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Biomedical subjects

Ye Zhang

Publications and source records attributed to Ye Zhang.

At least 91 records · Page 5Linked to original sources
PubMed2003

[Pathological features of light chain nephropathy].

OBJECTIVE: To investigate the pathologic features and diagnostic algorithm of light chain nephropathy (LCN). METHODS: Seven cases of LCN were studied by light microscopy, electron microscopy and immunolabeling of light chains (kappa, lambda) by immunofluorescence and immunoelectron microscopy. RESULTS: The histopathology of 7 cases by light microscopy was variable, with 3 cases showing nodular glomerulosclerosis, 1 case showing mild to moderate mesangial proliferation, and 3 cases showing cast nephropathy with minimal glomerular change. Immunofluorescence study revealed positive staining of a single type of light chain in mesangium (nodular pattern) or along glomerular basement membrane (linear), along tubular basement membrane and around arteriolar walls in all the 7 cases. Ultrastructurally, electron-dense granular deposits were identified in mesangium, subendothelial aspect of glomerular basement membrane, outer aspect of tubular basement membrane and arteriolar walls. Immunogold labeling of light chains showed distinct labeling of a single type light chain in the granular electron-dense materials (5 cases being kappa-positive and 2 being lambda-positive). CONCLUSIONS: LCN typically shows nodular glomerulosclerosis. The ultrastructural change is characteristic and important for diagnosis. Immunolabeling of light chains by immunofluorescence and immunoelectron microscopy carries further diagnostic value, especially in cases with minimal light microscopic change.

Adult↗
PubMed2003

[Origin of hemagglutinin and neuraminidase gene of swine influenza A H1N1 viruses].

OBJECTIVE: To understand the origin of hemagglutinin (HA), and neuraminidase (NA) gene of swine influenza A (H1N1) viruses isolated in pigs in mainland China in 2002 and reveal the reason of pathogenesis of them in pigs. METHODS: The target gene amplified by PCR,PCR product was linked with PGEM-T Easy Vector(Promega company, USA) at 4? degrees C, the recombined plasmid was transferred into DH 10B bacteria, positive colonies were selected and identified them with restriction enzyme. Afterwards, they were sent to Liu He Tong company in Beijing for testing nucleotide sequence. Finally, phylogenetic analysis of the sequencing data was performed with MegAlign (Version 1.03)and Editseq (Version 3.69) software. RESULTS: The HA and NA genes of three strains of swine influenza A (H1N1) viruses isolated from pigs in China were closely related to those of swine influenza A (H1N1) virus, but different from those of avian or human influenza A (H1N1) virus. The swine strain of influenza A (H1N1) virus isolated in 2002 was derived from swine influenza A (H1N1) virus circulated in pigs in China in 1991. Since the antigenic drifts of HA and NA proteins of the new isolates occurred, their activity in pigs is increasing and they can cause disease in pigs. CONCLUSION: The HA and NA genes of three strains of influenza A (H1N1) virus tested were identified to be derived from those of swine influenza A (H1N1) virus. The increased activity and pathogenesis of them in pigs were most likely due to antigenic drifts of HA and NA proteins of the new isolates.

Amino Acid Sequence↗
PubMed2003

[Characterization of internal genes of two strains of influenza A (H9N2) virus isolated from men].

BACKGROUND: To understand the characteristics of internal genes of two strains of influenza A(H9N2) virus isolated from men and on the basis of these to reveal the origin of these two strains of influenza A(H9N2)virus. METHODS: The target gene was amplified by RT-PCR,the PCR product was ligated with P GEM-T Vector (Promega Company, USA) at 4 degrees, the recombined plasmid was transferred into dH5a bacteria, and the positive colonies were selected and identified with restriction enzyme. Afterwards, they were sent to Liu He Tong Company in Beijing for nucleotide sequencing. Finally, phylogenetic analysis of the sequencing data was performed with MegAlign (version 1.03)and Editseq (Version 3.69) softwares. RESULTS: Internal genes of the two strains of H9N2 virus were G9 lineage. There was a slight difference in nucleotide sequence in PA gene between the two strains, whereas another five gene segments were identical to each other. CONCLUSION: The genomes of the two strains of influenza A(H9N2)virus were G9 lineage.They were transmitted to men separately from different avian sources with different characteristics of gene of influenza A(H9N2) virus, respectively.

Animals↗
PubMed2003

[Expression variation and mutation analysis of exon 9 and 10 in amyloid precursor protein gene in Alzheimer's disease].

To explore the expression differences of exon 9 and 10 in Amyloid Precursor Protein gene(APP9 approximately 10) in Alzheimer's disease,and detect the probable point mutation appeared in cDNA fragment of APP9 approximately 10 in the Shanghai Han people.semi-quantitative competitive RT-PCR technique was performed to detect the expression of APP9 approximately 10 in peripheral lymphocyte, and the Apolipoprotein E gene(ApoE) and Presenilin 1(PS1)gene were genotyped with PCR-RFLP method. We also analyzed the point mutation in APP9 approximately 10 cDNA through the denatured gel electrophoresis. The results are as follows:1. While compared with healthy controls,expression of APP9 approximately 10 mRNA was significantly enhanced in Alzheimer disease; 2.APOE*epsilon4 allele, the most common genetic risk factor for AD, did not affect the Expression of APP9 approximately 10 mRNA, whereas the APP9 approximately 10 mRNA expression might be increased by the allele 1 of PS1 gene, another probable susceptibility gene of AD.3. No point mutation in APP9 approximately 10 cDNA was detected. In our samples, the expression of APP9 approximately 10 mRNA in AD was significantly different from that of controls, suggesting that the change of peripheral APP9 approximately 10 mRNA expression might be another bio-marker used in clinical diagnosis for AD.

English Abstract↗
PubMed2002

Monogene and polygene therapy for the treatment of experimental prostate cancers by use of apoptotic genes bax and bad driven by the prostate-specific promoter ARR(2)PB.

We have shown that adenovirus-mediated manipulation of apoptotic genes such as bax could be a therapeutic option for prostate cancer. Unfortunately, the response of experimental prostate tumors to a single therapeutic gene of the apoptotic pathway is short-lived, and most of these tumors relapse after a short period of time. In this investigation we present data generated with adenovirus AvARR(2)PB-Bad, in which the apoptotic gene bad was placed under the control of the dihydrotestosterone (DHT)-inducible third-generation probasin-derived promoter ARR(2)PB. This therapeutic virus was given alone or in combination with other therapeutic viruses to a variety of in vitro and in vivo experimental models of prostate cancer. On infection with AvARR(2)PB-Bad, DHT-induced Bad overexpression occurred specifically in androgen receptor-positive (AR(+)) cells of prostatic derivation. The apoptotic effect of AvARR(2)PB-Bad (group 1) was compared with that of AvARR(2)PB-Bax (which overexpresses the apoptotic protein Bax) (group 2), with that of the combination AvARR(2)PB-Bad plus AvARR(2)PB-Bax (group 3), and with that of the control virus AvARR(2)PB-CAT (group 4) in the cell line LNCaP. In addition to identifying the modality of apoptosis induction by overexpressed Bad, the results suggested that group 3 contained more apoptotic cells than any other group. In additional studies, AR(+) androgen-dependent LNCaP cells or AR(+) and androgen-independent C4-2 cells were injected subcutaneously into nude mice. Four groups of six LNCaP or C4-2 tumors were treated with the same combinations of viruses discussed above for groups 1, 2, 3, and 4. Treatment resulted in decreased tumor size in groups 1, 2, and 3 compared with group 4. There was a better response in group 3 compared with group 2, and in group 2 compared with group 1. A better response in group 3 was confirmed during a 8-week follow-up period, in which no treatment was administered. Two LNCaP and C4-2 tumors of group 3 disappeared at the end of treatment and did not recur after an 8-week follow-up period. The data suggest that polygene therapy with apoptotic molecules is more effective in experimental models of androgen-dependent or -independent prostate cancer than monogene therapy.

Adenoviridae↗
PubMed2002

A novel class of nonbiaryl atropisomeric P,O-ligands for palladium-catalyzed asymmetric allylic alkylation.

[structure: see text]. A novel class of nonbiaryl atropisomeric P,O-ligands possessing an N,N-dialkyl-1-naphthamide skeleton has been synthesized via an efficient chemical resolution process. It represents the first example of axially chiral P,O-ligands devoid of central chirality. Up to 94.7% ee was obtained for the Pd-catalyzed asymmetric allylic alkylation (AAA). Effects of solvent, base, and the bulk of the C8 oxygen group of the P,O-ligand on the AAA reaction were examined.

Journal Article↗
PubMed2002

RANTES-mediated chemokine transcription in astrocytes involves activation and translocation of p90 ribosomal S6 protein kinase (RSK).

RANTES (regulated on activation normal T cell expressed and secreted) (> or =10 ng/ml) stimulates the induction of KC and other chemokines in astrocytes. Elements of the signal transduction pathway controlling this response were identified. RANTES induced phosphorylation of MEK, ERK1/2, p90 ribosomal S6 kinases (RSK), and cAMP-response element-binding protein (CREB) in astrocytes. U0126, a pharmacological inhibitor of MEK, blocked the phosphorylation of the downstream elements ERK, RSK, and CREB, inhibited chemokine synthesis, and reduced transcription from a KC promoter construct. Dominant negative mutants of RSK or CREB blocked the transcription driven by the KC promoter. Finally, RANTES treatment induces nuclear translocation of phosphorylated RSK in astrocytes. This novel role for RSK in signaling chemokine responses and synthesis in astrocytes may contribute to the amplification mechanisms responsible for prolonging inflammatory responses in the central nervous system.

Animals↗
PubMed2002

The signalling pathway for BCG-induced interleukin-6 production in human bladder cancer cells.

Intravesical bacillus Calmette-Guerin (BCG) is currently the therapy of choice for superficial bladder cancer with a 60-70% response rate. Induction of cytokine production (e.g. IL-6, etc.) by BCG has been found in patient's urine in vivo as well as bladder cancer cell lines. However, the signalling mechanisms are still unclear. In this study, we investigated the effect of BCG on cAMP production and its role in regulating interleukin-6 expression in the human bladder cancer cell line, MGH. After 1 hr exposure to BCG, IL-6 gene expression in MGH cells increased by 2.5-3-fold and cAMP production increased by 8-10-fold in a time- and dose-dependent manner. BCG-induced cAMP production was inhibited by both antifibronectin antibody and an adenylate cyclase inhibitor, SQ22536 in a dose-dependent way. In the presence of SQ22536, IL-6 expression in MGH cells was also greatly reduced. Furthermore, cAMP-dependent kinase inhibitors H7 and HA1004 also inhibited BCG-induced IL-6 expression in MGH, with HA1004 being much less effective than H7. Thus, BCG induces cAMP production and may regulate interleukin-6 expression partially via a cAMP-dependent pathway in human bladder cancer cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2002

CD4-deficient T helper cells are capable of supporting somatic hypermutation and affinity maturation of germinal center B cells.

Collaborative interactions between B lymphocytes and CD4+ helper T cells are necessary for the induction of Ab responses to most protein Ag and for the generation of memory B cells in germinal centers. To study the role of the CD4 molecule in the germinal center response and in the development of B cell memory, we have investigated T helper function in the initiation and maturation of humoral immunity in CD4-deficient mice. In the absence of CD4+ T cells, immunization with thymus-dependent Ag was able to induce germinal center formation and Ig somatic hypermutation. In addition, Ag-driven affinity maturation and development of B cell memory were largely intact in CD4-deficient mice. Thus, CD4-deficient T helper cells are able to collaborate with Ag-activated B cells to elicit the germinal center reaction, switch on the mutational machinery, and deliver signals necessary for B cell memory development.

Animals↗
PubMed2002

RANTES stimulates inflammatory cascades and receptor modulation in murine astrocytes.

Cultured mouse astrocytes respond to the CC chemokine RANTES by production of chemokine and cytokine transcripts. Stimulation of astrocytes with 1 nM RANTES or 3-10 nM of the structurally related chemokines (eotaxin, macrophage inflammatory protein-1alpha and -beta [MIP-1alpha, MIP-1beta]) induced transcripts for KC, monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-alpha), MIP-1alpha, MIP-2, and RANTES in a chemokine and cell-specific fashion. Synthesis of chemokine (KC and MCP-1) and cytokine (TNF-alpha) proteins was also demonstrated. RANTES-mediated chemokine synthesis was specifically inhibited by pertussis toxin, indicating that G-protein-coupled chemokine receptors participated in astrocyte signaling. Astrocytes expressed CCR1 and CCR5 (the redundant RANTES receptors). Astrocytes derived from mice with targeted mutations of either CCR1 or CCR5 respond after RANTES stimulation, suggesting multiple chemokine receptors may separately mediate RANTES responsiveness in astrocytes. Preliminary data suggest activation of the MAP kinase pathway is also critical for RANTES-mediated signaling in astrocytes. Treatment with RANTES specifically modulated astrocyte receptors upregulating intercellular adhesion molecule 1 (ICAM-1) and downregulating CX3CR1 expression. Thus, after chemokine treatment, astrocytes release proinflammatory mediators and reprogram their surface molecules. The combined effects of RANTES may serve to amplify inflammatory responses within the central nervous system.

Animals↗
PubMed2002

A comparison of two impedance cardiographs using head-up tilting and trend analysis.

OBJECTIVES: To compare the performances of two impedance cardiographs, the RheoCardioMonitor (RCM) and the BoMed NCCOM3, using trend analysis. This involved a series of head-up tilts, a simulation of the stroke volume (SV) and cardiac output (CO) response, calculation of prediction errors and cumulative sums (Cusum). METHODS: Eight healthy male volunteers, aged 27-37 years, were tilted on four occasions to angles of 55 degrees, 15 degrees, 30 degrees and 55 degrees, whilst recording SV and CO every 10-sec. Baseline and percentage changes with tilting were calculated. A simulation of the tilt response was constructed, and from this residuals (observed-predicted) and prediction errors ((observed-predicted)/predicted) x 100% were calculated at 10-sec intervals. Trend analysis was performed by multiple analysis of the variance of serial measurements and graphically assessing changes in serial SV prediction errors, using Cusums. Results are presented as mean (range or SD). RESULTS: Baseline values for RCM-SV were 76 (35-94) ml and for CO 4.7 (2.8-6.1) litre x min(-1). For BoMed-SV they were 113 (90-164) ml and for CO 7.2 (5.5-11.9) litre x min(-1). Head-up tilting to 55 degrees resulted in a 32 (12)% decrease in RCM-SV and a 21 (11)% decrease in BoMed-SV (p < 0.01). Prediction errors for RCM-SV were (6.5 (4.9)%) and for BoMed-SV (6.8 (5.2)%) (p = 0.048). Cusum analysis showed that in 84% of tests, impedance measurements remained within +/- 10% of the initial calibration. There was no difference between devices (chi2 = 0.92). CONCLUSIONS: Simulation of a physiological response, such as that to head-up tilting, and using a trend analysis based on prediction errors and Cusum, is a useful technique. The trending abilities of the RCM and BoMed were similar.

Cardiac Output↗
PubMed2002

Antimicrobial activity and stability to proteolysis of small linear cationic peptides with D-amino acid substitutions.

Antimicrobial peptides contribute to innate host defense against a number of bacteria and fungal pathogens. Some of antimicrobial synthetic peptides were systemically administered in vivo; however, effective protection has so far not been obtained because the effective dose of peptides in vivo seems to be very high, often close to the toxic level against the host. Alternatively, peptides administered in vivo may be degraded by certain proteases present in serum. In this study, D-amino acids were substituted for the L-amino acids of antimicrobial peptides to circumvent these problems. Initially a peptide (L-peptide) rich in five arginine residues and consisting of an 11-amino acid peptide (residues 32-42) of human granulysin was synthesized. Subsequently, the L-amino acids of the 11-amino acid peptide were replaced partially (D-peptide) or wholly (AD-peptide) with D-amino acids. Activity and stability to proteolysis, in particular, in the serum of antimicrobial peptides with D-amino acid substitutions were examined. Peptides with D-amino acid substitutions were found to lyse bacteria as efficiently as their all-L-amino acid parent, L-peptide. In addition, the peptide composed of L-amino acids was susceptible to trypsin, whereas peptides containing D-amino acid substitutions were highly stable to trypsin treatment. Similarly, the peptide consisting of L-amino acids alone was also susceptible to fetal calf serum (FCS), however, protease inhibitors restored the lowered antimicrobial activity of the FCS-incubated peptide. Thus, D-amino acid substitutions can make antimicrobial peptides resistant to proteolysis, suggesting that the antimicrobial peptides consisting of D-amino acids are potential candidates for clinical therapeutic use.

Amino Acid Substitution↗
PubMed2002

[RhoA gene expression in colorectal carcinoma].

OBJECTIVE: To investigate the expression of RhoA mRNA in colorectal neoplasms. METHODS: Total RNA was extracted from 42 surgically resected specimens of colorectal caricinoma and normal mucosa close to the lesions. Afier the optimal reverse transcription polymerase chain reaction (RT-PCR) condition was found, the mRNA expression levels of the RhoA gene in the lesions and the normal mucosa were examined semi-quantitatively and the relation between these expression levels and clinical pathological markers was compared. RESULTS: The expression of RhoA gene mRNA in lesion of colorectal carcinoma was significantly higher than that in contiguous normal mucosa (1.8 +/- 0.6 vs 0.9 +/- 0.4, P < 0.01). The ratio of RhoA expression in neoplasm to that in contiguous mucosa was 2.02 +/- 0.82. Based on this ratio the 42 patients were divided into two groups: overexpression group (19 cases) and high-expression group (23 cases). In the overexpression group the lesions of 14 cases were in Dukes C and Dukes D stages, and lymph node metastasis was found in 13 cases. In the high-expression group, only 9 out of the 23 cases were in advanced stage and 8 cases showed lymph-node metastasis. Chi-squared test analysis demonstrated a significant difference in both aspects between these two groups (P < 0.05). The difference in number of metastatic lymph nodes between the two groups was statistically significant (P < 0.01). Mutation was not found in the RhoA gene sequence examined. CONCLUSION: RhoA gene may play an important role in colorectal carcinogenesis and correlate with invasion and metastasis of colorectal carcinoma.

Adult↗
PubMed2002

[Characterization of genome of A/Guangzhou/333/99(H9N2) virus].

BACKGROUND: To understand the characterization of genome of a strain of avian influenza A H9N2 virus repeatedly isolated from a child with influenza illness. Thereafter to reveal the origin of this H9N2 virus. METHODS: Viruses were passed in embryonated hen eggs and virion RNA was extracted from allantoic fluid and reverse transcribed to synthesize cDNA. cDNA was amplified by PCR and the PCR product was purified with a purification kit. Afterwards RNA sequence analysis was performed by dideoxynucleotide chain termination and a cloning method. Finally, phylogenetic analysis of the sequencing data was performed with MegAlign (Version 1.03) and Editseg (Version 3.69) softwares. RESULTS: Genome of A/Guangzhou/333/99 (H9N2) virus was closely related to avian influenza A H9N2 virus, but obvious difference from that of A/Duck/Hong Kong/Y439/97(H9N2) virus, as well as its genome did not include any RNA segment derived from human influenza A virus. However, the genes encoding the HA,NA,NP and NS proteins of A/Guangzhou/333/99 virus were derived from those of G9 lineage virus, the rest genes encoding the M and three polymerase (PB2,PB1 and PA) proteins were derived from G1 lineage strain. CONCLUSIONS: A/Guangzhou/333/99 virus was a reassortant derived from reassortment betweenG9 and G1 lineages of avian influenzaA(H9N2) viruses. Therefore, the most possibility is that it is derived from avian influenza A virus directly. The results do not only demonstrate that avian influenza A (H9N2) virus could infect men, but also firstly prove that the genetic reassortment could be occurred between different genetic lineages of avian influenza A (H9N2) viruses in the nature.

Animals↗
PubMed2002

[Detection of human herpes virus 8 in Kaposi sarcoma using polymerase chain reaction and single stranded probe in situ hybridization with a tyramide signal amplification system].

OBJECTIVE: To study the relationship between Kaposi's sarcoma (KS) and human herpes virus 8 (HHV8; Kaposi's sarcoma-associated herpes virus), and to develop an in situ hybridization (ISH) technique effective for clinical pathological diagnosis. METHODS: Polymerase chain reaction (PCR) technique was used to synthesize a digoxigenin-labeled single stranded DNA probe specific for HHV8 open reading frame 72 cyclin D homolog gene encoded mRNA as the probe accompanying with a tyramide signal amplification system (TSA) for ISH assay. Totally 20 formalin-fixed and paraffin-embedded samples from 14 cases of KS from Danish patients were collected for HHV8 detection. In order to compare the result obtained, all of these cases were checked simultaneously using PCR technique. RESULTS: HHV8 was detected in 10 of 14 (71%) KS cases, of which 8 cases were positive for HHV8 by both ISH and PCR. In ISH, HHV8 hybridization signal was seen as a dot or patch located in the nuclei of both the neoplastic spindle cells and the endothelial cells. HHV8 was found in lesions in all the stages of KS including early patch, plaque and late nodular or tumor lesions, as well as in the primary and metastatic lesions. All the control cases showed a relevant positive or negative results. CONCLUSIONS: The results further confirmed that there is a strong association between Kaposi's sarcoma and HHV8. The ISH technique with single stranded probe and TSA would be helpful in clinical pathological diagnosis for HHV8 infected diseases, such as KS, primary effusion lymphoma and multicentric Castleman's disease.

Adolescent↗
PubMed2002

[A novel test for diagnosis of influenza].

OBJECTIVE: To set up a novel, simple, sensitive, specific, repeatable and rapid assay for diagnosis of influenza. METHODS: Monolayers of MDCK cells were inoculated with the specimens for amplifying viral yield, the feature of receptors on cell surface was changed by treatment of neuraminidases of influenza A and B viruses. Afterward, based on the lectin binds to receptors on cell surface with strict specificity,the phenomenon of red blood cell aggregation was observed under the conventional microscope. Finally, the tested results could be determined by the extent of red blood cell aggregation. RESULTS: There was a complete (%) consistency rate (100%) for viral isolation between new and routine tests. In general, the results were detected with new assay within 20 h. The sensitivity of new assay was over 100-10,000 times higher than that of routine method. Meanwhile, the novel test could not only be used for rapid diagnosis in the clinic, but also be used for influenza surveillance. The best concentration of red blood cells was 1 in the detection assay. The testing result was not effected by red blood cells taken from either different red blood cell type of human or different individual of guinea pigs. CONCLUSIONS: The novel method has several advantages: simple, high sensitivity and specificity, accurate and suitable for multiple purposes.

Animals↗
PubMed2001

Regulation of human osteocalcin promoter in hormone-independent human prostate cancer cells.

Osteocalcin (OC) is a small (6 kDa) polypeptide whose expression was thought to be limited to mature osteoblasts. The discovery of OC expression in prostate cancer specimens led us to study the regulation of OC gene in androgen-independent metastatic human prostate PC3 cells. An 800-bp human OC (hOC) promoter-luciferase construct exhibited strong basal and vitamin D-induced activity in OC-positive human prostate and osteosarcoma cell lines. Through deletion analysis of the hOC promoter, the functional hierarchy of the cis-acting elements, OSE1, OSE2, and AP-1/VDRE, was established in PC3 cells (OSE1 > AP-1/VDRE > OSE2). By juxtaposing dimers of these 3 cis-elements, we produced a minimal hOC promoter capable of displaying high tissue specific activity in prostate cancer cells. Our study demonstrated three groups of transcription factors, Runx2, JunD/Fra-2, and Sp1, responsible for the high hOC promoter activity in PC3 cells by binding to the OSE2, AP-1/VDRE, and OSE1 elements, respectively. Among the three groups of transcription factors, the expression levels of Runx2 and Fra-2 are higher in the OC-positive PC3 cells and osteoblasts, compared with the OC-negative LNCaP cells. Interestingly, unlike the mouse OC promoter, the OSE1 site in hOC promoter is regulated by members of Sp1 family instead of the osteoblast-specific factor Osf1. The molecular basis for androgen-independent prostate cancer cells behaving like mature osteoblasts may be explained by the interplay and coordination of these transcription factors under the tight regulation of autocrine and paracrine mediators.

Base Sequence↗