To investigate the effect of thiopental sodium on the release of glutamate and gamma-aminobutyric acid (GABA) from synaptosomes in the prefrontal cortex, synaptosomes were made, the spontaneous release and the evoked release by 30 mmol/L KCl or 20 micromol/L veratridine of glutamate and GABA were performed under various concentrations of thiopental sodium (10-300 micromol/L), glutamate and GABA concentrations were determined by reversed-phase high-performance liquid chromatography. Our results showed that spontaneous release and evoked release of glutamate were significantly inhibited by 30 micromol/L, 100 micromol/L and 300 micromol/L thiopental sodium, IC50 of thiopental sodium was 25.8 +/- 2.3 micromol/L for the spontaneous release, 23.4 +/- 2.4 micromol/L for KCl-evoked release, and 24.3 +/- 1.8 micromol/L for veratridine-evoked release. But GABA spontaneous release and evoked release were unaffected. The study showed that thiopental sodium with clinically related concentrations could inhibit the release of glutamate, but had no effect on the release of GABA from rats prefrontal cortical synaptosomes.
Glutamic Acid/*metabolism ; Hypnotics and Sedatives/pharmacology ; Prefrontal Cortex/*metabolism ; Rats, Sprague-Dawley ; Synaptosomes/*metabolism ; Thiopental/*pharmacology ; gamma-Aminobutyric Acid/*metabolism

AIM: To investigate the dynamic changes of ATPases and NOS activities and NO production at different anesthesia phases using thiopental and propofol andifferent anesthetic phases (induction, anesthesia, restoration, and awake), the activities of NOS and ATPase and NO production in cortex and brain stem were meagroup. RESULTS: Ca2+ -ATPase and Na+ ,K+ -ATPase activities in the cortex and brain stem were significantly decreased after administration ofthiopental and propofol,especially at induction, anesthesia, or even restoration phase of thiopental group (P＜0.05, P＜0.01) and at anesthesia phase of propofol group (P＜0.05). NOS activities and NO production decreased from induction to restoration phase with thiopental and propofol anesthesia (P＜0.01). The parameters were returned near to the normal at awaken phase. CONCLUSION: Activities of ATPases and NOS and the production of NO may mediate the anesthesia effects of thiopental and propofol in the rat cortex and brain stem.

Aim To investigate the effect of thiopental sodium on the release of glutamate and GABA from synaptosomes of rats prefrontal cortex. Methods Synaptosomes were made from rats prefrontal cortex and incubated with artificial cerebral and spinal fluid (aCSF), then divided into five groups: group base release (Base), group thiopental sodium 10 ?mol?L -1 (THS 10), group thiopental sodium 30 ?mol?L -1 (THS 30), group thiopen tal sodium 100 ?mol?L -1 (THS 100) and group thiopental sodium 300 ?mol? L -1 (THS 300). Various concentrations of thiopental sodium were added to aC SF, the release of glutamate and GABA were performed under 37℃ and measured using reversed-phase high-performance liquid chromatography (RP-HPLC). When Ca 2+-independent release of glutamate and GABA were studied, Ca 2+ was omitted from aCSF.Results Compared with Base, thiopental sodium 30 , 100 and 300 ?mol?L -1 inhibited Ca 2+-dependent release of gluta mate evoked by KCl or veratridine significantly (P

Background: The prevalence of ulcerative colitis (UC) in China has significantly increased in recent years,and Toll-like receptor 4 (TLR4) may be closely related to the development of UC.Aims: To study the effect of vitamin D3 on expression of TLR4 in the intestinal mucosa in colitis model in rats.Methods: Thirty Sprague-Dawley rats were randomly divided into normal control group,model group and vitamin D3 group.Rats in model group and vitamin D3 group were given trinitro-benzene-sulfonic acid (TNBS) to induce colitis model.Rats in vitamin D3 group were given vitamin D3.HE staining was performed,and disease activity index (DAI) and colon histopathological score were evaluated,the expression of TLR4 was measured by immunohistochemistry.Results: Compared with normal control group,DAI and histopathological score in model group were significantly increased (P＜0.05),and expression of TLR4 was significantly increased (P＜0.05).After giving vitamin D3,DAI and histopathological score were significantly decreased (P＜0.05),and expression of TLR4 was significantly decreased (P＜0.05).Conclusions: The expression of TLR4 is increased in colon tissue in colitis model in rats,which may be involved in the pathogenesis of UC.Vitamin D3 can alleviate intestinal inflammation via inhibiting expression of TLR4,thereby playing a role in the adjunctive therapy of UC.

Objective To explore the values of various surgical techniques in the treatment of secondary hepatocarcinoma.Methods One hundred thirty-four patients with secondary hepatocarcinoma were respectively divided into three groups,hepatectomy(group Ⅰ), other surgical treatments(group Ⅱ) and chemotherapy or/and interventional therapy(group Ⅲ). Retrospective analysis was performed to all patients above mentioned.The three groups were compared each other for survival rate.Results The survival rate among three groups was significantly different.There was a higher survival rate in hepatectomy group.Conclusions Hepatectomy is the most effective method to cure secondary hepatocarcinoma.

Objective To investigate the effect of thiopental sodium (TPS) on spontaneous and KCl-evoked glutamate release from prefrontal cortical synaptosomes in rats and the effect of bicuculline on this effect ofTPS.Methods SD rats of both sexes (200-250 g) were decapitated and brains were removed. The prefrontalcortex was dissected and added to ice-cold sucrose solution and homogenized. The homogenate was centrifuged at1000 g at 0℃-4℃ for 5 min. The supernatant was again centrifuged at 12 000 g for 20 min. The sediment wascrude synaptosomes, which was added to artificial cerebro-spinal fluid (ACSF). The crude synaptosomes weredivided into 5 groups (n = 8): control group and 4 TPS groups. In control group no TPS was added while in TPSgroups different concentrations of TPS was added and the final concentration of TPS was 10, 30, 100, 300?mol?L~(-1) respectively. The synaptosomes were then placed with or without KCl in water bath at 37℃ for 15 min. Thespontaneous or KCl-evoked glutamate release was measured using high-performance liquid chromatograph (HPLC).In another set of experiment bicuculline 0. 1 mmol?L~(-1) was added to ACSF in each group before 15 min water bathto see if it could antogonize the effect of TPS on glutamate release. Results TPS 30, 100 and 300 ?mol?L~(-1)could significantly inhibit the spontaneous or KCl-evoked glutamate release compared with control group (P0.05). Bicuculline 0. 1 mmol?L~(-1) had no effect on the glutamate release in control group but could antagonize the inhibitory effect of TPS on glutamate release. Afteraddition of bicucculline the glutamate released in control group was not significantly different from that in the TPSgroups.Conclusion TPS sodium can inhibit the spontaneous or KCl-evoked glutamate release from prefrontalcortical synaptosomes in a concentration-dependent manner. The inhibitory effect is mediated by GABA_A receptors.

Objective To study the expressions of SKP2 and p27 in gastric carcinoma and pericancerous tissues and to detect the relationship between their expressions and clinicopathological features. Methods Forty-nine cases of gastric carcinoma spicemen and 20 cases of tissue adjacent to the carcinoma were cut and made into paraffin-embedded slices. The expressions of SKP2 and p27 were then detected by SP immunohistochemical method. Results The positive expression rate and score of SKP2 were both significantly higher in the gastric carcinoma tissues than those in pericancerous tissues (P

To investigate the effect of propofol on the release of glutamate and gamma-aminobutyric acid (GABA) from rat hippocampal synatosomes, synaptosomes was made from hippocampus and incubated with artificial cerebrospinal fluid (aCSF). With the experiment of Ca(2+)-dependent release of glutamate and GABA, dihydrokainic acid (DHK) and nipectic acid were added into aCSF. For the observation of Ca(2+)-independent release of glutamate and GABA, no DHK, nipectic acid and Ca2+ were added from aCSF. The release of glutamate and GABA were evoked by 20 micromol/L veratridine or 30 mmol/L KCI. The concentration of glutamate and GABA in aCSF was measured by using high-performance liquid chromatography (HPLC). 30, 100 and 300 micromol/L propofol significantly inhibited veratridine-evoked Ca(2+)-dependent release of glutamate and GABA (P < 0.01 or P < 0. 05). However, propofol showed no effect on elevated KCl-evoked Ca(2+)-dependent release of glutamate and GABA (P > 0.05). Veratridine or elevated KCI evoked Ca(2+)-independent release of glutamate and GABA was not affected significantly by propofol (P > 0.05). Propofol could inhibit Ca(2+)-dependent release of glutamate and GABA. However, it has no effect on the Ca(2+)-independent release of glutamate and GABA.
Anesthetics, Intravenous/pharmacology ; Calcium/metabolism ; Glutamic Acid/*biosynthesis ; Hippocampus/*metabolism ; Propofol/*pharmacology ; Rats, Sprague-Dawley ; Synaptosomes/*metabolism ; gamma-Aminobutyric Acid/*biosynthesis

Objectives To analyze the clinical and pathological characteristics of gastric submucosal tumors (GSMTs), and evaluate the safety and efficacy of endoscopic treatment for GSMTs. Methods 61 patients with GSMTs were selected from June 2014 to September 2012 by endoscopy and ultrasonography;they were all treated by endoscopic therapy; pathological examination was took in all removed tumors, the tumors which could be the gastric stromal tumor were furtherly examined by molecular biology technique of immunohistochemistry. Result In 61 cas-es, 39 cases are female patients, accounting for 63.93%;the tumors located at the stomach fund accounted for 52.46%(32/61), at the gastric corpus for 21.31%(13/61), at the gastric antrum for 11.48 %(7/61), at cardia for 14.75%(9/61); 10 cases were treated by Endoscopic submucosal dissection, 21 by endoscopic submucosal excavation, 27 by Endoscopic full-thickness resection, 3 by Submucosal tunnelling endoscopic resection; in all 61 cases, 2 were changed to laparoscopic treatment because one tumor was too big and broke the Serous and another was located at mucus Lake of gastric fund, 1 occurred postoperative bleeding and was treated by laparoscopy successfully, 1 oc-curred postoperative perforation and was treated by endoscopy successfully; after pathological and immunohisto-chemical analysis, 34 tumors were identified as gastric stromal tumor and all of them in risk classification were at very low risk, 11 were leiomyoma, 5 were lipoma, 3 were heterotopic pancreas, 5 were calcifying fibrous pseudotu-mor, 2 were inflammatory fibroid polyps, and 1 was angiomatous proliferation; gastric stromal tumor at gastric fundus account for 73.53 % (25/34), at gastric corpus for 11.76 % (4/34), at gastric antrum for 5.88 % (2/34) and at cardia for 8.82 %(3/34). Conclusion Most GSMTs are found in female and commonly lack of specific clinical symptoms;GMSTs are commonly located at gastric fund and most of them are gastric stromal tumors, vast majority of gastric stromal tumors in the risk classification are at very low risk;the endoscopic resection is a mini-invasive, safe and ef-fective treatment for GSMTs.

Objective To establish adult rat auditory epithelial cell culture and try to find precursor cells of auditory hair cells in vitro. Methods With refinement of culture media and techniques, cochlear sensory epithelial cells of adult rat were cultured. Immunocytochemistry and Bromodeoxyuridine (BrdU)labeling were used to detect properties and mitotic status of cultured cells. Results The cultured auditory epithelial cells showed a large, flat epithelial morphotype and expressed F-actin and cytokeratin, a subset of cells generated from auditory epithelium were labeled by calretinin, a specific marker of early hair cell. Conclusion Adult rat auditory epithelium can be induced to generate hair cell-like cells by nature culture, this phenomenon suggests that progenitor cells may exist in rat cochlea and they may give birth to new hair cells. Whether these progenitor cells are tissue specific stem cells is still need more study.