Search PubMed⌕ Search

Biomedical subjects

G Xiao

Publications and source records attributed to G Xiao.

At least 55 records · Page 3Linked to original sources
PubMed2000

[Application of bio-electrical impedance analysis in the compensation period of intracranial pressure increasing].

In the compensation period of intracranial pressure increasing, brain impedance rises continuously while cerebrospinal fluid volume changes. Along with the illness progressing, intracranial pressure would rise obviously, but the intracranial component relative volume would go near to constant; at the same time, brain impedance fluctuates around a baseline and there appears an inflection point on the impedance track record curve after the compensation period.

Electric Impedance↗
PubMed2000

[The change of intestinal microcirculation blood flow and its relationship with bacterial translocation in burned rats receiving delayed fluid resuscitation].

OBJECTIVE: To investigate the change of intestinal microcirculation blood flow and its relationship with bacterial translocation in burned rats receiving delayed fluid resuscitation. METHODS: Twenty-four Wistar rats inflicted by 30% TBSA III degree followed by delayed fluid resuscitation were taken as the model. The rats were randomly divided into four groups, i.e. burn shock without resuscitation (BSNR), delayed resuscitation (fluid given from 8 hours postburn, DR), immediate resuscitation (IR), and sham operation (SO). The incidence of bacterial translocation, intestinal microcirculation blood flow volume of intestinal wall at terminal ileum as well as the change of systemic mean arterial pressure were monitored. RESULTS: The incidence of bacterial translocation in DR group (54.2%) was significantly higher than that in IR group (P < 0.01), but no remarkable difference with that in BS group (P < 0.05). In addition, microcirculation blood flow of intestinal wall recovered to some degree at 4 hours after delayed fluid resuscitation but far below that in IR group at the same time point. Nevertheless, the systemic mean arterial blood pressure had restored to the normal range at that time. CONCLUSION: The incidence of intestinal bacterial translocation sustained at high level after burn shock with delayed fluid resuscitation, which might be the result of delayed improvement of microcirculation blood flow of the intestinal wall.

Animals↗
PubMed2000

[The relationship between postburn gene expression of modulators in gut associated lymph tissue and the change in IgA plasma cells].

OBJECTIVE: To investigate the relationship between the postburn change in IgA plasma cells and those of IL- 4 and IL-6 in gut associated lymph tissue (GALT). METHODS: One hundred and twenty -- five SPF mice were enrolled in the study and randomly divided into three groups -- normal control (A), microbial inoculation (B) and microbial inoculation followed by burn injury. (C) In groups Band C, the mice were gavaged with candida albicans, and the mice in group C, were inflicted with 20% TBSA III degree burn at the 14th day after inoculation. The mice were sacrificed thereafter on 1, 2 and 3 postburn days and the samples were obtained aseptically. The number of candida albicans adhering to intestinal mucosal membrane was counted. The number of IgA plasma cells in lamina propria was determined by immunohistochemical staining. The gene expression of IL-4 in Peyer patch was detected by dothybridization and that of IL-6 in lamina propria was determined by insitu hybridization. RESULTS: (1) The postburn gene expression of IL-4 in Peyer patch decreased, but the IL-6 level in intestinal lamina propria increased. (2) The number of IgA plasma cells in lamina propria decreased significantly, but the adherence of candida albicans to intestinal mucous membrane increased obviously. CONCLUSION: The decrement of postburn gene expression of IL-4 in Peyer patch might lead to IgA plasma cell decrease, resulting in the increase of candida albicans adhering to intestinal mucosal membrane.

Animals↗
PubMed2000

[Study on the pharmacokinetics of Imipenem cilastatin in burn patients during the acute phase].

OBJECTIVE: To investigate the pharmacokinetic characteristics of Imipenem/cilastatin in burn patients during the acute phase. METHODS: Imipenem concentrations in the plasma, blister and, interstitial fluids and urine of 6 burn patients (P group) were determined during the acute phase by high performance liquid chromatography after the first initial dose. Pharmacokinetic parameters were thus produced and statistically analyzed by program package STAT 5. Ten healthy volunteers served as control group (C group). RESULTS: Compared to those in control group, pharmacokinetic parameters of Imipenem exhibited evident difference, such as prolonged half-life [(1.56 plus minus 0.55) h vs (1.06 plus minus 0.24) h] and enlarged distributing volume (16.16 plus minus 4.26) vs (13.96 plus minus 7.10). Imipenem could be detected in the blister and interstitial fluids of burn patients 1 hr after the initial dose. Renal clearance of Imipenem was positively correlated to creatinine clearance (r = 0.5834). CONCLUSION: The intervals between doses should better be prolonged when loaded-dosage of Imipenem was administered in burn patients during the acute phase. Imipenem could penetrate II and III degree burn wound when given in the acute phase. Attention should be paid to renal function when Imipenem was given.

Adult↗
PubMed2000

[Chemical study of Alpinia officinarum].

Seven compounds were isolated from Alinia officinarum Hance and were identified as beta-sitoterol, 1,7-diphenyl-5-ol-3-heptone, 1-phenyl-7-(3'-methoxyl-4'-hydroxyl) phenyl-5-ol-3-heptone, glandin, kaempferol-4'-methylether and 3,4-dihydroxylbenzoic acid by IR, 1HNMR, 13CNMR, FAB-MS and EA. Among these compounds, 3,4-dihydroxylbenzoic acid was the first time obtained from Alpinia officinarum Hance. Furthermore, 1-phenyl-7-(3'-methoxyl-4'-hydroxyl) phenyl-5-ol-3-heptone and a new compound 1,7-diphenyl-3,5-heptandiol-phenyl-7-(3'-methoxyl-4'-hydroxyl) phenyl-3,5-heptaxdiol were obtained from 1,7-diphenyl-5-ol-3-heptone and 1-phenyl-7-(3'-methoxyl-4'-hydroxyl) phenyl-5-ol-3-heptone via chemical reductions.

Alpinia↗
PubMed1999

Calreticulin is transported to the surface of NG108-15 cells where it forms surface patches and is partially degraded in an acidic compartment.

Although calreticulin (Crt) is primarily localized to the endoplasmic reticulum (ER), our results using biotinylation and immunocytochemical methods indicate that a small but significant amount of Crt is present and forms large patches on the surface of NG108-15 cells (a mouse neuroblastoma-rat glioma hybrid cell line). (35)S-labelled Crt molecules begin to reach the cell surface after only 10 min of labelling and disappear slowly from the cell surface. After 4 hr of labelling, approximately half of the newly synthesized Crt molecules are on the cell surface. We believe that some Crt molecules may escape from the KDEL receptor-mediated salvage pathway as they are synthesized and proceed through the secretory pathway to the cell surface. Immunoprecipitation from the culture medium shows that Crt is not released from the cell surface to the medium, suggesting tight binding to surface molecules. NH(4)Cl can block the degradation of Crt; therefore, Crt is presumably degraded in the lysosome pathway. However, blockage of the disappearance of surface Crt is less efficient than that of internal Crt. This suggests that the disappearance of Crt from the cell surface may not be due solely to its degradation, but may reflect transport into another cell compartment such as the ER.

Animals↗
PubMed1999

Roles of tyrosine 158 and lysine 165 in the catalytic mechanism of InhA, the enoyl-ACP reductase from Mycobacterium tuberculosis.

The role of tyrosine 158 (Y158) and lysine 165 (K165) in the catalytic mechanism of InhA, the enoyl-ACP reductase from Mycobacterium tuberculosis, has been investigated. These residues have been identified as putative catalytic residues on the basis of structural and sequence homology with the short chain alcohol dehydrogenase family of enzymes. Replacement of Y158 with phenylalanine (Y158F) and with alanine (Y158A) results in 24- and 1500-fold decreases in k(cat), respectively, while leaving K(m) for the substrate, trans-2-dodecenoyl-CoA, unaffected. Remarkably, however, replacement of Y158 with serine (Y158S) results in an enzyme with wild-type activity. Kinetic isotope effect studies indicate that the transfer of a solvent-exchangeable proton is partially rate-limiting for the wild-type and Y158S enzymes, but not for the Y158A enzyme. These data indicate that Y158 does not function formally as a proton donor in the reaction but likely functions as an electrophilic catalyst, stabilizing the transition state for hydride transfer by hydrogen bonding to the substrate carbonyl. A conformational change involving rotation of the Y158 side chain upon binding of the enoyl substrate to the enzyme is proposed as an explanation for the inverse solvent isotope effect observed on V/K(DD-CoA) when either NADH or NADD is used as the reductant. These data are consistent with the recently published structure of a C16 fatty acid substrate bound to InhA that shows Y158 hydrogen bonded to the substrate carbonyl group and rotated from the position it occupies in the InhA-NADH binary complex [Rozwarski, D. A., Vilcheze, C., Sugantino, M., Bittman, R., and Sacchettini, J. C. (1999) J. Biol. Chem. 274, 15582-15589]. Finally, the role of K165 has been analyzed using site-directed mutagenesis. Replacement of K165 with glutamine (K165Q) and arginine (K165R) has no effect on the enzyme's catalytic ability or on its ability to bind NADH. However, the K165A and K165M enzymes are unable to bind NADH, indicating that K165 has a primary role in cofactor binding.

Amino Acid Substitution↗
PubMed1999

KDEL proteins are found on the surface of NG108-15 cells.

Although KDEL proteins are primarily localized to the endoplasmic reticulum (ER), we have employed surface biotinylation method to demonstrate that the KDEL proteins calreticulin (Crt), protein disulfide isomerase (PDI) and the 78-kDa glucose regulated protein (GRP78) are found on the surface of the NG108-15 cell line. In contrast, the 94-kDa glucose regulated protein (GRP94), another KDEL protein, is not found on the cell surface. Calnexin (Cnx), a type-1 integral transmembrane ER protein which is partially homologous to Crt but lacks the KDEL sequence, is not detected on the cell surface either. While only small amounts of the total GRP78, PDI and Crt molecules exist on the cell surface at steady state, a significant fraction of the newly synthesized molecules are transported to the cell surface and transport of these proteins is inhibited by treatment with brefeldin A. The surface GRP78 contains the KDEL sequence. On the cell surface, GRP78, PDI and Crt associate with other proteins and form complexes of different sizes. Surface Crt is found to be essential for the neurite formation when NG108-15 cells are induced to differentiate using dibutyryl cAMP.

Amino Acid Sequence↗
PubMed1999

Heteronuclear NMR and crystallographic studies of wild-type and H187Q Escherichia coli uracil DNA glycosylase: electrophilic catalysis of uracil expulsion by a neutral histidine 187.

The nature of the putative general acid His187 in the reaction catalyzed by Escherichia coli uracil DNA glycosylase (UDG) was investigated using X-ray crystallography and NMR spectroscopy. The crystal structures of H187Q UDG, and its complex with uracil, have been solved at 1.40 and 1.60 A resolution, respectively. The structures are essentially identical to those of the wild-type enzyme, except that the side chain of Gln187 is turned away from the uracil base and cannot interact with uracil O2. This result provides a structural basis for the similar kinetic properties of the H187Q and H187A enzymes. The ionization state of His187 was directly addressed with (1)H-(15)N NMR experiments optimized for histidine ring spin systems, which established that His187 is neutral in the catalytically active state of the enzyme (pK(a) <5.5). These NMR experiments also show that His187 is held in the N(epsilon)()2-H tautomeric form, consistent with the crystallographic observation of a 2.9 A hydrogen bond from the backbone nitrogen of Ser189 to the ring N(delta)()1 of His187. The energetic cost of breaking this hydrogen bond may contribute significantly to the low pK(a) of His187. Thus, the traditional view that a cationic His187 donates a proton to uracil O2 is incorrect. Rather, we propose a concerted mechanism involving general base catalysis by Asp64 and electrophilic stabilization of the developing enolate on uracil O2 by a neutral His187.

Binding Sites↗
PubMed1999

Structural basis and mechanism of enoyl reductase inhibition by triclosan.

The enoyl-acyl carrier protein reductase (ENR) is involved in bacterial fatty acid biosynthesis and is the target of the antibacterial diazaborine compounds and the front-line antituberculosis drug isoniazid. Recent studies suggest that ENR is also the target for the broad-spectrum biocide triclosan. The 1.75 A crystal structure of EnvM, the ENR from Escherichia coli, in complex with triclosan and NADH reveals that triclosan binds specifically to EnvM. These data provide a molecular mechanism for the antibacterial activity of triclosan and substantiate the hypothesis that its activity results from inhibition of a specific cellular target rather than non-specific disruption of the bacterial cell membrane. This has important implications for the emergence of drug-resistant bacteria, since triclosan is an additive in many personal care products such as toothpastes, mouthwashes and soaps. Based on this structure, rational design of triclosan derivatives is possible which might be effective against recently identified triclosan-resistant bacterial strains.

Anti-Bacterial Agents↗
PubMed1999

Crystal structure of Escherichia coli uracil DNA glycosylase and its complexes with uracil and glycerol: structure and glycosylase mechanism revisited.

The DNA repair enzyme uracil DNA glycosylase (UDG) catalyzes the hydrolysis of premutagenic uracil residues from single-stranded or duplex DNA, producing free uracil and abasic DNA. Here we report the high-resolution crystal structures of free UDG from Escherichia coli strain B (1.60 A), its complex with uracil (1.50 A), and a second active-site complex with glycerol (1.43 A). These represent the first high-resolution structures of a prokaryotic UDG to be reported. The overall structure of the E. coli enzyme is more similar to the human UDG than the herpes virus enzyme. Significant differences between the bacterial and viral structures are seen in the side-chain positions of the putative general-acid (His187) and base (Asp64), similar to differences previously observed between the viral and human enzymes. In general, the active-site loop that contains His187 appears preorganized in comparison with the viral and human enzymes, requiring smaller substrate-induced conformational changes to bring active-site groups into catalytic position. These structural differences may be related to the large differences in the mechanism of uracil recognition used by the E. coli and viral enzymes. The pH dependence of k(cat) for wild-type UDG and the D64N and H187Q mutant enzymes is consistent with general-base catalysis by Asp64, but provides no evidence for a general-acid catalyst. The catalytic mechanism of UDG is critically discussed with respect to these results.

Amino Acid Sequence↗
PubMed1999

Suppression of breast cancer growth and metastasis by a serpin myoepithelium-derived serine proteinase inhibitor expressed in the mammary myoepithelial cells.

A serpin was identified in normal mammary gland by differential cDNA sequencing. In situ hybridization has detected this serpin exclusively in the myoepithelial cells on the normal and noninvasive mammary epithelial side of the basement membrane and thus was named myoepithelium-derived serine proteinase inhibitor (MEPI). No MEPI expression was detected in the malignant breast carcinomas. MEPI encodes a 405-aa precursor, including an 18-residue secretion signal with a calculated molecular mass of 46 kDa. The predicted sequence of the new protein shares 33% sequence identity and 58% sequence similarity to plasminogen activator inhibitor (PAI)-1 and PAI-2. To determine whether MEPI can modulate the in vivo growth and progression of human breast cancers, we transfected a full-length MEPI cDNA into human breast cancer cells and studied the orthotopic growth of MEPI-transfected vs. control clones in the mammary fat pad of athymic nude mice. Overexpression of MEPI inhibited the invasion of the cells in the in vitro invasion assay. When injected orthotopically into nude mice, the primary tumor volumes, axillary lymph node metastasis, and lung metastasis were significantly inhibited in MEPI-transfected clones as compared with controls. The expression of MEPI in myoepithelial cells may prevent breast cancer malignant progression leading to metastasis.

Adult↗
PubMed1999

Gene expression profiles in HTLV-I-immortalized T cells: deregulated expression of genes involved in apoptosis regulation.

Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent of adult T-cell leukemia, an acute and often fatal T-cell malignancy. A key step in HTLV-I-induced leukemigenesis is induction of abnormal T-cell growth and survival. Unlike antigen-stimulated T cells, which cease proliferation after a finite number of cell division, HTLV-I-infected T cells proliferate indefinitely (immortalized), thus facilitating occurrence of secondary genetic changes leading to malignant transformation. To explore the molecular basis of HTLV-I-induced abnormal T-cell survival, we compared the gene expression profiles of normal and HTLV-I-immortalized T cells using 'gene array'. These studies revealed a strikingly altered expression pattern of a large number of genes along with HTLV-I-mediated T-cell immortalization. Interestingly, many of these deregulated genes are involved in the control of programmed cell death or apoptosis. These findings indicate that disruption of the cellular apoptosis-regulatory network may play a role in the HTLV-I-mediated oncogenesis.

Apoptosis↗
PubMed1999

Cloning of a 2.5 kb murine bone sialoprotein promoter fragment and functional analysis of putative Osf2 binding sites.

Bone sialoprotein (BSP) is an extracellular matrix protein that is intimately associated with the process of biomineralization. Osf2, a member of the Cbf/runt family of transcription factors, is required for the development of osteoblasts in vivo and has been reported to stimulate the transcription of BSP when overexpressed in mesenchymal cell lines. To investigate the role of Osf2 in BSP expression, we cloned a 2.5 kb fragment of a 5' untranscribed sequence from the murine BSP gene and evaluated it for putative Osf2 binding sites. This promoter, which was able to direct 5- to 10-fold higher levels of luciferase reporter expression in osteoblastic cells than in nonbone cell lines, contains two consensus core binding sites for members of the Cbf/runt family. One, at -61 relative to the start of transcription, is within a region having 75% overall sequence identity with the rat and human BSP promoters. The other is located at -1335, outside this highly conserved region. Neither site is completely conserved in the rat or human sequences. Only the -1335 site was able to bind a protein in nuclear extracts of osteoblastic cells, and this protein was identified as Osf2. Despite this in vitro binding ability, we detected no significant enhancer activity in the -1335 element when placed in front of a minimal osteocalcin promoter driving a luciferase reporter gene in osteoblastic cells nor any loss in transcriptional activity of a 5' promoter deletion which eliminated this element as compared with the full-length 2.5 kb promoter. These results suggest that Osf2 binding to the BSP promoter is not essential for its osteoblast-selective expression.

3T3 Cells↗
PubMed1999

Isolation and characterization of MC3T3-E1 preosteoblast subclones with distinct in vitro and in vivo differentiation/mineralization potential.

A series of subclonal cell lines with high or low differentiation/mineralization potential after growth in the presence of ascorbic acid (AA) were derived from murine MC3T3-E1 cells. Subclones were characterized in terms of their ability to mineralize a collagenous extracellular matrix both in vitro and in vivo and express osteoblast-related genes. When compared with nonmineralizing cells, mineralizing subclones selectively expressed mRNAs for the osteoblast markers, bone sialoprotein (BSP), osteocalcin (OCN), and the parathyroid hormone (PTH)/parathyroid hormone-related protein (PTHrP) receptor. In contrast, alkaline phosphatase mRNA was present in certain nonmineralizing as well as mineralizing subclones, suggesting that its expression may be subject to different controls from other osteoblast markers. Only highly differentiating subclones exhibited strong AA-dependent induction of a transiently transfected OCN promoter-luciferase reporter gene, indicating that there was a good correlation between mRNA levels and transcriptional activity. Consistent with its postulated role in biomineralization, BSP as measured by Western blotting was only present in mineralizing subclones. After implantation into immunodeficient mice, highly differentiating subclones formed bone-like ossicles resembling woven bone, while poorly differentiating cells only produced fibrous tissue. Interestingly, subclones with both high and low differentiation potential produced similar amounts of collagen in culture and expressed comparable basal levels of mRNA encoding Osf2/Cbfa1, an osteoblast-related transcription factor. Although some strongly differentiating cells exhibited a modest AA-dependent up-regulation of Osf2/Cbfa1 mRNA, there was no clear relationship between levels of this message and induction of mRNAs for other differentiation markers. Thus, the mere presence of Osf2/Cbfa1 in a subclone was not sufficient for osteoblast differentiation. These subclones will be very useful for studying critical events in osteoblast differentiation and mineralization.

Animals↗
PubMed1999

[Experimental study of the effect of dexamethasone on pulmonary diffuse hemorrhage and energy metabolism of mitochondria in the liver of guinea pig infected with leptospirosis].

This experiment was designed to study the curative effect of dexamethasone on leptospirosis with pulmonary diffuse hemorrhage (PDH) in guinea pig model. The guinea pigs were randomly divided into four groups: the infected group, all animals developed PDH(n = 10); the infected plus treated group(n = 10); the treated control group(n = 10); and the normal control group(n = 10). The gross and microscopic observations in lung, liver and kidney were made. Also, ultrastructural changes of mitochondria in liver were examined, and the lactic acid level and mitochondrial ATPase activity in liver were determined. The results showed that there was significant difference in mortality, in gross and microscopic changes in lung, liver and kidney, and in the changes of mitochondrial ultrastructures, ATPase activity and lactic acid level in liver between the infected group and the infected plus treated group (P < 0.01). These findings suggest that the pharmacologic dose of dexamethasone injected intravenously in the early stage of PDH may have some beneficial effect on the emergency treatment of leptospirosis with PDH. The mechanism appears to be related to its effect on the inhibition of glycolysis and increasing oxidative phosphorylation in mitochondria.

Adenosine Triphosphatases↗
PubMed1999

[Pathogenetic effect of platelet activating factor on enterogenic endotoxemia after burn].

OBJECTIVE: To investigate the effects of platelet activating factor (PAF) on the occurrence of enterogenic endotoxemia after burn. METHODS: The relationship between changes of PAF and enterogenic endotoxima was observed on a model of rats with 30% TBSA III degree burn. RESULTS: The intestinal permeability and plasma endotoxin were significantly elevated and were positively correlated with the increase of PAF in the intestinal tissue and blood. PAF antagonist treatment significantly decreased the intestinal permeability and the levels of plasma endotoxin. After intravenous injection of enogenous PAF to healthy rats, the intestinal permeability and plasma endotoxin were also markedly increased, which was significantly depended on the dose of PAF. CONCLUSION: PAF is one of the important factors for the occurrence of postburn enterogenic endotoximia.

Animals↗