Comparison of mannitol and hypertonic saline in treatment of intracranial hypertension of rabbits / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To compare the effects of mannitol and hypertonic saline (HS) in treatment of intracranial hypertension (ICH) of rabbits.</p><p><b>METHODS</b>The animal mode of ICH was established by perfusing artificial cerebrospinal fluids (aCSF) with controlled pressure into the cerebral ventricles of rabbits. The mean arterial pressure, respiratory rate, tidal volume, perfusion rate of aCSF and water content of cerebrum were investigated in rabbits with ICH after a single bolus of 20% mannitol (5 ml/kg), 7.5% HS (2.2 ml/kg) or 23.4% HS (2.2 ml/kg).</p><p><b>RESULTS</b>After the intracranial pressure was elevated from 15 cmH₂O to 75 cmH₂O, the mean arterial pressure was increased and the tidal volume was decreased. After treatment by 20% mannitol, 7.5% HS or 23.4% HS, the increased percentage of mean arterial pressure and the decreased percentage of tidal volume were similar to the changes in control group. However, the perfusion rate of CSF was increased and water content of cerebrum was decreased after treatment by either 20% mannitol or 23.4% HS, but not by 7.5% HS. No different effects were found between 20% mannitol and 23.4% HS.</p><p><b>CONCLUSION</b>With the similar osmotic burden, 20% mannitol is more effective in treating ICH than 7.5% HS. With higher osmotic load, the efficacy of HS is enhanced, and 23.4% HS may be used as an alternative to mannitol in treatment of ICH.</p>

Therapeutic effect of in vitro 5-aza-2'-deoxycytidine combined with imatinib on gastrointestinal stromal tumor / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the impact of 5-aza-2'-deoxycytidine(5-aza-CdR) combined with imatinib on the proliferation, motility, invasion, and apoptosis of gastrointestinal stromal tumors(GIST) cells in vitro.</p><p><b>METHODS</b>MTT assay was used to investigate the effect of the two agents on proliferation of GIST882. Plate colony forming assay was used to determine the number of colony-forming. Motility and invasion abilities were tested to evaluate the inhibitory effect of each agent. Flow cytometry was used to observe apoptosis and cell cycle.</p><p><b>RESULTS</b>5-aza-CdR or imatinib effectively inhibited the growth of GIST882 cells in concentration- and time-dependent manner. The inhibitory rate of combined treatment using 5-aza-CdR and imatinib was significantly higher than that of 5-aza-CdR or imatinib alone(P<0.05). After treatment for 48 h, the apoptosis rates of 5-aza-CdR group (1000 μg/L) and imatinib group (100 μmol/L) were (11.7±1.2)% and (14.6±0.8)%, respectively. Compared with the control group (2.8±0.3)%, the difference was statistically significant(P=0.000). Furthermore, the difference in apoptosis rate was significant between combined treatment group (19.4±1.1)% and single drug treatment group(vs. 5-aza-CdR group, P=0.000, vs. imatinib group, P=0.013). 5-aza-CdR raised G0/G1 ratio and reduced S ratio of GIST882. Imatinib and combined group had no apparent influence on the cell cycle of GIST882 cells.</p><p><b>CONCLUSION</b>5-aza-CdR may be a potential agent of GIST treatment in the near future.</p>

Prognostic value of P16 gene methylation and P16 protein expression in gastrointestinal stromal tumor / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To study the methylation status of P16 gene promoter and the expression of P16 protein in gastrointestinal stromal tumors(GIST) and to explore the prognostic value.</p><p><b>METHODS</b>Methylation status of the P16 promoter was detected by methylation- specific polymerase chain reaction (MSP) and the expression of P16 protein by immunohistochemistry in 62 patients with GIST.</p><p><b>RESULTS</b>The status of P16 gene methylation and the expression of P16 protein were significantly different among the patients with different subclassification of GIST using Fletcher's scheme (P < 0.05, P < 0.01). And there were significant differences in progressive disease (PD) among various levels of P16 expression (P < 0.01). P16 gene methylation was closely related to P16 protein. P16 gene methylation accounted for 75% in the tumor tissue with less than 50% P16 positive cells, and accounted for only 10% in the tumor tissue with more than 50% P16 positive cells (P< 0.01).</p><p><b>CONCLUSION</b>P16 immunohistochemical assessment can be used as a prognostic index for GIST. The patients with more than 50% fraction of cells with low P16 immunostaining have poor prognosis.</p>