with agar (70% for 0% agar, 94% for 1% agar, and 93% for 1.2% agar, respectively). The development rate to blastocysts, however, was not different among the treatments. In experiment II, the developmental rates to the morula and blastocyst stages were 81%, 89%, and 28% for the chimeric embryos with parthenogenetic:IVF blastomere ratios of 2:6, 4:4, and 6:2, respectively. In experiment III, the developmental rate to the morula and blastocyst stages was 60% and 65% for the two 4-cell and four 8-cell chimeric embryos compared with 10% for intact 8-cell parthenogenetic embryos and 15% for intact 16-cell parthenogenetic embryos. To verify participation of parthenogenetic and the cells derived from the male IVF embryos in blastocyst formation, 51 embryos (hatching and hatched) were karyotyped, resulting in 27 embryos having both XX and XY chromosome plates in the same sample, 14 embryos with XY and 10 embryos with XX. The viability and the percentage of zona-free chimeric embryos at 24 hr following cryopreservation in EG plus T with 10% PVP were significantly greater than those cryopreserved without PVP (89% vs. 56%). Pregnancies were diagnosed in both stations after the transfer of chimeric blastocysts. Twin male (stillbirths) and single chimeric calves were delivered at the Yamaguchi station, with each having both XX and XY chromosomes detected. Three pregnancies resulted from the transferred 40 chimeric embryos at the Louisiana station. Two pregnancies were lost prior to 4 months and one phenotypically-chimeric viable male calf was born. We conclude that the IVF-derived blastomeres were able to stimulate the development of bovine parthenogenetic blastomeres and that the chimeric parthenogenetic bovine embryos were developmentall
Animals↗
Angiopoietin-1 and its receptor Tie-2 participate in the regulation of capillary-like tubule formation and survival of endothelial cells.
Angiopoietin-1 (Ang-1) and its receptor Tie-2, a trans-membrane tyrosine kinase uniquely expressed by endothelial cells, are shown by null mutation studies to be essential to developmental angiogenesis. The phenotypic abnormalities in these knockout animals suggest that Tie-2 signaling is necessary for the maintenance and expansion of the primitive capillary network. We present in vitro evidence indicating that the Ang-1/Tie-2 system participates in the regulation of capillary tubule formation and is necessary for the survival of confluent endothelial cells. Although recombinant Ang-1, which induces Tie-2 phosphorylation, has no effect on the proliferation of endothelial cells, treatment of confluent adult bovine aortic endothelial cells (ABAE) cells grown on collagen gels with Ang-1 (100 ng/ml) causes the cells to migrate into the collagen gel and form capillary-like tubules. The tubule-forming effect of Ang-1 is similar to the effect caused by FGF-2. A soluble form of the Tie-2 extracellular domain, in fivefold molar excess, blocks Ang-1-induced tubule formation. Specific elimination of Tie-2 protein expression in cultured ABAE cells as a result of transfection with an antisense oligonucleotide causes cell death in a dose-dependent manner (IC(50) = 50 nM). The antisense treatment has no effect on cells that do not express Tie-2. Cells treated with antisense oligonucleotide show a sixfold increase in the rate of apoptosis as assessed by in situ end labeling of fragmented DNA. These findings are consistent with the view that Ang-1/Tie-2 signaling is essential for both angiogenesis and endothelial cell survival.
3T3 Cells↗
VEGI, a novel cytokine of the tumor necrosis factor family, is an angiogenesis inhibitor that suppresses the growth of colon carcinomas in vivo.
A novel member of the tumor necrosis factor (TNF) family has been identified from the human umbilical vein endothelial cell cDNA library, named vascular endothelial growth inhibitor (VEGI). The VEGI gene was mapped to human chromosome 9q32. The cDNA for VEGI encodes a protein of 174 amino acid residues with the characteristics of a type II transmembrane protein. Its amino acid sequence is 20-30% identical to other members of the TNF family. Unlike other members of the TNF family, VEGI is expressed predominantly in endothelial cells. Local production of a secreted form of VEGI via gene transfer caused complete suppression of the growth of MC-38 murine colon cancers in syngeneic C57BL/6 mice. Histological examination showed marked reduction of vascularization in MC-38 tumors that expressed soluble but not membrane-bound VEGI or were transfected with control vector. The conditioned media from soluble VEGI-expressing cells showed marked inhibitory effect on in vitro proliferation of adult bovine aortic endothelial cells. Our data suggest that VEGI is a novel angiogenesis inhibitor of the TNF family and functions in part by directly inhibiting endothelial cell proliferation. The results further suggest that VEGI maybe highly valuable toward angiogenesis-based cancer therapy.
Amino Acid Sequence↗