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Biomedical subjects

S G Zhu

Publications and source records attributed to S G Zhu.

13 recordsLinked to original sources
PubMed2005

Human papillomavirus type 16 E7 peptide(38-61) linked with an immunoglobulin G fragment provides protective immunity in mice.

OBJECTIVE: To explore whether the recombinant protein (Human papillomavirus (HPV) type16 E7 peptide(38-61) linked with an immunoglobulin G fragment) will generate protective immunity in mouse model. METHODS: In our study, we combined the HPV16 E7 peptide(38-61) with a murine IgG heavy chain constant region to construct a chimeric protein compound, which was highly expressed as inclusion bodies in a bacterial expression system with Escherichia coli. The purified chimeric protein was injected into C57BL/6 mice and the efficiency of the chimeric vaccine candidate was evaluated by antibody response assay, T cell proliferation assay, CTL assay, tumor challenge assay and therapeutic experiment. RESULTS: The chimeric vaccine candidate was able to induce anti-HPV antibodies as well as to elicit HPV16 E7-specific CTLs and T cell proliferation in a pre-clinical mouse model. It was also able to effectively protect mice against the challenge of HPV16-positive tumor cells, and to eradicate HPV16-expressing tumors in mice. CONCLUSIONS: The chimeric protein vaccine can induce E7-specific immune responses and protect mice against challenge of HPV16-positive tumor, even eradicate developed tumor. The results indicated a possibility to use the chimeric protein vaccine to protect human against HPV infection.

Animals↗
PubMed2000

Interleukin-1 promotes expression and phosphorylation of neurofilament and tau proteins in vivo.

Slow-release, IL-1-impregnated pellets implanted in rat cerebral cortex to simulate chronic overexpression of IL-1 significantly increased relative tissue levels of tau mRNA and of tau immunoreactivity in neuronal cell bodies and in swollen dystrophic neurites that also overexpressed phosphorylated and nonphosphorylated neurofilament epitopes. In addition, rats with IL-1-impregnated pellets, but not control rats or those with sham pellets, showed focal immunoreactivity for hyperphosphorylated tau epitopes present in paired helical filaments. Our results are consistent with an important driving role for IL-1 in the pathogenesis of Alzheimer-type neuronal and neuritic changes.

Animals↗
PubMed1999

Increased interleukin-1beta converting enzyme expression and activity in Alzheimer disease.

Increased expression of interleukin-1 in Alzheimer disease (AD) has been implicated as a driving force in neurodegenerative cascades that underlie the formation of neuritic plaques and neurofibrillary tangles, the spread of these neuropathological lesions across cerebral cortical regions, and the accompanying neuronal cell injury and loss. The beta isoform of interleukin-1 is generated from an inactive, 33-kDa precursor through the action of a specific interleukin-1beta converting enzyme (ICE), also known as caspase-1. We used mesial temporal tissue (hippocampus and parahippocampal cortex) obtained postmortem from Alzheimer and control patients for determinations of endogenous tissue ICE activity and for Western immunoblot analysis of tissue ICE concentrations. ICE activity in Alzheimer tissue was elevated 50-100% (p < 0.002, or better, at incubation times of 30 min to 10 h), and ICE protein level was elevated 180% (p = 0.01). Parahippocampal cortex of Alzheimer patients showed increased numbers of neurons with in situ evidence of DNA damage. Increased DNA degradation was also evident upon electrophoresis of isolated DNA. Overexpression and increased activity of ICE may contribute to neurodegeneration in AD through generation of biologically active interleukin-1, with consequent activation of interleukin-1-driven neurodegenerative cascades.

Alzheimer Disease↗
PubMed1991

[Porencephaly. A report of 45 cases].

In 45 cases of porencephaly 35 were male and 10 female. Their age ranged from 80 days to 58 years (mean 14 years). In this series, symptoms were observed 80 days to 22 years before diagnosis. twenty-four cases were premature delivery, difficult labour or birth trauma. 14 cases had a history of head injury. 36 cases had congenital porencephalic cyst and 9 had post-traumatic porencephaly. The main symptoms and signs of porencephaly were dementia, speech defect, intracranial hypertension, hydrocephalus, epilepsy, ataxia or paralysis. etc. It is suggested that CT scan is very useful in the diagnosis of porencephaly, and section of cerebral cortex, opening of cyst, continuous drainage or shunting operation should be done as soon as the diagnosis was made.

Adolescent↗
PubMed1990

Lamotrigine protects against kainate but not ibotenate lesions in rat striatum.

Pretreatment of rats with 8-16 mg/kg of lamotrigine 1 h before intrastriatal injections of 2 nm of kainic acid significantly attenuated the neurotoxicity as evidenced by measurements of striatal choline acetyltransferase and glutamate decarboxylase activities. No significant effect was seen on the toxicity of intrastriatal injections of quinolinic acid or ibotenic acid. These differential effects are further evidence that these neurotoxins act at different excitatory amino acid receptors and that the neurotoxicity of kainate is uniquely dependent on neuronally released glutamate.

Animals↗
PubMed1990

gamma-Glutamyltransferase activity is unchanged in acutely quinolinate-lesioned rat neostriatum but is elevated in Huntington's disease caudate.

gamma-Glutamyltransferase (GGT; gamma-glutamyl transpeptidase) was measured in the neostriata of rats 5-7 days after local injections of 0-150 nmol of quinolinic acid. In contrast to the high levels seen in studies on the caudate in a few Huntington's disease cases, GGT activity showed no significant relation to the amount of quinolinic acid injected or to the extent of neuronal loss, as indicated by assays of choline acetyltransferase and glutamate decarboxylase on the same striatal homogenates. The chronicity of the degenerative disease, contrasted with the acuteness of the lesion, may explain the difference.

Animals↗
PubMed1990

Immunostaining of human brain capillaries by antibodies to very late antigens.

Normal and neurologically diseased brain tissue was stained with antibodies directed against very late antigens (VLAs) 1, 2, 3, 5, 6, their common beta 1-subunit, and three extracellular proteins: collagen type IV, laminin and fibronectin. Strong staining of capillaries was obtained in both normal and pathological tissue with antibodies to collagen type IV and its putative receptor VLA-1; laminin and its putative receptor VLA-6; and the common VLA beta 1-subunit. Only residual plasma in vessels was stained with the antibody to fibronectin. Negative staining was obtained with antibodies to the fibronectin receptor VLA-5 and VLA-3. Trace staining was obtained with the antibody to VLA-2.

Alzheimer Disease↗
PubMed1990

Preliminary crystallographic analysis of deshexapeptide (B25-B30) insulin.

Satisfactory single crystals of deshexapeptide (B25-B30) insulin for X-ray crystal structure analysis have been grown in citrate buffer by the method of hanging-drop gas phase diffusion. The crystal belongs to the monoclinic system with space group C2. The unit cell constants are a = 42.6 A, b = 37.9 A, c = 27.2 A, beta = 125.4 degrees and there is only one molecule of deshexapeptide insulin in an asymmetric unit.

Crystallography↗
PubMed1989

Effect of MK-801, kynurenate, glycine, dextrorphan and 4-acetylpyridine on striatal toxicity of quinolinate.

Measurements of striatal choline acetyltransferase (ChAT) and glutamic acid decarboxylase (GAD) activities indicated that systemic administration of 4-8 mg/kg of MK-801 to rats completely blocked neuronal damage due to intrastriatal injections of 75-150 nmol of quinolinic acid. Similar experiments with 0-2 mg/kg MK-801 suggested the ED50 might be between 1 and 1.5 mg/kg for protection against 50 nmol of intrastriatal quinolinic acid, and between 2 and 3 mg/kg for 75 nmol. Repeated pretreatment with kynurenate (3 x 300 mg/kg) gave significant but not complete protection against similar doses of quinolinic acid, with the protective effect being greater for GAD than for ChAT. Glycine appeared to potentiate the effect of high doses of quinolinic acid on ChAT and the other pretreatments tested (dextrorphan, dextromethorphan, 4-acetylpyridine) had no significant effect.

Animals↗
PubMed1988

Tetrahydroaminoacridine potentiates neurotoxicity of quinolinic acid in rat striatum.

Intraperitoneal injection of 5 mg/kg of tetrahydro-9-amino-acridine (THA) in rats 1 h before intrastriatal injection of 50-150 nmol of quinolinic acid potentiated the local neurotoxicity as indicated by measurements of striatal levels of glutamate decarboxylase and choline acetyltransferase. A larger dose (10 mg/kg) THA had no significant effect. The results are discussed in terms of THA's binding to various elements of the NMDA/sigma receptor complex and reported data on such binding are confirmed.

Aminoacridines↗
PubMed1985

Gene amplification in Tetrahymena thermophila: formation of extrachromosomal palindromic genes coding for rRNA.

Tetrahymena thermophila contains in the macronucleus multiple copies of extrachromosomal palindromic genes coding for rRNA (rDNA) which are generated from a single chromosomal copy during development. In this study we isolated the chromosomal copy of rDNA and determined the structure and developmental fate of the sequence surrounding its 5' junction. The result indicates that specific chromosomal breakage occurs at or near the 5' junction of rDNA during development. The breakage event is associated with DNA elimination and telomeric sequence addition. Similar results were also found previously for the 3' junction of this gene. These results could explain how the extrachromosomal rDNA is first generated. Near both junctions of the chromosomal rDNA, a pair of 20-nucleotide repeats was found. These sequences might serve as signals for site-specific breakage. In addition, we found a pair of perfect inverted repeats at the 5' junction of this gene. The repeats are 42 nucleotides long and are separated by 28 nucleotides. The existence of this structure provides a simple explanation for the formation of the palindromic rDNA.

Base Sequence↗