Influence of mild hypothermia on apoptotic protease activating factor-1 protein expression in the hippocampal CA1 area and learning and memory functions of rats after diffuse brain injury / 中华神经医学杂志

Objective To investigate the influence of mild hypothermia on the apoptotic protease activating factor-1 (Apaf-1) protein expression in the hippocampal CA1 area and learning and memory functions of rats after diffuse brain injury (DBI). Methods Forty-eight male Wistar rats were equally randomized into normal group, sham-operated group, brain injury group and mild hypothermia treatment group (n=12). Rats in the normal group did not receive any treatment; rats in the sham-operated group only received anesthesia, and incision and suture of scalp; rats in the brain injury group and mild hypothermia treatment group were induced the DBI models according to Marmarou method; and rats in the mild hypothermia treatment group were performed hypothermia with ice blanket and ice bag to control the rectal temperature within 30.0-31.0 ℃ for 2 h. After DBI for 2 weeks, the times of searching refuge platform and the protein expression of Apaf-1 were compared among the 4 groups. Results The times of searching refuge platform in the normal group, sham operated group, brain injury group and mild hypothermia treatment group were (10.1 ±1.9), (10.3±1.8), (3.8±2.3) and (6.9±1.1), respectively,with significant differences between each 2 groups (P<0.05). The protein expression of Apaf-1 in the brain injury group and mild hypothermia treatment group was obviously higher than that in the other groups (P<0.05), and significantly lower protein expression of Apaf-1 in the mild hypothermia rats was noted as compared with that in the brain injury rats (P<0.05). Conclusion Mild hypothermia might play a protective role by inhibiting neuronal apoptosis for rats with DBI through the Apaf-1 pathway,which can improve learning and memory abilities.

Antitumor activity of F90, an epidermal growth factor receptor tyrosine kinase inhibitor, on glioblastoma cell line SHG-44 / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Over-expression of epidermal growth factor receptor (EGFR) is thought to be related to cell proliferation, invasion, metastasis, resistance to chemoradiotherapy and poor prognosis of various human cancers. Forty percent to fifty percent of glioblastoma multiforme (GBM) possess deregulated EGFR, which may contribute to the aggressive and refractory course of GBM. Therefore, blockade of EGFR signal transduction may be a promising treatment strategy for GBM.</p><p><b>METHODS</b>MTT assay, cell growth curve assay and tumor xenograft model were used to evaluate the antitumor activity of F90 against SHG-44 in vitro and in vivo. Western blot assay was applied to evaluate the expression of p-EGFR, p-ERK1, p-JNK, p-P38, Bcl2 and P53 proteins.</p><p><b>RESULTS</b>F90 inhibited the cell proliferation in a dose-dependent manner in vitro. The growth of SHG-44 tumor xenografts was suppressed by F90 at a high dose level (100 mg x kg(-1) x d(-1)). Phosphorylation of EGFR and activated downstream signaling proteins, such as ERK1, JNK and P38, were found to be depressed after incubation with F90 for 48 hours in vitro. Down-regulated Bcl2 protein and up-regulated P53 protein were also observed.</p><p><b>CONCLUSIONS</b>The results demonstrate that F90 is effective in inhibiting the proliferation of SHG-44 cells in vitro and tumor growth in vivo, suggesting that F90 may be a new therapeutic option for treatment of GBM.</p>

Transthoracic echocardiography in transcatheter closure of atrial septal aneurysm combined with secoundum-type atrial septal defect / 中南大学学报(医学版)

OBJECTIVE@#To explore the value of transthoracic echocardiography (TTE) in transcatheter closure of atrial septal aneurysm (ASA) combined with secoundum-type atrial septal defect (ASD).@*METHODS@#Fourteen patients (3 males and 11 females) who had ASA combined with secoundum-type ASD were diagnosed by TTE or transesophageal echocardiography. The ASA projected to the right atrium in all patients. The width of basilar part was 13 approximately 24 (18.5+/-3.9) mm, and the vertical extent was 7 approximately 11(9.7+/-1.8) mm. Ten patients combined with single hole ASD and 4 patients with multiple hole ASD. Blood shifting from the left atrium to the right atrium was displayed in color Doppler in all patients. All patients were treated by transcatheter closure under the guiding of X fluoroscopy and TTE, and examined with TTE during the follow-up.@*RESULTS@#Transcatheter closure was successfully performed by 14 occluders in all patients. No residual shunt was detected immediately by TTE after the procedure in all patients. During the 6 approximately 12 month follow-up, no residual shunt or occluder shifting was found, the dimensions of the heart became normal in 11 patients (79%) and were significantly decreased in 4.@*CONCLUSION@#Transcatheter closure is feasible in patients with ASA combined with secoundum-type ASD, and extra attention must be paid to the specialty. TTE is very important in case selection before transcatheter closure, and it may be used to monitor and guide the procedure during transcatheter closure.

Effects of valsartan and indapamide on plasma cytokines in essential hypertension / 中南大学学报(医学版)

OBJECTIVE@#investigate and compare the effect of valsartan and indapamide on inflammatory cytokines in hypertension.@*METHODS@#Forty-one untreated patients with mild to moderate hypertension and 20 age and sex-matched normotensives were enrolled in this study. Hypertensives were treated with indapamide 1.5 mg/d (n=20) or valsartan 80 mg/d (n=21) for 4 weeks, and blood samples for determining monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-1 (MIP-1alpha), sP-selectin, asymmetric dimethylarginin (ADMA), angiotensin II (Ang II), and 6-keto-PGF1alpha were collected before the treatment and 4 weeks after the treatment.@*RESULTS@#Hypertensives exhibited significantly higher blood pressure, as well as elevated plasma levels of MCP-1, MIP-1alpha, sP-selectin and serum level of ADMA compared with the normotensives. Nevertheless, there was no significant difference in serum 6-keto-PGF1alpha and Ang II between the hypertensives and the normotensives. After the treatment with indapamide or valsartan for 4 weeks, both the systolic and diastolic blood pressures, though still higher than those of the normotensives, decreased markedly. After the treatment with indapamide for 4 weeks, MCP-1, MIP-1alpha and sP-selectin slightly decreased, but not statistically significant (P>0.05). Those cytokines decreased significantly after being treated with valsartan for 4 weeks [(19.16+/-3.11) pg/mL vs (16.08+/-2.67) pg/mL, P0.05).@*CONCLUSION@#The levels of MCP-1, MIP-1alpha, sP-selectin and ADMA were elevated in mild to moderate hypertensives. Valsartan and indapamide have similar blood pressure lowering effect. Valasartan exerts more significant effect on cytokines than indapamide does.

Protective effect of losartan on injury induced by ox-LDL in endothelial cells and the relationship with asymmetric dimethylarginine / 中南大学学报(医学版)

OBJECTIVE@#To investigate the protective effect of losartan against on injury induced by ox-LDL in endothelial cells and the relationship with asymmetric dimethylarginine (ADMA).@*METHODS@#Endothelial injury was induced by incubation with ox-LDL 100 mg/L in cultured HUVECs for 24 h, and the levels of ADMA, lactate dehydrogenase (LDH), nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) in the conditioned medium were measured. The activity of dimethylarginine dimethylaminohydrolase (DDAH) of cultured endothelial cells was also determined.@*RESULTS@#Incubation of endothelial cells with ox-LDL 100 mg/L for 24 h induced a marked elevation of the levels of ADMA, LDH and TNF-alpha in the conditioned medium and a significant decrease in the activity of DDAH and the content of NO (P < 0.05). Pretreatment with losartan (10(-8) - 10(-6) mmol/L) significantly inhibited the increased levels of ADMA, LDH and TNF-alpha, attenuated the decreased levels of NO and the decreased activity of DDAH induced by ox-LDL (P < 0.05).@*CONCLUSION@#Losartan may preserve ox-LDL-induced endothelial cell injury by increasing the DDAH activity and decreasing the ADMA level.