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Biomedical subjects

Z G Liu

Publications and source records attributed to Z G Liu.

At least 19 recordsLinked to original sources
PubMed2003

Self-modulation of light in piezoelectric crystals.

Spectroscopic measurements were used to monitor the optical interference of ordinary (o-ray) waves with extraordinary (e-ray) waves by incidence of plane-polarized light and transmission through piezoelectriccrystals (alpha-quartz, LiNbO3, and LiTaO3). This observation confirms that the rotations of the vibration planes of the o- and e-ray waves originate from the dynamic gratings induced by the electric field of the incident light. This is a self-modulation process of the polarized incident light in piezoelectric crystals.

Journal Article↗
PubMed2001

Comparison of nitric oxide release and endothelium-derived hyperpolarizing factor-mediated hyperpolarization between human radial and internal mammary arteries.

BACKGROUND: Arterial grafts for CABG have been used increasingly, and the radial artery (RA) has become a preferable graft, secondary to the internal mammary artery (IMA). In the present study, we investigated and compared NO release and endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization for IMA and RA. METHODS AND RESULTS: IMA and RA segments taken from CABG patients were placed in an organ chamber. An NO-sensitive electrode (to directly measure NO release) or intracellular glass microelectrode (to measure membrane potential) was used to study NO or EDHF in response to acetylcholine (ACh) and bradykinin (BK) before and after incubation with indomethacin (a cyclooxygenase inhibitor), N(G)-nitro-L-arginine (an NO synthase inhibitor), and oxyhemoglobin (an NO scavenger). The resting membrane potential of the smooth muscle cells of IMA and RA was -58+/-0.84 (n=61) and -61+/-1.3 (n=46) mV, respectively (P=0.03). BK-induced EDHF-mediated hyperpolarization in the IMA was significantly greater than that in RA (BK 10(-)(7) mol/L: -10.9+/-1.5 [n=7] versus -5.8+/-0.9 [n=6] mV, P=0.04). The basal (16.8+/-1.9 versus 11.1+/-1.0 nmol/L, n=12, P=0.02) and stimulated releases of NO in IMA were significantly greater for BK (44.3+/-4.0 versus 25.8+/-3.6 nmol/L, n=8, P=0.004) and lasting longer for ACh (9.5+/-2.0 versus 6.6+/-3.6 minutes, n=12, P=0.03) than those in RA. CONCLUSIONS: The basal and stimulated releases of NO and EDHF-mediated hyperpolarization in the IMA are significantly greater than that in the RA. The lower capacity of NO release may contribute to the susceptibility of RA to the perioperative vasospasm and may have an impact on the long-term graft patency.

Acetylcholine↗
PubMed2001

Direct measurement of nitric oxide release from saphenous vein: abolishment by surgical preparation.

BACKGROUND: Surgical preparation (distension) of the saphenous vein (SV) is applied routinely during harvesting in coronary artery bypass grafting (CABG). However, mechanical distension may impair the endothelium, which plays an important role in long-term patency. The present study investigated the effect of surgical preparation of the SV on nitric oxide (NO) release from the endothelium by direct measurement of NO. METHODS: Saphenous vein segments taken from CABG patients were cut open longitudinally and placed in an organ chamber. An NO-sensitive electrode and NO meter were used to directly measure NO release induced by acetylcholine (ACh) and bradykinin (BK) from the surgically prepared veins (PV) compared with the control (nondistended) veins. RESULTS: The basal release of NO in the PV group was significantly lower than that in the control group (3.4 +/- 1.4 nM, n = 9 versus 9.9 +/- 2.8 nM, n = 13, p = 0.002). The maximum concentrations of NO release induced by ACh and BK in the PV group were also significantly lower than those in the control veins (for ACh 10(-6) mol/L: 9.6 +/- 3.1 nM, n = 8 versus 41.9 +/- 11.2 nM, n = 12, p = 0.005; for BK 10(-8) mol/L: 8.3 +/- 3.7 nM, n = 7 versus 37.9 +/- 6.1 nM, n = 9, p = 0.003). Further, the duration of NO release in the PV group was significantly shorter than that in control veins (1.5 +/- 1.3 minutes, n = 8 versus 8.1 +/- 1.9 minutes, n = 8, p < 0.001). CONCLUSIONS: Surgical preparation almost abolishes NO release by the SV and this may significantly contribute to the low long-term patency rate of the vein graft.

Endothelium, Vascular↗
PubMed2001

Cellular responses to tumor necrosis factor.

TNF is a proinflammatory cytokine that plays an important role in many physiological and pathological conditions through the regulation of immunological reactions. Many of TNF functions have been proven to be cell type-specific, and the specificity of TNF-induced cellular responses in a given cell is determined by the specific intracellular signaling pathways that are activated by TNF. Although current information is insufficient to sort out how the cell type specificity is controlled by the different intracellular signaling pathways, a number of signaling pathways that are commonly activated in many types of cells by TNF have been revealed. This review weighs the current knowledge of these TNF-induced signaling pathways.

Animals↗
PubMed2000

Difference in endothelium-derived hyperpolarizing factor-mediated hyperpolarization and nitric oxide release between human internal mammary artery and saphenous vein.

BACKGROUND: The greater nitric oxide (NO) release that occurs in the internal mammary artery (IMA) when compared with the saphenous vein (SV) has been suggested by more endothelium-dependent relaxation in the IMA or measured by bioassay; however, no direct measurement of NO- or endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization has been reported. The present study measured such hyperpolarization, as well as NO release, in these vessels. METHODS AND RESULTS: IMA (n=46) and SV (n=61) segments taken from patients undergoing coronary surgery were studied in the organ chamber. Hyperpolarization (by intracellular glass microelectrode) and NO release (by NO-sensitive electrode) in response to acetylcholine and bradykinin, with and without incubation with N(G)-nitro-L-arginine, indomethacin, and oxyhemoglobin, were measured. The resting membrane potential of the smooth muscle cells from the IMA (58+/-0.8 mV; n=15) was higher than that in those from the SV (-62+/-0.9 mV; n=23; P:=0.0001). The EDHF-mediated hyperpolarization induced by acetylcholine (10(-5) mol/L: -9.4+/-1.5 mV in IMA, n=10, versus -4. 5+/-1.0 mV in SV, n=17; P:<0.01) and bradykinin (10(-7) mol/L: -10. 9+/-1.5 mV in IMA, n=8, versus -5.1+/-0.5 mV in SV, n=8; P:<0.01) and the basal release of NO (16.8+/-1.6 nmol/L in IMA, n=13, versus 9.9+/-2.8 nmol/L in SV, n=13; P:<0.001) were significantly greater in the IMA than in the SV. The duration of acetylcholine- and bradykinin-induced NO release was longer in the IMA than in the SV. CONCLUSIONS: The basal release of NO and EDHF-mediated hyperpolarization were significantly greater in the IMA than in the SV. In addition, the duration of the stimulated release of NO was longer in the IMA than in the SV. These differences may contribute to the superior long-term patency of IMA grafts.

Acetylcholine↗
PubMed2000

Disruption of hsp90 function results in degradation of the death domain kinase, receptor-interacting protein (RIP), and blockage of tumor necrosis factor-induced nuclear factor-kappaB activation.

The death domain kinase, receptor interacting protein (RIP), is one of the major components of the tumor necrosis factor receptor 1 (TNFR1) complex and plays an essential role in tumor necrosis factor (TNF)-mediated nuclear factor kappaB (NF-kappaB) activation. The activation of NF-kappaB protects cells against TNF-induced apoptosis. Heat-shock proteins (Hsps) are chaperone molecules that confer protein stability and help to restore protein native folding following heat shock and other stresses. The most abundant Hsp, Hsp90, is also involved in regulating the stability and function of a number of cell-signaling molecules. Here we report that RIP is a novel Hsp90-associated kinase and that disruption of Hsp90 function by its specific inhibitor, geldanamycin (GA), selectively causes RIP degradation and the subsequent inhibition of TNF-mediated IkappaB kinase and NF-kappaB activation. MG-132, a specific proteasome inhibitor, abrogated GA-induced degradation of RIP but failed to restore the activation of IkappaB kinase by TNF, perhaps because, in the presence of GA and MG-132, RIP accumulated in a detergent-insoluble subcellular fraction. Most importantly, the degradation of RIP sensitizes cells to TNF-induced apoptosis. These data indicate that Hsp90 plays an important role in TNF-mediated NF-kappaB activation by modulating the stability and solubility of RIP. Thus, inhibition of NF-kappaB activation by GA may be a critical component of the anti-tumor activity of this drug.

Apoptosis↗
PubMed2000

The preclinical pharmacologic study of dopamine transporter imaging agent [99mTc]TRODAT-1.

The purpose of this study was to investigate the pharmacologic characteristics of TRODAT-1 (2beta-((N,N'-bis(2-mercaptoethyl)ethylene diamino)methyl), 3beta-(4-chlorophenyl)tropane) labeled with [99mTc] as an imaging agent for dopamine transporter (DAT). Radiochemical purity of [99mTc]TRODAT-1 was over 90%. The partition coefficients in octanol and buffer were 2.12 and 2.19 at pH 7.0 and 7.4, respectively. Animal studies have been performed in rats, rabbits, and normal and hemi-Parkinsonian model monkeys. Biodistribution displayed moderate uptake in rat brain (0.28 %ID/organ at 2 min) and the striatal uptake was 0.193, 0.142, and 0.136 %ID/g at 2, 60, and 120 min, respectively. The ratios of striatal/cerebellar (ST/CB) uptake were 2.4, 4.45, and 2.45 %ID/g at 60, 120, and 240 min, respectively. The major radioactivity was excreted by the hepatobiliary system. Blood clearance kinetics was performed in rabbits, and the initial half-life of 1.18 min and late half-life of 367.8 min were obtained. Brain single photon emission computed tomography imaging studies in normal monkeys showed the ratios of ST/CB uptake were 1.56-2.0 %ID/g and indicated that both uptake and retention in the striatal area were associated with the DAT. The imaging of hemi-Parkinsonian model monkeys also displayed the expected selectivity, the highest uptake being observed in the basal ganglia area of the normal side. Thereby, it is suggested that [99mTc]TRODAT-1 is a safe and useful imaging agent for localization of the presynaptic DAT in the brain.

Animals↗
PubMed2000

Long-term phenotypic correction of rodent hemiparkinsonism by gene therapy using genetically modified myoblasts.

Rat myoblasts were genetically modified to express tyrosine hydroxylase (TH) and produce dopamine in culture. Implanting TH gene-transfected myoblasts into the denervated striatum of 6-OHDA-lesioned rats significantly decreased rotational asymmetry by 50 to approximately 60%. Improvement persisted for up to 13 months. Genetically modified cells could survive and express transgene in the striatum as demonstrated by RT-PCR and immunohistochemical stain-ing. The dopamine content in the striatum tissue of the gene therapy group recovered to 49% of the normal level and was 25-fold higher than that of a control group receiving parental cells. Neither tumor formation nor immunorejection was observed in this study. These results show that myoblasts may be useful as gene carriers for ex vivo gene therapy in the CNS. Gene Therapy (2000) 7, 445-449.

Animals↗
PubMed2000

The death domain kinase RIP is essential for TRAIL (Apo2L)-induced activation of IkappaB kinase and c-Jun N-terminal kinase.

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) (Apo2 ligand [Apo2L]) is a member of the TNF superfamily and has been shown to have selective antitumor activity. Although it is known that TRAIL (Apo2L) induces apoptosis and activates NF-kappaB and Jun N-terminal kinase (JNK) through receptors such as TRAIL-R1 (DR4) and TRAIL-R2 (DR5), the components of its signaling cascade have not been well defined. In this report, we demonstrated that the death domain kinase RIP is essential for TRAIL-induced IkappaB kinase (IKK) and JNK activation. We found that ectopic expression of the dominant negative mutant RIP, RIP(559-671), blocks TRAIL-induced IKK and JNK activation. In the RIP null fibroblasts, TRAIL failed to activate IKK and only partially activated JNK. The endogenous RIP protein was detected by immunoprecipitation in the TRAIL-R1 complex after TRAIL treatment. More importantly, we found that RIP is not involved in TRAIL-induced apoptosis. In addition, we also demonstrated that the TNF receptor-associated factor 2 (TRAF2) plays little role in TRAIL-induced IKK activation although it is required for TRAIL-mediated JNK activation. These results indicated that the death domain kinase RIP, a key factor in TNF signaling, also plays a pivotal role in TRAIL-induced IKK and JNK activation.

Animals↗
PubMed2000

[The construction and expression of two humanized scFv-urokinase fusion genes].

By using PCR and DNA recombination, two fusion genes of humanized mouse anti-human fibrin scFv and low molecular weight single chain urokinase (Scu-PA-32K) was constructed. The difference of these two fusion genes lay in the linker between two moieties, one was (Ala)3 and another was (Gly4Ser)3. These two fusion genes were both overexpressed in E. coli with the expression level at 30%. Both expression products showed the activity of binding antigen D-Dimer and activating plasminogen after the denaturation and renaturation, but under general refolding conditions, the one with linker (Gly4Ser)3 showed better effect in the renaturation of fusion protein.

Animals↗
PubMed2000

[A study of effects of head-down bed-rest simulated weightlessness on phonetic features of Chinese].

OBJECTIVE: To study the changes of phonetic features of Chinese speech during head-down bed-rest (HDBR) simulated weightlessness. METHOD: During -6 degrees HDBR in 6 healthy subjects (20-30 years), acoustic-phonetic features were analyzed. RESULT: The duration of utterance was slightly increase in the first two days, and recovered after the fourth day of HDBR; mean energy decreased along with time of bed rest, t-tests showed that the decrease in energy of utterances was very significant; a decrease in fundamental frequencies under HDBR was also significant. CONCLUSION: There were certain changes in the acoustic phonetic features under HDBR, some of them were significant.

Adult↗
PubMed2000

[The capability of IL-1 in the induction of chemokine production by murine thymic epithelial cell (MTEC1) clones].

To analyze the capability of IL-1 and IL-6 in the induction of chemokine (CF) production by mouse thymus epithelial cell (MTEC1) clones, MTEC1 cells were cloned through one cell culture and individual cell clones were established in long term culture referred to as MTEC1-DW clones. The constitutive production of IL-1, IL-6 and CF by MTEC1-DW clones was evaluated and the patterns of the cytokine production determined. Addition of exogenous IL-1 or IL-6 or both to the cultures of those MTEC1-DW clones that are unable to produce CF, and incubated for 2 days, then, to assess the chemotactic activity in the cell culture supernatants (SNs). In the opposite, addition of anti-IL-1 mAb(s) to the cultures of those MTEC1-DW clones that can produce IL-1 and CF to neutralize secreted IL-1 then, to test chemotactic activity in the SNs after 2-day incubation. The results showed that in the MTEC1-DW clones which were unable to constitutively produce IL-1 or CF, addition of IL-1 could induce these cloned cells to produce CF with high chemotactic activity. By constrast, addition of anti-IL-1 mAb(s) to those MTEC1-DW clones that constitutively produce IL-1 and CF could significantly inhibit them to produce CF. IL-6 only exhibited weak activity in the induction of CF production by those cloned cells. Therefore, in the cytokine network regulation, CF production is mainly induced by endogenously produced IL-1 in MTEC1 cells.

Animals↗
PubMed1999

Cleavage of the death domain kinase RIP by caspase-8 prompts TNF-induced apoptosis.

Although the molecular mechanisms of TNF signaling have been largely elucidated, the principle that regulates the balance of life and death is still unknown. We report here that the death domain kinase RIP, a key component of the TNF signaling complex, was cleaved by Caspase-8 in TNF-induced apoptosis. The cleavage site was mapped to the aspartic acid at position 324 of RIP. We demonstrated that the cleavage of RIP resulted in the blockage of TNF-induced NF-kappaB activation. RIPc, one of the cleavage products, enhanced interaction between TRADD and FADD/MORT1 and increased cells' sensitivity to TNF. Most importantly, the Caspase-8 resistant RIP mutants protected cells against TNF-induced apopotosis. These results suggest that cleavage of RIP is an important process in TNF-induced apoptosis. Further more, RIP cleavage was also detected in other death receptor-mediated apoptosis. Therefore, our study provides a potential mechanism to convert cells from life to death in death receptor-mediated apoptosis.

Adaptor Proteins, Signal Transducing↗
PubMed1999

Signaling by proinflammatory cytokines: oligomerization of TRAF2 and TRAF6 is sufficient for JNK and IKK activation and target gene induction via an amino-terminal effector domain.

Interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) stimulate transcription factors AP-1 and NF-kappaB through activation of the MAP kinases JNK and p38 and the IkappaB kinase (IKK), respectively. The TNF-alpha and IL-1 signals are transduced through TRAF2 and TRAF6, respectively. Overexpressed TRAF2 or TRAF6 activate JNK, p38, or IKK in the absence of extracellular stimulation. By replacing the carboxy-terminal TRAF domain of TRAF2 and TRAF6 with repeats of the immunophilin FKBP12, we demonstrate that their effector domains are composed of their amino-terminal Zn and RING fingers. Oligomerization of the TRAF2 effector domain results in specific binding to MEKK1, a protein kinase capable of JNK, p38, and IKK activation, and induction of TNF-alpha and IL-1 responsive genes. TNF-alpha also enhances the binding of native TRAF2 to MEKK1 and stimulates the kinase activity of the latter. Thus, TNF-alpha and IL-1 signaling is based on oligomerization of TRAF2 and TRAF6 leading to activation of effector kinases.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed1998

Characterization of microstructural morphology of austempered ductile iron by electron microscopy.

Mechanical properties of austempered ductile iron (ADI) are mainly controlled by its unique microstructure. The objectives of this paper are to characterize the microstructural morphology and the phase distribution of ADI using scanning electron microscopy (SEM) and transmission electron microscopy (TEM) and to determine the mechanism of strengthening and toughening of ADI. The experimental results show that, in the microstructure of ADI composing of upper bainite, retained austenite, graphitic nodule, and a small amount of martensite, the upper bainite is composed of sub-units of ferrite in the shape of "wheat ears" on which the "wheat grains" grow at an angle of about 60 degrees to the long axis of the "wheat ears." The retained austenite is connected with each other in the shape of a continuous net. The wheat-ear like bainite with a homogeneous distribution in the continuous austenite net plays an important role to the strengthening and toughening of ADI. The metastable austenite appears in the shape of a large plate in which the martensite is preferentially formed. The appearance of martensite can be suppressed at the time when retained austenite remains stable, which is of benefit to the continuity and homogeneity of austenite net.

Dental Alloys↗
PubMed1998

[30 kD MCP-1 protein produced by mouse thymic epithelial cell line MTEC1].

A medullary type mouse thymic epithelial cell line MTEC1 can produce chemokines. Crude culture supernant of MTEC1 cells was concentrated by controlled-pore glass beads. One of these chemotactic proteins was isolated from MTEC1 supernatant and purified to homogeneity by heparin-Sepharose affinity chromatography, cation-exchange FPLC and Reverse Phase-HPLC. The chemotactic factor for both lymphocytes and monocytes was identified as a 30 kD protein by SDS-PAGE analysis under reducing conditions. After cleavage of the NH2-terminally blocked protein with formic acid, the amino acid sequence of the internal fragment was analyzed and found to be identical to the amino acid sequence of mouse MCP-1/JE. The protein was hence identified as a glycosylated MCP-1/JE-like chemokine secreted by thymic epithelial cells. The characterization of chemokines produced by thymic stromal cells will benefit the analysis of the mechanism of thymus homing and the finding of new chemokines.

Amino Acid Sequence↗
PubMed1997

[Multiple types of cytokines secreted by a mouse fetal liver stromal cell line].

A murine fetal liver stromal cell line, called MFLC, has been established and maintained in DME supplemented with 10%NCS for 2 years. Without exogenous stimulation, the MFLC cells spontaneously secreted several types of cytokines, including IL-6, GM-CSF and chemotactic factor. Of which, IL-6 and chemotactic factor were abundant, GM-CSF at low level. Biological activities of IL-7 and IL-3 were not detected in the MFLC cell's supernatants. MFLC-SN induced colony formation of murine bone marrow cells in a dose dependent fashion in which mixed granulocyte/macrophage/megakaryocyte colonies(CFU-GMM) and granulocyte/macrophage colonies(CFU-GM) were dominant. MFLC-SN also sustained colony formation of bone marrow cells taken from 5-Fu injected mice, suggesting that there was a biological activity similar to SCF in MFLC-SN. The cytokines secreted by MFLC might play an important role in T cell early development in fetal liver. These results will be useful for us to analyse the mechanism of T cell development in fetal liver and to study the cytokine network regulation.

Animals↗