Biomedical subjects

Hui Yuan

Publications and source records attributed to Hui Yuan.

24 records · Page 2Linked to original sources

PubMed2004

[The clinical value of quantitative analysis of plasma Epstein-Barr virus DNA in patients with nasopharyngeal carcinoma].

OBJECTIVE: To elucidate the clinical value of quantitative analysis of plasma cell-free EBV-DNA in patients with nasopharyngeal carcinoma (NPC) . METHODS: Using fluorescence quantitative polymerase chain reaction (FQ-PCR), the copies of EBV-DNA in 66 plasma samples of pre- and post-treated NPC patients were examined, and compared with 30 normal controls. The relationships between the copies of free EBV-DNA and tumor stage, metastases load, as well as short-term therapeutic response were analyzed. RESULTS: The positive percentage and copies of plasma EBV-DNA of NPC patients (66.7%, Median 522.0) were significantly higher than those of normal controls (10.0%, Median 0). Among the pre-treated patients, plasma EBV-DNA copies in stage III-IV patients (Median 3130.0) were higher than those were in stage I-II (Median 400.0), and the copies of N2-3 patients (Median 3250.0) were higher than those were in N0-1 patients (Median 400.0). And then the level of post-treated patients (Median 0) was lower than that of pre-treated patients (Median 522.0). Depending on the evaluation of therapeutic response, post-treated patients could be classified as two different categories, patients whose tumor regressed satisfyingly and those with remaining lesions. It was found that EBV-DNA copies of the former (Median 0) were lower than those of the latter (Median 2083.0). CONCLUSIONS: FQ-PCR determination of plasma EBV-DNA may become a promising marker to monitor the course of this disease.

Adult↗

PubMed2003

Effects of extract of Ginkgo biloba on spasms of the basilar artery and cerebral microcirculatory perfusion in rats with subarachnoid hemorrhage.

This study was aimed at investigating the effects of extract of Ginkgo biloba (EGb) on cerebral vasospasm and microcirculatory perfusion after subarachnoid hemorrhage (SAH). An endovascular piercing method was used to induce Wistar rat SAH models, and animals were divided into sham-operated, vehicle controls, and EGb-treated groups. EGb was injected intraperitoneally 30 minutes before operation and was repeated every 6 hours, with a single dose of 15 mg/kg bw. Diameters of basilar arteries before and after operation were measured. Microcirculatory blood perfusion of parietal lobe cortex was detected using a laser Doppler flow-meter probe within 24 hours. Endothelin-1 levels in both plasma and brain tissue were detected at different time points. The results showed that SAH caused an immediate drop in microcirculatory blood flow in vehicle controls, which persisted for 24 hours. Endothelin-1 levels in both plasma and brain tissue increased after SAH. EGb partly reversed spasms of the basilar artery and antagonized a drop in microcirculatory blood flow. EGb also prevented an increase in endothelin-1 both in plasma and in brain tissue. In conclusion, EGb, by antagonizing the overproduction of endo- thelin-1, partly reverses cerebral vasospasm and improves microcirculation, and thus relieves secondary ischemic brain injury after experimental SAH.

Animals↗

PubMed2003

The effects of nimodipine on regional cerebral blood flow, brain water and electrolyte contents in rats with subarachnoid hemorrhage.

Secondary cerebral ischemic injury is a major cause of mortality and disability from subarachnoid hemorrhage (SAH). In this study, the protective effects of nimodipine were investigated. Rat SAH models were divided into a sham-operated group, a saline-controlled, and a nimodipine-treated group by an endovascular piercing method. Nimodipine, 100 microg/kg BW was injected intraperitoneally 30 minutes before operation and was repeated every 6 hours. Dynamic changes in cortical regional cerebral blood flow (rCBF) using a laser Doppler flow-meter probe, and somatosensory evoked potentials (SEP) were estimated. Brain water content, sodium, potassium and calcium contents at different time points were determined. rCBF, latency of SEP, brain water and electrolyte contents did not statistically change in sham-operated rats. In saline-controlled rats, rCBF decreased immediately after SAH, and stabilized at low levels within 24 hours. The latency of SEP delayed gradually after SAH. Brain water and sodium increased, while potassium decreased at 6 hours and 24 hours. Brain calcium content increased significantly from 1 hour to 24 hours after induction of SAH. Extents of alterations of the above parameters caused by SAH in the nimodipine-treated group were less than those in the saline-controlled group, statistically. In conclusion, nimodipine partly prevents a decrease in cerebral blood supply and attenuates secondary cerebral ischemic injury after SAH.

Animals↗

PubMed2003

The effect of cerebral lymphatic blockage on cortex regional cerebral blood flow and somatosensory evoked potential.

Disputes on the significance of cerebral lymphatic drainage pathways under physiological and pathophysiological conditions still exist. The purpose of this experiment is to investigate the influence of cerebral lymphatic blockage on cerebral blood flow and cortex somatosensory evoked potential. Wistar rat cerebral lymphatic blockage models were established by removing cervical lymphatic nodes after obstructing their input and output tubes. Animals were divided randomly into a sham-operated group and a cerebral lymphatic-blockage group. Regional cerebral blood flow in different regions of the cortex were detected using a laser-Doppler flowmeter probe, and cortex evoked potential was detected using an electromyogram and evoked potential instrument before the operation, then 1 day, 5 days and 7 days after the operation. Results showed that the sham operation had no obvious effect on regional cerebral blood flow and the latency of somatosensory evoked potential. From 1 day to 7 days after cerebral lymphatic obstruction, regional cerebral blood flow in different cortical regions decreased markedly (P<0.01). Latency of somatosensory evoked potential was significantly delayed on the 5th and 7th day after blockage of cerebral lymphatic drainage (P<0.01). We concluded that cerebral lymphatic drainage may play an important role in maintaining the equilibrium of the internal environment of the brain, and blockage of this pathway results in cerebral ischemia.

Animals↗

PubMed2003

L-arginine improves cerebral blood perfusion and vasomotion of microvessels following subarachnoid hemorrhage in rats.

The purpose of this study is to investigate the effect of L-arginine (L-Arg) on cerebral blood perfusion and vasomotion (perfusion motion) in microvessels following subarachnoid hemorrhage (SAH). Rat noncraniotomy SAH models were used and animals were divided into sham-operated, saline-treated, and L-Arg-treated groups. L-Arg was injected intraperitoneally 30 minutes before the operation and repeated every 6 hours, with a single dose of 0.5 g/kg bw. Dynamic changes in regional cerebral blood flow (CBF) and vasomotion within 24 hours were measured using a laser Doppler flow-meter probe. Serum nitric oxide (nitrite/nitrate) and plasma endothelin-1 levels were also measured at different time points within 24 hours. Morphologic changes in neurons in the hippocampus CA1 region were examined. SAH gave rise to an immediate and persistent decrease in CBF in saline-treated rats. Abnormal vasomotions with decreased frequency and amplitude were observed. Serum nitric oxide decreased, while plasma endothelin-1 increased significantly. Neurons in the hippocampus CA1 region were severely damaged. The above pathological alterations in the L-Arg-treated group were alleviated. It was concluded that L-Arg, which increases cerebral blood perfusion and improves vasomotions of microvessels by enhancing nitric oxide levels and decreasing endothelin-1 levels in blood, exerts a protective effect on secondary cerebral ischemic injury following experimental SAH.

Animals↗

PubMed2002

[Oxidative stress of cooking oil fume on rat type II lung cells].

The relationship between the oxidative stress and damages in rat type II lung cells exposed to cooking oil fume (COF) was studied. The cytotoxicity, DNA cross-links and DNA single strand breaks could be observed in the cells exposed to COF. The contents of MDA were increased and GSH were decreased significantly with exposure doses of COF and with time dependence. Pretreatment with antioxidant N-acetylcysteine (NAC) could reduce the toxicity of COF to the cells. The results suggested that cytotoxicity and DNA damages of rat type II lung cells induced by cooking oil fume might be related to the oxidative stress and the possible pathways might be the formation of lipid peroxides and interfering the GSH anti-oxidative systems of the cells.

Animals↗