[Progress in the epidemiologic study of variant Creutzfeldt-Jakob disease].
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Animals↗
Biomedical subjects
Yu Zhu
Publications and source records attributed to Yu Zhu.
Structural and functional conservation of error-free DNA postreplication repair in Schizosaccharomyces pombe.
DNA postreplication repair (PRR) is a cellular process by which cells survive replication-blocking lesions without removing the lesion. In the budding yeast Saccharomyces cerevisiae, MMS2 plays a key role in the error-free PRR pathway: the mms2 null mutant displays an increased spontaneous mutation rate and sensitivity to a variety of DNA damaging agents. In contrast, its human homologs appear to play a different role. In order to address whether the MMS2-mediated PRR pathway is conserved in eukaryotes, we isolated a Schizosaccharomyces pombe cDNA homologous to MMS2, which we named spm2(+). Using spm2(+) as a bait in a yeast two-hybrid screen, we identified a fission yeast cDNA homologous to UBC13 from various species and named it spu13(+). Two-hybrid analysis confirmed physical interaction between Spm2 and Spu13, and between Spm2 and budding yeast Ubc13. Genetic analysis shows that both spm2(+) and spu13(+) are able to functionally complement the corresponding budding yeast mutants. Furthermore, deletion of either spm2(+), spu13(+) or both genes from fission yeast results in an increased sensitivity to DNA damaging agents, suggesting that spm2(+) and spu13(+) indeed function in PRR. The fact that the spm2(-) spu13(-) double mutant showed sensitivity similar to that of the single mutant indicates that these two gene products act at the same step. Hence, our data strongly support the hypothesis that the PRR function mediated by UBC13-MMS2 is conserved throughout eukaryotes.
Amino Acid Sequence↗
A stable and sensitive genotoxic testing system based on DNA damage induced gene expression in Saccharomyces cerevisiae.
A sensitive and stable genotoxic testing system has been developed based on the induction of a Saccharomyces cerevisiae RNR3-lacZ reporter gene expression in response to a broad range of DNA-damaging agents and agents that interfere with DNA synthesis. All 11 tested known carcinogenic and genotoxic agents, ranging from DNA alkylating agents, oxidative chemicals and radiations, were able to induce RNR3-lacZ expression at a sublethal dose. In particular, a potent colon carcinogen, 1,2-dimethyl hydrazine (SDMH), was not detected as a mutagen by a standard Ames test, but was able to induce RNR3-lacZ expression. In contrast, both non-mutagenic and non-genotoxic chemicals tested were unable to induce RNR3-lacZ expression. We have compared three yeast DNA damage-inducible genes for their sensitivity and inducibility, and found that RNR3 is more sensitive than RNR2 and MAG1. The effects of damage dose, post-treatment incubation time and cell growth stage on RNR3-lacZ expression have also been determined and optimized. In order to create a stable and user-friendly testing system, we integrated the RNR3-lacZ cassette into the yeast genome and demonstrated that its inducibility is indistinguishable from that of plasmid-based studies.
Animals↗
Two-dimensional rhombohedral grid coordination polymers [M(bbbt)(2)(NCS)(2)](n)(M = Co, Mn, or Cd; bbbt = 1,1'-(1,4-butanediyl) bis-1H-benzotriazole): synthesis, crystal structures, and third-order nonlinear optical properties.
In this paper, treatment of 1,1'-(1,4-butanediyl) bis-1H-benzotriazole (bbbt) and KSCN with Co(II), Mn(II), or Cd(II) afforded three two-dimensional rhombohedral grid coordination polymers [M(bbbt)(2)(NCS)(2)](n)(M = Co, 1; Mn, 2; Cd, 3). The two-dimensional rhombohedral grids are parallel to the crystallographic ac plane. The rhombohedral grid consists of 44-membered rings of M(4)(bbbt)(4), and gives the dimensions of 12.913 x 10.764 A for polymer 1, 13.106 x 10.797 A for polymer 2, and 13.256 x 10.870 A for polymer 3. The three polymers' third-order nonlinear optical (NLO) properties were determined by Z-scan technique in DMF solution. The results show that all three polymers show very large NLO absorption and strong NLO refraction properties. The third-order NLO absorptive coefficients alpha(2) are 5.4 x 10(-9) m W(-1) for polymer 1, 5.2 x 10(-9) m W(-1) for polymer 2, and 5.0 x 10(-9) m W(-1) for polymer 3. The alpha(2) values are larger than those of all the reported cluster compounds. The NLO refractive index values n(2) of the three polymers are 5.73 x 10(-19), 3.55 x 10(-19), and 3.07 x 10(-19) m(2) W(-1), respectively. Their hyperpolarizability gamma values are calculated to be 2.40 x 10(-30) esu for polymer 1, 1.52 x 10(-30) esu for polymer 2, and 1.50 x 10(-30) esu for polymer 3. The gamma values are comparable to those of clusters and better than those of organometallic compounds, semiconductors, and fullerene.
Journal Article↗
Initiation and development of experimental autoimmune neuritis in Lewis rats is independent of the cytotoxic capacity of NKR-P1A+ cells.
Natural killer (NK) cells are implicated in T cell-mediated autoimmune diseases. Experimental autoimmune neuritis (EAN) is a CD4+ T cell-mediated animal model of the Guillain-Barré syndrome in human. The role of NK cells in the initiation and development of EAN remains unclear. In the present study, we demonstrate that anti-NKR-P1A monoclonal antibody (mAb) treatment in vivo did not affect the initiation and development of clinical EAN in Lewis rats induced by immunization with peripheral nerve myelin P0 protein peptide 180-199 and Freund's complete adjuvant, as well as the proportion of NKR-P1A+ cells (including NK cells and NKT cells) in the spleen. Furthermore, inflammatory cell infiltrations and demyelination in the peripheral nervous system (PNS) and in vitro P0 peptide 180-199-specific splenocyte proliferation were not different in anti-NKR-P1A mAb-treated rats compared to the control antibody-treated rats. The cytotoxic activity of NKR-P1A+ cells, determined by NK cell-sensitive K562 cells as target cells, decreased markedly in anti-NKR-P1A mAb-treated rats, suggesting that decrease of the cytotoxic activities of NKR-P1A+ cells is not sufficient to alter clinical EAN, although NKR-P1A+ cells may participate in the pathogenesis of T cell-mediated autoimmune diseases, such as EAN, by the mechanisms that involve the release of cytokines.
Animals↗
CD4 and CD8 T cells, but not B cells, are critical to the control of murine experimental autoimmune neuritis.
Experimental autoimmune neuritis (EAN) is a T cell-mediated autoimmune disease of the peripheral nervous system that duplicates the clinical, pathological, and electrophysiological features of Guillain-Barré syndrome in humans. However, the molecular pathogenesis of EAN remains controversial. Therefore, for this study, we induced EAN with P0 protein peptide 180-199 in CD4(-/-), CD8(-/-), CD4(-)8(-), and B cell knockout (microMT) mice to further investigate the roles of these cells in EAN. Our results showed that the severity of clinical signs and histopathological manifestations of EAN and the T cell response to P0 peptide 180-199 in CD4(-/-) mice were significantly lower than those in their wild-type counterparts. CD8(-/-) mice also had a milder clinical course, less histopathological change, and a diminished T cell response to P0 peptide 180-199. However, more severe clinical and histopathological manifestations, a stronger T cell response to P0 peptide 180-199, and enhanced IFN-gamma production in the spleen were observed in the EAN of CD4(-)8(-) and microMT mice, but these were not obviously different from those of wild-type mice. Levels of IgG production were similar in sera from CD4(-/-), CD8(-/-), and CD4(-)8(-), and wild-type mice. These findings suggest that the induction and control of murine EAN are dependent on both CD4(+) and CD8(+) T cells and that B cells apparently do not perpetuate the related inflammatory demyelination.
Animals↗
Flash photolytic generation and study of 5-methoxy-o-quinone alpha-phenylethidet in aqueous solution: comparison of cis and trans isomer reactivity.
Cis and trans isomeric 5-methoxy-o-quinone alpha-phenylethides were generated by flash photolysis of o-hydroxybenzyl alcohol and o-hydroxystyrene precursors and their rates of decay were measured in aqueous solutions of perchloric acid, sodium hydroxide, and biphosphate (dihydrogen phosphate) ion and carbonate ion buffers. The data so obtained gave two parallel rate profiles displaced from one another by about an order of magnitude, the faster of which could be assigned to the cis isomer and the slower to the trans isomer. Both rate profiles showed acid catalyzed, uncatalyzed, and hydroxide ion catalyzed portions, with acid catalysis becoming saturated at the high acidity end of the range investigated. This saturation implies a pre-equilibrium mechanism involving quinone ethide protonation on carbonyl oxygen for the acid catalyzed process, and analysis of the data shows the trans isomer to be a slightly stronger base than the cis isomer. The fact that two separate rate profiles are observed implies that the cationic intermediates formed by substrate protonation in these acid catalyzed processes do not interconvert on the time scale of the quinone ethide decay reactions, and that in turn indicates that the former ethide bonds of the cationic intermediates have substantial double-bond character; a lower limit of 10 kcal mol(-1) may be estimated for the barrier to rotation about this bond.
Journal Article↗
Non-convulsive status epilepticus induced by tiagabine in a patient with pseudoseizure.
Tiagabine, a novel GABA reuptake inhibitor, has been reported to induce non-convulsive status epilepticus (NCSE) in patients with epilepsy. We report a 27 year old female with history of pseudoseizure documented by video-EEG monitoring who presented confusion while on 56 mg per day of tiagabine. Electroencephalography showed generalized sharp and slow wave discharges, consistent with NCSE. The NCSE was terminated by lorazepam and did not recur after tiagabine was discontinued. This case report suggests that tiagabine may induce NCSE in patients without epilepsy.
Adult↗
[Study on expression of norepinephrine and dopamine placental tissues of normal pregnancy and pregnancy induced hypertension syndrome].
OBJECTIVE: To study the distribution and levels of norepinephrine (NE) and dopamine (DA) in placenta tissues of normal pregnancy and pregnancy induced hypertension syndrome (PIH) and discuss the relationship of NE and DA with PIH. METHOD: Control group was consisted of thirty-one normal pregnancies divided into three stages (early, middle and late). Study group was consisted of thirty-eight women with PIH in mild, moderate and severe degrees. The distribution and levels of NE and DA in the placental tissues were detected by immunohistochemistry (SP) and computer image analysis. RESULTS: (1) In the control group, the levels of NE and DA located in the cell membrane and cytoplasm of cytotrophoblast were higher in early pregnancy than that located in the cell membrane and cytoplasm of syncytiotrophoblast and endothelium of capillary vessel in middle and late stages. The results in PIH were same as late stage in control group. (2) The expression of NE (1.595 +/- 0.018) and DA (1.552 +/- 0.067) were decreased gradually in early pregnancy than that of NE (1.488 +/- 0.019, 1.419 +/- 0.014, P < 0.01) and DA (1.305 +/- 0.023, 1.237 +/- 0.024, P < 0.01) in middle and late stages in control group; the expression of DA following with the PIH degrees were decreased (1.378 +/- 0.029 vs 1.305 +/- 0.023 vs 1.237 +/- 0.024, P < 0.01); the expression of NE following the PIH degrees were increased (1.494 +/- 0.018 vs 1.624 +/- 0.014 vs 1.917 +/- 0.044, P < 0.01). CONCLUSION: These findings suggested that NE and DA located in placental cytotrophoblast in early pregnancy and syncytiotrophoblast in middle and late stages and continuously distributed properly with the gestation. The level of NE increased with degrees PIH.
Adult↗
[Deeply carry out studies on diagnosis and treatment of traumatic optic neuropathy].
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Eye Injuries↗
[Analysis of 7-aminonitrazepam in urine by trimethylsilyl derivatization-gas chromatography/mass spectrometry].
A highly sensitive method has been developed for the analysis of 7-aminonitrazepam (7-ANIZ), the major metabolite of nitrazepam, in urine by trimethylsilyl derivatization-gas chromatography/mass spectrometry. Urine samples were extracted with ethyl ether-ethyl acetate (99:1, volume ratio). The extracts were derivatized with N,O-bis (trimethylsilyl) trifluoroacetamide, and the total ion current chromatograms of derivatives were acquired. 7-ANIZ was identified by the relative abundance of major characteristic ions in the mass spectrum of its derivative and the retention time of the mass chromatogram peaks of these characteristic ions. Based on the mass chromatogram of the base peak ion, quantification was performed using 7-aminoclonazepam (7-ACLZ) as the internal standard. The extraction efficiency of 7-ANIZ was 82.8%. The linear range was 10 microg/L - 500 microg/L. The limit of detection was 1.2 microg/L and the limit of quantification was 3.5 microg/L. The recoveries were 94.7% - 103.5%, and the RSDs were 3.9% - 5.4%. 7-ANIZ in the urine sample excreted by the subject over 96 h period after oral administration of 10 mg nitrazepam was measured. It is demonstrated that the method can be applied to the forensic identification.
Anti-Anxiety Agents↗