Biomedical subjects

Lei Yao

Publications and source records attributed to Lei Yao.

23 records · Page 2Linked to original sources

PubMed2003

[Electroacupuncture of 2 Hz induces long-term depression of synaptic transmission in the spinal dorsal horn in rats with neuropathic pain].

OBJECTIVE: To observe the effect of 2 Hz electroacupuncture (EA) on long-term depression (LTD) of synaptic transmission in the spinal dorsal horn in rats with neuropathic pain, so as to explore the central mechanisms of the antinociceptive effects of 2 Hz electroacupuncture on neuropathic pain. METHODS: The neuropathic pain models were produced by tight ligation of the L5/L6 spinal nerves in Sprague-Dawley rats. The C-fiber-evoked field potentials in the spinal dorsal horn were recorded with extracellular recording techniques. The parameters of the electroacupuncture were as follows: frequency of 2 Hz, wavelength of 0.6 ms, intensity of 1, 2, 3 mA lasting 10 min for each intensity, stimulation time of 30 min. The positive stimulating electrode was placed in acupoint "sanyinjiao" and the negative electrode in "zusanli". RESULTS: (1) 2 Hz electroacupuncture significantly decreased the amplitudes of C-fiber-evoked field potentials in the spinal dorsal horn in rats with neuropathic pain to (49.4 +/- 0.6)% of the control, compared with that (100.1 +/- 1.2)% of the control before EA (unpaired t test, P < 0.001, n = 6), which lasted for at least 3 hours. (2) This EA suppression on long-term depression of C-fiber-evoked field potentials in the spinal dorsal horn in rats with neuropathic pain could be blocked significantly by intravenous application of NMDA receptor antagonist MK-801 (0.5 mg.kg-1), or by opioid receptor antagonist naloxone (1 mg.kg-1). CONCLUSION: EA of 2 Hz could induce long-term depression of the nociceptive synaptic transmission in the spinal dorsal horn in rats with neuropathic pain. This kind of 2 Hz EA-suppression on LTD was NMDA receptor-dependent and the endogenous opioid system may be involved in it. These data indicate that the NMDA receptor-dependent LTD at the nociceptive sensory synapses in the spinal dorsal horn in rats with neuropathic pain induced by activating the endogenous opioid system may play the primary role in the antinociceptive effects of 2 Hz EA on neuropathic pain.

Acupuncture Points↗

PubMed2002

Anti-tumor activities of the angiogenesis inhibitors interferon-inducible protein-10 and the calreticulin fragment vasostatin.

Tumor growth depends upon an adequate supply of oxygen and nutrients achieved through angiogenesis and maintenance of an intact tumor vasculature. Therapy with individual agents that target new vessel formation or existing vessels has suppressed experimental tumor growth, but rarely resulted in the eradication of tumors. We therefore tested the combined anti-tumor activity of vasostatin and interferon-inducible protein-10 (IP-10), agents that differently target the tumor vasculature. Vasostatin, a selective and direct inhibitor of endothelial cell proliferation, significantly reduced Burkitt tumor growth and tumor vessel density. IP-10, an "angiotoxic" chemokine, caused vascular damage and focal necrosis in Burkitt tumors. When combined, vasostatin plus IP-10 reduced tumor growth more effectively than each agent alone, but complete tumor regression was not observed. Microscopically, these tumors displayed focal necrosis and reduction in vessel density. Combination therapy with the inhibitors of angiogenesis vasostatin and IP-10 is effective in reducing the rate of tumor growth but fails to induce tumor regression, suggesting that curative treatment may require supplemental drugs targeting directly the tumor cells.

Actins↗

PubMed2002

Regulation of endothelial cell branching morphogenesis by endogenous chemokine stromal-derived factor-1.

The chemokine stromal-derived factor-1 (SDF-1) and its unique receptor, CXCR4, are required for normal cardiovascular development, but a critical role for SDF-1 in postnatal vascular remodeling and the mechanisms underlying SDF-1/CXCR-4 vasculogenesis are unclear. Here we show that SDF-1 is expressed by the vascular endothelium from selected healthy and tumor tissues. In vitro, primary endothelial cells constitutively express SDF-1 that is detected in the cytoplasm, on the cell surface, and in the culture supernatant. Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) increase SDF-1 expression in endothelial cells. In functional studies, pertussis toxin and antibodies to SDF-1 or CXCR-4 disrupt extracellular matrix-dependent endothelial cell tube formation in vitro. This morphogenic process is associated with time-dependent modulation of surface CXCR-4 expression that changes from being diffuse to being polarized and subsequently lost. In vivo, pertussis toxin and neutralizing antibodies directed at SDF-1 inhibit growth factor-dependent neovascularization. These results indicate that SDF-1/CXCR-4 identifies VEGF- and bFGF-regulated autocrine signaling systems that are essential regulators of endothelial cell morphogenesis and angiogenesis.

Autocrine Communication↗

PubMed2002

Laminin binding to the calreticulin fragment vasostatin regulates endothelial cell function.

Vasostatin, the 1-180 amino acids NH(2) domain of calreticulin, inhibits endothelial cell proliferation, angiogenesis, and tumor growth, but the mechanisms underlying these effects are unclear. We show that endothelial cells express the extracellular matrix protein laminin, including chains alpha 5 and gamma 1 and that vasostatin specifically binds to laminin. When added to endothelial cell cultures, vasostatin specifically inhibits endothelial cell attachment to laminin and by this mechanism, can reduce subsequent endothelial cell growth induced by basic fibroblast growth factor. As an angiogenesis inhibitor that specifically disrupts endothelial cell attachment to components of the extracellular matrix, vasostatin has a unique potential as a cancer therapeutic.

Angiogenesis Inhibitors↗

PubMed2002

[The change in sensitivity of methicillin-resistant Staphylococcus aureus to vancomycin].

OBJECTIVE: To determine the shift of susceptibility of methicillin-resistant Staphylococcus aureus (MRSA) isolates to vancomycin in recent years. METHODS: Antimicrobial susceptibility was determined by disk diffusion test (K-B method). The t-test was used to compare the mean diameters of zone of inhibition. RESULTS: The clinical isolates of MRSA from 1994 to 2000 were 218, 187, 292, 237, 351, 886 and 652 in number respectively. The mean diameters (mm) of the inhibition zone of MRSA isolates each year were 19.9, 19.1, 18.6, 17.4, 18.4, 18.2 and 17.8. Comparison of the diameters of the inhibition zone of MRSA isolates (K-B method) showed that the mean diameter of the inhibition zone from the 652 MRSA isolates in 2000 was much less than that of the 218 MRSA isolates in 1994 and the difference was significant (P < 0.001). The resistant rates to chloramphenicol, ciprofloxacin, erythromycin, gentamicin, tetracycline and trimethoprim/sulfamethoxazole were 44.0%, 73.7%, 89.1%, 65.7%, 61.0% and 67.0%. CONCLUSION: Our observation demonstrated that the susceptibility of MRSA to vancomycin gradually decreased from 1994 to 2000. It is important to monitor the antimicrobial susceptibility of Staphylococcus aureus to vancomycin.

Anti-Bacterial Agents↗