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Biomedical subjects

Yan Wu

Publications and source records attributed to Yan Wu.

At least 145 records · Page 8Linked to original sources
PubMed2003

[Relation between helicobacter pylori L-form infection and tumor angiogenesis in human esophageal carcinoma].

OBJECTIVE: To investigate the correlation between helicobacter pylori L-form (Hp-L) infection in human esophageal carcinoma (EC) and tumor angiogenesis, and study the effect of Hp-L on the malignant biological behaviors of EC. METHODS: Hp-L was examined in 98 patients with EC and 30 controls by Gram stain, electronmicroscopic technique and immunohistochemical stain (ABC method). VEGF, p53 protein and microvessel density (MVD) were examined by immunohistochemical stain (SP method) with their relationship with the clinicopathologic factors analyzed. RESULTS: The positive rate of Hp-L was 60.2% in EC group. Two types of Hp-L were detected in the tissue of EC by electronmicroscopic technique, which lay in the outer or inner carcinoma cells. The positive rates of Hp-L, MVD, VEGF and p53 in the cancer group were significantly higher than those in control group (P < 0.005-0.001). The positive rates of MVD, VEGF and p53 in the Hp-L positive group of EC were significantly higher than those in Hp-L negative group (P < 0.005-0.001). The positive rate of Hp-L was correlated with MVD (r = 0.46, P < 0.01) and the expression of VEGF and p53 (r = 0.31, P < 0.01). The positive rate of Hp-L in the EC group was correlated with vessel invasion, depth of invasion, metastasis to the para-esophageal and distant lymph nodes except tumor size. CONCLUSION: Hp-L infection in EC is closely related with tumor angiogenesis and may be an important promoting factor in esophageal carcinoma growth, invasion and metastasis.

Adult↗
PubMed2003

[Overexpression of p21WAF1 and p53 in human lung adenocarcinoma cell line].

OBJECTIVE: To study the growth inhibitory effects of p21WAF1 and p53 overexpression in human lung adenocarcinoma cell line. METHODS: The p21WAF1 and p53 gene were transfected respectively into a human lung adenocarcinoma cell line, GLC-82. Flow cytometry (FLC), transmission electron microscopy (EM) and TUNEL technique were used to evaluate cell growth and identify apoptosis. RESULTS: The GLC-82 transfected by p21 plasmid showed increased cell number in G1 phase of cell cycle, decreased proliferation potential and decreased cloning efficiency. Apoptosis have not been detected neither on EM nor by TUNEL technique, whereas the GLC-82 infected by Ad-p53 showed significantly decreased proliferation potential and some of them even died, in addition apoptosis was confirmed by TUNEL technique. CONCLUSION: The results indicate that p21WAF1 and p53 can inhibit proliferation; p53 also can induce apoptosis of lung adenocarcinoma cell. Therefore, these two genes should have a wide application in gene therapy of tumors in future.

Adenocarcinoma↗
PubMed2003

[Forest gap characteristic in a coniferous-Picea likiangensis forest in the Yulong Snow Mountain Natural Reserve, Yunnan Province, China].

In this paper, some important parameters related to the gap disturbance regimes in a coniferous-Picea likiangensis forest in the Yulong Snow Mountain Natural Reserve, Yunnan Province were described. The results showed that expanded gaps occupied 42.5%, and canopy gaps occupied 28.8% of the land area in the forest. The frequency of gap disturbance was 35 gaps per hectares. There were 25% of small (gap area < 50 m2), 41% of middle (gap area 50-100 m2), and 34% of large (gap area > 100 m2) forest gaps. The most important manner of gap formation was the breakage at trunk base and its middle, and the secondly important manner was rotten. Gap maker in the forest was more than 80% of Picea likiangensis. The probability of making gaps was the greatest, when the big trees in the canopy layer got DBH 40-50 cm and height 15-25 m. Gaps formed by 1-2 gap makers was of 68.8%, and by 5 gap makers was seldom. The most of gap makers were 6 in a gap of the forest. The density of the seedlings in gap gradually increased with the forest gap from large to small.

Conservation of Natural Resources↗
PubMed2003

[Research on expression and control of p16 and p21 by wild-type p53 gene in two lung adenocarcinoma cell lines].

OBJECTIVE: To evaluate the potential of p53 gene therapy for lung cancer in nude mice. METHODS: Two lung adenocarcinoma cell lines L-18 and 95D were infected with adenovirus encoding wild-type p53 gene pAdCMV -p53 (Ad-p53 ) in vitro and in vivo. The antitumor effect of wild type p53 gene was assessed by cell growth curve, reverse transcriptase polymerase chain reaction (RT-PCR) analysis and TUNEL staining methods. RESULTS: The p53-specific growth inhibition and apoptosis of tumor cells were observed in both cell lines in vitro. By RT-PCR analysis, the increasing expression of p21 gene but not of p16 gene after p53 gene infection suggested that p21 gene played an important role in p53 gene induced cell apoptosis. The in vivo study revealed that celiac injection of p53 gene significantly inhibited the tumorigenesis in 95D and L-18 cells in nude mice. However, no obvious inhibition of tumorigenesis was observed after subcutaneous injection of p53 gene in L-18 cell line, compared with the inhibition noted in 95D cell line. CONCLUSION: The results showed the adenovirus-mediated antitumor therapy by means of p53 gene infection might be a potential way to inhibit cancer growth and induce tumor cell apoptosis.

Adenocarcinoma↗
PubMed2003

[Effects of tensile strain and loading time on the shape and cytoskeleton of the human periodontal ligament fibroblast measured by confocal laser scanning microscopy and immunity fluorescence technique].

UNLABELLED: The periodontal ligament fibroblast (PDLF) was cultivated artificially as the cell to be tested, and then it was loaded with mechanical stress-strain of different values and for different times. The cell and nucleus projected areas and shapes as well as the structure of cytoskeleton were tested by use of confocal laser scanning microscope and immunity fluorescence technique. Then the relationship among the stress-strain, the time, the shape and the structure of cytoskeleton of the PDLF was detected. RESULTS: In the trial groups of 0, 8%, 12%, 16% strain values, the cell and nucleus projected areas were proportional to strain (stress) and time. The diameter, density and order of the structure of cytoskeleton increased in the strain and time dependent fashion. In the trial group of 20% strain values, the cell and nucleus projected areas decreased with the increase of time, and the structure of cytoskeleton became disorderly. It was demonstrated in this study that the shape and structure of cytoskeleton of PDLF underwent regular changes when the PDLF was loaded with the mechanical stress-strain.

Cells, Cultured↗
PubMed2003

[Primary peritoneal malignant tumor: clinical analysis of 28 cases].

BACKGROUND & OBJECTIVE: Primary malignant peritoneal tumor is a kind of rare malignancy. Its morphology and clinical manifestations are very similar to the advanced ovarian cancer, therefore, they are usually misdiagnosed and the proper treatment were delayed. This paper analyzed the clinical characteristics, diagnosis, treatment, and prognosis of primary malignant peritoneal tumor. METHODS: The clinical data of 28 cases of primary peritoneal malignant tumor patients admitted between January 1996 to February 2002 in People's Hospital, Peking University, was analyzed retrospectively. There are 20 cases of primary peritoneal seropapillary adenocarcinoma, 8 cases of primary peritoneal malignant Muellerian tube tumor. Their age ranged from 33 to 74, with median age of 54. RESULTS: Among 28 patients, 22 were misdiagnosed preoperatively, the misdiagnose rate were 79%. In all cases, cytoreductive surgery were performed. Postoperative chemotherapy were given either with CAP regimen or TP regimen. Postoperative survival time was 1-83 months, the median survival time was 30 months. CONCLUSION: The recognition of this special tumor should be stressed, to improve early diagnosis and treatment. The authors suggest that cytoreductive surgery on time and postoperative adjuvant chemotherapy should be implemented to improve survival rate.

Adult↗
PubMed2003

Clinical spectrum of diffuse crescentic glomerulonephritis in Chinese patients.

OBJECTIVE: To investigate retrospectively the incidence, distribution of primary disease and clinicopathologic characteristics of diffuse crescentic glomerulonephritis (DCGN) in Chinese patients. METHODS: One hundred and seventy-two consecutive patients diagnosed as having DCGN out of 9828 cases of non-transplanting renal biopsies over sixteen years, were studied. DCGN is categorized into three types according to immunopathologic characteristics. The incidence of this disease, its primary diseases, clinical characteristics and serum antineutrophil cytoplasmic antibodies (ANCAs) were analyzed. RESULTS: The distribution of patients among the three classifications was 8.7% type I, 68.6% type II and 22.7% type III. Clinically, the majority of patients (69.8%) presented rapidly progressive glomerulonephritis (RPGN), but 30.2% manifested a chronic nephritic syndrome or chronic renal failure. In terms of related conditions, 93% were anemic, 61.6% had hypertension, 50.6% oliguria, 45.3% nephrotic syndrome, 43% uremic syndrome and 39.5% displayed gross hematuria. Those patients who were positive in serum for ANCAs had predominantly type III DCGN. Two cases with anti-GBM-antibody crescentic glomerulonephritis and three with lupus nephritis were also positive for ANCAs in serum. CONCLUSION: DCGN is not rare in Chinese patients. A majority of patients in our study presented with RPGN, but 30.2% manifested a chronic renal failure. Lupus patients with DCGN that were positive for ANCAs had more severe vasculitic lesions.

Adolescent↗
PubMed2003

[Chemical constituents from the leaves of Dalbergia hainanensis].

OBJECTIVE: To study the chemical constituents from the leaves of Dalbergia hainanensis. METHOD: Compounds were isolated by chromatographic techniques on silica gel and polyamide column. Their structures were elucidated by chemical and spectroscopic methods. RESULTS: Thirteen compounds were identified as 8-C-glucosylprunetin (1), 8-C-glucosylgenistein (2), 2-hydroxy-5-methoxy biochanin A (3), formononetin (4), 3,5-dimethoxy-4-hydroxybenzaldehyde (5), 1-O-beta-D-glucopyranosyl-(2S, 3S, 4R, 8Z)-2-[(2R)-2-hydroxyl docosylamino]-8-octadecene-1, 3, 4-triol (6), friedelin (7), taxaxerol (8), 3(-hydroxy-glutin-5-ene (9), ursolic acid (10), beta-sitosterol (11), daucosterol (12), lupeol (13). CONCLUSION: All the compounds were isolated from the plant for the first time.

Dalbergia↗
PubMed2002

Overexpression of wild-type breast cancer resistance protein mediates methotrexate resistance.

Previously, we have reported that a multidrug-resistant, mitoxantrone (MX)-selected cell line, MCF7/MX, is highly cross-resistant to the antifolate methotrexate (MTX), because of enhanced ATP-dependent drug efflux (E. L. Volk et al., Cancer Res., 60: 3514-3521, 2000). These cells overexpress the breast cancer resistance protein (BCRP), and resistance to MTX as well as to MX was reversible by the BCRP inhibitor, GF120918. These data indicated that BCRP causes the multidrug-resistance phenotype. To further examine the role of this transporter in MTX resistance, and in particular the role of amino acid 482, we analyzed a number of BCRP-overexpressing cell lines. MTX resistance correlated with BCRP expression in all of the cell lines expressing the wild-type transporter, which contains an Arg at position 482. In contrast, little or no cross-resistance was found in the MCF7/AdVp1000 and S1-M1-3.2 and S1-M1-80 cell lines, which contain acquired mutations at this position, R482T and R482G, respectively. Concomitantly, the greatest reduction in MTX accumulation was observed in the MCF7/MX cells (BCRP(Arg)) as compared with cells expressing the Thr and Gly BCRP variants. Furthermore, the reduction in drug accumulation was sensitive to BCRP inhibition by GF120918. In conclusion, we have demonstrated a novel role for BCRP as a mediator of MTX resistance and have provided further evidence for the importance of amino acid 482 in substrate specificity.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed2002

Identification, characterization, and functional study of the two novel human members of the semaphorin gene family.

We cloned two novel human transmembrane semaphorins, (HSA)SEMA6C and (HSA)SEMA6D, that belong to the class VI subgroup of the semaphorin family. The genes for SEMA6C and SEMA6D are mapped on chromosome 1q12-21.1 and 15q21.1, respectively. Among the adult tissues, SEMA6C is expressed only in skeletal muscle, whereas SEMA6D is expressed abundantly in kidney, brain, and placenta and moderately in the heart and skeletal muscles. During murine development, neither SEMA6C nor SEMA6D was expressed in embryonic day 10.5 (E10.5) embryos, but both were highly expressed in the areas of the lateral ventricle, the striatum, the wall of the midbrain, the pons/midbrain junction, and the choroid plexus of E13 embryos. Were neurons, neither axons nor astrocytes, highly expressed both semaphorins. Three isoforms of SEMA6C and five isoforms of SEMA6D derived from alternative splicing were identified, and their expression was regulated in a tissue- and development-dependent manner. Deletion analysis indicated that a sema domain and a PSI domain are integrally necessary for correct post-translation modification and subcellular localization. The extracellular domain of SEMA6C inhibited axonal extension of nerve growth factor-differentiated PC12 cells and induced the growth cone collapse of chicken dorsal root ganglion, rat hippocampal neurons, and rat cortical neurons in a dose-responsive manner. SEMA6D acted like SEMA6C except it had no significant effect on the growth cones of rat cortical neurons.

Alternative Splicing↗
PubMed2002

Revascularization of ischemic tissues by PlGF treatment, and inhibition of tumor angiogenesis, arthritis and atherosclerosis by anti-Flt1.

The therapeutic potential of placental growth factor (PlGF) and its receptor Flt1 in angiogenesis is poorly understood. Here, we report that PlGF stimulated angiogenesis and collateral growth in ischemic heart and limb with at least a comparable efficiency to vascular endothelial growth factor (VEGF). An antibody against Flt1 suppressed neovascularization in tumors and ischemic retina, and angiogenesis and inflammatory joint destruction in autoimmune arthritis. Anti-Flt1 also reduced atherosclerotic plaque growth and vulnerability, but the atheroprotective effect was not attributable to reduced plaque neovascularization. Inhibition of VEGF receptor Flk1 did not affect arthritis or atherosclerosis, indicating that inhibition of Flk1-driven angiogenesis alone was not sufficient to halt disease progression. The anti-inflammatory effects of anti-Flt1 were attributable to reduced mobilization of bone marrow-derived myeloid progenitors into the peripheral blood; impaired infiltration of Flt1-expressing leukocytes in inflamed tissues; and defective activation of myeloid cells. Thus, PlGF and Flt1 constitute potential candidates for therapeutic modulation of angiogenesis and inflammation.

Animals↗
PubMed2002

Placental growth factor reconstitutes hematopoiesis by recruiting VEGFR1(+) stem cells from bone-marrow microenvironment.

The mechanism by which angiogenic factors recruit bone marrow (BM)-derived quiescent endothelial and hematopoietic stem cells (HSCs) is not known. Here, we report that functional vascular endothelial growth factor receptor-1 (VEGFR1) is expressed on human CD34(+) and mouse Lin(-)Sca-1(+)c-Kit(+) BM-repopulating stem cells, conveying signals for recruitment of HSCs and reconstitution of hematopoiesis. Inhibition of VEGFR1, but not VEGFR2, blocked HSC cell cycling, differentiation and hematopoietic recovery after BM suppression, resulting in the demise of the treated mice. Placental growth factor (PlGF), which signals through VEGFR1, restored early and late phases of hematopoiesis following BM suppression. PlGF enhanced early phases of BM recovery directly through rapid chemotaxis of VEGFR1(+) BM-repopulating and progenitor cells. The late phase of hematopoietic recovery was driven by PlGF-induced upregulation of matrix metalloproteinase-9, mediating the release of soluble Kit ligand. Thus, PlGF promotes recruitment of VEGFR1(+) HSCs from a quiescent to a proliferative BM microenvironment, favoring differentiation, mobilization and reconstitution of hematopoiesis.

Animals↗
PubMed2002

[Adenovirus-mediated NT3 gene transfer protects spiral ganglion neurons from degeneration after noise trauma].

Numerous studies have shown that the health of spiral ganglion neurons is highly important for hearing. As a trophic factor of spiral ganglion neurons, neurotrophin 3 (NT3) is a potential candidate for prevention of spiral ganglion neuron degeneration in human. In our experiments, efficient transduction and long term expression of foreign gene of cochlea cells has been found with adenovirus carried lacZ gene (Ad-lacZ). A model of guinea pig deafness was made by intense noise exposure, which destroyed the entire organ of Corti in the middle part of the cochlea. Seven days after noise exposure, the animals were anesthetized and 1 10(8) recombinant adenoviral particles were injected into the scala tympani through the round window membrane. Animals inoculated with neurotrophin 3 adenovirus(Ad-NT3) were designated as the experimental group, animals inoculated with Ad-lacZ vector served as the control group. Four weeks after the inoculation of the virus, NT3 immunoreactivity was observed in the Ad-NT3 inoculated group. HE histochemical staining results showed that in the Ad-lacZ injected group, the neuronal degeneration was severer and the density of spiral ganglion neurons was significantly lower than those in the Ad-NT3 injected group. Our results demonstrate that with adenovirus-mediated overexpression NT3 may be developed into a new treatment to prevent secondary spiral ganglion degeneration following the damage to Corti organ.

Adenoviridae↗
PubMed2002

Crystal structure of shikimate kinase from Mycobacterium tuberculosis reveals the dynamic role of the LID domain in catalysis.

Shikimate kinase (SK) and other enzymes in the shikimate pathway are potential targets for developing non-toxic antimicrobial agents, herbicides, and anti-parasite drugs, because the pathway is essential in the above species but is absent from mammals. The crystal structure of Mycobacterium tuberculosis SK (MtSK) in complex with MgADP has been determined at 1.8 A resolution, revealing critical information for the structure-based design of novel anti-M. tuberculosis agents. MtSK, with a five-stranded parallel beta-sheet flanked by eight alpha-helices, has three domains: the CORE domain, the shikimate-binding domain (SB), and the LID domain. The ADP molecule is bound with its adenine moiety sandwiched between the side-chains of Arg110 and Pro155, its beta-phosphate group in the P-loop, and the alpha and beta-phosphate groups hydrogen bonded to the guanidinium group of Arg117. Arg117 is located in the LID domain, is strictly conserved in SK sequences, is observed for the first time to interact with any bound nucleotide, and appears to be important in both substrate binding and catalysis. The crystal structure of MtSK (this work) and that of Erwinia chrysanthemi SK suggest a concerted conformational change of the LID and SB domains upon nucleotide binding.

Adenosine Diphosphate↗
PubMed2002

Selective targeting of angiogenic tumor vasculature by vascular endothelial-cadherin antibody inhibits tumor growth without affecting vascular permeability.

Vascular endothelial-cadherin (VE-cadherin) is an endothelial cell-specific adhesion molecule that is localized exclusively at cell-cell contacts referred to as adherens junctions. VE-cadherin-mediated adhesion is crucial for proper assembly of vascular structures during angiogenesis as well as for maintenance of a normal vascular integrity. We have shown previously that a monoclonal antibody (BV13) to VE-cadherin not only inhibits the formation of vascular tubes during tumor angiogenesis but also disrupts adherens junctions of normal vasculature with a concomitant increase in vascular permeability. The goal of the current studies was to block VE-cadherin function during angiogenesis without disrupting existing junctions on normal endothelium. Using in vitro screening assays to test for functional blocking of adherens junction formation and in vivo assays to detect antibody effects on vascular permeability in normal tissues, we have identified a novel blocking antibody (E4G10) that inhibits VE-cadherin function during angiogenesis but does not disrupt existing adherens junctions on normal vasculature. E4G10 inhibited formation of vascular tubes in vivo in the Matrigel plug and corneal micropocket assays. E4G10 also inhibited tumor growth in three models of mouse and human tumors via an antiangiogenic mechanism. Examination of normal mouse and tumor tissues showed that E4G10 bound to endothelial cells in a subset of tumor vasculature but not to normal vasculature. Bromodeoxyuridine labeling experiments showed that E4G10 specifically targeted a subset of tumor endothelium that is undergoing active cell proliferation, which likely reflects the activated, angiogenic endothelium. These findings indicate that VE-cadherin can be selectively targeted during states of pathological angiogenesis, despite its ubiquitous distribution throughout the entire vasculature. Our data also suggest that antibody E4G10 recognizes VE-cadherin epitopes that are only accessible on endothelial cells forming new adherens junctions, such as in angiogenic tumor vasculature.

Adherens Junctions↗
PubMed2002

A novel homozygous point mutation in the COL17A1 gene in a Chinese family with generalized atrophic benign epidermolysis bullosa.

We describe a Chinese family with generalized atrophic benign epidermolysis bullosa (GABEB), a non-lethal variant of junctional epidermolysis bullosa. The proband was an offspring of consanguineous parents, had generalized blisters since birth and developed severe alopecia during early childhood. Ultrastructural examination of the proband's skin revealed fissures in the lamina lucida. Immunofluorescence assays using a monoclonal antibody recognizing the extracellular domain of the 180 kDa bullous pemphigoid antigen (BPAG2) showed loss of fluorescent signal in the basal membrane zone of the skin. DNA sequencing revealed a homozygous C-to-G transversion at nucleotide position 899 in exon 11 of the COL17A1 gene, which encodes BPAG2. This mutation results in serine to cysteine at position 265, which is located in a highly conserved region of the intracellular domain of BPAG2. We showed that the proband's father was heterozygous for this mutation. In addition, we found a novel polymorphic substitution of C-to-G at nucleotide position 798 in exon 10 of the COL17A1 gene, which results in an I233M change in BPAG2 and is a common polymorphic allele in a limited Chinese population.

Adult↗
PubMed2002

Five new diterpenoids from Pseudolarix kaempferi.

Five new diterpenoids, pseudolaric acids F (1), G (2), and H (3), 2',3'-dihydroxy-1'-propoxypseudolarate B (4), and 6'-O-acetylpseudolaric acid B O-beta-D-glucopyranoside (5), along with nine known diterpenoids, pseudolaric acids A, B, and C(1), deacetylpseudolaric acid C(2), deacetylpseudolaric acid A, methyl pseudolarate A, methyl pseudolarate B, pseudolaric acid A-O-beta-D-glucopyranoside, and pseudolaric acid B-O-beta-D-glucopyranoside, were isolated from the root bark of Pseudolarix kaempferi. Their structures and stereochemistry were elucidated mainly by spectral data, especially 2D NMR techniques.

Chromatography, Thin Layer↗