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Biomedical subjects

G Zhu

Publications and source records attributed to G Zhu.

At least 37 records · Page 2Linked to original sources
PubMed2001

[Relationship between serum 1,25-dihydroxyvitamin D and bone loss in postmenopausal women].

OBJECTIVE: To study the correlations between loss of activity and/or amont of serum 1,25-dihydroxyvitamin D(1,25(OH)2D) and 25-dihydroxyvitamin D(1,25(OH)2D) and bone loss in postmenopausal women, in order to reveal the possible pathophysiology of postmenopausal osteoporosis. METHODS: The serum levels of 1,25 (OH)2D, 25 (OH) D, PTH, and E2 in 57 postmenopausal women with osteoporosis and 37 postmenopausal women without osteoporosis were measured by radioimmunology. Their Dpd/Cr in urine was measured by ELISA. The bone mineral density (BMD) at lumbar spine (L2-4) was measured in each subject by DEXA. RESULTS: The serum 1,25(OH)2D in postmenopausal oeteoporotic women and non-osteoporotic women were 18 pg/ml +/- 6 pg/ml and 31 pg/ml +/- 14 pg/ml respectively (P < 0.01) The serum 25 (OH)2D in postmenopausal oeteoporotic women and non-osteoporotic women were 32 ng/ml +/- 9 ng/ml and 46 ng/ml +/- 17 ng/ml respectively (P < 0.01). Postmenopausal osteoporotic women had a lower estrogen concentration (P < 0.01), higher serum parathyroid hormone (PTH) (P < 0.01) and higher urinary Dpd/Cr level (P < 0.01). The level of serum 1,25(OH)2D was highly correlated with BMD in L2-4 for postmenopausal women (r = 0.693, P < 0.001). There was a close relationship between the serum level of 1,25(OH)2D and serum level of 25(OH)2D, suggesting an association between the two factors. CONCLUSION: The lower bone mass density was associated with lower level of serum 1,25-dihydroxyvitamin D, accompanied by reduced serum estrogen and elevated serum PTH in postmenopausal women. Those may be among the important pathphysiological changes of postmenopausal osteoporosis.

Aged↗
PubMed2001

The dynamics of bone marrow stromal cells in the proliferation of multipotent hematopoietic progenitors by substance P: an understanding of the effects of a neurotransmitter on the differentiating hematopoietic stem cell.

Communication within the hematopoietic-neuroendocrine-immune axis is partly mediated by neurotransmitters (e.g. substance P, SP) and cytokines. SP mediates neuromodulation partly through the stimulation of bone marrow (BM) progenitors. This study shows that SP, through the neurokinin-1 receptor, stimulates the proliferation of primitive hematopoietic progenitors: cobblestone-forming cells (CAFC, CD34+). This effect is optimal when macrophage is included within the fibroblast support. Indirect induction of IL-1 could be important in the proliferation of CAFC colonies by SP. Phenotypic and functional studies suggest that SP might directly interact with the CD34+/CD45(dim) population. These studies indicate that SP can initiate a cascade of biological responses in the BM stroma and stem cells to stimulate hematopoiesis.

Cell Differentiation↗
PubMed2001

A simulation study on the topotactic transformations from aluminophosphate AlPO(4)-21 to AlPO(4)-25.

Aluminophosphate AlPO(4)-21 (AWO), formulated /(CH(3))(2)NH(2)/[Al(3)P(3)O(12)(OH)], has been synthesized solvothermally by using dimethylamine as the template. Single-crystal X-ray diffraction analysis shows that AlPO(4)-21 crystallizes in the monoclinic space group P2(1)/n with a = 8.687(2) A, b = 17.428(5) A, c = 9.159(2) A, beta = 109.60(2) degrees, V = 1306.3(5) A(3), and Z = 4. XRD analysis shows that AlPO(4)-21 transforms to AlPO(4)-25 (ATV) upon calcination at 500 degrees C. The molecular dynamics simulation approach was used to investigate the topotactic transformations from AlPO(4)-21. The simulation study suggests that AlPO(4)-21 is energetically favored to transform to AlPO(4)-25, as well as other hypothetical forms, by the changing of the UUDD chains to the UDUD chains.

Journal Article↗
PubMed2001

Progressive depletion of peripheral B lymphocytes in 4-1BB (CD137) ligand/I-Ealpha)-transgenic mice.

Interaction of 4-1BB (CD137) and its ligand (4-1BBL) is thought to positively regulate cell-mediated and humoral immune responses. We have prepared transgenic mouse strains that express 4-1BBL cDNA under the control of MHC class II I-Ealpha promoter. The 4-1BBL-transgenic mice show progressive splenomegaly and selective depletion of B220(+) B cells accompanied with low levels of circulating IgG and defective humoral responses to Ag challenge. In addition, splenocytes from the transgenic mice fail to provide stimulation for allogeneic T cells in both lymphoproliferative and CTL responses in vitro, whereas their T cells remain functionally normal. Our results reveal unexpected functions of 4-1BBL in the regulation of humoral immune responses and Ag presentation.

4-1BB Ligand↗
PubMed2001

Protein kinase C epsilon suppresses Abeta production and promotes activation of alpha-secretase.

Deposition of plaques containing Abeta is considered important in the pathogenesis of Alzheimer's disease. Phorbol esters that activate protein kinase C (PKC) promote alpha-secretase-mediated processing of the beta amyloid precursor protein (APP), which generally reduces formation of Abeta. To determine which PKC isozymes mediate this process, we studied CHO cells that express human APP751. Phorbol 12-myristate, 13-acetate (PMA)-stimulated APP secretion, which was reduced by a general PKC inhibitor bisindoylmaleimide I, but not by Gö 6976, which inhibits PKCalpha, beta, gamma, and mu. Since PKCdelta and epsilon were the only other PMA-sensitive isozymes present, we studied cells that express selective peptide inhibitors of these isozymes. Expression of the PKCepsilon inhibitor inhibited PMA-induced APPs secretion and suppression of Abeta production. In contrast, the PKCdelta inhibitor had no effect. These results provide evidence that PKCepsilon decreases Abeta production by promoting alpha-secretase mediated cleavage of APP.

Alzheimer Disease↗
PubMed2001

Crystal structure of alpha-momorcharin in 80% acetonitrile--water mixture.

Crystals of alpha-momorcharin (MMC) were cross-linked and soaked in an 80% acetonitrile--water mixture and X-ray data were collected to 2.2 A resolution. MMC is a ribosome-inactivating protein with a sugar chain on Asn-227. In previous studies, the whole conformation of the sugar chain could not be obtained in the aqueous system. Here the structure of MMC in a low water system is shown to be similar to the native one, but the sugar chain on Asn-227 is defined by the electron density map. Several oxygen atoms of the oligosaccharide formed intramolecular hydrogen bonds to the protein moiety. The conformation of the residues in the active center is similar to that in the aqueous system. Our results show conformational alteration of the tetrasaccharide of MMC in organic media. They indicate that the oligosaccharides are more rigid in organic solvents. X-ray determination in organic media may be used to solve some structures of oligosaccharides linked to glycoproteins.

Acetonitriles↗
PubMed2001

Molecular cloning, phylogenetic analysis and three-dimensional modeling of Cu,Zn superoxide dismutase (CnSOD1) from three varieties of Cryptococcus neoformans.

Cryptococcus neoformans (Cn), causal agent of fungal meningoencephalitis, has three varieties with variable host predilection. To explore mechanisms for these pathogenic differences, we have characterized Cu,Zn SOD gene (CnSOD1). A Saccharomyces cerevisiae sod1Delta mutant was complemented with Cn var. grubii yeast expression library. The complementing clone had an ORF of 462 bp and the deduced 154 aa sequence showed 61% identity with S. cerevisiae SOD1 and 53-65% with other eukaryotic SOD1s. Cn var. grubii CnSOD1 cDNA was used to clone corresponding cDNAs from var. neoformans and var. gattii. ORFs from three varieties revealed 20-29% differences in deduced aa (s) with a significant 6% non-synonymous aa substitution between Cn var. grubii and Cn var. gattii. Cosmid library screening and PCR cloning were used to obtain genomic SOD1, which was split by five introns with identical placements and a typical 5' splice junction sequence, GTNNGY. These introns also showed a large nt variation among the three Cn varieties. Phylogenetic analyses revealed CnSOD1 to be in a group distinct from other eukaryotic SOD1s and with a significant divergence of the var. grubii from var. gattii. The CnSOD1 -deduced protein was modeled based on the crystal structure of S. cerevisiae SOD1, which showed an excellent fit. Most of the non-synonymous aa substitutions occurred on the outside of the molecule and these may contribute to differences in antigenicity among the three varieties. Notably, Cn var. neoformans and var. gattii Cu,Zn SOD had three substitutions of glycine (Gly26, Gly92 and Gly123 for Asn26, Ser92 and Ser123) that may contribute to the observed lower thermostability of this enzyme vis-a-vis Cn var. grubii. This is the first nucleotide and structural comparison of a protein-encoding gene from the three Cn varieties, which may provide a framework for future studies on the role of Cu,Zn SOD in Cn pathogenesis.

Amino Acid Sequence↗
PubMed2001

RELT, a new member of the tumor necrosis factor receptor superfamily, is selectively expressed in hematopoietic tissues and activates transcription factor NF-kappaB.

The members of tumor necrosis factor receptor (TNFR) superfamily have been designated as the "guardians of the immune system" due to their roles in immune cell proliferation, differentiation, activation, and death (apoptosis). This study reports the cloning of a new member of the TNFR superfamily, RELT (Receptor Expressed in Lymphoid Tissues). RELT is a type I transmembrane glycoprotein with a cysteine-rich extracellular domain, possessing significant homology to other members of the TNFR superfamily, especially TNFRSF19, DR3, OX40, and LTbeta receptor. The messenger RNA of RELT is especially abundant in hematologic tissues such as spleen, lymph node, and peripheral blood leukocytes as well as in leukemias and lymphomas. RELT is able to activate the NF-kappaB pathway and selectively binds tumor necrosis factor receptor-associated factor 1. Although the soluble form of RELT fusion protein does not inhibit the one-way mixed lymphocyte reaction, immobilized RELT is capable of costimulating T-cell proliferation in the presence of CD3 signaling. These results define a new member of the TNFR superfamily that may be a potential regulator of immune responses.

Amino Acid Sequence↗
PubMed2001

Characterization of a heavy metal ATPase from the apicomplexan Cryptosporidium parvum.

P1-ATPases are transporters which pump heavy metals across membranes, either to provide enzymes with essential cofactors or to remove excess, toxic metal cations from the cytosol. The first protist P1-ATPase (CpATPase2) has been isolated from the apicomplexan Cryptosporidium parvum, an opportunistic pathogen of AIDS patients. This single copy gene encodes 1260 amino acids (aa), predicting a protein of 144.7 kDa. Reverse transcription-polymerase chain reaction (RT-PCR) and western blot analysis confirmed CpATPase2 expression. Immunofluorescence microscopy of C. parvum sporozoites using rabbit antiserum raised against a glutathione-S-transferase (GST) fusion protein suggests that CpATPase2 is associated with the plasma- and cytoplasmic membranes. The protein shares greatest overall sequence similarity to previously characterized copper P1-ATPases. Expression and subsequent biochemical analyses of the N-terminal heavy metal binding domain (HMBD, GMxCxxC) of CpATPase2 as a maltose-binding protein (MBP) in Escherichia coli reveals that the protein specifically binds reduced copper, Cu(I), in vitro and in vivo, and that the cysteine residues of HMBD are responsible for heavy metal coordination. Overall, these data show that the apicomplexan C. parvum possesses a heavy metal P-ATPase transporter with a specificity for reduced copper. Since this discovery represents the first time a heavy metal P-ATPase has been identified and characterized from a protist, further molecular and biochemical studies are needed to understand the roles heavy metal P-ATPases play in heavy metal metabolism and potential virulence for this and other apicomplexa.

Adenosine Triphosphatases↗
PubMed2001

B7-H1 costimulation preferentially enhances CD28-independent T-helper cell function.

B7-H1 is a recently described B7-like molecule that costimulates T-cell growth and cytokine secretion without binding to CD28, cytotoxic T-lymphocyte antigen-4 (CTLA-4), and inducible costimulator (ICOS). In this report, a mouse homologue of human B7-H1 is identified, and its immunologic functions are studied in vitro and in vivo. Mouse B7-H1 shares 69% amino acid homology to the human counterpart. Similar to human B7-H1, mouse B7-H1 can be induced to express on macrophages, T cells, and B cells and to enhance T-cell proliferation and secretion of interleukin-10 (IL-10), interferon-gamma, and granulocyte-macrophage colony-stimulating factor but not IL-2 and IL-4. Furthermore, B7-H1 preferentially costimulates CD4+ T cells independently of CD28 and enhances mixed lymphocyte responses to allogeneic antigens. In contrast to B7-1, expression of B7-H1 on murine P815 tumor cells by transfection fails to increase allogeneic and syngeneic cytolytic T-cell responses in vitro and in vivo. Administration of B7-H1Ig fusion protein, however, enhances keyhole limpet hemocyanin- specific T-cell proliferation and 2,4,6-trinitrophenyl-specific immunoglobulin G2a antibody production. The study thus identifies a unique costimulatory pathway that preferentially affects T-helper cell functions.

Amino Acid Sequence↗
PubMed2001

Fudenine, a C-terminal truncated rat homologue of mouse prominin, is blood glucose-regulated and can up-regulate the expression of GAPDH.

Messenger RNA differential display was applied to screen for the blood glucose-regulated genes in SD rat skeletal muscle. The rat homologue of the mouse prominin was thus identified. Comparing to its mouse and human homologues, fudenine was C-terminal truncated due to a single nucleotide deletion. However, its mitochondrial energy transfer signature peptide PQDLVKKLI remained intact. Fudenine, an 592-amino acid containing, 66-kDa glycoprotein, is a novel plasma membrane protein with four transmembrane segments flanking by two large glycosylated extracellular domains. Although it is devoid of the last transmembrane domain comparing to its homologues, fudenine also locates in cell membrane by transfection of fusion plasmid pFudenine-EGFP into CBRH7919 cell and L-6TG cell. Overexpression of fudenine in CBRH7919 cell line up-regulated the mRNA level of GAPDH (3-phosphate glyceraldehyde dehydrogenase), while long-term glucose exposure resulted to reduced GAPDH expression. Since high blood glucose level induced the expression of fudenine in skeletal muscle, which in turn up-regulated the expression of GAPDH, we propose that fudenine might be a candidate gene for diabetes mellitus.

AC133 Antigen↗
PubMed2001

X-Ray study on an artificial mung bean inhibitor complex with bovine beta-trypsin in neat cyclohexane.

The active trypsin inhibiting component, SPC1, was obtained during the synthesis of a 22-residue peptide with three disulfide bridges according to the mimic mung bean Bowman-Birk type inhibitor. The K(i) value of SPC1 is 1.2x10(-7) M. In order to determine the topological structure of SPC1, X-ray diffraction studies were carried out on the complex of SPC1 with bovine beta-trypsin. Only the binding loop of SPC1 resolved at 2.2 A resolution due to conformational flexibility of the other residues [1]. The amino acid sequence was re-determined and electrospray mass spectroscopy was also performed to ensure that no cleaving occurred on SPC1 and the primary sequence of SPC1 is correct. Because the protein is more rigid in nonaqueous medium as has been proved by others [2], we treated the complex of SPC1 with neat cyclohexane and then subjected it to X-ray diffraction analysis, and the result showed that all the 22 residues of SPC1 were located in the electron density map. So the topological structure of SPC1 has been determined, suggesting that crystal treatment with cyclohexane may be used as a method to determine the conformation of the disordered regions in protein crystal structures.

Amino Acid Sequence↗
PubMed2001

Girl with phenotypic abnormalities and a de novo, apparently balanced translocation 46,XX,t(5;10)(q35.2q11.2).

We describe a three-year-old girl with a triangular face, epicanthus, midfacial hypoplasia, apparently low-set ears, a small mouth with thin vermilion border, and a small chin, hypermobile joints, developmental delay with insecure gait, dystonic movement disorder, speech defect, and a history of unexplained undernutrition. She has a de novo, apparently balanced translocation t(5;10)(q35.2;q11.2). Using fluorescence in situ hybridization (FISH), we located the breakpoints in the 1.5-Mb area defined by YAC 753f5 (5q35.2) and within the approximately 2-Mb interval between 10cen and YAC 933a3 (10q11.21).

Child, Preschool↗
PubMed2001

Adenosine receptor subtypes modulate two major functional pathways for hippocampal serotonin release.

To clarify the mechanisms of interaction between adenosine A(1) receptor (A1-R) and adenosine A(2) receptor (A2-R) on neurotransmitter release, this study determined the functional interactions among adenosine receptors (AD-Rs), voltage-sensitive Ca(2+) channels (VSCCs), protein kinases (PKs), and synaptic proteins [N-ethylmaleimide-sensitive factor (NSF) attachment protein (SNAP) receptors] on hippocampal serotonin release using in vivo microdialysis in freely moving rat. Basal serotonin release was regulated by two functional complexes: N-type VSCC (N-VSCC)/calcium-phospholipid-dependent protein kinase (PKC)/syntaxin (major pathway) and P-type VSCC (P-VSCC)/cyclic AMP-dependent protein kinase (PKA)/synaptobrevin (minor pathway). However, K(+)-evoked serotonin release was regulated by N-VSCC/PKC/syntaxin (minor pathway) and P-VSCC/PKA/synaptobrevin (major pathway). A1-R antagonists increased basal serotonin release, which was reduced by inhibitors of N-VSCC, PKC, and syntaxin predominantly and by inhibitors of PKA and synaptobrevin weakly, but was not affected by P-VSCC inhibitor. In the presence of A1-R antagonist, A2-R agonists increased basal serotonin release, which was inhibited by inhibitors of P-VSCC, PKA, and synaptobrevin predominantly and reduced by inhibitors of N-VSCC, PKC, and syntaxin weakly. Under the condition of activation of adenylate cyclase in the absence of A1-R antagonists, A2-R agonists increased basal serotonin release. A1-R antagonist and A2-R agonist enhanced K(+)-evoked serotonin release, which was inhibited by inhibitors of P-VSCC, PKA, and synaptobrevin predominantly. These results suggest that an activation of A1-R suppresses serotonin release via inhibition of both N-VSCC/PKC/syntaxin and P-VSCC/PKA/synaptobrevin pathways, and an activation of A2-R stimulates serotonin release via enhancement of the P-VSCC/PKA/synaptobrevin pathway. Therefore, PKA activity plays an important role in the interaction between A1-R and A2-R on hippocampal serotonin release.

Adenylyl Cyclases↗
PubMed2001

Surface-renewable cobalt(II) hexacyanoferrate-modified graphite organosilicate electrode and its electrocatalytic oxidation of thiosulfate.

Cobalt(II) hexacyanoferrate (CoHCF) was deposited on graphite powder by an in situ chemical deposition procedure and then dispersed into methyltrimethoxysilane-derived gels to prepare a surface-renewable CoHCF-modified electrode. The electrochemical behavior of the modified electrode in different supporting electrolyte solutions was characterized by cyclic voltammetry. In addition, square-wave voltammetry was employed to investigate the pNa-dependent electrochemical behavior of the electrode. The CoHCF-modified electrode showed a high electrocatalytic activity toward thiosulfate oxidation and could thus be used as an amperometric thiosulfate sensor.

Journal Article↗
PubMed2001

Sol-gel-derived carbon ceramic electrode containing 9,10-phenanthrenequinone, and its electrocatalytic activity toward iodate.

9,10-Phenanthrenequinone (PQ) supported on graphite powder by adsorption was dispersed in propyltrimethoxysilane-derived gels to yield a conductive composite which was used as electrode material to fabricate a PQ-modified carbon ceramic electrode. In this configuration, PQ acts as a catalyst, graphite powder guarantees conductivity by percolation, the silicate provides a rigid porous backbone, and the propyl groups endow hydrophobicity and thus limit the wetting region of the modified electrode. Square-wave voltammetry was exploited to investigate the pH-dependent electrochemical behavior of the composite electrode and an almost Nernstian response was obtained from pH 0.42 to 6.84. Because the chemically modified electrode can electrocatalyze the reduction of iodate in acidic aqueous solution (pH 2.45), it was used as an amperometric sensor for the determination of iodate in table salt. The advantages of the electrode are that it can be polished in the event of surface fouling, it is simple to prepare, has excellent chemical and mechanical stability, and the reproducibility of surface-renewal is good.

Journal Article↗
PubMed2001

Heterologous expression of the single-mutation glucose isomerase (GIG138P) gene in Streptomyces lividans and its genetic instability.

A 1.3-kb PstI-BamHI fragment containing the single-mutation glucose isomerase (GIG138P, GI1) gene and its natural promoter was inserted into PstI-BglII linearized Streptomyces vector pIJ702. The ligation mixture was then introduced into Streptomyces lividans TK54 protoplasts; transformants were identified based on their thiostrepton resistance (ThR) and insertional inactivation of the melanin phenotype; and three white colonies, XY-2, 6, and 9, harboring recombinant expression plasmid pYH703, were obtained. Enzyme assay and SDS-PAGE analysis indicated that the GI1 gene was expressed, the intracellular GI1 specific activity was 6 U/mg, and GI1 accounted for 20% of the soluble proteins in S. lividans. Restriction analysis and Southern blot of pYH703 showed the existence of plasmid deletion, presumably owing to the interaction between the mel and GI1 sequences. Continuous liquid cultures of the recombinant strain demonstrated that the GI1 specific activity and GI1 expression in S. lividans decreased, and more obviously under non-selective conditions.

Aldose-Ketose Isomerases↗