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Objective@#To investigate the effect of dopamine (DA) on the glutamate (Glu) uptake ability of neural cells, as well as its effect on cognitive impairment in rats with minimal hepatic encephalopathy (MHE) via related pathways.@*Methods@#A total of 45 Sprague-Dawley rats were randomly divided into control group, MHE model group, and DA intervention model group, with 15 rats in each group. The rats in the MHE model group were given intraperitoneal injection of thioacetamide (TAA), those in DA intervention model group were given intraventricular injection of DA, and those in the control group were given intraperitoneal injection of physiological saline, with a frequency of twice a week for 8 weeks. Cerebral microdialysis was used to measure the change in the content of Glu in the brain in MHE rats and rats with DA intervention; RT-PCR and Western blotting were used to measure the relative mRNA and protein expression of trace amine-associated receptor 1 (TAAR1) and excitatory amino acid transporter 2 (EAAT2); the changes in the expression of EAAT2 and extracellular Glu level were measured after intracerebroventricular injection of TAAR1 siRNA and TAAR1 plasmid in MHE rats and rats with DA intervention. One- way analyses of variance for comparison among different groups were performed, categorical data between groups were compared using nonparametric tests.@*Results@#Compared with the control group, the MHE model group had significant increases in the content of DA in liver tissue, plasma, and brain tissue (4.90 ± 0.13 ng/g vs 1.20 ± 0.13 ng/g, P < 0.05; 16.32 ± 1.01 pmol/ml vs 5.50 ± 0.82 pmol/ml, P < 0.05; 732.45 ± 78.85 ng/g vs 387.00 ± 23.36 ng/g, P < 0.05). There was a significant increase in the extracellular Glu level within 40-120 minutes after intracerebral injection of DA in the DA intervention model group. Compared with the control group, the MHE model group and the DA intervention model group had a significant increase in the relative protein expression of TAAR1 (3.72 ± 0.50/4.18 ± 0.43 vs 0.96 ± 0.40, both P < 0.05) and a significant reduction in the expression of EAAT2 (0.46 ± 0.16/0.51 ± 0.20 vs 0.92 ± 0.11, P = 0.013 and 0.036). Compared with the model group treated with empty vector, the MHE model group and the DA intervention model group had a significant increase in the relative protein expression of EAAT2 after TAAR1 siRNA intervention (0.86±0.142 vs 0.56 ± 0.060, P = 0.028; 0.99 ± 0.056 vs 0.43 ± 0.098, P = 0.0010) and a significant reduction in the extracellular Glu level in the brain at 60-120 minutes after injection, while after TAAR1 plasmid intervention, the MHE model group and the DA intervention model group had a significant reduction in the relative protein expression of EAAT2 (0.20 ± 0.040 vs 0.48 ± 0.08, P = 0.006; 0.24 ± 0.05 vs 0.54 ± 0.07, P = 0.004) and a significant increase in the extracellular Glu level in brain at 60-100 minutes after injection.@*Conclusion@#DA interacts with TAAR1 in brain tissue to induce extracellular accumulation of Glu, thus leading to the disorder of the TAAR1-EAAT2 signaling pathway in brain tissue and ultimately injuring the cognitive function of MHE rats.
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Objective To investigate the distribution and change in antimicrobial resistance of pathogens causing blood-stream infection,so as to provide reference for rational antimicrobial use.Methods The isolation and antimicrobial resistance of major pathogens from blood culture specimens from a tertiary first-class hospital in 2012-2015 were analyzed statistically.Results A total of 4 780 isolates were detected,the top five species were Escherichia coli (n = 1 008, 21.09%),Klebsiella pneumoniae (n = 624,13.05%),Acinetobacter baumannii (n = 452,9.46%),Staphylococcus aureus (n=437,9.14%),and Pseudomonas aeruginosa (n=247,5.17%).The percentage of gram-negative bacilli, gram-positive cocci,fungi,and others were 62.05%,29.31%,7.76%,and 0.88% respectively.The resistance rates of Klebsiella pneumoniae to ertapenem and imipenem increased from 4.50% in 2012 to 46.79% and 33.94% in 2015(both P<0.01).The resistance rates of Acinetobacter baumannii to cefepime,ceftazidime,tobramycin,gentamicin,and imipenem were 86.50%,80.56%,78.10%,79.87%,and 84.29% respectively;resistance rates to amikacin in 2012-2015 were 0, 10.22%,39.85%,and 21.30% respectively(P<0.01);resistance rates to minocycline in four years were 0-7.52% (P<0.01 ).Conclusion The main pathogens causing bloodstream infection are gram-negative bacilli,Acinetobacter baumannii is highly resistant to cephalosporins and carbapenems,resistance rates of Klebsiella pneumoniae to carbapenems increased rapidly.Broad-spectrum antimicrobial agents must be used cautiously to reduce the selective pressure of antimicrobial agents.
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Objective To explore the possibility of gelatin sponge as supporter of central nervous tissue engineering. Methods Primary NSCs were isolated from forebrain of neonatal Sprague Dawley rats and cuhured in serum-free medium for long-term survival in vitro. Neural stem cells were divided into absorbable gelatin sponge group and control group.Observe their morphology and proliferation.Immunofluorescence technique were used to test the results of differentiation of two groups of neural stem cells. Resultes NSCs in absorbable gelatin sponge group and control group survived and there was no conspicuous change in shape and quality. The rates of survival cell were 91.6％ and 92.8％ respectively, which was no significant difference between them.NSCs could adherented to the surface of the gelatin sponge and well-grown.After induced differentiation,NSCs started to shrink and stretch,axons grown and connected with each other,till form network structure.The expression of neuroglia cell marker GFAP and neuron cell marker NSE could be detected by immunofluorescence assay. Couclusion Neural stem cells and gelatin sponge can mixed and cultivating together in vitro.NSCs is no conspicuous change.It is suggested that absorbable gelatin sponge can serve as the carrier of the tissue engineering of central nervous system.
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Objective To study the antidepression action of curcumin and to explore its mechanism. Methods Mouse reserpine-induced depression model and mouse tetrabenazine-induced acquired despair model were used to observe the effect of curcumin on relieving depression. According to the hypothesis of monoamine, the effect of curcumin on activating monoamine, and inhibiting reuptake of monoamine neurotransmitters and monoamine oxidase inhibitor (MAOI) were observed. Results Curcumin in the dose of 50 mg/kg and more can relieve melancholic symptoms in mice induced by reserpine and tetrabenazine. Curcumin had no direct activation on monoamine either had no obvious inhibition on reuptake of monoamine neurotransmitters of noradrenalin, 5-hydroxytriptamine and dopamine . However, Curcumin had an obvious effect on improving rat forelimb spasm induced by tryptamine hydrochloride. Conclusion Curcumin acts like a kind of monoamine oxidase inhibitor, which exerts antidepression action by inhibiting monoamine oxidase activity and increasing the concentration of monoamine neurotransmitter in brain.