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L J Guo

Publications and source records attributed to L J Guo.

14 recordsLinked to original sources
PubMed2002

Coherent electron transport in a Si quantum dot dimer.

We show that the coherence of charge transfer through a weakly coupled double-dot dimer can be determined by analyzing the statistics of the conductance pattern, and does not require a large phase coherence length in the host material. We present an experimental study of the charge transport through a small Si nanostructure, which contains two quantum dots. The transport through the dimer is shown to be coherent. At the same time, one of the dots is strongly coupled to the leads, and the overall transport is dominated by inelastic cotunneling processes.

Journal Article↗
PubMed2001

Magnetically induced reconstruction of the ground state in a few-electron Si quantum dot.

We report unexpected fluctuations in the positions of Coulomb blockade peaks at high magnetic fields in a small Si quantum dot. The fluctuations have a distinctive sawtooth pattern: as a function of magnetic field, linear shifts of peak positions are compensated by abrupt jumps in the opposite direction. The linear shifts have large slopes, suggesting formation of the ground state with a nonzero angular momentum. The value of the momentum is found to be well defined, despite the absence of the rotational symmetry in the dot.

Journal Article↗
PubMed2001

Effect of phenolic alkaloids from Menispermum dauricum on myocardial-cerebral ischemia-reperfusion injury in rabbits.

AIM: To explore the mechanism underlying the effect of phenolic alkaloids from Menispermum dauricum (PAMd) on simultaneous myocardial-cerebral ischemia-reperfusion injury in rabbits. METHODS: Both left anterior descending coronary artery and bilateral carotid arteries were occluded to induce myocardial-cerebral ischemia-reperfusion injury in rabbits. At 30 min after ischemia, the occlusion was removed and shed blood was rapidly reinfused. Two mL of blood was taken fr om femoral artery at 10 min before ischemia, 1, 10, and 30 min after ischemia, and 1, 10, 30, 60, 120, 180, and 240 min after reperfusion. Each rabbit was sacrificed at the end of reperfusion, and left ventricle, hippocampus, cortex, and cerebellum were taken out. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. RESULTS: At 10 min after reperfusion, MDA content in serum was significantly higher and SOD activity was lower in ischemia-reperfusion (I-R) group than those of control group (P < 0.05). After administration of PAMd, MDA content was lower and SOD activity was higher in serum than those of I-R group (P < 0.05). Both MDA content and SOD activity in tissues had the similar results with those in serum. CONCLUSION: PAMd could attenuate the injury induced by lipid peroxidation and enhance the activity of SOD, thus PAMd might play a protective role in simultaneous myocardial-cerebral ischemia-reperfusion injury.

Alkaloids↗
PubMed1996

No subacute thrombosis and femoral bleeding complications under full anticoagulation in 150 consecutive patients receiving non-heparin-coated intracoronary Palmaz-Schatz stents.

Intracoronary stenting has been shown to have better immediate and long-term clinical outcomes and less restenosis than standard balloon angioplasty. However, the benefit was achieved at the cost of higher rates of coronary thrombosis, bleeding complications, the need for anticoagulation, and longer hospital stay. For the latter reasons there is a tendency to replace the anticoagulants by antiplatelet agents alone after stenting. However, we prospectively monitored 150 consecutive patients (133 men, 17 women, mean age 58.5 years) from two centers since February 1993. They all had coronary artery disease and underwent percutaneous implantation of non-heparin-coated Palmaz-Schatz coronary stents under a full but lower dose of anticoagulation. The femoral approach was used in all patients except one. In the 150 patients, 200 stents were implanted in 165 target arteries with 172 lesions. Stenting was performed without the guidance of intravascular ultrasonography; high-pressure poststenting inflation was used in only 17.3% of patients with less than optimal angiographic results. Coronary angiography was performed at baseline, immediately after the procedure, and after 6 months (mean 207 +/- 53.6 days SD) of stenting. The mean (+/-SD) coronary minimum luminal diameter increased from 0.52 0.31 mm to 3.13 +/- 0.42 mm immediately after stenting was performed and was 2.12 +/- 0.91 mm at 6 months. There was a 0% subacute thrombosis rate and a 0% femoral bleeding complication rate in the whole series. Only three (2%) major events occurred: one Q-wave myocardial infarction from closure of an angioplasty site distal to the stent on a very long lesion, one cerebrovascular accident, and one noncoronary-related death. The only patient who underwent the brachial approach had hematoma; otherwise no other minor event occurred. The mean hospital stay was 4.5 days in one of the two study centers. The long-term clinical follow-up rate was 97.3%. The mean (+/- SD) clinical follow-up period was 589 +/- 363 days. Clinical symptoms improved; the percentage of patients who had angina according to the Canadian Cardiovascular Society functional class II, III, and IV was 31.3%, 44.7%, and 4%, respectively, before stenting was performed and was reduced to 4.7%, 3.7%, and 0%, respectively at 6-month follow-up after stenting was performed. The 6-month angiographic restudy rate was 90.6%, and the restenosis rate was 18.3%. In contrast to other reported series, these results support the idea that with careful puncture technique and meticulous postoperative wound care, intracoronary stenting can be successfully performed with the patient under full anticoagulation without major risks of bleeding and femoral vascular complications. Furthermore with a full but comparatively lower dose of anticoagulation, subacute thrombotic complications can be reduced to 0% even with non-heparin-coated stents without the use of intravascular ultrasound guidance and without the use of adjunctive high-pressure poststenting inflation in most patients. The restenosis rate and long-term clinical outcomes remained very favorable.

Acute Disease↗
PubMed1996

[A study on the change of myocardial neuropeptide Y release induced by electric stimulation and myocardial ischemia in guinea pig heart].

Electrical stimulation of the left stellate ganglion in guinea pig heart evoked a calcium-dependent, exocytotic release of neuropeptide Y (NPY). Stimulation after 10 min of global ischemia (S2), compared with control period stimulation (S1), had no significant effect on the NPY release. The release of NPY produced by the same stimulation after 20 min of ischemia was inhibited to certain extent (S2/S1: 0.72, P < 0.05), whereas the inhibition of NPY release disappeared after 5 min of reperfusion (with a S2/S1 of 1.01). Ischemia alone, without electric stimulation, did not apparently induce NPY release, suggesting that electrical stimulation may induce a calcium-dependent, exocytotic release of NPY. It is further suggested that the inhibition of NPY release may be produced by some metabolites and the abolishment of the inhibition after reperfusion may be due to washout of the metabolites.

Animals↗
PubMed1995

Serotonin outflow in the hypothalamus of conscious rats: origin and possible involvement in cardiovascular control.

The push-pull technique was used to investigate the effects of neuroactive compounds and experimentally induced blood pressure changes on the release of endogenous serotonin in the posterior hypothalamic area of the rat. Hypothalamic superfusion with artificial cerebrospinal fluid which contained 80 mM K+ or 1 microM veratridine enhanced the rate of serotonin release. Superfusion with tetrodotoxin (5 microM) led to a pronounced decrease in the serotonin release rate. Increases in blood pressure elicited by intravenous infusions of noradrenaline (3-4 micro g/kg/min) or phenylephrine (10 microg/kg/min) enhanced the release of serotonin in the hypothalamus. Similarly, the serotonin release rate was enhanced by hypervolaemia. Decreases in blood pressure elicited by intravenous administration of nitroprusside (30-40 microg/kg/min) or chlorisondamine (3 mg/kg) reduced the release of serotonin. Likewise, the serotonin release rate was decreased by hypovolaemia. With one exception (hypothalamic superfusion with tetrodotoxin) neither neuroactive drugs, nor experimentally elicited blood pressure changes modified the release rate of the metabolite 5-hydroxyindoleacetic acid (5-HIAA). These findings show that changes in blood pressure lead to counteractive alterations in the release of serotonin. Thus, serotoninergic neurons of the posterior hypothalamus seem to be involved in the homeostasis of blood pressure by exerting a hypotensive function. At least in the hypothalamus, the concentration of 5-HIAA in the superfusate does not seem to be a reliable marker for the activity of serotoninergic neurons.

Animals↗
PubMed1995

Ionic and haemodynamic changes influence the release of the excitatory amino acid glutamate in the posterior hypothalamus.

The push-pull technique was used to investigate the release of the excitatory amino acid glutamate in the posterior hypothalamic area of the conscious rat. The hypothalamus was superfused through the push-pull cannula with artificial cerebrospinal fluid (CSF), and the superfusate was collected in time periods of 10 min when ionic conditions in the CSF were changed, or in short periods of 3 min when blood pressure changes were evoked. The mean glutamate release rate was 2.8 +/- 0.7 pmol/min. Depolarization by hypothalamic superfusion with CSF containing 50 mM K+ enhanced the release of glutamate in the presence of Ca2+. The K(+)-induced release was attenuated by 40% when the hypothalamus was superfused with Ca(2+)-free CSF. Replacement of Ca2+ by Mg2+ abolished the K(+)-induced release of glutamate. Hypovolaemia elicited by haemorrhage enhanced the release rate of glutamate. Similarly, a hypotension elicited by i.v. injection of chlorisondamine (3 mg/kg) led to a pronounced and permanent enhancement in glutamate release. The effects of hypovolaemia and chlorisondamine on glutamate release were abolished in aortic denervated rats, indicating that this response is due to a decrease of impulse generation in baroreceptors. A hypervolaemia elicited by blood infusion did not affect the release of glutamate. Similarly, a pronounced pressor response to phenylephrine (15 micrograms/kg per minute) infused intravenously for 9 min was ineffective. The results show that the K(+)-induced release of glutamate in the hypothalamus is dependent on the presence of Ca2+. The increase in glutamate release rate by hypovolaemia or chlorisondamine suggests that the glutamatergic neurons in the posterior hypothalamic area respond to unloading of aortic baroreceptors and possess a counteracting, hypertensive function.

Animals↗
PubMed1995

[Effects of gamma-aminobutyric acid on isolated dog cerebral arteries].

The present experiments were designed to investigate the effects of gamma-aminobutyric acid (GABA) on isolated dog cerebral arteries (basilar artery). On addition of agonists phenylephrine 10 mumol.L-1, 5-HT 10 mumol.L-1, or KCl 25 mmol.L-1, the isometric tension of the contraction increased 0.51 +/- 0.18 g, 0.33 +/- 0.12 g and 0.57 +/- 0.16 g. After GABA at 50 mumol.L-1, the contraction was shown to decrease 0.27 +/- 0.15 g, 0.19 +/- 0.07 g and 0.17 +/- 0.06 g, the maximal relaxation were 45.49% +/- 20.4%, 58.60% +/- 12.96% and 27.75% +/- 15.78%, respectively. But it showed no effect on the contraction induced by high concentration of KCl (45 mmol.L-1). GABA also showed a potent relaxation on the contraction induced by cold Krebs solution (T 28 +/- 0.5 degrees C). The finding suggest that GABA can inhibit the muscle tone induced by various agonists and cooling in isolated dog basilar artery.

Animals↗
PubMed1995

Effects of hemodynamic changes on taurine release from posterior hypothalamus of freely moving rats.

AIM: To study the effects of blood volume and vascular resistance on taurine release. METHODS: We used push-pull superfusion technique in the posterior hypothalamus of conscious freely moving rats. Taurine was determined in the superfusate by HPLC with fluorescence detection following automatic precolumn o-phthaldialdehyde (OPA) derivatization. RESULTS: Hypervolemia increased the release of taurine in the hypothalamus. Intravenous infusion of levarterenol (3 micrograms kg-1 min-1) elicited a pronounced pressor response and an increase in the release of taurine. Conversely, a controlled hemorrhagic hypotension or iv infusion of nitroprusside (30 micrograms kg-1 min-1) elicited a hypotension and a decrease in the release of taurine from the posterior hypothalamus. CONCLUSION: In the posterior hypothalamus, taurine might play an important role in central blood pressure regulation.

Animals↗
PubMed1994

[Effects of arterial blood pressure change on release of GABA in the posterior hypothalamus conscious of freely moving rats].

Push-pull superfusion technique was used to investigate the release of endogenous gamma-aminobutyric acid (GABA) in the posterior hypothalamus of the conscious, freely moving rat in response to peripherally applied drugs or experimentally induced blood pressure changes. The rise in blood pressure elicited by intravenous infusion of phenylephrine (15 micrograms.kg-1.min-1) or blood (3 ml/100 g) was associated with an increased rate of GABA release in the posterior hypothalamus. Hypotension produced by nitroprusside (30 micrograms.kg-1.min-1), chlorisondamine (3 mg.kg-1,iv) and controlled bleeding (3 ml/100 g) led to a counteracting decrease in hypothalamic GABA outflow. This finding suggests that GABAergic neurons of the conscious, freely moving rat in the posterior hypothalamus are involved in cardiovascular control and possess a hypotensive function.

Animals↗
PubMed1993

Taurine release in the hypothalamus is altered by blood pressure changes and neuroactive drugs.

The release of endogenous taurine was determined in the posterior hypothalamus of the conscious, freely moving rat by using the push-pull superfusion technique. At the start of superfusion, the outflow of endogenous taurine declined rapidly with a half-time of 7.9 min and reached a steady state after approximately 1 h. Thereafter, the release rate was constant and amounted to 2.6 +/- 0.3 pmol/min. During depolarization either with K+ (50 or 90 mM) or veratridine (1 or 10 microM), taurine outflow was increased in a concentration-dependent way. Hypothalamic superfusion with tetrodotoxin (1 microM) elicited a sustained decrease in the taurine release to 60% of the control values. Intravenous infusion of noradrenaline led to a rise in blood pressure (45 mm Hg) and enhanced the release of taurine in the hypothalamus. A fall of blood pressure (30 mm Hg) caused by an intravenous infusion of nitroprusside diminished taurine outflow. The results suggest that a considerable amount of the taurine detected is released from hypothalamic neurons. Changes in the release rate of taurine by experimentally induced alterations of blood pressure indicate that, in the posterior hypothalamus, the amino acid might play an important role as a neurotransmitter or neuromodulator possessing a hypotensive function.

Animals↗