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Biomedical subjects

P Sheng

Publications and source records attributed to P Sheng.

At least 19 recordsLinked to original sources
PubMed2000

Locally resonant sonic materials

We have fabricated sonic crystals, based on the idea of localized resonant structures, that exhibit spectral gaps with a lattice constant two orders of magnitude smaller than the relevant wavelength. Disordered composites made from such localized resonant structures behave as a material with effective negative elastic constants and a total wave reflector within certain tunable sonic frequency ranges. A 2-centimeter slab of this composite material is shown to break the conventional mass-density law of sound transmission by one or more orders of magnitude at 400 hertz.

Journal Article↗
PubMed2000

Robust photonic band gap from tunable scatterers

We show theoretically and experimentally that photonic band gaps can be realized using metal or metal-coated spheres as building blocks. Robust photonic gaps exist in any periodic structure built from such spheres when the filling ratio of the spheres exceeds a threshold. The frequency and the size of the gaps depend on the local order rather than on the symmetry or the global long range order. Good agreement between theory and experiment is obtained in the microwave regime. Calculations show that the approach can be scaled up to optical frequencies even in the presence of absorption.

Journal Article↗
PubMed1997

An ATP-gated cation channel with some P2Z-like characteristics in gastric smooth muscle cells of toad.

1. Whole-cell and single-channel currents elicited by extracellular ATP were studied in freshly dissociated smooth muscle cells from the stomach of the toad Bufo marinus using standard patch clamp and microfluorimetric techniques. 2. This ATP-gated cation channel shares a number of pharmacological and functional properties with native rat myometrium receptors, certain native P2Z purinoceptors and the recently cloned P2X7 purinoceptor. But, unlike the last two, the ATP-gated channel does not mediate the formation of large non-specific pores. Thus, it may represent a novel member of the P2X or P2Z class. 3. Extracellular application of ATP (> or = 150 microM) elicited an inward whole-cell current at negative holding potentials that was inwardly rectifying and showed no sign of desensitization. Na+, Cs+ and, to a lesser degree, the organic cation choline served as charge carriers, but Cl- did not. Ratiometric fura-2 measurements indicated that the current is carried in part by Ca2+. The EC50 for ATP was 700 microM in solutions with a low divalent cation concentration. 4. ATP (> or = 100 microM) at the extracellular surface of cell-attached or excised patches elicited inwardly rectifying single-channel currents with a 22 pS conductance. Cl- did not serve as a charge carrier but both Na+ and Cs+ did, as did choline to a lesser extent. The mean open time of the channel was quite long, with a range in hundreds of milliseconds at a holding potential of -70 mV. 5. Mg2+ and Ca2+ decreased the magnitude of the ATP-induced whole-cell currents. Mg2+ decreased both the amplitude and the activity of ATP-activated single-channel currents. 6. ADP, UTP, P1, P5-di-adenosine pentaphosphate (AP5A), adenosine and alpha, beta-methylene ATP (alpha, beta-Me-ATP) did not induce significant whole-cell current. ATP-gamma-S and 2-methylthio ATP (2-Me-S-ATP) were significantly less effective than ATP in inducing whole-cell currents, whereas benzoylbenzoyl ATP (BzATP) was more effective. BzATP, alpha, beta-Me-ATP, ATP-gamma-S and 2-Me-S-ATP induced single-channel currents, but a higher concentration of alpha, beta-Me-ATP was required. 7. BzATP did not induce the formation of large non-specific pores, as assayed using mag-fura-2 as a high molecular mass probe.

Adenosine Triphosphate↗
PubMed1997

[Via the submandible: cervical glossopharyngeal neurectomy and histomorphology findings].

Three cases of serious idiopathic glossopharyngeal neuralgia are reported. They were treated with cervical glossopharyngeal neurectomy via the submandible. The resected nerve tissue was detected under light and microscope. The pathological change was found in the form of myelinoclasis. The present article is intended to introduce a method via the submandible, comparing the intracranial and extracranial approach. We think the procedure via the submandible is a method more safe, simple and therefore, worthy to be recommended.

Female↗
PubMed1996

Nitric oxide is a mediator of methamphetamine (METH)-induced neurotoxicity. In vitro evidence from primary cultures of mesencephalic cells.

METH is a monoaminergic toxic that destroys dopamine terminals in vivo. Oxidative mechanisms associated with DA metabolism are thought to play an important role in its toxic effects. These ideas were supported by the demonstration that CuZn-superoxide dismutase (CuZnSOD) transgenic mice were protected against the toxic effects of the drug. In the present study, we sought to determine if nitric oxide (NO) production was also involved in METH-induced neurotoxicity using primary cultures obtained from fetal rat mesencephalon. METH caused dose- and time-dependent cell death in vitro. Blockade of nitric oxide (NO) formation with several nitric oxide (NO) synthase blockers attenuated METH-mediated toxicity. Moreover, inhibition of ADP-ribosylation with nicotinamide and benzamide also provided protection against the toxicity of the drug. These results, together with our previous results in transgenic mice, support a role for free radicals in METH-induced toxic effects.

Animals↗
PubMed1996

Retrovirus-mediated transfer of the human O6-methylguanine-DNA methyltransferase gene into a murine hematopoietic stem cell line and resistance to the toxic effects of certain alkylating agents.

O6-Methylguanine-DNA methyltransferase (MGMT) is an important DNA repair protein that plays a key role in cancer chemotherapy by alkylating agents such as carmustine (BCNU) and Dacarbazine (DTIC). Therapy by BCNU and DTIC is reduced by dose-limiting hematological toxicity as a result of low MGMT repair activity in bone marrow cells. In this study, we have constructed a Moloney murine leukemia virus retroviral vector containing the human mgmt gene. High-titer retrovirus producer cells lines have been generated. Retroviral-mediated transfer of the human mgmt gene into murine multi-potent hematopoietic stem cells, FDCP-1, resulted in the expression of a high level of MGMT activity. In comparison with the control cells that were transduced with the parent vector, the MGMT-expressing clones were considerably more resistant to the cytotoxicity of the methylating agents, such as N-methyl-N'-nitro-N-nitrosoguanidine, N-nitroso-N-methyl-urea, and temozolomide, as well as the chloroethylating agents 1-(2-chloroethyl)-1-nitrosourea and BCNU. The protection provided by MGMT could be eliminated by the MGMT inactivator O6-benzylguanine. Thus, the principal lethal lesions produced by these alkylating agents in the murine hematopoietic stem cells and the MGMT deficiency in these cells can be complemented by retroviral-mediated gene transduction.

3T3 Cells↗
PubMed1996

AP-1 DNA-binding activation by methamphetamine involves oxidative stress.

Methamphetamine (METH) caused dose-dependent increases in AP-1 DNA-binding activity in both nontransgenic (Non-Tg) and CuZn-SOD transgenic (SOD-Tg) mice. However, the increases in SOD-Tg mice were less prominent than those observed in Non-Tg animals. The time-course of METH-induced AP-1 changes was similar in both strains of mice. AP-1 binding activity showed an initial increase at 1 h, peaked at 3 h, and then gradually declined. AP-1 binding activity was back to normal by the 72-h time point. Regional analyses of METH effects revealed increases in the caudate putamen and cerebellum, with the striatum showing relatively higher METH-induced AP-1 DNA-binding activation. These regional effects were also attenuated in the SOD-Tg mice. These data indicate that METH-induced stimulation of AP-1 DNA-binding depends on cellular redox status. These results are consistent with in vitro studies that have reported that several transcription factors are regulated through redox mechanisms.

Animals↗
PubMed1996

Methamphetamine-induced neurotoxicity is associated with increased striatal AP-1 DNA-binding activity in mice.

Multiple injections of methamphetamine (METH) produce long-lasting neurotoxic effects on the nigrostriatal dopamine (DA) system. The drug also causes increases in AP-1 DNA-binding activity in mice. In the present study, we tested the idea that toxic doses of METH might cause long-term increases in AP-1 DNA-binding. Mice were given 10 mg/kg of METH 2, 3 or 4 times at a 2 h interval in 1 day. Striatal DA levels were markedly decreased at 3 h and 24 h in all injection groups. After 1 week, striatal DA level recovered to near control in the METH x2 group, but were still significantly decreased in the METH x3 and x4 groups. Similar drug administration schedules caused increases in AP-1 DNA-binding activity at the 3 h time point in all groups. The AP-1-binding activity almost returned back to control level in the x2 and x3 injection groups at the 24 h and 1 week time point, but there were still increased levels of AP-1-binding activity in the METH x4 group. These findings raise the possibility that METH-induced neurotoxicity might involve prolonged activation of AP-1 transcription factor. This might be related to the report that c-fos or c-jun activation may be important in some models of neurodegeneration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Environmental radiation real-time monitoring system permanently installed near Qinshan Nuclear Power Plant.

An environmental radiation real-time monitoring system with high pressure ionization chamber was developed. It has been installed permanently in the vicinity of Qinshan Nuclear Power Plant, the first built in mainland China. The system consists of four basic components: environmental radiation monitors; data communication network; a data processing center; and a remote terminal computer situated in Hangzhou. It has provided five million readings of environmental radiation levels as of January 1993.

Air Pollutants, Radioactive↗
PubMed1995

Involvement of oxidative and L-arginine-NO pathways in the neurotoxicity of drugs of abuse in vitro.

1. Inhibitors of nitric oxide (NO) formation or ADP-ribosylation attenuate methamphetamine (METH)- and methylenedioxymetamphetamine (MDMA)-induced neurotoxicity on dopaminergic and serotonergic cells in primary cultures. 2. They also prevent METH-induced reactive gliosis in dopaminergic cultures. 3. Overexpression of superoxide dismutase (SOD) in cells obtained from SOD-transgenic mice also attenuates drug-induced toxicity. 4. These data indicate a role for oxygen-based and NO free radicals in the mechanisms of cell death associated with drugs of abuse in vitro.

Adenosine Diphosphate Ribose↗
PubMed1994

Methamphetamine (METH) causes reactive gliosis in vitro: attenuation by the ADP-ribosylation (ADPR) inhibitor, benzamide.

We examined the effects of methamphetamine (METH) in an in vitro model of rat fetal mesencephalic cells. METH causes loss of dopamine (DA) cells and neuronal process degeneration. In addition, the drug causes an increase in reactive gliosis as shown by the number of cells that stain for and by the intensity of staining with a glial fibrillary acidic protein (GFAP) antibody. Co-incubation of METH-treated cells with benzamide, which is a known inhibitor of ADP-ribosylation (ADPR), attenuated METH effects on both DA and glial cells. However, the effects of benzamide were somewhat more prominent on the glial cells. These results suggest that ADP-ribosylation may play a very important role in the development of reactive gliosis after the administration of neurotoxic agents.

Adenosine Diphosphate Ribose↗
PubMed1994

Attenuation of methamphetamine-induced neurotoxicity in copper/zinc superoxide dismutase transgenic mice.

Administration of methamphetamine (METH) to rats and nonhuman primates causes loss of terminals in the nigrostriatal dopaminergic system. The mechanism by which METH causes its neurotoxicity is not known. To evaluate further the role of oxyradicals in METH-induced neurotoxicity, we have tested its effects in CuZn superoxide dismutase (SOD) transgenic (Tg) mice, which express the human CuZnSOD gene. In non-Tg mice, acute METH administration causes significant decreases in levels of dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the striata and cortices of non-Tg mice. In contrast, there were no significant decreases in cortical or striatal DA in the SOD-Tg mice. The effects of METH on DOPAC were also attenuated in both structures of these SOD-Tg mice. Chronic METH administration caused decreases in levels of striatal DA and DOPAC in the non-Tg mice, whereas the SOD-Tg mice were not affected. These results suggest that METH-induced dopaminergic toxicity in mice may be secondary to increased production of reactive oxygen species such as the superoxide radical.

3,4-Dihydroxyphenylacetic Acid↗