1.Effect of propofol on glutamate and gamma-aminobutyric acid release from rat hippocampal synaptosomes.
You, SHANG ; Shanglong, YAO ; Yinming, ZENG ; Hongliang, LIU ; Junli, CAO
Journal of Huazhong University of Science and Technology (Medical Sciences) 2005;25(6):700-2
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
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Calcium/metabolism
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Glutamic Acid/*biosynthesis
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Hippocampus/*metabolism
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Propofol/*pharmacology
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Rats, Sprague-Dawley
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Synaptosomes/*metabolism
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gamma-Aminobutyric Acid/*biosynthesis
2.Incidence of needlestick injury in Chinese nursing interns: a Meta-analysis
Haiqiu SUN ; Junli YOU ; Gangmei CHEN ; Xianchai HONG
Chinese Journal of Practical Nursing 2014;30(10):37-40
Objective To systematically assess the incidence of needlestick injury in Chinese nursing interns.Methods Research articles published on China Academic Journal Electronic Retrieval Database (CNKI),Chinese Scientific Journals Full-text Database (VIP),Wanfang DATA,ISI Web of Knowledge,PUBMED,OVID,Springer and other databases before 2013 were searched,which were relevant to needlestick injury in Chinese nursing interns.Using STATA 12.0 software,pooled estimates were summarized by Meta-analysis.Results 61 articles were included in this study,which covered a total of 15 451 nursing interns.Meta-analysis showed that the pooled incidence of needlestick injury in nursing interns was 65%,95%CI=60%~71%.Although the incidence declined year by year in recent decade,it was still higher than 55%.However,the injury reporting rate was 22%,95% CI=16%~29%.Conclusions Needlestick injury showed a high incidence in Chinese nursing interns,but declined slightly year by year.However,the injury reporting rate was still very low.
3.Characteristics of glucose metabolism in non-obese and obese women with polycystic ovarian syndrome
Yuhua SHI ; Dongni ZHAO ; Junli ZHAO ; Li YOU ; Hong LIU ; Mei SUN ; Zijiang CHEN
Chinese Journal of Obstetrics and Gynecology 2010;45(8):575-577
Objective To investigate characteristics of glucose metabolism of non-obese and obese women with polycystic ovary syndrome (PCOS). Methods From May 2006 to April 2009, 1928 PCOS patients treated in Reproductive Medicine Center of Shandong Provincial Hospital Affiliated to Shandong University were enrolled in this study, which were divided into 901 cases [body mass index (BMI) ≥25 kg/m2] in obese group and 1027 cases in non-obese (BMI < 25 kg/m2) group. The prevalence of type 2 diabetes mellitus (T2DM), oral glucose tolerance test, impaired fasting glucose (IFG), impaired glucose tolerance(IGT) were compared between the two groups. Results (1) Blood glucose levels: at the time of fasting, 30, 60, 120 and 180 minutes, the levels of glucose were (5. 3±1.1), (9. 0±2. 4), (9. 3±4. 4),(7.5±2.8) ,(5.3±1.8)mmol/L in obese group and (5.0±0. 8) ,(8.4±3.5),(8.0±4.2),(6.5±3.2) ,(4. 9±1.6) mmol/L in non-obese group, which all showed statistical difference at every time point (P < 0. 01). (2)The level of insulin: at the time of fasting, 30, 60, 120 min, the level of insulin were (13±7), (81±51), (102±65), (83±63) mU/L in obese group and (8±5) ,(57±35) ,(62±44),(46±39) mU/L in non-obese group, which all showed statistical differenceatevery time point (P <0. 01). However, at time point of 180 minutes, the level of insulin did not exhibit significantly difference between obese and non-obese group (P > 0. 05). (3) The prevalence of abnormal glucose metabolism: the rate of IFG was 4. 98% (96/1928). The rate of abnormal glucose tolerance was 23. 08% (445/1928). The rate of IGT were 13.05% (134/1027) in non-obese group and 24. 20% (218/901) in obese group,which also showed remarkable difference (P < 0. 01). The rate of T2DM were 2. 53% (26/1027) in nonobese group and 7.44% (67/901) in obese group, which reached significant difference (P < 0. 01).Conclusion Abnormal glucose metabolism was observed more frequently in overweight or obese PCOS women.
4.Role of sonic hedgehog signaling pathway in spinal neurons in morphine tolerance in mice
Junli YAO ; Su LIU ; You LYU ; Peiyu CAO ; Longjian YAN ; Hui SU ; Gongjian LIU
Chinese Journal of Anesthesiology 2017;37(2):175-179
Objective To evaluate the role of sonic hedgehog (SHH) signaling pathway in spinal neurons in morphine tolerance (MT) in mice.Methods Pathogen-free healthy female Kunming mice,weighing 20-25 g,aged 8-10 weeks,were used in the study.MT was induced with morphine 10 mg/kg injected subcutaneously twice a day for 7 consecutive days.The experiment was performed in two parts.Experiment Ⅰ Forty-eight mice were randomly assigned into 2 groups:control group (group C,n =8) and MT group (group M,n=40).The thermal pain threshold (TPT) was measured at 1 day before morphine injection and 1,3,5,7 and 14 days after the end of injection.Eight mice in each group were sacrificed at 2 h after measurement of TPT at each time point after the end of injection in group M or at 2 h after the last measurement of TPT in group C,and the lumbar segment (L4-6) of the spinal cord was removed.Experiment Ⅱ Forty-eight mice were randomly assigned into 6 groups (n=8 each):SHH inhibitor cyclopamine plus MT group (group CP+M),cyclopamine solvent plus MT group (group D1 +M),SHH agonist SAG plus MT group (group SAG+M),SAG solvent plus MT group (group D2+M),MT plus cyclopamine group (group M+CP) and morphine plus cyelopamine solvent group (group M+D1).At 15 min before morphine injection,cyclopamine 10 mg/kg was injected subcutaneously in group CP+M,and SAG 5 mg/kg was injected subcutaneously in group SAG+M.Cyclopamine 10 mg/kg was injected subcutaneously once a day during the 1-3 days after the end of morphine injection in group M+CP.The TPT was measured before injection of morphine,at 30 min after the first injection of morphine every day and at 1-3 days after the end of morphine injection.The animals were sacrificed at 2 h after the last measurement of TPT,and the lumbar segment (L4-6) of the spinal cord was removed for determination of the expression of SHH signaling pathway-related proteins SHH,ptch1,smo,gli1 and gli3 using Western blot.Results Experiment Ⅰ Compared with group C,the TPT was significantly decreased at 1 and 3 days after the end of morphine injection (P<0.05),no significant change was found in TPT at 5-14 days after the end of morphine injection (P>0.05),and the expression of SHH,smo and glil at 1-5 days after the end of morphine injection,of ptchl at 1 and 3 days after the end of morphine injection and of gli3 at 7 days after the end of morphine injection was up-regulated in group M (P<0.05).Experiment Ⅱ Compared with group D1+M,the TPT was significantly increased,the expression of SHH,ptchl,smo and glil was down-regulated,and gli3 expression was up-regulated in group C P+M (P<0.05).Compared with group D2+M,the TPT was significantly decreased,the expression of SHH,ptch1,smo and glil was up-regulated,and gli3 expression was down-regulated in group SAG+M (P<0.05).There was no significant difference in the parameters mentioned above between group M+CP and group M+D1 (P>0.05).The TPT was significantly lower on 3rd-7th days after beginning of morphine injection and 1-3 days after the end of morphine injection than at 30 min after the first injection of morphine in group CP+M (P<0.05).Conclusion The mechanism underlying the development of MT is partially related to activation of SHH signaling pathway in spinal neurons of mice,however,the maintenance mechanism has no marked relationship with it.
5.Renal pathological characteristics in cirrhotic patients
Chinese Journal of Internal Medicine 2020;59(11):898-901
This study is aim to analyze pathological characteristics of kidneys in cirrhotic patients with renal disease. Fifty-six cirrhotic patients with various renal diseases at Peking University First Hospital who underwent percutaneous renal biopsy from January 2010 to September 2019 were evaluated retrospectively. Immunoglobulin A nephropathy (IgAN) was the most common type of kidney biopsy (23 cases, 41.1%). Different pathologic types were often overlapping. More than 60% patients were treated with steroids and/or immunosuppressants, and 1 patient with anti-CD20 monoclonal antibody. Percutaneous renal biopsy is important for the diagnosis and treatment in cirrhotic patients with renal disease.
6.Effect of Propofol on Glutamate and γ-aminobutyric Acid Release from Rat Hippocampal Synaptosomes
You SHANG ; Shanglong YAO ; Yinming ZENG ; Hongliang LIU ; Junli CAO
Journal of Huazhong University of Science and Technology (Medical Sciences) 2005;25(6):700-702
To investigate the effect of propofol on the release of glutamate and γ-aminobutyric acid (GABA) from rat hippocampal synatosomes, synaptosomes was made from hippocampus and incubated with artificial cerebrospinal fluid (aCSF). With the experiment of Ca2+-dependent release of glutamate and GABA, dihydrokainic acid (DHK) and nipectic acid were added into aCSF. For the observation of Ca2+-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 20μmol/L veratridine or 30 mmol/L KCl. The concentration of glutamate and GABA in aCSF was measured by using high-performance liquid chromatography (HPLC). 30, 100 and 300 μmol/L propofol significantly inhibited veratridine-evoked Ca2+-dependent release of glutamate and GABA (P<0.01 or P<0.05). However, propofol showed no effect on elevated KCl-evoked Ca2+-dependent release of glutamate and GABA (P>0.05). Veratridine or elevated KCl evoked Ca2+ -independent release of glutamate and GABA was not affected significantly by propofol (P>0.05). Propofol could inhibit Ca2+-dependent release of glutamate and GABA. However, it has no effect on the Ca2+-independent release ofglutamate and GABA.