Basic & Clinical Medicine

Mesenchymal stem cell, cancer stem cell and cancer

Hui QIAN; Wen-rong XU

2008, 28(9): 897-903.

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Recent theorys suggest the existence of cancer stem cell (CSC), a subpopulation of cells with tumorigenic potential that is lacked in the rest of the cells within this tumor. It has been reported that the occurrence of some tumors closely related to mesenchymal stem cell as origin of stroma cell. This review discuss the relationship among mesenchymal stem cell, cancer stem cell and cancer.

Molecular characteristics of leukemia stem cells and up-dating therapeutic strategy

Ying GU; Xi QIU; Rong-zhen XU

2008, 28(9): 904-907.

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Drug resistance and relapse are two major causes for treatment failure of leukemia, but their mechanisms remain elusive. Recently, increasing evidence shows that there is a subset of leukemia stem cells apart from immature leukemia cells in leukemia patients. These cancer stem cells are not responsible to conventional chemotherapeutic agents, and may be the root of drug resistance and relapse of leukemia. Permanent cure of leukemia need elimination of these leukemia stem cells. We describe molecular characteristics of leukemia stem cells and possible target therapeutic strategies in this review.

Progress in Ovarian Cancer Stem Cells Research

Wei HE; Qing-xia FAN; Zhen-he SUO

2008, 28(9): 908-913.

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Cancer stem cells are characterized by self-renewal and multi-differentiation potential, which play an important role in initiation, progression and metastasis of tumor. Interest in cancer stem cells is rapidly increasing, and the existence of such cells in various of tumors has been verified during the recent years. The progress of ovarian cancer stem cells research is reviewed in this article, which suggests that better solutions on isolation and identification of ovarian cancer stem cells are critical tasks currently, and primary cells culture may play a key role in these issues.

Tumor stem cells and targeting cancer therapy

Shu-li WEI Shi-neng ZHANG

2008, 28(9): 914-919.

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The hypothesis of tumor stem cells believes that a small proportion of cells which have the stemness property reside in tumor. This population is the reason of tumor formation, growth, metastasis and relapse. Only the therapy targeting this population could make tumors curable. At present, most anti-cancer protocols merely kill the majority of differentiated tumor cells and hardly affect the tumor stem cells. That is why most of the therapies do not achieve good results. Disrupting the pathways and niche which regulate the tumor stem cells' self-renewal, or inducing the tumor stem cells' differentiation, or targeting the surface markers which distinguish the tumor stem cells from normal stem cells are all probable strategies.

Regulatory T cells in patients with early new-onset systemic lupus erythematosus

Biao ZHANG; Xuan ZHANG; Fu-lin TANG Li-ping ZHU; Yin LIU

2008, 28(9): 920-924.

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Objective To investigate the expression of FOXP3 and CD25 in CD4+ T cells of peripheral blood from patients of early new-onset systemic lupus erythematosus(SLE) before and after treatment. Methods Forty-four early new-onset SLE patients including twenty-four with active disease (SLEDAI≥10), twenty with low active disease (SLEDAI<5) were enrolled in this study. Twenty-one healthy volunteers were also included as controls. Peripheral blood samples before and after treatment were collected. Cell populations of CD4+CD25+T cells, CD4+CD25highT cells and CD4+FOXP3+T cells were quantified and the expression of CD25 in CD4+FOXP3+T cells and FOXP3 in CD4+CD25highT cells were also analyzed. Results Peripheral blood CD4+CD25+T cells and CD4+CD25highT cells in active new-onset lupus patients (3.95%~13.04%, 0.04%~1.34%) were significantly lower than in low active lupus patients (7.27%~24.48%, 0.14%~3.07%) (P<0.05,P<0.01); Though there was no significantly difference of CD4+FOXP3+T cells in active (7.46%~17.38%) and in low active (5.30%~23.00%) new-onset lupus patients, both were significantly higher than in normal controls(2.51%~12.94%) (P<0.01,P<0.01); CD25 expression in CD4+FOXP3+T cells in active lupus patients (25.24%~62.47%) was significantly lower than in low active untreated lupus patients(30.35%~75.25%) and normal controls(54.83%~86.38%) (P<0.05, P<0.05). Meanwhile, Mean fluorescent intensity (MFI) of FOXP3 in CD4+CD25highT cells from patients with new-onset SLE was significantly lower than from normal control（100.52~160.92 vs. 122.58~198.10., P=0.012）. CD4+CD25highT cells increased significantly in active lupus patients after corticosteroid treatment. Conclusions The disproportional expression between CD25high and FOXP3+ in CD4+T cells may play an important role in imbalance of immune homeostasis in new-onset patients with active SLE.

-Synuclein regulates mitochondrial complex I activity of respiratory chain of rats

Guang-wei LIU; Juan-juan YIN; Xin LI; Sheng-nan XIE; Yao-hua LI; Shun YU

2008, 28(9): 925-929.

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Objective To study the expression of mitochondrial -Synuclein ( -SYN) in different rat brain regions and its effect on complex I activity of respiratory chain. Methods Immunoblot analysis was used to examine the expression level of mitochondrial -SYN in different brain regions and the transportation of -SYN into isolated mitochondria. The mitochondrial complex I activity of respiratory chain was measured by measuring the change of NADH maximal absorbance at 340 nm. Results -SYN was found to localize in mitochondria throughout the rat brain, with the amount being varied in different brain regions. Incubation of recombinant -SYN protein with isolated mitochondria led to transportation of this protein into mitochondria. Incubation of -SYN protein with isolated mitochondria decreased the complex I activity of respiratory chain in a dose-dependent manner. Conclusion The amount of mitochondrial -SYN is varied in different brain regions. Mitochondrial -SYN may come from the transportation of cytoplasmic -SYN and may regulate the complex I activity of respiratory chain.

Effects Of Superparamagnetic Iron Oxide On Proliferation And Neural Differentiation Of Human Mesenchymal Stem Cells

Chang-jun WANG; Shan LU; Ming FENG; Qin HAN; Jun-ji WEI; Ren-zhi WANG; Chun-hua ZHAO

2008, 28(9): 930-935.

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Objective To label Flk-1+CD31-CD34- human Mesenchymal Stem Cells (hMSCs) with Superparamagnetic Iron Oxide (SPIO) and evaluate the effect of SPIO on proliferation and neural differentiation of labeled cells. Methods hMSCs were incubated with SPIO (50mg/L) and PLL (1.5mg/L) overnight(12-18 hours). Both labeled and unlabeled cells went through growth curve test，Trypan blue staining and flow cytometer to evaluate the effects of SPIO on cell proliferation，cell viability and surface markers. Immunofluorescence assay was conducted for neuron and neuroglia specific cell surface markers after neural induction protocols were used. Results Cell viability results of two groups were both more than 90% in the following 7 days. There was no significant difference on cell viability and growth curve test between two groups. The results of flow cytometer showed that both labeled and unlabeled cells expressed CD44, CD105 and Flk-1 markers, while CD31 and CD34 were negative. After neural induction, the statistical analysis of A value for all the markers showed no significant difference between the two groups. Methods: hMSCs were incubated with Feridex (50mg/L) and PLL (1.5mg/L) overnight(12-18 hours). Both labeled and unlabeled cells went through growth curve test Trypan blue staining and flow cytometer to evaluate the effects of Feridex on cell proliferation，cell viability and surface markers. Immunofluorescence assay was conducted for neuron and neuroglia specific cell surface markers after two kinds of neural induction protocols were used. Results：After incubated with Feridex and PLL overnight, the labeling rate of hMSCs could be 96％. Cell viability results of two groups were both more than 90% in the following 7 days，indicating that Feridex didn’t cause significant cell death. There was no significant difference on cell viability and growth curve test between two groups. The results of flow cytometer showed that both labeled and unlabeled cells expressed CD44, CD105 and Flk-1 markers, while CD31 and CD34 were negative. According to the two kinds of neural induction protocols, the statistical analysis of OD for all the markers showed no significant difference between the two groups. Conclusions: Incubated with Feridex(50mg/L) and PLL(1.5mg/L) overnight could effectively label hMSCs. Feridex shows no significant influence on cell viability, proliferation, cell surface markers and neural differentiation. Feridex, as MRI cellular contrast, is safe and efficient.Conclusions SPIO, as MRI cellular contrast, is safe and efficient.

Effects of Magonol on Body Weight and Insulin Resistance of High-fat-fed Obese Rats

Zhen GUO; Liang-jie YUAN; Xia LU; Mei-ling LIN; Tian-zhen ZHENG; Wei LI

2008, 28(9): 936-939.

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Obejective To study the effects of magnolol on body weight and insulin resistance of high-fat-fed rats and to discuss the possible mechanism. Methods SD rats were randomized into 4 groups: (1) normal control group fed with ordinary diet and administered normal saline, (2) high-fat-fed group administered normal saline, (3) and (4) groups fed with high fat diet and administered high and low concentration of aqueous suspension of magnolol diluted by normal saline respectively. Food intake was monitored daily and body weight was weighed weekly at the set time. At the end of the eighth week, All rats were fasted for 12 hours to collect blood for measuring biochemical Indexes, including glucose, insulin, free fatty acid(FFA), total antioxidative ability（T-AOC）, malondialdehyde(MDA) and so on . Result The body weights of rats in low dose group administered magnolol were lower than that of high-fat-fed group from the fourth week on（P<0.05）. Compared with high-fat-fed group, the serum levels of insulin, FFA and MDA reduced in each group administered magnolol（P<0.05）. Conclusion Magnolol can inhibit the weight gain caused by high-fat diet, reduce serum levels of MDA, FFA and insulin and improve the inlusin resistance and metabolism disorders.

SNP 45(T/G) of adiponectin gene polymorphism and genetic susceptibility to type 2 diabetes mellitus

Ying-li WEI; Lan-jie HE; Zheng-hao HUO; Wei ZHAO

2008, 28(9): 940-943.

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Objective To investigate the association of single nucleotide polymorphisms (SNP)45T/G in the adiponectin gene with type 2 diabetes of Han nationality in Ningxia.. Methods PCR- RFLP method was used to determine the distributions of alleles and genotypes frequencies of SNP45T/G polymorphisms in adiponectin gene in 100 type 2 diabetic patients and 101 normal subjects .Results The distribution of both genotypes and alleles frequencies of the SNP45 polymorphisms were significantly different between two groups(GG genotype:13% vs 3% ,P<0.05;G allele;76% vs 24%, P<0.05). Conclusion The results suggest that SNP45 in adiponectin gene was associated with type 2 diabetes of Han nationality in Ningxia. Individuals with SNP45 GG genotypes of adiponectin gene have high susceptibility to type 2 diabetes.

Proliferation of renal cells induced by NF-κB/COX-2 signal pathway in diabetic nephropthy

Shu-xia LIU; Yu-jun ZHANG; Jing-kun ZHANG; Qing-juan LIU; Li-juan TANG; Hui-jun DUAN

2008, 28(9): 944-948.

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Objective To investigate the correlation between NF-κB/COX-2 signal pathway and cell proliferation in diabetic nephropathy. Methods Uninephrectomized STZ-induced male Wister rats were used. Using immunohistochemistry to detect NF-κB and COX-2 protein expressions in diabetic kidneys at the week of 16 . HKC were cultured separately in normal or high glucose medium for 24,48,72h.The expression of NF-κB and COX-2 protein was detected by flow cytometry and the expression of PCNA was detected by immunocytochemical staining. Results 1 Volum of glomeruli, mesangial matrix, thickness of glomerular and tubular basement membrane increased in diabete group; 2 COX-2 were positively expressed in cytoplasm of tubules and glomeruli by immunohistochemistry. Compared with control group, the expression of COX-2 was higher; activated NF-κB were positively expressed in nucli of both tubules and glomeruli, There was weak stainings for in control group, while enhanced stainings were observed in DM, there was positive correlation between NF-κB and COX-2. 3 Compared with those in HKC cultured in the medium with normal level glucose, the stainings were strengthened for PCNA in HKC exposed to high glucose from 24h . 4 By FCM , the expression of NF-κB and COX-2 in HKC cultured in high glucose medium was higher than that in normal glucose medium ; the expression of NF-κB and PCNA was positively correlated with the expression of COX-2. Conclusion Activating NF-κB and elevating the expression of COX-2 play an important role in regulating cell proliferation , which may be one of the injury mechanisms of the renal cells during diabetic nephropathy.

Double protect functions of rat Sertoli cells to co-encapsulated hepatocytes in vitro

Hai-long LIN; Yong-ping CHEN; Ming-hua ZHENG; Yue-e HE; Yu HUANG; Lan-man XU

2008, 28(9): 949-952.

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Objective To evaluate the nourishment and immune privilege effects of Sertoli cells to co-encapsulated hepatocytes. Methods The hepatocytes and Sertoli cells were alone encapsulated or co-encapsulated in various ratio of 100:1、50:1、20:1、10:1, and co-cultured for 21 days in vitro. The secretion of albumin and urea was analyzed, and the morphology of encapsulated cells was observed by microscopy, then to determine the best mixed ratio of hepatocytes to Sertoli cells. Splenocyte proliferation response was assessed to evaluate Sertoli cell's immune privilege function to hepatocytes by CCK-8. Results Sertoli cells could elevate hepatocyte's secretion of albumin and urea when they were co-encapsulated with each in appropriate ratio (P<0.01), and prolonged the survival time of hepatocytes. The mixed ratio of 20:1 get the best effect at secretion of albumin and urea . Capsules contained hepatocytes initiated significant splenocyte proliferation response, in spite of more significant to hepatocytes group (P<0.01). Sertoli cells could inhibit splenocyte proliferation obviously. Conclusion Co-encapsulated hepatocytes with Sertoli cells is an available approach to sustain hepatocyte's function、morphology and survival, and inhibit impairment of immune response partially.

Effcects of Interleukin-1β on the expression of VEGF In A549 cells lines

Lan-yan ZHU; Ping CHEN; Yun-sheng JIANG

2008, 28(9): 953-956.

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Abstract: Objective To investigate the effect of interleukin-1β(IL-1β) on the expression of VEGF in A549 cells lines. Methods: A549 cells were incubated with IL-1βin the presence or absence of Celecoxib. After indicated incubation time, cells were harvested to detect VEGFmRNA by reverse transcription-polymerase chain rection (RT-PCR), and the medium was collected to determine the concentration of VEGF protein by enzyme-linked immunosorbent assay (ELISA).Results: After treated with IL-1β, the expression of VEGF mRNA and protein in A549 cells were significantly higher than that in the control group(P＜0.05); IL-1β upregulate the expression of VEGF mRNA, protein in a time-dependent and dose-dependent manner in A549 cells, after incubation 24 hours, VEGF expression were up to high. After Celecoxib intervention, VEGF expression were decrease than control group(IL-1βinduced), the difference was significance(P＜0.05); with the concentration of Celecoxib step up, VEGF expression were decrease in dose-dependent manner, and the difference within different group was significance(P＜0.05. Conclusions： These results suggest that IL-1β upregulate VEGF expression in A549 cells lines，the mechanism may be at transcriptional level; Celecoxib down-regulated IL-1β induced VEGF expression in A549 cells lines.

Snail1 expression increased in the renal tissues of diabetic rats

Kai-yun FANG; Jing-lei LOU; Ying XIAO; Ming-juan SHI; Hua-zhen GUI; Bing GUO; Guo-zhong ZHANG

2008, 28(9): 957-963.

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Objective To explore the expression of snail1 in renal tissues of diabetic rats ,and to investigate its contribution to the progression of diabetic nephropathy.Methods Rats were randomly divided into control groups,DM and insulin-treated groups . The protein and(or) mRNA expression of Snail1，E-cadherin, α-SMA and FN in renal tissue were detected. Results The Snail1 protein strongly positive stainings were observed in renal tubules of DM rats. In DM rats α-SMA tubules staining were seen from 16th week. The proteins and mRNA of Snail1 and FN were significantly up-regulated in renal cortex of diabetic rats（P＜0.05）, while down-regulated in the insulin-treated diabetic rats （P＜0.05）. The expression of E-cadherin protein and mRNA were contrary to the snail1.Conclusion These findings suggest that snail1 expression is up-regulated in the renal tubules of rats with DM , which may involve in the pathogenesis of diabetic nephropathy by inducing FN and tubular epithelial-mesenchymal transition.

Tyrosine kinase Src mediates Notch-1 activation in BxPC3 pancreatic cancer cells

Xiao-yan YANG; Yu-xiang ZHANG; Zhe-sheng WANG

2008, 28(9): 964-968.

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Objective To observe the effect of tyrosine kinase Src on activating Notch-1 protein in pancreatic cancer cell line - BxPC3. Methods Notch-1 expression and c-Src expression were inhibited by siRNA interference, and the activation of Src was inhibited by its inhibitor PP2. The growth rate of BxPC3 cells was measured by MTT. The changes of Notch-1 NICD level and Src protein level were measured by Western blot. Results The growth of BxPC3 cells decreased after inhibiting Notch-1 expression, as well as the cells were treated with PP2. The level of Notch-1 NICD decreased both after inhibiting c-Src expression and after Src activation was inhibited by PP2. Conclusion In BxPC3 cells, tyrosine kinase Src promotes the level of Notch-1 NICD, which directly influences the cell growth.

Tamoxifen inhibit cell proliferation and currents of sodium channel in glioma cell line SHG-44

Shuai WANG; Bao-hua JIAO

2008, 28(9): 969-972.

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Objective To explore the effects of tamoxifen on the proliferation of SHG-44 glioma cells and the currents of sodium channel. Methods The cellular activity was detected by MTT test.The alteration of cellular proliferation and apoptosis was dectected by flow cytometer. Whole-cell patch clamp technique was used to record the Na currents.Results After treatment with tamoxifen,the cells became aging and shedding.The total sum of them decreased.The cells in G2/M cell cycle was more than that in control and the apoptosis ration increased. Tamoxifen could significantly decrease the amplitude of Na currents of SHG-44 cell line.This block effect was dose dependent and voltage dependent.When the holding potential was 0mV, 8μmol/L tamoxifen could block this currents 69%.The half inhibition concentration(IC50) was 5.54μmol/L. Conclusion Tamoxifen can inhibit SHG-44 glioma cells proliferation.The inhibion of sodium channel may be one of its mechanisms.

Nicotinamide Enhances the Effect of None Focused Ultrasound on the Death of Human Pulmonary Carcinoma Cell Line GLC-82

Jian-lian GUO; Hong SHEN

2008, 28(9): 973-977.

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Objective To determine the sensitization of Nicotinamide (NA) on None Focused Ultrasound (NFU) on GLC-82 cells in vitro. Methods The experiments were divided into A、B、C and D four groups, group A was negative control, group B was treated with NA, group C was irradiated with NFU, group D was treated with both NFU and NA; MTT assay was used to evaluate the cytotoxicity of NA and its sensitivity for NFU on GLC-82 cells quantified by calculating the sensitive enhancement ratios (SER); Morphologic change of cells were observed with light microscope, fluorescence microscope and scanning electron microscope；Flow cytometry was performed to determine the percentage changes of apoptosis and distributional percentage of the cell cycle of GLC-82 cells in response to NFU, NA and the effect of its intervention to NFU. Results The cytotoxicity of NA increased in a dose-dependent manner after 24-hour treatment, with the optimal dose range of 1 mg/ml-5 mg/ml. A sub-toxic dose of NA at 3 mg/ml was used in the subsequent experiments; After treatment with NA plus NFU, microvilli and filipodium of GLC-82 cells reduced, shortened and shrunk into corpuscule-shape; The apoptosis rate of group D was more than group B and C, with cell cycle arrested at phase S and G2；Conclusion NA can obviously enhance the effect of NFU on GLC-82 cells, which provided evidence for NA as a sensitization to NFU in clinic.

Dexamethasone inhibited the expression of RANTES in the lungs of asthmatic mice

Ye-qing ZHANG; Shu-yang ZHU; Li-li LV; Qi-nan ZHU; Jia ZHU

2008, 28(9): 978-981.

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Objective :To study the effect of dexamethasone on the protein and mRNA expression of RANTES in asthmatic mice. Methods: Thirty female BALB/c mice were randomly divided into three groups(10 mice in each group) : control group\asthmatic group \dexamethasone group . Bronchoalveolar lavage fliud (BALF) were collected for counting cells and the percentage of eosinophils (EOS); RANTES concentrations in BALF and serum were measured by ELISA.The pathologic changes of bronchi and the left lung tissue were evaluated and stained with hematoxylin and eosin(HE), Immunohistochemistry was used to measure the level of RANTES protein in the lung tissues of asthmatic mice.In situ hybridization was used to measure the level of RANTES mRNA in the lung tissues of asthmatic mice.Results :The total cells、percentage of EOS、concentrations of RANTES in BALF and serum in asthmatic group was significantly different from control group (P<0.01); Dexamethasone group were significantly different from asthmatic group (P<0.01). The expressions of RANTES protein and RANTES mRNA around the lung tissue of asthmatic group were significantly elevated than those of control group (P<0.01), the epithelial cell was the chief expression cell, the expressions of RANTES protein and RANTES mRNA around the lung tissue of dexamethasone group were significantly lower than those of asthmatic group (P <0.01).Conclusion: Dexamethasone demonstrates anti-inflammatory effects partly by downregulating the expressions of RANTES protein and RANTES mRNA.

Recombinant adenovirus vector delivered report gene expression in rats kidney through different way

Lin LI; Fang WU; Hong LI

2008, 28(9): 982-985.

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Objective To investigate expression of recombinant adenovirus(rAV) vector-mediated report gene in kidney, and seek for the best way of rAV vector-mediated gene transfer in vivo. Methods Thirty Sprague-Dawley(SD) rats were divided into 5 groups randomly. rAV－GFP(1013viral particales·L-1 ) was injected through different ways. 2, 7 and 14d after injection, the GFP expression in left kidney, right kidney, liver and lung was evaluated by fluorescence microscope and computer software. Results GFP gene expressed in kidey and 7d after injection expression reach peak, through intraperitoneal and caudal vein injection expressions were most; through renal artery has the best target. Conclusion rAV vector-mediated report gene could be transducted in kidney. The rAV-mediated transgene expression in kidney is a potential strategy in treatment kidney diseases and different ways have their own characteristics.

Significance of MMP-9 and TIMP-1 in human nasal polyps

Gang XUE; Yang LU; Jing-fang WU; Bo LIU; Jun-xu REN

2008, 28(9): 986-987.

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Effects of Ethanol on Proliferation and CYP450 Isoform Expressions in Hepatic Stellate Cells by Gene Array Assays

Zhang-xiu LIAO; Hui WANG; Jie PING; Yong WU

2008, 28(9): 988-989.

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Increase of leukotrienes C4 scretion in human umbilical vein endothelial cells treated by oxidized low density lipoprotein

Wu-sheng ZHU; Guang-yi ZHOU; Hua-jun ZHANG; Xiao-wei MAO; Bing LUO; Ge-lin XU; Xin-feng LIU

2008, 28(9): 990-991.

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Changes in serum levels of IL-18 and IFN-γ in relapsing remitting multiple sclerosis

Jie LV; Jun WANG

2008, 28(9): 992-993.

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Pathophysiology role of angiotensin converting enzyme 2

Jing HONG; Min NIE; Mei-li SUN; Da-wang WANG

2008, 28(9): 994-997.

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The rennin angiotensin system had been recognized for many years as a key regular of systemic blood pressure and the metabolism of water and salt. Angiotensin converting enzyme 2(ACE2) was the first human homolog of Angiotensin converting enzyme which efficiently hydrolyzed the angiotensin II to vasodilator angiotensin l-7.ACE2 is now implicated in cardiovascular ,renal, lung disease and serves as a receptor for Severe Acute Respiratory Syndrome coronavirus.

Rep78/68 protein of adeno-associated virus

Tian-hui LIU; Hong YOU

2008, 28(9): 998-1000.

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Rep78/68 is a nonstructural protein of adeno-associated virus. It has been found to inhibit a variety of viruses and tumor transformation. In addition, it has spreading effect on the proliferation and metabolism of host cells. Here, we reviewed the latest advances of this protein.

Role of retrograde messenger NO in long-term potentiation

Wei LU; Rui-bin SU; Jin LI

2008, 28(9): 1001-1003.

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As an important messenger molecule, NO exists in both peripheral and central nervous system (CNS). Recently NO was proved to play a critical role in CNS, especially in synaptic plasticity. As a kind of retrograde messenger, it plays some roles in the induction and maintenance of LTP through activation of downstream pathway or molecules, such as NO-cGMP-PKG, ADPRT and C-FOS.

Progress of the vector for mediating RNA interference in mammals

Xiang-e LONG; Zhao-hui GONG

2008, 28(9): 1004-1006.

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RNA interference (RNAi) is a process that functions to inhibit the specific gene expression via the degradation of the target mRNA induced by the double strand RNA. The use of RNAi in mammals as a tool to study gene function has rapidly developed in recent years. Here we described the novel progress and applications of the vector for mediating RNAi in mammals.

Research on the connection between pathophysiological experiment teaching and clinics

Ya-nan JIANG; Yan-yan ZHANG; Ji-min ZHAO; Ping CHEN; You-tian HUANG; Zi-ming DONG

2008, 28(9): 1007-1008.

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The connection between pathophysiological experiment practice and clinics plays primary role in strengthening students' abilities in doing and clinical thinking. It also enables them to understand the mechanisms underlying the development of diseases. Through the experimental design, designed questions and case discussion, pathophysiological experiment teaching can be integrated with clinics and arouse students' enthusiasm. All above is the basis of clinical teaching.

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