Search PubMed⌕ Search

Biomedical subjects

Z Guan

Publications and source records attributed to Z Guan.

At least 55 records · Page 3Linked to original sources
PubMed1999

Chain walking: A new strategy to control polymer topology

Ethylene pressure has been used to control the competition between isomerization (chain walking) and monomer insertion processes for ethylene coordination polymerization catalyzed by a palladium-alpha-diimine catalyst. The topology of the polyethylene varies from linear with moderate branching to "hyperbranched" structures. Although the overall branching number and the distribution of short-chain branching change very slightly, the architecture or topology of the polyethylene changes from linear polyethylene with moderate branches at high ethylene pressures to a hyperbranched polyethylene at low pressures.

Journal Article↗
PubMed1999

Depletion of hematogenous macrophages promotes partial hindlimb recovery and neuroanatomical repair after experimental spinal cord injury.

Traumatic injury to the spinal cord initiates a series of destructive cellular processes which accentuate tissue damage at and beyond the original site of trauma. The cellular inflammatory response has been implicated as one mechanism of secondary degeneration. Of the various leukocytes present in the spinal cord after injury, macrophages predominate. Through the release of chemicals and enzymes involved in host defense, macrophages can damage neurons and glia. However, macrophages are also essential for the reconstruction of injured tissues. This apparent dichotomy in macrophage function is further complicated by the overlapping influences of resident microglial-derived macrophages and those phagocytes that are derived from peripheral sources. To clarify the role macrophages play in posttraumatic secondary degeneration, we selectively depleted peripheral macrophages in spinal-injured rats during a time when inflammation has been shown to be maximal. Standardized behavioral and neuropathological analyses (open-field locomotor function, morphometric analysis of the injured spinal cord) were used to evaluate the efficacy of this treatment. Beginning 24 h after injury and then again at days 3 and 6 postinjury, spinal cord-injured rats received intravenous injections of liposome-encapsulated clodronate to deplete peripheral macrophages. Within the spinal cords of rats treated in this fashion, macrophage infiltration was significantly reduced at the site of impact. These animals showed marked improvement in hindlimb usage during overground locomotion. Behavioral recovery was paralleled by a significant preservation of myelinated axons, decreased cavitation in the rostrocaudal axis of the spinal cord, and enhanced sprouting and/or regeneration of axons at the site of injury. These data implicate hematogenous (blood-derived) macrophages as effectors of acute secondary injury. Furthermore, given the selective nature of the depletion regimen and its proven efficacy when administered after injury, cell-specific immunomodulation may prove useful as an adjunct therapy after spinal cord injury.

Animals↗
PubMed1999

Mechanisms through which PDGF alters intracellular calcium levels in U-1242 MG human glioma cells.

PDGF-BB induces a rapid, sustained increase in intracellular calcium levels in U-1242 MG cells. We used several calcium channel blockers to identify the types of channels involved. L channel blockers (verapamil, nimodipine, nicardipine, nitrendipine and taicatoxin) had no effect on PDGF-BB induced alterations in intracellular calcium. Blockers of P, Q and N channels (omega-agatoxin-IVA, omega-conotoxin MVIIC and omega-conotoxin GVIA) also had no effect. This indicates that these channels play an insignificant role in supplying the Ca2+ necessary for PDGF stimulated events in U-1242 MG cells. However, a T channel blocker (NDGA) and the non-specific (NS) calcium channel blockers (FFA and SK&F 9365) abolished PDGF-induced increases in intracellular calcium. This indicates that PDGF causes calcium influx through both non-specific cationic channels and T channels. To study the participation of intracellular calcium stores in this process, we used thapsigargin, caffeine and ryanodine, all of which cause depletion of intracellular calcium stores. The PDGF effect was abolished using both thapsigargin and caffeine but not ryanodine. Collectively, these data indicate that in these human glioma cells PDGF-BB induces release of intracellular calcium from caffeine- and thapsigargin-sensitive calcium stores which in turn lead to further calcium influx through both NS and T channels.

Becaplermin↗
PubMed1999

The protective role of plasmalogens in iron-induced lipid peroxidation.

The role of plasmalogens in iron-induced lipid peroxidation was investigated in two liposomal systems. The first consisted of total brain phospholipids with and without plasmalogens, and the second of phosphatidylethanolamine/phosphatidylcholine liposomes with either diacyl- or alkenylacyl-phosphatidylethanolamine. By measuring thiobarbituric acid reactive substances, oxygen consumption, fatty acids and aldehydes, we show that plasmalogens effectively protect polyunsaturated fatty acids from oxidative damage, and that the vinyl ether function of plasmalogens is consumed simultaneously. Furthermore, the lack of lag phase, the increased antioxidant efficiency with time, and the experiments with lipid- and water-soluble azo compounds, indicate that plasmalogens probably interfere with the propagation rather than the initiation of lipid peroxidation, and that the antioxidative effect cannot be related to iron chelation.

Azo Compounds↗
PubMed1999

Decrease and structural modifications of phosphatidylethanolamine plasmalogen in the brain with Alzheimer disease.

Several lipid modifications, some of which were attributed to oxidative stress, have been reported in the brains of patients with Alzheimer disease (AD). To evaluate this possibility, all phospholipids and their ether subclasses from the frontal cortex, hippocampus, and the white matter of AD brain were analyzed by high performance liquid chromatography and gas chromatography. The total phospholipid in the frontal cortex and hippocampus decreased on a DNA basis by about 20% and this change was essentially explained by a selective decrease in phosphatidylethanolamine and phosphatidylcholine. The lower content of phosphatidylethanolamine was due to a specific decrease in the plasmalogen subclass. Phosphatidylethanolamine plasmalogen was also the only lipid exhibiting major structural modifications: a significant decrease in polyunsaturated fatty acids and oleic acid as well as a shift of the aldehyde pattern from 18:1 to 18:0. The only modification observed in the other phospholipids was a decrease in oleic acid in diacyl-phosphatidylethanolamine and diacyl-phosphatidylcholine. None of these changes were observed in the white matter. Both the vinyl ether bond of phosphatidylethanolamine plasmalogen and polyunsaturated fatty acids are major targets in oxidative stress; thus, these specific lipid modifications strongly support the involvement of free radicals in the pathogenesis of AD.

Aged↗
PubMed1999

Evaluation of the inhibition of other metalloproteinases by matrix metalloproteinase inhibitors.

Two series of compounds synthesized as specific matrix metalloproteinase (MMP) inhibitors have been evaluated for their inhibition of non-MMPs. In a series of substituted succinyl hydroxamic acids, some were found to be significant (IC50 < 1 microM) inhibitors of leucine (microsomal) aminopeptidase, neprilysin (3.4.24.11), and thermolysin. Macrocyclic compounds in which the alpha carbon of the succinyl hydroxamate is linked to the side chain of the P2' amino acid were found to be good inhibitors of aminopeptidase, but not of neprilysin or thermolysin. Compounds of neither series were found to be significant inhibitors of angiotensin converting enzyme or carboxypeptidase A.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Gender differences in late positive components evoked by human faces.

Event-related potentials (ERPs) were recorded in male and female participants in response to 32 male and 32 female faces. Participants were instructed to simply look carefully at each face; after ERP collection they were asked to rate each face on a 5-point attractiveness scale. A positive correlation between average rating and average P300 scores to opposite sex faces was observed in male (r = .40) and in preovulatory (r = .41) and postovulatory (r = .44) female subjects. Correlations to same sex faces were only found in postovulatory females (r = .61). Male participants showed a much larger average P300 than did female participants, and the P300 evoked in female participants was unexpectedly larger to female than to male faces. Neither task relevance nor stimulus probability is a plausible explanations for these findings because they were experimentally controlled. These results support the emotional value hypothesis, according to which classical P300 processes reflect an affective evaluation of the stimulus, which in turn produces context updating.

Adolescent↗
PubMed1999

[Experimental study and preliminary clinical application of bacterial collagenase in catabolizing scars].

OBJECTIVE: To investigate the mechanism of collagenase in degradation of hypertrophic scars and observe the clinical effects of this therapy. METHODS: Both animal experiment and clinical trial were conducted. RESULTS: The injection of collagenase into the hypertrophic scar tissues in nude mice resulted in 86% volume reduction after two injections within two weeks, while the control tissues reduced only by 35% during the same time. Clinically, 13 cases were treated with intralesional injection of bacterial collagenase. The volume reduction rate was 46.92% in average within two weeks. The volume reduction in 4 of 13 cases was above 50%. Three to sixteen months' follow-up of five patients revealed that only one case of keloid recurred after treatment in the second month. Examinations of histological sections and TEM showed the dissolved collagen fiber clearly. CONCLUSION: Collagenase can degrade collagen fiber directly. The prompt significant effects and the mild complications make it a prospective therapy.

Adolescent↗
PubMed1999

The effects of classic antipsychotic haloperidol plus the extract of ginkgo biloba on superoxide dismutase in patients with chronic refractory schizophrenia.

OBJECTIVES: To explore the association between schizophrenic symptoms and superoxide dismutase (SOD), and to investigate the effect of classic antipsychotic haloperidol plus the extract of Ginkgo biloba (EGb) on SOD. METHODS: In 54 patients with chronic refractory schizophrenia, 27 were treated with haloperidol plus EGb (group 1), and the rest received haloperidol plus placebo (group 2). Superoxide dismutase (SOD) levels of these patients were measured before and after treatment and compared with the levels of 25 healthy volunteers. Therapeutic efficacy was equated with a change in clinical rating scores assessed by standardized measurement tools including the Scale for Assessment of Positive Symptoms (SAPS) and the Scale for Assessment of Negative Symptoms (SANS). RESULTS: Patients in group 1 improved significantly as demonstrated by scores from both SAPS and SANS, while those in group 2 only by scores from SANS. Assessed by SAPS, the response of patients receiving haloperidol plus EGb was more significant than those receiving haloperidol only. SOD levels before treatment in all patients were significantly higher than those in normal controls. After treatment, SOD levels decreased significantly in group 1 but not in group 2. In addition, before treatment, SOD levels in all patients correlated significantly with SAPS score. The levels of SOD measured before treatment were also correlated with the improvement of patients as measured by SAPS and SANS after 12 weeks. CONCLUSIONS: EGb may enhance the efficacy of classic antipsychotic haloperidol on schizophrenia, especially on positive symptoms. It may work through an antioxidant efficacy that is involved in the therapeutic mechanism.

Adult↗
PubMed1999

[Reinfusion of autologous shed blood after joint replacement].

OBJECTIVE: To evaluate the results of reinfusion of autologous shed blood after joint replacement. METHODS: From February 1996 to March 1998, we selected 36 patients for 56 joint replacements. Apart from preoperative donation of autologous blood, all patients received transfusion of unwashed autologous drained blood from hips and knees after arthroplasty. The CBCIIConstaVac blood conservation system was used to salvage shed blood. Among the patients, 8 hips and 48 knees were involved. 12 patients had rheumatoid arthritis, 16 osteoarthritis, 5 ankylosing spondylitis, and 3 other arthritis. RESULTS: 36 patients received 24 260 ml (50%) autologous shed blood, 9 700 ml (20%) reserved autologous blood, and 14 600 ml (30%) allogenic blood. 15 patients experienced transient febrile reaction at the time of reinfusion, no other clinic abnormalities were discovered after reinfusion. CONCLUSIONS: Reinfusion of autologous shed blood is a safe and effective to decrease the use of allogenic blood and avoid the complications of its transfusion.

Adult↗
PubMed1999

[Study on the steroid constituents of soft coral Lobophytum microspiculatum].

The soft coral Lobophytum microspiculatum collected from Xisa Islands of the South China Sea was immersed in and extracted with ethyl alcohol and the extract was concentrated, and then partitioned between ethyl acetate and water. The portion soluble in ethyl acetate was subjected to column chromatography over Sillca H, eluted with a step gradient of EtOAc and petroleum ether. The sterols were obtained from 20% EtOAc-petroleum ether eluent portion. By means of GC/MS method, the sterols were identified to be: cholesta-26-methyl-ol; ergosta-8, 22-dien-3 beta-ol, 24-methyl; ergosta-5, 22-dien-3 beta-ol, 23, 24-dimethyl; cholesta-5,22(23)-dien-3 beta-ol, 22,24-dimethyl; cholesterol; ergosta-5,22-dien-3 beta-ol, 24-methyl; ergosta-5,22-dien-3 beta-ol, 22,24-dimethyl, 24-methyl-cholesterol; ergosta-7-en-3 beta-ol, 24-methyl; nor-ergosta-7-en-3 beta-ol and gorgosterol. Among them cholest-5,22(23)-3 beta-ol, 22,24-dimethyl (4) is a new compound which was found at the first time from the nature. This finding gave a further prove for the biogenesis path way of gorgosterol.

Animals↗
PubMed1999

[Study on relative factors in endoscopic sinus surgical procedure].

OBJECTIVE: In order to investigate the factors which affect the operative treatment effect of FESS. METHOD: 215 cases suffered functional endoscopic sinus surgery (FESS) from May 1994 to December 1997 were analysed. RESULT: The clinical curative rate was 75.8% and the improving rate was 96.3%. CONCLUSION: The effect shows that surgical procedure is closely related to following factors: mechanic of operation, drugs taken in pre-operation, kinds of anesthsia, clinical stage of chronic sinusitis, nasal poplys and skill of surgeons.

Adolescent↗
PubMed1998

Interleukin-1beta-induced cyclooxygenase-2 expression requires activation of both c-Jun NH2-terminal kinase and p38 MAPK signal pathways in rat renal mesangial cells.

The inflammatory cytokine interleukin-1beta (IL-1beta) induces cyclooxygenase-2 (Cox-2) expression with a concomitant release of prostaglandins from glomerular mesangial cells. We reported previously that IL-1beta rapidly activates the c-Jun NH2-terminal/stress-activated protein kinases (JNK/SAPK) and p38 mitogen-activated protein kinase (MAPK) and also induces Cox-2 expression and prostaglandin E2 (PGE2) production. The current study demonstrates that overexpression of the dominant negative form of JNK1 or p54 JNK2/SAPKbeta reduces Cox-2 expression and PGE2 production stimulated by IL-1beta. Similarly, overexpression of the kinase-dead form of p38 MAPK also inhibits IL-1beta-induced Cox-2 expression and PGE2 production. These results suggest that activation of both JNK/SAPK and p38 MAPK is required for Cox-2 expression after IL-1beta activation. Furthermore, our experiments confirm that IL-1beta activates MAP kinase kinase-4 (MKK4)/SEK1, MKK3, and MKK6 in renal mesangial cells. Overexpression of the dominant negative form of MKK4/SEK1 decreases IL-1beta- induced Cox-2 expression with inhibition of both JNK/SAPK and p38 MAPK phosphorylation. Overexpression of the kinase-dead form of MKK3 or MKK6 demonstrated that either of these two mutant kinases inhibited IL-1beta-induced p38 MAPK phosphorylation and Cox-2 expression but not JNK/SAPK phosphorylation and activation. This study suggests that the activation of both JNK/SAPK and p38 MAPK signaling cascades is required for IL-1beta-induced Cox-2 expression and PGE2 synthesis.

Animals↗
PubMed1998

Induction of cyclooxygenase-2 by the activated MEKK1 --> SEK1/MKK4 --> p38 mitogen-activated protein kinase pathway.

The mitogen-activated protein kinase (MAPK) cascade is believed to function as an important regulator of prostaglandin biosynthesis. Previously we reported that interleukin-1beta induces activation of JNK/SAPK and p38 MAPK with concomitant up-regulation of cyclooxygenase (Cox)-2 expression and prostaglandin E2 (PGE2) synthesis. Our experiments demonstrate that overexpression of DeltaMEKK1 (a constitutively active truncation mutant of MEKK1 containing the C-terminal 324 amino acids) increases Cox-2 expression and PGE2 production which is completely blocked by SC68376, a pharmacologic inhibitor of p38 MAPK. DeltaMEKK1 overexpression results in activation of both c-Jun N-terminal kinases/extracellular signal-regulated kinases (JNK/SAPK) and p38 MAPK. Furthermore, activation of MEKK1 increases SEK1/MKK4 but not MKK3 or MKK6 activity. These findings suggest that MEKK1 --> SEK1/MKK4 may function as an upstream kinase capable of activating both p38 MAPK and JNK/SAPK with subsequent induction of Cox-2 expression and PGE2 production. We also found that overexpression of the constitutively active form of SEK1 (SEK1-ED) increases both p38 MAPK and JNK/SAPK phosphorylation, and increases PGE2 production and Cox-2 expression. By comparison, overexpression of the dominant negative form of SEK1 (SEK1-AL) decreases the phosphorylation of both p38 MAPK and JNK/SAPK and reduces Cox-2 expression. Together, this data suggests a potential role for the MEKK1 --> SEK1/MKK4 --> p38 MAPK -->--> Cox-2 cascade linking members of the MAPK pathway with prostaglandin biosynthesis.

3T3 Cells↗
PubMed1998

Creatine kinase: essential arginine residues at the nucleotide binding site identified by chemical modification and high-resolution tandem mass spectrometry.

Phenylglyoxal is an arginine-specific reagent that inactivates creatine kinase (CK). Previous results suggest that modification of the dimeric enzyme at a single arginine residue per subunit causes complete inactivation accompanied by the loss of nucleotide binding; the actual site of modification was not identified. Here, high-resolution tandem mass spectrometry (MS/MS) was used to identify three phenylglyoxal-modified Arg residues in monomeric rabbit muscle CK. Electrospray ionizaton Fourier-transform MS of the phenylglyoxal-modified CK that had lost approximately 80% activity identified three species: unmodified, once-modified (+116 Da), and twice-modified (+232 Da) enzyme in a ratio of approximately 1:4:1. MS/MS restricts the derivatized sites to P122-P212 and P283-V332, whereas MS of Lys-C digestions revealed two modified peptides, A266-K297 and G116-K137. The only Arg in A266-K297 is Arg-291 (invariant), whereas MS/MS of modified G116-K137 shows that two of the three sites Arg-129, Arg-131, or Arg-134 (all invariant) can contain the modification. The recently reported x-ray crystal structure for the octameric chicken mitochondrial CK indicates that its nucleotide triphosphate-binding site indeed contains the equivalent of R291, R129, and R131 reported here to be at the active site of rabbit muscle CK.

Animals↗