Objective To investigate the treatment effect of gamma knife radiosurgery for hypothalamic hamartomas. Methods Gamma knife radiosurgery was performed in 9 patients with gelastic seizures. Collimator helmets (4 and 8 mm) were used and a radiosurgery plan was designed to cover 90% of the hamartoma at the 40%~55% isodose curve with the center dose of 28~40 Gy and the margin dose of 12~18 Gy. The clinical outcome was evaluated with the Tan’s scale. Results No complications due to gamma knife radiosurgery occurred. A follow-up from 24 to 54 months showed effectiveness in 7 patients, disappearance of seizure in 1 patient, rare occurrence in 3 patients, significantly reduced occurrence in 2 patients, improvement in seizure control in 1 patient, but ineffectiveness in 2 patients. Conclusion As an approach to the treatment of hypothalamic hamartomas, gamma knife is a safe and cost-effective therapy with rare side effects for hypothalamic harmatomas.

Objective To investigate the effects of human umbilical cord mesenchymal stem cells (UC-MSCs) on vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6) expression in acute myocardium infarction (AMI) rats. Methods The human UC-MSCs were cultured to the 4th generation for experiment. Sixty male Sprague-Dawley (SD) rats were randomly divided into sham group, AMI model group and UC-MSCs group, with 20 in each group. AMI animal model was produced by ligation of anterior descending coronary artery; in the sham group, the threading vein was gone below without ligation. In UC-MSCs group 2×106 UC-MSCs were infused through the caudal vein at 24 hours after successful model production. The animals were sacrificed after 7 days; the myocardial tissue and coronary artery below the ligation line were harvested. The mRNA and protein expressions of IL-6 in myocardium were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western Blot. The positive expression of VEGF in coronary artery was observed by immunohistochemisty. Results Compared with the sham group, the mRNA and protein expressions of IL-6 in myocardium in AMI model group were increased significantly (gray value: 0.732±0.131 vs. 0.321±0.080, 0.678±0.191 vs. 0.286±0.061, both P < 0.05). Compared with the AMI model group, the mRNA and protein expressions of IL-6 in myocardium in UC-MSCs group were decreased significantly (gray value: 0.300±0.104 vs. 0.732±0.131, 0.312±0.101 vs. 0.678±0.191, both P < 0.05). Observation under light microscope, the VEGF positive cells in AMI model group was increased significantly compared with the sham group (cells/HP: 21.1±2.2 vs. 7.6±1.3, P < 0.05), the VEGF positive cells in UC-MSCs group were increased significantly compared with the AMI model group (cells/HP: 41.5±3.1 vs. 21.1±2.2, P < 0.05). Conclusion Human UC-MSCs could promote angiogenesis by the improvement of VEGF in coronary artery and inhibit the inflammation by the reduction of IL-6 in rats with AMI.

Objective To investigate the dynamic changes of metallothionein(MTs)gene expression and explore the important significance of MTs during hepatocarcinogenesis.Methods One hundred and twenty-five SPF 5 -8-week old male C57BL/6J mice were randomly divided into control group and model group.Diethylnitrosamine (DEN) was given to the mice at a dose of 100 mg/kg, ip, and 50 mg/kg, ip, in the first and next week, respectively.The mice were given ethanol (53%, 5 mL/kg/day, 5 days/week) from the third week of experiment till 35 weeks.At 1, 3, 9, 13, 24 and 35 weeks of the experiment, liver samples were taken for histopathological examination of liver damages and incidence of HCC. The liver index and malondialdehyde (MDA) of liver homogenate were determined.All liver tissue samples were examined by histopathology using hematoxylin and eosin (HE), Masson and reticular fiber staining.Real-time RT-PCR was used to analyze the mRNA expression level of liver metallothionein-1 /2 (MT-1 /2) in different periods.Results Progressive liver damages in model group mice were identified in different periods.Hepatocytes abnormal tission and abnormal liver plate structure, architecture often characteristic of HCC could be seen in approximately 50% of mice at 35 weeks.In addition to these, a higher liver index also were seen at 35 weeks.Increased MDA levels in the mouse liver tissues were observed in each stage.Real-time RT-PCR analysis showed that significantly increased transcription of MT-1 and MT-2 at 1, 3 and 9 weeks, then gradually declined and even below the normal level.Conclusions MTs gene expression levels in mouse liver tissues are changed from significantly increased in the early stage of injury to decreased expression combined with distinct fibrosis. Our findings further demonstrate that the down-regulation of MTs level is closely correlated with hepatocarcinogenesis.

AIM:To discover the effect of MCPH1 on the DNA damage induced by ionizing radiation in esoph-ageal cancer cells.METHODS:ECA109 cancer cells were radiated at dose of 8 Gy.The nuclear foci of relevant factors were detected 1 h after irradiation in the ECA109 cells after silence of MDC1 gene.A cell line was established that was sta-ble low expression of MCPH1.The nuclear foci induced by ionizing radiation after silence of MCPH1 were determined.RE-SULTS:The MCPH1 gene silenced ECA109 cell line was successfully constructed.A strong relationship between MDC1, MCPH1 andγ-H2AX was observed 1 h after 8 Gy irradiation.Silence of MDC1 did not affect the nuclear foci formation ofγ-H2AX and MCPH1.The nuclear foci of MDC1 but notγ-H2AX significantly reduced after silencing of MCPH1.CON-CLUSION:MCPH1 is located in the downstream of H2AX and upstream formation of MDC1, and regulates the nuclear fo-ci formation of MDC1 during DNA damage response.

[ ABSTRACT] AIM:To investigate the inhibitory effect of Am80 on neointima hyperplasia in carotid arteries after balloon injury and to observe the interaction between Krüppel-like factor 4 (KLF4) and retinoic acid receptorα(RARα). METHODS:Neointima hyperplasia in carotid arteries was observed by hemotoxylin and eosin staining.The expression of KLF4 and cyclin D1 was examined by immunostaining and Western blotting analysis.To detect the interaction between KLF4 and RARαin the vascular tissue, the injured arteries were harvested, and the protein extracts were prepared and subjected to co-immunoprecipitation assay.RESULTS:Compared with injured group, Am80 significantly reduced neointi-mal hyperplasia and the thickness ratio of intima to media.Am80 not only up-regulated KLF4 or RARαexpression in caro-tid arteries, but also increased the interaction between KLF4 and RARαat tissue levels.CONCLUSION:Am80 inhibits neointima hyperplasia in carotid arteries after balloon injury by promoting the interaction between KLF4 and RARα.

AIM: To investigate the expression, distribution and significance of nuclear factor κB (NF-κB) in experimental hepatic fibrosis.METHODS: Wistar rats were randomly divided into normal control group, hepatic fibrisis model group and the pyrrolidine-1-dithiocarboxylic acid ammonium sail (PDTC) group. The PDTC group was treated with subcutaneous injection of carboan tetrachloride, and treated with PDTC by oral administration. The content of hydroxyproline was measured. Endotoxin was determined with a Limulus amebocyte lysate test kit. The alanine aminotransferase (ALT) in plasma was measured by laishi method. The content of malondialdehyde (MDA) in liver tissue was detected by means of TBA method. The expression of NF-κB was determined by immunohistochemistry. The expression of connective tissue growth factor (CTGF) was measured by Western blotting.RESULTS: In control group, just a small amount of NF-κB p65 was expressed in the cytoplasm of a few hepatocytes around central veins. In model group, the positive staining of NF-κB p65 was expressed in cytoplasm and nucleus, mainly in fibrous stepta, hepatic sinusoid and partial vascular endothelial cells, part of proliferating ductular epithelial cells and impaired hepatocytes. The positive staining began to increase from the first week. The expression of NF-κB in the liver tissues in PDTC group was lower than that in model control group (P<0.05). The ET levels and expression of NF-κB and CTGF began to increase significantly in liver fibrosis group. The levels of plasma ET and expression of NF-κB and CTGF were correlated positively with each other. In PDTC group, ET content in plasma increased significantly at first, then began to decline at the end of the test. The expression of NF-κB and CTGF in liver tissues in PDTC groups was lower than that in model group. Furthermore, the expression of NF-κB in liver tissues in PDTC group was correlated positively with CTGF. The levels of plasma ET were not correlated with the expression of NF-κB and CTGF.CONCLUSION: ET may up-regulate the expression of CTGF by activating NF-κB.

Objective:To investigate the correlation between endothelial dysfunction and cardiomyocyte apoptosis during myocardial ischemia-reperfusion.Methods:A total of 63 male rats were selected to establish the rat model of myocardial ischemia-reperfusion by the ligation of the left anterior descending(LAD)coronary artery to simulate myocardial ischemia.Rats were divided into the control group and group Ⅰb, group Ⅰa, group Ⅱb, group Ⅱa, group Ⅲb and group Ⅲa.Control rats were treated only with LAD threading without ligation.In observation group, at 30, 90, 120 min after LAD ligation(marked as Ⅰ, Ⅱ, Ⅲ group respectively), loosen the ligation to simulate ischemia-reperfusion.In the observation group, captopril sublingual injection of 0.25 mg/kg before ligation were marked as group b, and as group a with no captopril injection.The circulating endothelial cells(CEC), endothelin(ET), nitric oxide(NO)and the apoptosis rate of cardiomyocytes in each group were measured.Results:The CEC and ET levels showed a continuous upward trend, and a NO level showed a continuous downward trend from group Ⅰa to Ⅱa to Ⅲa as compared with the control group( P<0.05). After using preventive intervention of captopril, the CEC and ET levels were lower and NO levels were higher in group Ⅱb and Ⅲb than in group Ⅱa and Ⅲa, respectively( P<0.05). The apoptotic rate of cardiomyocytes was higher in group Ⅰa than in the control group, and the apoptotic rate from high to low were from group Ⅲa[(235.71±40.25)%]to group Ⅱa[(197.28±43.56)%]to group Ⅰa[(138.55±32.87)%]and to the control group[(5.81±2.02)%]( P<0.05). The apoptotic rate of cardiomyocytes was lower in group Ⅱb[(125.67±26.51)%]and Ⅲb[(124.91±33.28)%]than in group Ⅱa and Ⅲa, respectively( P<0.05). Conclusions:The ischemia-reperfusion can cause endothelial dysfunction and the apoptosis of cardiomyocytes, and there is a close relationship between the degree of this lesions and the duration of ischemia-reperfusion.While, the appropriate application of angiotensin converting enzyme inhibitor can inhibit the damage of cardiomyocytes to a some extent.

AIM:To investigate the expression,distribution and significance of nuclear factor ?B (NF-?B) in experimental hepatic fibrosis.METHODS:Wistar rats were randomly divided into normal control group,hepatic fibrisis model group and the pyrrolidine-1-dithiocarboxylic acid ammonium sail (PDTC) group. The PDTC group was treated with subcutaneous injection of carboan tetrachloride,and treated with PDTC by oral administration. The content of hydroxyproline was measured. Endotoxin was determined with a Limulus amebocyte lysate test kit. The alanine aminotransferase (ALT) in plasma was measured by laishi method. The content of malondialdehyde (MDA) in liver tissue was detected by means of TBA method. The expression of NF-?B was determined by immunohistochemistry. The expression of connective tissue growth factor (CTGF) was measured by Western blotting.RESULTS:In control group,just a small amount of NF-?B p65 was expressed in the cytoplasm of a few hepatocytes around central veins. In model group,the positive staining of NF-?B p65 was expressed in cytoplasm and nucleus,mainly in fibrous stepta,hepatic sinusoid and partial vascular endothelial cells,part of proliferating ductular epithelial cells and impaired hepatocytes. The positive staining began to increase from the first week. The expression of NF-?B in the liver tissues in PDTC group was lower than that in model control group (P

This study was aimed to explore the molecular mechanism of nano-realgar in treatment of systematic lupus erythematosus (SLE) lupus nephritis (LN). Intragastric administration of equal volume of high-, middle-, low-dose nano-realgar suspension, and normal saline (NS) were given to MRL/lpr mice, respectively. The observations were made on levels of ANA, ds-DNA antibody, IgG and IgM in blood serum, as well as TWEAK, NF-κB, MCP-1 mRNA and protein expression levels in renal tissues. The results showed that compared with the NS group, levels of ANA, ds-DNA antibody, IgG and IgM were obviously reduced (P < 0.05); the levels of TWEAK, NF-κB and MCP-1 mRNA were obviously reduced (P < 0.05); the protein expression levels of TWEAK, NF-κB and MCP-1 mRNA were obviously reduced (P < 0.05) in the high-, middle-, low-dose nano-realgar group. It was concluded that nano-realgar intervened the TWEAK-NF-κB signal pathway through downregulating MCP-1 expression among MRL/lpr mice, in order to reduce the levels of ANA, ds-DNA antibody, IgG and IgM for relieving autoimmune damages in the treatment of SLE (LN).

Objective To evaluate HCC family history on recurrence and survival of HCC patients after curative hepatectomy. Methods The family history,postoperative recurrence rate,1,2 and 5 year survival rate of 79 HCC patients who received surgical resection were collected.Patients were divided into two groups:34 cases in familial aggregation HCC group (FH group ) and 45 cases in non- familial aggregation HCC group (NH group).All these HCC patients were followed up for 3 months to10 years after surgery,and the median follow-up period was 48.5 months.We analyzed the survival rate of HCC patients by Kaplan -Meier survival curve to compare the postoperative recurrence rate and survival rate between two groups. Results 34 cases of HCC probands came from 33 families,and there were 104 cases of HCC patients in these families,an average of 3.2 cases per family.There were 6 families in which 3 or more cases developed HCC,and there were 13 families in which father or (and) mother had HCC accounting for 39.4％.The six months,1 year,2 year posthepatectomy recurrence rate in FH group was 15.1％,22.3％,40.1％,significantly higher than NH group of 10.3％,17.4％,25.6％ (x2 =5.762,6.434,5.987,P ＜0.05),and 1,2,5 year's survival rate in FH group was 57％,46％,40.3％,much lower than NH group of 85.3％,75.2％ and61.5％ (x2 =8.986,9.765,7.634,P＜0.05). Conclusions Family history of HCC affects the prognosis of HCC patients after surgery. Patients with HCC family history have higher postoperative recurrence rate and worse prognosis than that of patients who do not have HCC family history.