2.The effects of enteral immunonutrition on immunological function and inflammatory responses in severe scalded rats
Chen CAI ; Guanghua GUO ; Guohui LI ;
Parenteral & Enteral Nutrition 1997;0(01):-
Objectives:To investigate the effects of enteral immunonutrition (Stresson) on immunological function and inflammatory responses in severe scalded rats. Methods:Sixty four SD rats inflicted by 30% TBSA Ⅲ degree scalds were randomly divided into enteral immunonutrition(EIN) and enteral nutrition (EN) groups.Animals of both groups were fed isocaloric enteral nutrition. Lymphocyte subsets, serum levels of immunoglobulins,endotoxin,IL 6,TNF ? were determined on the 1st,4th,7th and 10th day postburn. Results:CD3 + ,CD4 + ,CD4 + /CD8 + in EIN group were higher( P
3.Effects of droperidol on sodium currents in isolated rat dorsal root ganglion neurons
Meng CHEN ; Xinliang ZHUANG ; Guohui XU
Chinese Journal of Anesthesiology 1994;0(03):-
Objective To investigate the effects of droperidol on the Na+ currents in rat dorsal root ganglion neurons.Methods The rat dorsal root ganglion neurons were enzymatically dissociated. Whole-cell patch-clamp technique was applied to record Na+ current. Results 3-300?mol?L-1 Droperidol inhibited the sodium currents by 14.12%-78.46% (P0.05, n =7).Conclusions Droperidol inhibits Na+ currents in rat dorsal root ganglion neurons in a concentration- and voltage-dependent manner. The results suggest that the concentration of epidural droperidol clinically applied during epidural patient control analgesia may enhance the analgesic effects.
4.Characteristics of Muscular Power Changes of Knee Joint and Static Balance in Elderly with Knee Osteoarthritis
Guohui XU ; Jiejiao ZHENG ; Xiuen CHEN
Chinese Journal of Rehabilitation Theory and Practice 2009;15(12):1153-1155
Objective To explore the characteristics of muscular power changes of knee joint and static balance in the elderly patients with knee osteoarthritis(KOA).Methods Isokinetic test and computerized static posturography were performed in 59 patients with KOA(KOA group) and 50 age-matched controlled subjects(conrtol group). The parameters were recorded.Results Peak torque, total work, average power and torque acceleration energy significantly decreased in KOA group compared with the control group at the low velocity of concentric pattern(P<0.05), while hamstring/quadriceps value increased statistically(P<0.05);The values of covered area, length of path, length/area statistically increased in KOA group compared with the control group only when eyes closed (P<0.01), and so did it in KOA group when eyes closed compared with eyes opened(P<0.05); There was significant relationship between length/area and hamstring/quadriceps value.Conclusion The ability of balance declined as knee muscular power decreased in the patients with KOA, especially the non-spontaneous decrease of extensor and flexor power of the knee joint.
5.Regulation of histone acetylation and apoptosis by trichostatin in HL-60 cells.
Xingang, LI ; Weikai, CHEN ; Junxia, GU ; Guohui, CUI ; Yan, CHEN
Journal of Huazhong University of Science and Technology (Medical Sciences) 2004;24(6):572-4
In order to examine the strong anticancer action and low toxicity of Trichostatin A (TSA), the effect of TSA was examined on the growth inhibition, acetylation of histone H3 and apoptosis in HL-60 cells by employing MTT, immunocytochemical techniques, and Annexin-V-FITC/ PI assay. Our results showed that TSA could inhibit proliferation of HL- 60 cells in a time- and dose-dependent manner, and the IC50 at the 36th h was 100 ng/ml. The apoptosis-inducing effect of TSA on HL-60 cells was also time- and dose-dependent. But it didn't demonstrate apparent apoptosis induction in NPBMNCs within specific dose and time range. Both of the acetylation of histone H3 in HL-60 cells and NPBMNCs increased significantly (P<0.05) after treated with 100 ng/ml TSA for 4 h. However, there was no significant differences between the two groups (P>0.05). It is concluded that TSA can inhibit growth and induce apoptosis of HL-60 cells in a time- and dose-dependent manner, and is able to selectively induce apoptosis in HL-60 cells but does not respond in NPBMNCs under the same conditions. The difference of TSA between HL-60 cells and NPBMNCs can't be explained by the regulation of histone acetylation.
Acetylation
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Antineoplastic Agents/pharmacology
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Apoptosis/*drug effects
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HL-60 Cells
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Histone Deacetylases/antagonists & inhibitors
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Histone Deacetylases/*chemistry
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Hydroxamic Acids/*pharmacology
6.Effect of Exercise Practice on Balance Ability of Elder
Jiejiao ZHENG ; Shangmin ZHAO ; Xiuen CHEN ; Peifang LU ; Guohui XU
Chinese Journal of Rehabilitation Theory and Practice 2008;14(1):73-73
Objective To study the factors related with balance ability of the elder.Methods 37 persons above 60 years were assessed with the balanced function reflectoscope reflector,grouped according to their exercise practice.Results The length of locus and length/envelope area as eyes closed increased significantly compared with that as eyes opened in the less exercise group(P<0.05),while they were increased significantly compared with those in the more exercise group either when eyes closed or opened(P<0.05).Conclusion The exercise practice can improve the balances function of the old persons.
7.Study of Simulation Application of Simulink Pharmacokinetic Compartment Model
Wei CHEN ; Yu WANG ; Xiaofei FEI ; Langui XIE ; Guohui LI
China Pharmacist 2015;(5):736-740
Objective:To dynamically describe the drug concentration change in different time in vivo to understand the in vivo be-havior patterns and rules of drugs, provide reference for performing individual treatment and avoiding adverse drug reactions and lay foundation for dynamic description of physiological pharmacokinetic model. Methods:A two-compartment model was established using Simulink dynamic simulation and used in curve fitting and parameter estimation. The results from the model were compared with those from 3P97 software. Results:There was no significant difference between the results from the dynamic model and those from 3P97 soft-ware. Conclusion:The dynamic model can be used to dynamically simulate two-compartment model for oral administration. The re-sults from the dynamic simulation are more direct, and can correct the fitting error in 3P97 software.
8.Effects of midazolam on macroscopic voltage-gated potassium currents in rat sympathetic neurons
Qinghong MAO ; Xinliang ZHUANG ; Meng CHEN ; Jun TANG ; Guohui XU ;
Chinese Journal of Clinical Pharmacology and Therapeutics 2000;0(03):-
AIM: To explore the influence of different concentration midazolam on the macroscopic voltage gated potassium currents and to discuss the relationship between potassium currents and inhibitory effect of clinical relevant concentration midazolam on sympathetic nervous system. METHODS: Superior sympathetic ganglion neurons were dissociated enzymatically from 7 to10 day old rat. Experiments were performed about 5 h after plating at room temperature (20- 24 ℃ ). Appropriate solution was chosen to separate the K + current from the other transmembrane currents. 1 ?mol?L -1 TTX was applied to the extracelluar solution to block the Na + current. Midazolam was also resolved in extracelluar solution to get various concentration ( 0.1 , 0.3 ,3,10,50,100 ?mol?L -1 ). Currents were recorded with the patch clamp technique in whole cell configuration using glass electrodes with a tip resistance of 2- 4 M . Potassium currents were evoked by test pulse from -100 mV to +30 mV with holding potential -80mV. Data were analyzed using Clampfit 6.0 and Oringih 5.0 software. Whole cell current records were corrected for leakage and capacitance by using the P/5 protocol. RESULTS: Midazolam dose dependently inhibited the whole cell potassium currents. Clinical relevant concentration midazolam ( 0.3 ?mol?L -1 ) only reduced the peak currents by 3.89 %(P= 0.88 ). The concentration required to produce 50% current inhibition(IC 50 ) was 76.065 ?mol?L -1 . CONCLUSION: Midazolam inhibits the whole cell potassium current significantly and dose dependently, but clinical relevant concentration midazolam has minor effect on the potassium currents, indicating that the inhibitory effect of midazolam on potassium current is not related to the suppression of activity of sympathetic system.
9.Effect of Gambogic acid on the regulation of hERG channel in K562 cells in vitro.
Guohui, CUI ; Wenxiu, SHU ; Qing, WU ; Yan, CHEN
Journal of Huazhong University of Science and Technology (Medical Sciences) 2009;29(5):540-5
Overexpression of human ether-脿-go-go (eag) related gene (hERG) has been found in a broad range of human leukemia cell lines and primary human leukemia. The block of hERG protein might be a potential therapeutic strategy for leukemia. Gambogic acid (GA) has recently exhibited marked anti-tumor potency on solid tumors of various derivations. Here, we investigated the anti-leukemia effects of GA and its relation to the regulation of hERG in K562 leukemia cells in vitro. K562 cells were treated with various concentrations of GA (0.125-8.0 micromol/L) for 0-72 h. MTT assay was used to evaluate the inhibition effect of GA on the growth of K562 cells. Cell apoptosis was measured through both Annexin-V FITC/PI double-labeled cytometry and transmission electron microscopy. Cell cycle regulation was studied by a propidium iodide method. RT-PCR and Western blot were applied to detect the expression level of hERG in K562 cells. GA presented striking growth inhibition and apoptosis induction potency on K562 cells in vitro in a time- and dose-dependent manner. The IC(50) value of GA for 24 h was 2.637+/-0.208 micromol/L. Moreover, GA induced K562 cells arrested in G(0)/G(1) phase, accordingly, cells in S phase decreased gradually, and no obvious changes were found in G(2)/M phase cells. Under the transmission electron microscopy, apoptotic bodies containing nuclear fragments were found in GA-treated K562 cells. After treatment with GA of 2.0 micromol/L for 24 h, the percentage of apoptotic cells was increased from 4.09% to 18.47% (P<0.01). Overexpression of hERG channel was found in K562 cells, while GA could down-regulate it at both protein and mRNA levels (P<0.01). It was concluded that GA exhibited its anti-leukemia effects partially through down-regulating the expression level of hERG channel in K562 cells, suggesting that GA may be a potential agent against leukemia with a mechanism of blocking hERG channel.
10.Wortmannin inhibits K562 lukemic cells by regulating PI3k/Akt channel in vitro.
Qing, WU ; Yan, CHEN ; Guohui, CUI ; Yiquan, CHENG
Journal of Huazhong University of Science and Technology (Medical Sciences) 2009;29(4):451-6
The inhibitory effect of wortmannin on leukemic cells and the possible mechanisms were examined. K562 cells were treated with wortmannin of various concentrations (3.125-100 nmol/L) for 0-72 h. MTT assay was used to evaluate the inhibitory effect of wortmannin on the growth of K562 cells. Cell apoptosis was detected by both Annexin-V FITC/PI double-labeled cytometry and transmission electron microscopy (TEM). The expression of p-Akt, T-p-Akt, NF-kappaBp65 and IKK-kappaB was determined by Western blotting and reverse transcription-polymerase chain reaction (RT-PCR). Our results showed that wortmannin obviously inhibited growth and induced apoptosis of K562 cells in vitro in a time- and dose-dependent manner. The IC(50) value of wortmannin for 24 h was 25+/-0.14 nmol/L. Moreover, wortmannin induced K562 cells apoptosis in a dose-dependent manner. TEM revealed typical morphological changes of apoptosis in wortmannin-treated K562 cells, such as chromatin condensation, karyopyknosis, karyorhexis and apoptotic bodies. Additionally, several important intracellular protein kinases such as p-Akt, NF-kappaBp65 and IKK-kappaB experienced degradation of various degrees in a dose-dependent manner both at protein level and transcription level when cultured with wortmannin, but the expression of total Akt showed no change. It is concluded that wortmannin can inhibit the proliferation and induce apoptosis of K562 leukemia cells possibly by down-regulating the survival signaling pathways (PI3K/Akt and NF-kappaB channels).