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Biomedical subjects

G Zhang

Publications and source records attributed to G Zhang.

At least 73 records · Page 4Linked to original sources
PubMed2002

Heavy metals in agricultural soils of the Pearl River Delta, South China.

There is a growing public concern over the potential accumulation of heavy metals in agricultural soils in China owing to rapid urban and industrial development and increasing reliance on agrochemicals in the last several decades. Excessive accumulation of heavy metals in agricultural soils may not only result in environmental contamination, but elevated heavy metal uptake by crops may also affect food quality and safety. The present study is aimed at studying heavy metal concentrations of crop, paddy and natural soils in the Pearl River Delta, one of the most developed regions in China. In addition, some selected soil samples were analyzed for chemical partitioning of Co, Cu, Pb and Zn. The Pb isotopic composition of the extracted solutions was also determined. The analytical results indicated that the crop, paddy and natural soils in many sampling sites were enriched with Cd and Pb. Furthermore, heavy metal enrichment was most significant in the crop soils, which might be attributed to the use of agrochemicals. Flooding of the paddy soils and subsequent dissolution of Mn oxides may cause the loss of Cd and Co through leaching and percolation, resulting in low Cd and Co concentrations of the paddy soils. The chemical partitioning patterns of Pb, Zn and Cu indicated that Pb was largely associated with the Fe-Mn oxide and residual fractions, while Zn was predominantly found in the residual phase. A significant percent fraction of Cu was bound in the organic/sulphide and residual phases. Based on the 206Pb/207Pb ratios of the five fractions, it was evident that some of the soils were enriched with anthropogenic Pb, such as industrial and automobile Pb. The strong associations between anthropogenic Pb and the Fe-Mn oxide and organic/sulphide phases suggested that anthropogenic Pb was relatively stable after deposition in soils.

Agriculture↗
PubMed2002

Kindling induces the mRNA expression of methyl DNA-binding factors in the adult rat hippocampus.

We have investigated the gene expression responses of a family of methyl CpG-binding domain-containing factors (MeCP2, MBD1, MBD2, and MBD3) in the hippocampus of electrically kindled rats. Expression was examined in both amygdala- and partial perforant-pathway-kindled subjects, 24 h and 28 days following the final stimulation. In general, the responses of MBDs 2 and 3 paralleled each another, both temporally and spatially. The expression of both genes was significantly elevated in all hippocampal subfields at 24 h following either the fifth stage 5 seizure (amygdala kindling) or the 15th stimulation of the perforant pathway. This induced expression was transient, however, as the expression of both genes returned to control levels by 28 days. This pattern of response contrasted to that observed for MeCP2 and MBD1. MeCP2 displayed no change in expression either 24 h or 28 days after amygdala kindling, but did display a late-developing, significant increase in expression in the dentate gyrus at 28 days following perforant-pathway kindling. The expression of MBD1 was unchanged by partial perforant-pathway kindling, but was induced in the dentate gyrus 28 days after amygdala kindling. These results demonstrate that electrical kindling alters the hippocampal expression of methyl DNA-binding factors, but does not affect each factor equivalently. The responsive patterns observed suggest that this family of transcriptional regulators can be differentially altered in the hippocampus by seizure activity.

Amygdala↗
PubMed2002

Expression and function of A1 adenosine receptors in the rat hippocampus following transient forebrain ischemia.

We investigated how transient cerebral ischemia affects the gene expression, immunoreactive protein levels, and the function of the A1 subtype of adenosine receptor in the rat hippocampus at different times following reperfusion. A1 receptor mRNA levels were altered significantly in different hippocampal subfields as early as 6 h following insult. However, these changes in mRNA levels were not paralleled at the protein level, as western blotting with A1 receptor-specific antibodies revealed that hippocampal A1 adenosine receptor prevalence did not differ from sham control at either 6 or 24 h following insult. The lack of change in A1 receptor prevalence was consistent with functional examinations, as only marginal changes were observed in the ability of A1 receptors to attenuate excitatory post-synaptic potentials in the CA1 subfield at 24 h following reperfusion. These data illustrate that although the mRNA expression levels of the A1 adenosine receptor are altered by transient cerebral ischemia, the immunoreactive prevalence and function of this receptor are maintained in the post-ischemic hippocampus at times preceding the death of the vulnerable neurons.

Animals↗
PubMed2002

Transient forebrain ischemia alters the mRNA expression of methyl DNA-binding factors in the adult rat hippocampus.

We have examined how transient cerebral ischemia affects the mRNA expression of a family of methyl CpG-binding domain (MBD)-containing factors in the rat hippocampus. Our results show that each member of this family is affected by cerebral ischemia challenge, but with differing patterns of responsiveness. At 3, 6 and 12 h following reperfusion, MeCP2 and MBD1 expression is maintained at control levels throughout the hippocampus. At 24 h, MeCP2 and MBD1 are induced in both the CA1 and CA3 subfields. This delayed pattern of induction is in contrast to the responses of MBD2 and MBD3. Both MBD2 and MBD3 display significant changes in expression at early times following reperfusion, although their changes are opposite in direction. MBD2 expression is induced throughout the hippocampal formation at 6 h, and remains elevated at 12 and 24 h. MBD3 expression decreases as early as 3 h following insult in the CA3 and dentate gyrus, and the decreased expression remains in the vulnerable CA1 subfield at 6, 12, and 24 h. Taken together, these results are the first to illustrate that the expression of methyl DNA-binding factors are affected by challenges to the brain, and they also illustrate that each methyl DNA-binding factor responds differently to cerebral ischemic challenge. As each of these family members is associated either directly or indirectly with the inhibition of gene transcription, our results suggest that following cerebral ischemia the normal pattern of transcriptional inhibition provided by these factors may be altered in the hippocampus.

Age Factors↗
PubMed2002

Expression of the mel gene from Pseudomonas maltophilia in Bacillus thuringiensis.

AIMS: The objective of this work was to express a novel mel gene, responsible for melanin formation, in Bacillus thuringiensis. METHODS AND RESULTS: A novel mel gene from Pseudomonas maltophilia was sub-cloned into B. thuringiensis using a shuttle vector plasmid and electroporation. Results revealed that the mel gene was expressed under the control of the CryIIIA promoter in B. thuringiensis and conferred u.v. protection on the recipient strain. CONCLUSIONS: The novel mel gene from Ps. maltophilia expressed in B. thuringiensis conferred u.v. protection on the recipient strain. SIGNIFICANCE AND IMPACT OF THE STUDY: Products containing B. thuringiensis for pest control are sensitive to u.v. degradation. As melanin has the ability to act as a u.v. absorber, a recombinant B. thuringiensis strain producing melanin provides a new stability for B. thuringiensis preparations.

Bacillus thuringiensis↗
PubMed2002

Physical map of the chromosome 6q22 region containing the oculodentodigital dysplasia locus: analysis of thirteen candidate genes and identification of novel ESTs and DNA polymorphisms.

Oculodentodigital dysplasia (ODDD) is an autosomal dominant condition with congenital anomalies of the craniofacial and limb regions and neurodegeneration. Genetic anticipation for the dysmorphic and neurologic features has been inferred in a few families. Our previous linkage studies have refined the ODDD candidate region to chromosome 6q22-->q23. In an attempt to clone the ODDD gene, we created a yeast artificial chromosome contig with 31 redundant clones spanning the region and identified and ordered candidate genes and markers. Fluorescent IN SITU hybridization mapped two of these YAC clones to chromosome 6q22.2 telomeric to a known 6q21 fragile site, excluding it as a possible cause of the suggested anticipation. We performed mutation analysis on thirteen candidate genes - GRIK2, HDAC2, COL10A1, PTD013, KPNA5, PIST, ROS1, BRD7, PLN, HSF2, PKIB, FABP7, and HEY2. Although no mutations were found, we identified 44 polymorphisms, including 28 single nucleotide polymorphisms. Direct cDNA selection was performed and fifty-five clones were found to contain sequences that were not previously reported as known genes or ESTs. These clones and polymorphisms will assist in the further characterization of this region and identification of disease genes.

Abnormalities, Multiple↗
PubMed2001

Targeted PEG-based bioconjugates enhance the cellular uptake and transport of a HIV-1 TAT nonapeptide.

We previously described the enhanced cell uptake and transport of R.I-K(biotin)-Tat9, a large ( approximately 1500 Da) peptidic inhibitor of HIV-1 Tat protein, via SMVT, the intestinal biotin transporter. The aim of the present study was to investigate the feasibility of targeting biotinylated PEG-based conjugates to SMVT in order to enhance cell uptake and transport of Tat9. The 29 kDa peptide-loaded bioconjugate (PEG:(R.I-Cys-K(biotin)-Tat9)8) used in these studies contained eight copies of R.I-K(biotin)-Tat9 appended to PEG by means of a cysteine linkage. The absorptive transport of biotin-PEG-3400 (0.6-100 microM) and the bioconjugate (0.1-30 microM) was studied using Caco-2 cell monolayers. Inhibition of biotin-PEG-3400 by positive controls (biotin, biocytin, and desthiobiotin) was also determined. Uptake of these two compounds was also determined in CHO cells transfected with human SMVT (CHO/hSMVT) and control cells (CHO/pSPORT) over the concentration ranges of 0.05-12.5 microM and 0.003-30 microM, respectively. Nonbiotinylated forms of these two compounds, PEG-3350 and PEG:(R.I-Cys-K-Tat9)8, were used in the control studies. Biotin-PEG-3400 transport was found to be concentration-dependent and saturable in Caco-2 cells (K(m)=6.61 microM) and CHO/hSMVT cells (K(m)=1.26 microM). Transport/uptake was significantly inhibited by positive control substrates of SMVT. PEG:(R.I-Cys-K(biotin)Tat9)8 also showed saturable transport kinetics in Caco-2 cells (K(m)=6.13 microM) and CHO/hSMVT cells (K(m)=8.19 microM). Maximal uptake in molar equivalents of R.I-Cys-K(biotin)Tat9 was 5.7 times greater using the conjugate versus the biotinylated peptide alone. Transport of the nonbiotinylated forms was significantly lower (P<0.001) in all cases. The present results demonstrate that biotin-PEG-3400 and PEG:(R.I-Cys-K(biotin)Tat9)8 interact with human SMVT to enhance the cellular uptake and transport of these larger molecules and that targeted bioconjugates may have potential for enhancing the cellular uptake and transport of small peptide therapeutic agents.

Animals↗
PubMed2001

[Effects of hepatitis G virus coinfection on hepatic pathological changes of patients with chronic hepatitis B: a long-term comparative study].

OBJECTIVE: To observe the long-term effect of hepatitis G virus (HGV) coinfection on hepatic pathological changes of patients with chronic hepatitis B (CHB) and explore the pathogenicity of HGV. METHODS: Menghini method liver biopsy was performed on 45 patients with CHB twice with an interval of 5 years on a voluntary basis. The liver tissue of 21 cases was HGV nonstructural region 5 (HGV NS5) antigen positive by peroxidase anti-peroxidase (PAP) immunohistochemical staining assay (HGV coinfection group) in these two tests, and 24 cases were negative (HGV noncoinfection group). There was no significant difference in age, sex, course of disease, amount of serum HBV-DNA by competitive quantitative polymerase chain reaction assay and severity of hepatic pathological leisions between these two groups (P < 0.05) and they were treated with the same scheme and without sustained curative effeect. The hepatic pathological changes of the two groups after 5 years were compared and analysed retrospectively. RESULTS: There was no significant difference in basic hepatic pathological change, severity of inflammatory activity grade and fibrosis stage in these two groups. The numbers of cases of inflammatory activity grade G1, G2, G3, and G4 were 3, 7, 7, and 4 in HGV coinfection group, and 5, 8, 7, and 4 in HGV noncoinfection group in the beginning of observation; and were 3, 5, 7, and 6 in HGV coinfection group, and 4, 6, 8, and 6 in HGV noncoinfection group after 5 years. The numbers of cases in fibrosis stages S1, S2, S3, and S4 were 4, 7, 7, and 3 in HGV coinfection group, and 6, 8, 6, and 4 HGV noncoinfection group in the beginning of observation; and were 3, 6, 5, 7 in HGV coinfection group, and 4, 7, 5, and 8 in HGV noncoinfection group after 5 years (P > 0.05). CONCLUSION: HGV coinfection does not lead to the activation of hepatic pathological changes and does not speed up the progression of fibrosis in patients with CHB. HGV coinfection does not play an obvious role in long-term hepatic pathological changes of patients with CHB. HGV has at most a mild hepatic pathogenicity.

Adult↗
PubMed2001

Extracellular signal-regulated kinase and c-Jun N-terminal protein kinase in ischemic tolerance.

The alterations and involvement of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal protein kinase (JNK) activation were examined in the hippocampal CA1 region in a rat model of global brain ischemic tolerance. Western blotting study showed that ERK activation (diphosphorylation) level was decreased (3.75-, 0.56-, and 0.23-fold vs sham control) and JNK activation level was increased (3.82-, 4.63-, and 5.30-fold vs sham control) 3 days after more severe ischemic insults (6 min, 8 min, and 10 min of ischemia, respectively). These alterations were significantly prevented by pretreatment with preconditioning ischemia, which also provided neuronal protection against ischemic injury. Inhibition of ERK activation after preconditioning ischemia by PD98059, a specific ERK kinase inhibitor, significantly prevented the inhibitory effects of preconditioning ischemia on both JNK activation and ischemic injury. The results suggest that ERK activation after preconditioning ischemia may result in the prevention of JNK activation and thus be involved in the protective responses in ischemic tolerance in hippocampal CA1 region.

Animals↗
PubMed2001

Gene polymorphisms of homocysteine metabolism-related enzymes in Chinese patients with occlusive coronary artery or cerebral vascular diseases.

The mutations in homocysteine (Hcy) metabolism-related enzyme genes including methylenetetrahydrofolate reductase (MTHFR) C677T, cystathionine beta-synthase (CBS) 844ins68, and methionine synthase (MS) A2756G have been identified as genetic risk factors for thromboembolic events. It has been noticed that these gene mutations have heterogeneous distributions among different ethnic groups or geographic areas. The data on the prevalence of the gene mutations in Chinese population is not yet available. In the present study, we have investigated the frequency of the MTHFR C677T, CBS 844ins68, and MS A2756G mutations in 102 patients with ischemic stroke (IS), 73 patients with myocardial infarction (MI) and 100 healthy controls. The distributive frequencies of the gene variations are as follows: In the IS, MI and control groups, the mutant homozygote for MTHFR C677T is 15 (14.7%), 8 (11.7%) and 16 (16.0%), respectively, and the T allele frequency is 37.7%, 33.6% and 39.5%, respectively; the heterozygote for CBS 844ins68 is 1 (1.0%), 1 (1.4%) and 5 (5.0%), respectively; the heterozygote for MS A2756G is 18 (17.6%), 14 (19.2%) and 17 (17.0%), and the G allele frequency is 8.8%, 11.0% and 9.5%, respectively. The carrier of both MS A2756G and MTHFR C677T (combined mutations) is 14 (12.7%), 8(11.0%) and 12(12.0%), respectively. There is no statistically significant difference between the patient groups and the control group in the frequencies of these single mutation or combined mutations. The heterozygosity of CBS 844ins68 yields an odds ratio (OR) of 0.19 (95% confidence interval (CI) 0.02-1.43) for IS and 0.26 (95% CI 0.03-2.31) for MI. The T allele of MTHFR C677T yields an OR of 0.93 for IS (95% CI 0.62-1.39) and 0.77 for MI (95% CI 0.50-1.21). The G allele of MS A2756G yields an OR of 0.92(95% CI 0.47-1.81) for IS and 1.17 (95% CI 0.58-2.37) for MI. Our results suggest that neither single mutation nor combined mutations in MTHFR C677T, CBS 844ins68 and MS A2756G represent an independent risk factor for increasing IS and coronary artery disease risks in Chinese population. However, CBS 844ins68 may be a protective factor against vascular thromboembolic disease. The prevalence of CBS 844ins68 and MS A2756G in Chinese population is obviously lower than in Western Caucasian population.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2001

The shorter zinc finger protein ZNF230 gene message is transcribed in fertile male testes and may be related to human spermatogenesis.

The zinc finger gene family represents one of the largest in the mammalian genome, with several of these genes reported to be involved in spermatogenesis. A newly discovered gene has been identified that is expressed abundantly in the testicular tissue of fertile men as determined by mRNA differential display. The gene encodes a C(3)HC(4)-type zinc finger protein motif (ring finger motif) consistent with a role in pre-meiotic or post-meiotic sperm development. The gene was named ZNF230 and mapped to the short arm of chromosome 11 (11p15). ZNF230 has two transcripts, of 1 kb and 4.4 kb in length. The shorter 1 kb transcript was only detected in testicular tissue whereas the longer 4.4 kb transcript was not detected in testis but was found in several other tissues. The lack of detectable ZNF230 expression in azoospermic patients by reverse transcriptase-mediated PCR analysis is interpreted to mean that this gene is involved in maintaining normal human male fertility.

Amino Acid Sequence↗
PubMed2001

Enhanced auditory reversal learning by genetic activation of protein kinase C in small groups of rat hippocampal neurons.

The hippocampus has a central role in specific types of learning, but there is only limited evidence identifying the requisite molecular changes in ensembles of hippocampal neurons. To investigate the role of protein kinase C (PKC) pathways in hippocampal mediated learning, a constitutively active, catalytic domain of rat PKC betaII was delivered into hippocampal dentate granule neurons using a Herpes Simplex Virus (HSV-1) vector. This PKC causes a long-lasting, activation-dependent increase in neurotransmitter release from cultured cells. Activation of PKC pathways in a small percentage (< or =0.26%) of dentate granule neurons was sufficient to enhance rat auditory discrimination reversal learning. The affected neurons altered hippocampal physiology as revealed by elevated NMDA receptor densities in specific hippocampal areas. Thus, these results directly suggest that activation of PKC pathways in a specific hippocampal area alters rat auditory discrimination reversal learning. Because each rat may contain a unique pattern of affected neurons, there appears to be considerable flexibility and/or redundancy in the groups of neurons that can modify learning.

Animals↗
PubMed2001

Regulatory activity of distal and core RNA elements in Tombusvirus subgenomic mRNA2 transcription.

Positive-strand RNA viruses that encode multiple cistrons often mediate expression of 3'-encoded open reading frames via RNA-templated transcription of subgenomic (sg) mRNAs. Tomato bushy stunt virus (TBSV) is a positive-strand RNA virus that transcribes two such sg mRNAs during infections. We have previously identified a distal element (DE), located approximately 1100 nucleotides upstream from the initiation site of sg mRNA2 transcription, part of which must base pair with a portion of a core element (CE), located just 5' to the initiation site, for efficient transcription to occur (Zhang, G., Slowinski, V., and White, K. A. (1999) RNA 5, 550-561). Here we have analyzed further this long distance RNA-RNA interaction and have investigated the regulatory roles of other subelements within the DE and CE. Our results indicate that (i) the functional base-pairing interaction between these elements occurs in the positive strand and that the interaction likely acts to properly position other subelements, (ii) two previously undefined subelements within the DE and CE are important and essential, respectively, for efficient sg mRNA2 accumulation, and (iii) the production of (-)-strand sg mRNA2 can be uncoupled from the synthesis of its (+)-strand complement. These data provide important insight into the mechanism of sg mRNA2 transcription.

RNA, Messenger↗
PubMed2001

[Electric pulse mediated high efficient gene transfer].

OBJECTIVE: To study gene transfer mediated by electric pulse and optimize the parameters of electric pulse in vivo. METHODS: 10 micrograms plasmid pcD2/LacZ was injected into the quadriceps of 220 Kunming mice. One to two minutes after the DNA injection electric pulse with different parameters was given to the injection site. Three days after, activity of beta-galactosidase was measured, and the expression of Laz2 gene in muscle was determined by histochemical staining. RESULTS: The activity of beta-galactosidase in electric pulse group (131.6 U/mg +/- 86.6 U/mg protein) was 30 fold higher than that in direct injection group (4.9 U/mg +/- 1.0 U/mg protein) (P < 0.05). Histochemical analysis of muscles injected with a LacZ expression plasmid also showed that in vivo electric pulse increased both the number of positively stained muscle fibers and the density of staining. When the electric pulse was with the parameters of 200 V/cm, 40 ms, 6 pulses and 1HZ, maximal gene expression was achieved. CONCLUSION: Electric pulse, with optimal parameters, increases gene expression. Electric pulse makes much more gene expression than mere intramuscular DNA injection.

Animals↗
PubMed2001

Nuclear translocation of extracellular signal-regulated kinases in neuronal excitotoxicity.

Subcellular distributions of extracellular signal-kinases (ERK1/2), including their activated form (p-ERK1/2), were investigated in glutamate-induced apoptotic-like death in cultured rat cortical neurons by Western immunoblot and immunocytochemistry. During 15 min glutamate exposure, p-ERK1/2 was increased in both cytosol and nuclear extracts, but prominently so in nuclear extracts. Simultaneously, ERK1/2 were mildly decreased in cytosol (to 0.7-fold vs sham control), largely increased in nuclear extracts (to 6.2-fold vs sham control), but not changed in total cell extracts. Immunocytochemistry studies also showed a large increase in nuclear and a mild decrease in cytosol extracts of ERK1/2 at 15 min of exposure. After glutamate exposure, all the above changes reverted simultaneously. The nuclear increase of ERK1/2 was largely prevented by inhibition of ERK1/2 activation, but prolonged by elongation of ERK1/2 activation. These observations suggest that stimulation of glutamate receptors in cortical neurons may incur an activation-dependent transient nuclear translocation of ERK1/2, which might be involved in excitotoxicity through a simultaneous strong elevation of p-ERK1/2 in nucleus.

Active Transport, Cell Nucleus↗
PubMed2001

NMDA receptor activation results in tyrosine phosphorylation of NMDA receptor subunit 2A(NR2A) and interaction of Pyk2 and Src with NR2A after transient cerebral ischemia and reperfusion.

Transient ischemia increases tyrosine phosphorylation of N-methyl-D-aspartate (NMDA) receptor. Several tyrosine kinases are involved in this process. In this study, effect of ischemia and reperfusion (I/R) on tyrosine phosphorylation of NMDA receptor subunit 2A (NR2A) and the interaction of two tyrosine kinases, Src and Pyk2, with NR2A was investigated. Four-vessel occlusion was used to produce transient (15 min) cerebral ischemia in SD rats. Tyrosine phosphorylation of NR2A in hippocampus was enhanced after 15 min of reperfusion and reached its peak level at 6 h of reperfusion. The increase sustained for at least 24 h. Src and Pyk2 co-immunoprecipitated with NR2A and the binding increased after I/R, which also reached a peak at 6 h of reperfusion. Besides, Src and Pyk2 were activated after I/R. These increases were prevented by ketamine, a selective NMDA receptor antagonist, which was administered to the SD rats 20 min before ischemia. Moreover, Src and Pyk2 coprecipitated with each other. These data show that NR2A, Src and Pyk2 might form a protein complex in vivo and the interaction suggests a possible mechanism of signal transduction in the postischemic hippocampus.

Animals↗
PubMed2001

A novel deletion mutation of the EXT2 gene in a large Chinese pedigree with hereditary multiple exostosis.

Hereditary multiple exostoses (EXT) is an autosomal dominant disease characterized by the formation of cartilage-capped prominences (exostoses) that develop from the juxta-epiphyseal regions of the long bones. 3 genes are known to be involved in the formation of exostoses. Among them, EXT1 and EXT2, which encode enzymes that catalyse the biosynthesis of heparan sulfate, an important component of the extracellular matrix, are responsible for over 70% of the EXT cases. A large Chinese family with hereditary multiple exostoses has been analysed and the disease-causing mutation has been found. Blood samples were obtained from 69 family members, including 23 affected individuals. The EXT phenotype was shown to be linked to the EXT2 gene by using 2-point linkage analysis. After polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP) analysis and DNA sequencing, a previously unreported deletion of a G in exon 3 of EXT2 gene was observed. This deletion co-segregated with the disease phenotype, suggesting that it is the disease-causing mutation in this family. Furthermore, in at least 4 members chondrosarcoma occurred after either an operation or injury of the exostosis and 3 of them died of the malignancy in the family. Whether the operation or injury was responsible for the malignant transformation still needs further study.

Base Sequence↗