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Biomedical subjects

J Yang

Publications and source records attributed to J Yang.

At least 505 records · Page 28Linked to original sources

Interleukin-1beta inhibits gamma-aminobutyric acid type A (GABA(A)) receptor current in cultured hippocampal neurons.

Interleukin-1beta (IL-1beta), a polypeptide immune mediator, is induced within the central nervous system in response to a variety of pathological stimuli, including systemic infection, hypoxia, brain trauma, and seizure. IL-1beta action on the gamma-aminobutyric acid type A (GABA(A)) inhibitory neurotransmitter receptor was investigated in whole cell patch-clamped cultured hippocampal neurons. Application of IL-1beta at concentrations encountered in pathophysiological conditions (1-10 ng/ml; 59-590 pM) irreversibly decreased the peak magnitude of current elicited by 30 microM GABA. Current inhibition was IL-1beta concentration- and time-dependent and was prevented by a specific IL-1beta type I receptor antagonist. No significant changes in current kinetics or reversal potential were observed. The IL-1beta depression of GABA current was inhibited by high concentrations of nonspecific kinase inhibitors staurosporine (500 nM) and 1-(5-isoquinolinyl-sulfonyl)-2-methylpiperazine (H-7; 50 microM), but not by a protein kinase C selective inhibitor calphostin C (5 microM). We conclude that IL-1beta inhibits GABA(A) receptor function in hippocampal neurons by the involvement of an unidentified kinase. This blockade of the GABA(A) inhibitory neurotransmitter receptor may underlie the central nervous system hyperexcitability seen in many pathophysiological conditions.

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

Detailed allelic loss mapping on 7q32 in nasopharyngeal carcinoma.

OBJECTIVE: The present research group had found high frequency of loss of heterozygosity(LOH) of D7S500-D7S495 on chromosome band 7q32 in nasopharyngeal carcinoma, this study was conducted to further find the deletion region. METHODS: Higher density of loci on 7q32 in 30 tumors was studied by using microsatellite analysis. RESULTS: The frequency of LOH was 63.3%. The highest frequency of LOH was identified at the loci of D7S500-D7S509-D7S495, among which a common deletion of D7S509 was found. CONCLUSION: A putative tumor suppressor gene may be present around D7S509.

Chromosomes, Human, Pair 7↗

[Experiments on elimination of the noise in NEMG by adopting wavelet transform].

Wavelet transform (WT) is a promising technique for time-frequency analysis. By decomposing signals into elementary building blocks that are well localized both in time and frequency, the WT can characterize the local regularity of signal. In this paper, we process the needle electrode electromyography (NEMG) signal with noise by adopting WT and have completed the contrast experiments. The results show that WT is an effective method by which high frequency noise and baseline drift in NEMG can successfully be eliminated by selecting proper transform scales of WT.

Electromyography↗

Expression of human single-chain variable fragment antibody against non-structural protein 3 of hepatitis C virus antigen in e.coli.

OBJECTIVE: To express human single-chain variable fragment (ScFv) antibody against non-structural protein 3 (NS(3)) of hepatitis C virus in E.coli. METHODS: The recombinant phages were panned by NS(3) antigen which was coated in a microtiter plate. After five rounds of biopanning, 66 clones were identified specific to NS(3) antigen. E.coli host XL(1)-Blue was transformed and induced by IPTG. The specificity of ScFv was evaluated by ELISA and dot blot hybridization. RESULTS: ScFv-NS(3) DNA digestion and sequencing data showed that the ScFv gene was composed of 750bp. ELISA and dot blot hybridization demonstrated that the soluble human single-chain Fv antibody to hepatitis C virus NS(3) antigen could combine different origins of NS(3) antigen. CONCLUSION: NS(3)-ScFv antibody expressed by E.coli host XL(1)-Blue has the activity and specificity to combine different origins of HCV NS(3) antigen.

Escherichia coli↗

[TBX5 mutation in Chinese patients with Holt-Oram syndrome].

OBJECTIVE: To analyse TBX5 mutation in Chinese patients with Holt-Oram syndrome(HOS). METHODS: Seven HOS families were analysed with single strand conformation polymorphism(SSCP) and sequencing. RESULTS: Three SSCP changes were detected and identified as the TBX5 gene mutation at three new sites. One of the changes is a frameshift mutation caused by a base cytidine deletion at the cDNA sequence of 416, which altered all the codons after the point, thus it can not encode the protein of normal amino acid sequence; another is a missense mutation induced by a base substitution(C-->A) at the cDNA sequence of 145, which made the codon of that point change from CAG-->AAG, and encoded amino acid changed from glutamine(Gln) to lysine(Lys), consequently the change weakened the function of TBX5 protein; the third is also a missense mutation which resulted from a base substitution (T-->C) at the cDNA sequence of 161, this change made the codon of that point change from ATC-->ACC, it changed the encoded amino acid from isoleucine(Ile) to threonine(Thr), which reduced the function of TBX5 protein. CONCLUSION: HOS in Chinese is caused by mutation in TBX5.

Abnormalities, Multiple↗

Retinal damage induced by cisplatin in neonatal rats and mice.

PURPOSE: The morphologic response of the retina at different neonatal ages to various doses of cis-platinum(II)diamminedichloride (cisplatin) was examined in rats and mice. METHODS: Cisplatin was given to rats at a dose of 1, 3 or 5 mg/kg at 0 days or 5 mg/kg at 7 or 14 days of age, and to mice at 0.5, 1.5, 3 or 6 mg/kg at 0 days or 6 mg/kg at 7 or 14 days of age, and the animals examined 12 and 24 hrs, and 3 and 7 days after the treatment. RESULTS: In both species, regardless of gender, with > or = 3 mg/kg cisplatin treatment (lethal dose) at day 0, retinal damage characterized by the appearance of aggregations of TUNEL-positive cells scattered in the undifferentiated neuroblastic layer was seen at 24 hrs, and led to rosette formation at day 3 and 7 (retinal dysplasia). At the ultrastructural level, neuroblastic cells showed condensation of chromatin and shrinkage of the cytoplasm, and rosettes encircled by an outer limiting membrane. Cell debris phagocytosed by pigment epithelial cells was seen. However, cisplatin at < 3 mg/kg in 0-day-old animals or at high dose in > or = 7-day-old animals caused no damage to the retina. CONCLUSIONS: A critical period (day 0) for the administration and a threshold dose (> or =3 mg/kg) of cisplatin in the development of retinal damage in rats and mice was seen. Although the cisplatin dose necessary to damage the retina caused a high incidence of mortality, it was below the human therapeutic dose.

Aging↗

Preliminary studies on parkin gene deletion at exons 1 to 6 in Chinese patients with praecox Parkinson's disease.

OBJECTIVE: To search parkin gene deletion mutations at exons 1 to 6 in Chinese patients with praecox Parkinson's disease (PPD) and analyze them together with the clinical features of PPD. METHODS: DNA was extracted from peripheral blood of PPD patients; deletion mutations of parkin gene were identified by PCR amplification and agarose gel electrophoresis. The clinical data were analyzed together with the above information. RESULTS: Out of 21 patients, 2 had exon 1 deletion, 2 exon 4 deletion, and 1 exon 6 deletion. The mean age of the patients with deletion mutation was 45.7+/-1.8 years. All of the patients who had parkin gene deletion mutation had tremor, rigidity and bradykinesia, but athetosis and family history of PD were not found. In additon, the deletion mutations of parkin gene at exons 2, 3, 5, were not found. CONCLUSION: There are deletion mutations of parkin gene at exons 1,4,6 in PPD of Chinese, and such deletions generally happen on middle-aged patients.

Adolescent↗

Study on polymorphism of MICA exon 5 microsatellite in Shanghai Han population.

OBJECTIVE: To investigate the polymorphism distribution of MICA gene exon 5 microsatellite in Shanghai Han population and study the relationship of MICA gene and its closely linked gene HLA B. METHODS: The microsatellite polymorphism of MICA exon 5 in 175 unrelated healthy individuals were investigated using PCR-heteroduplex analysis. RESULTS: (1)There are 5 alleles of the microsatellite polymorphism in exon 5 of the MICA gene in Shanghai Han population, the gene frequency of MICA*A5 is the highest(39.14%), the next is MICA*A5.1(22.29%). (2)There is strong linkage disequilibrium between the HLA-B and MICA STR loci, e.g. MICA*A5 and HLA-B15, MICA*A4 and HLA-B27. CONCLUSION: The polymorphism distribution of MICA gene and the linkage disequilibrium between MICA and HLA-B have deviations in different ethnic groups.

China↗

Effect of batroxobin on expression of c-Jun in left temporal ischemic rats with spatial learning and memory disorder.

The effect of Batroxobin on expression of c-Jun in left temporal ischemic rats with spatial memory disorder was investigated by means of Morri's water maze and immunohistochemistry methods. The results showed that the mean reaction time and distance of temporal ischemic rats for searching a goal were significantly longer than those of sham-operated rats, and at the same time c-Jun expression of left temporal ischemic region was significantly increased. However, the mean reaction time and distance of Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of c-Jun immune reactive cells of Batroxobin-treated rats was also less than that of ischemic group. In conclusion, Batroxobin can improve spatial memory disorder in temporal ischemic rats, and the down-regulation of the expression of c-Jun is probably related to the neuroprotective mechanism.

Animals↗

DNA methylation in the regulation of T cell LFA-1 expression.

Inducing T cell LFA-1 overexpression by transfection, or by treatment with DNA methylation inhibitors including 5-azacytidine, procainamide and hydralazine, causes MHC-specific T cell autoreactivity in vitro and autoimmunity in vivo. How DNA methylation inhibitors increase LFA-1 expression is unknown. In this report we identify a mechanism by which DNA methylation affects LFA-1 expression. Nuclear run-on assays demonstrated that inhibiting DNA methylation increased transcription of CD11a but not CD18 or beta-actin mRNA. CD11a mRNA stability was not affected. Transfection of hypomethylated cells with reporter constructs containing the CD11a promoter showed no role for overexpression of transcription factors. However, the CD11a promoter demethylated following treatment with DNA methyltransferase inhibitors, and in vitro methylation of the construct suppressed its expression. Together, these results indicate that DNA methylation inhibitors can cause LFA-1 overexpression directly by demethylating the CD11a promoter. This mechanism could contribute to T cell autoreactivity, and potentially to autoimmunity.

Azacitidine↗

Ridge preservation of dentition with severe periodontitis.

Severe loss of alveolar bone height and width can occur following the removal of teeth with advanced periodontitis. This compromise of the alveolar bone can limit the options available for achieving an acceptable dental restoration. Two case reports are presented of alveolar ridge augmentation after tooth removal and before implant placement using bone grafting and a biodegradable membrane. The resultant alveolar ridges in both patients were adequate for the placement of dental implants.

Adult↗

Molecular modeling on human CCR5 receptors and complex with CD4 antigens and HIV-1 envelope glycoprotein gp120.

AIM: To investigate the interaction between human CCR5 receptors (CCR5) and HIV-1 envelope glycoprotein gp120 (HIV-1 gp120) and HIV-1 receptor CD4 antigens (CD4). METHODS: The structurally conserved regions (SCR) of human CCR5 was built by the SYBYL/Biopolymer module using the corresponding transmembrane (TM) domain of bacteriorhodopsin (bR) as the template. The coordinates for amino-terminal residue sequence, and carboxyl-terminal residue sequence, extracellular and cytoplasmic loops were generated using LOOP SEARCH algorithm. Subsequently the structural model was merged into the complex with HIV-1 gp120 and CD4. RESULTS: Human CCR5 interacted with both an HIV-1 gp120 and CD4. The N-terminal residues (especially Met1 and Gln4) of human CCR5 contacted with CD4 residues, mainly with one span (56-59) of CD4 in electrostatic interaction and hydrogen-bonds. The binding sites of human CCR5 were buried in a hydrophobic center surrounded by a highly basic periphery. On the other hand, direct interatomic contacts were made between 7 CCR5 residues and 6 gp120 amino-acid residues, which included van der Waals contacts, hydrophobic interaction, and hydrogen bonds. CONCLUSION: The interaction model should be helpful for rational design of novel anti-HIV drugs.

CD4 Antigens↗

Effects of batroxobin on spatial learning and memory disorder of rats with temporal ischemia and the expression of HSP32 and HSP70.

The effect of Batroxobin on spatial memory disorder of left temporal ischemic rats and the expression of HSP32 and HSP70 were investigated with Morri's water maze and immunohistochemistry methods. The results showed that the mean reaction time and distance of temporal ischemic rats in searching a goal were significantly longer than those of the sham-operated rats and at the same time HSP32 and HSP70 expression of left temporal ischemic region in rats was significantly increased as compared with the sham-operated rats. However, the mean reaction time and distance of the Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of HSP32 and HSP70 immune reactive cells of Batroxobin-treated rats was also less than that of the ischemic group. In conclusion, Batroxobin can improve spatial memory disorder of temporal ischemic rats; and the down-regulation of the expression of HSP32 and HSP70 is probably related to the attenuation of ischemic injury.

Animals↗

Expression of vascular endothelial growth factor during the early stage of maxillofacial blast injury.

OBJECTIVE: To determine the expression and the change of vascular endothelial growth factor (VEGF) and its acceptor KDR during the early stage of maxillofacial blast injury. To evaluate the effect of VEGF on traumatic wound healing. METHODS: The rabbit model of maxillofacial blast injury was made by KTY-04 blasting cap. The expression of VEGF and KDR in wound tissue was determined by ABC immunohistochemistry of 6 hours, 1 day, 2 days, 3 days, 5 days, and 7 days after injury. The results were compared with preinjury groups. RESULTS: In the wound tissue of the maxillofacial blast injury, the expression of VEGF rose steadily during the first week after the injury. Compared with normal tissue, the wound tissue showed differences by the first day after injury, and showed significant differences by the third day (P < 0.01). The differences reached a peak at the seventh day after injury. The expression of KDR showed no difference within 3 days after injury when compared to normal tissue. Between 5 and 7 days after injury, the protein was more strongly expressed. CONCLUSION: The stage of the VEGF expression at the maxillofacial blast injury site is similar to the angiopoietic stage during would healing, and KDR expression also occurs during that period. VEGF takes part in angiogenic cascades of traumatic wound healing and is produced as an auxiliary action to the regeneration of blood vessels.

Animals↗

Interaction between human interleukin-16 and CD4 receptor of HIV-1.

AIM: To study the interaction between human interleukin-16 (IL-16) and the receptor CD4 (T-lymphocyte differentiation antigen) of human immunodeficiency virus type 1 (HIV-1). METHODS: Two structurally conserved regions (SCRs) of human IL-16 were built by the SYBYL/Biopolymer module using the corresponding transmembrane (TM) domain of human interleukin-4 (HIL-4) and HIL-2 as the templates. The coordinates for amino-terminal residue sequence, carboxyl-terminal residue sequences, and cytoplasm loops were generated using Biopolymer's LOOP SEARCH algorithm. RESULTS: HIL-16 first formed a homodimer, then contacted with CD4 dimer further forming a dimeric complex. Subsequently, the dimeric complex constructed the tetrameric complex by two disulfide bridges between the cysteines of HIL-16 (Cys31-Cys31). CONCLUSION: The interaction model is useful to propose the action mechanism of HIL-16 and is beneficial for rational designing of novel anti-HIV drugs.

Amino Acid Sequence↗

[Distribution of TT virus genotypes in blood donors of northern China].

OBJECTIVE: To analyse the distribution of TT virus (TTV) genotypes in the blood donors of Northern China. METHODS: TTV DNA was detected using nested-PCR and its PCR products were cloned into the pGEM-T vector for sequencing. The sequences were analysed using ClustalX and Neighbor joining programs. RESULTS: Nucleotide identity of the 12 strains of Chinese TTV isolated was 53%-95%. Nucleotide homology between the representatives of genotype 1a and 1b [TX011(O), TA278] and the 12 strains of TTV was 55%-94% and 55%-75%, respectively. Of the 12 Chinese TTV isolates, eight were classified as genotype 1b, three as unknown genotype X and one as unknown genotype Y, which accounted for 66.7%, 25% and 8.3%, respectively. CONCLUSIONS: An exceptional degree of genetic heterogeneity was displayed in TTV nucleotide sequences and they could be, at least, classified as three genotypes. Genotype 1b may be the main prevalent genotype in blood donors of Northern China.

Amino Acid Sequence↗

[Cell cycle G2 arrest, cell death and nuclear localization induced by human immunodeficiency virus type 1 protein R (VPR) in cervical cancer cells].

OBJECTIVE: To explore the possibility of using Vpr as a biological agent for anticancer therapy. METHODS: A HIV-1 wild type Vpr and a mutant VprX gene were expressed and tested in a cervical cancer HeLa cell line. The ability of Vpr to induce cell cycle G2 arrest and cell death was measured by flow cytometric analysis. Nuclear localization of Vpr was visualized by fluorescent light emitted from the green fluorescent protein (GFP) -Vpr fusion protein. RESULTS: Consistent with early reports, Vpr, not VprX, induced G2 arrest. However, both Vpr and VprX were able to induce cell death in HeLa cells. We also demonstrated that the nuclear localization of Vpr could be determined by using a GFP-Vpr fusion protein. CONCLUSIONS: This is the first report documenting in mammalian cells that G2 arrest and cell death induced by Vpr are two independent functions. The unique biological properties of Vpr shown in cervical cancer cells suggest that Vpr may be a useful biological agent for anti -cancer therapy.

Cell Death↗