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Q Si

Publications and source records attributed to Q Si.

At least 19 recordsLinked to original sources
PubMed2001

Locally critical quantum phase transitions in strongly correlated metals.

When a metal undergoes a continuous quantum phase transition, non-Fermi-liquid behaviour arises near the critical point. All the low-energy degrees of freedom induced by quantum criticality are usually assumed to be spatially extended, corresponding to long-wavelength fluctuations of the order parameter. But this picture has been contradicted by the results of recent experiments on a prototype system: heavy fermion metals at a zero-temperature magnetic transition. In particular, neutron scattering from CeCu6-x Aux has revealed anomalous dynamics at atomic length scales, leading to much debate as to the fate of the local moments in the quantum-critical regime. Here we report our theoretical finding of a locally critical quantum phase transition in a model of heavy fermions. The dynamics at the critical point are in agreement with experiment. We propose local criticality to be a phenomenon of general relevance to strongly correlated metals.

Journal Article↗
PubMed2001

Differential regulation of microglial NO production by protein kinase C inhibitors.

Nitric oxide (NO) produced by microglia has been implicated in the pathogenesis of various central nervous system diseases; however, the intracellular signal pathways for the production of NO are not well known. Protein kinase C (PKC) plays a key role in a variety of signal transduction processes. To elucidate how PKC regulates microglial NO production, we examined the effects of PKC inhibitors on lipopolysaccharide (LPS)-stimulated NO production by primary cultured rat microglia. Staurosporine, a non-selective PKC inhibitor, increased LPS-induced production of NO at 0.1-10 nM range of concentration. Protein kinase A (PKA) inhibitor, H89, did not affect LPS-induced NO production, suggesting that staurosporine effect is not mediated by inhibition of PKA. However, other two PKC inhibitors, whose specificities for PKC isoforms were different, Gö6976 and Ro-32-0432, exhibited different effects on NO production from staurosporine; the former inhibited and the latter showed no effect. Interestingly, an activator of PKC, phorbol 12-myristate 13-acetate (PMA) also increased LPS-induced production of NO at 1-10 nM range of concentration, suggesting that prolonged incubation with PMA caused down-regulation of PKC. These results indicate that the inhibition or down-regulation of some PKC isoforms causes the enhancement of NO production. The different effects of PKC inhibitors on the NO production suggest that the different PKC isoforms play different roles in regulation of NO production in microglia.

Animals↗
PubMed2000

A serum factor enhances production of nitric oxide and tumor necrosis factor-alpha from cultured microglia.

The pathological activation of microglia has been implicated in ischemic neuronal damage and some neurodegenerative diseases; however, the mechanism of microglial activation is not well understood. Previously, we showed that a serum factor, albumin, increased O(2)(-) production by cultured microglia (Si et al., 1997, Glia 21: 413-418). In the present study, we found that serum also enhanced lipopolysaccharide (LPS)-induced production of nitric oxide and tumor necrosis factor-alpha, which are other important neurotoxins released by activated microglia. In the presence of 0.1% normal rat serum, the half-effective concentration for LPS decreased from 300 to 1 ng/ml. The factor seemed to be a relatively high-molecular-weight protein because the factor was retained after a molecular sieve (50 kDa) membrane separation. The factor was labile to trypsinization and heat treatment at 72 degrees C for 5 min but was stable at 56 degrees C for 60 min. Several purified serum proteins including albumin could not mimic the enhancing effect of serum. Acute-phase serum showed a potent enhancing effect at a 10 times lower concentration than the normal serum. By gel filtration chromatography, the enhancing effect observed was a single peak at about 60 kDa. These results suggest that some serum protein infiltrates into brain parenchyma after blood-brain barrier disruption and such protein may result in neuronal damage by activating microglia to release neurotoxins in some central nervous system diseases.

Animals↗
PubMed1998

Differential regulation of microglial activation by propentofylline via cAMP signaling.

A pathological microglial activation is believed to contribute to progressive neuronal damage in neurodegenerative diseases by the release of potentially toxic agents and by triggering reactive astrocytic changes. Using cultured microglia from neonatal rat brains, we investigated the mode of propentofylline action in strengthening cAMP-dependent intracellular signaling. We compared this action with the effects of dibutyryl-cAMP, a cell-permeable cAMP analog. Propentofylline inhibited lipopolysaccharide (LPS)-induced release of both tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta in a dose-dependent manner within the therapeutic low micromolar range. However, LPS-induced release of IL-6 and NO were not affected by propentofylline. All these differential effects of propentofylline on LPS-induced microglial release were mimicked by the addition of dibutyryl-cAMP. Microglial proliferation and phorbol myristate acetate (PMA)-induced O2- release were also dose-dependently inhibited by propentofylline as well as dibutyryl-cAMP. These results suggest that propentofylline, probably via reinforcement of cAMP intracellular signaling, alters the profile of the newly adopted immune properties in a way that it inhibits potentially neurotoxic functions while maintaining beneficial functions. This differential regulation of microglial activation may explain the neuroprotective mechanism exerted by propentofylline.

Animals↗
PubMed1995

Effect of colchicine on hepatic glycosaminoglycan metabolism in mice infected with Schistosoma japonicum.

AIM: To study the effect of colchicine on hepatic glycosaminoglycan (GAG) metabolism in mice infected with Schistosoma japonicum. METHODS: The amount of GAG was measured in the liver of mice infected with Schistosoma japonicum for 6-16 wk and treated with colchicine. RESULTS: Six weeks after infection, the GAG content of infected mice's livers and uninfected control was 14 +/- 2 micrograms/g liver and 4 +/- 1 microgram/g liver, respectively. The GAG content reached a peak about 6 times of the normal level in the 10th wk after infection, being 56 +/- 9 micrograms/g and 10 +/- 1 microgram/g for infected and uninfected mice respectively, and then declined. Treatment of infected mice with colchicine reduced the total GAG content to 22 +/- 3 micrograms/g liver, but not suppress the GAG content below the normal level in the 10th wk. Microscopic hepatic egg granuloma. CONCLUSION: Colchicine may exerts its GAG reduction effect through the suppression of granuloma formation.

Animals↗
PubMed1994

Role of collagen metabolism changes in the pathogenesis of pulmonary hypertension in rats and its reversibility.

Pulmonary arterial pressure (PAP) was increased obviously in rats after 3 days of normobaric hypoxic exposure and reached a maximum at 14 days of hypoxia. It remained at the same level during prolonged hypoxic exposure of up to 21 days. Right ventricular weight (RV/LV+S) and hydroxyproline (HP) content in the pulmonary artery began to increase at day 7. HP content had increased much faster than the relative rate of increase of PAP after 14 days, but HP content in the thoracic aorta showed no change. The relative proportion of type I to III collagen increased significantly, and compliance of the pulmonary vessels obviously decreased. All parameters returned to the normal range within 14 days after recovery from hypoxia, except for HP content as expressed per vessel. 764-3 treatment obviously attenuated most of the changes caused by hypoxia, though it had no effect on compliance of the pulmonary vessels. It is suggested that collagen, especially type I collagen, accumulation may play an important role in maintaining pulmonary hypertension. 764-3 has certain protective effects and may be useful in the treatment of early chronic obstructive pulmonary disease.

Animals↗
PubMed1993

Hemodynamic and nonhemodynamic mechanism of experimental pulmonary edema in rats and the effect of anisodamine and tetramethylpyrazine--electron microscopic observation and measurement of pulmonary arterial, pulmonary arterial wedge and systemic arterial pressure (Part 2).

The pulmonary edema (PE) induced by adrenaline (AD) administration is similar to neurogenic PE. Anisodamine (ADM, 654-2, 30 mg/kg) and tetramethylpyrazine (TMP, 120 mg/kg) have shown significant preventive effects. Electron microscopic observation was carried out to study the changes of microvascular permeability, and the dynamic change of mean pulmonary arterial pressure (PAP, 40 rats), mean pulmonary arterial wedge pressure (PAWP, 20 rats) and mean carotid arterial pressure (CAP) were also measured. The results suggested that both ADM and TMP have significant inhibitory effects on PAWP and CAP increase, as well as on the damage responsible for the increase of microvascular and alveolar permeability.

Adrenergic alpha-Agonists↗
PubMed1993

Hemodynamic and nonhemodynamic mechanisms of experimental pulmonary edema in rats and the effect of anisodamine and tetramethylpyrazine. Part 1: Survival rate, pulmonary index, pathological change and pulmonary vascular permeability.

Pulmonary edema (PE) which is similar to the neurogenic type was induced by adrenaline (AD) administration (0.1 mg/kg) in rats. Acute progressive respiratory distress, cyanosis and dyspnea occurred. All the experimental animals in the PE group died within 20 min after AD injection, with a pulmonary index (PI) of 1.70 +/- 0.47 (mean +/- S) which was much higher than that in the normal group. The mortality rate was 100%. It was found that in rats with PE, a protein-rich fluid filled the alveolar and interstitial spaces, and ecchymosis occurred. The capillary permeability as estimated by Evans blue injection showed that Evans blue from extraction fluid and bronchoalveolar lavage (BAL) in the PE rats was at a much higher level than that in the normal control (NC) rats. In anisodamine (ADM, 654-2) and tetramethylpyrazine (TMP) treated rats, almost all the damage was diminished or absent, and the mortality rates were decreased from 100% to 4.4% and 20%, respectively. 654-2 and TMP could significantly inhibit the increase of pulmonary permeability.

Animals↗