新辅助化疗联合肿瘤细胞减灭术治疗Ⅲ～Ⅳ期卵巢癌的疗效分析

目的 探讨新辅助化疗联合肿瘤细胞减灭术治疗Ⅲ～Ⅳ期卵巢癌的疗效.方法 回顾性分析60例Ⅲ～Ⅳ期卵巢癌的临床治疗相关资料,根据采用的治疗方法不同分为对照组30例和化疗组30例,其中对照组患者仅行肿瘤细胞减灭术,观察组患者术前进行新辅助化疗后再行肿瘤细胞减灭术.比较分析两组患者的肿瘤体积、腹腔积液量、术中出血量、手术时间和住院时间等相关指标,并观察疗效.结果 观察组患者的肿瘤体积、腹腔积液量、术中出血量、手术时间和住院时间等指标与对照组相比均显著降低(P＜0.05);观察组患者的临床疗效显优于对照组,观察组的总有效率为73.3％,显著高于对照组(43.4％).结论 Ⅲ～Ⅳ期卵巢癌患者肿瘤细胞减灭术之前,进行2～3个疗程的化疗可减少腹腔积液量和术中出血量,缩短手术时间和住院时间,提高临床疗效.     

参芪复方对糖尿病大血管病变GK大鼠PI3-K/Akt信号通路的影响

目的探讨参芪复方防治糖尿病大血管病变的作用机制。方法以Wistar大鼠18只作为空白组,73只GK大鼠随机分为4组:GK组18只、模型组19只、阿托伐他汀组18只、参芪复方组18只。模型组、阿托伐他汀组、参芪复方组给予一氧化氮合酶(NOS)抑制剂L-NAME0.1mg/(ml.d),加入饮用水中进行糖尿病大血管病变造模,造模同时开始给药。35天后观测主动脉形态,检测血清C反应蛋白(CRP)含量和腹主动脉PI3-KP85a、AktmRNA表达量变化情况。结果参芪复方中药可减轻模型大鼠动脉粥样硬化的病理改变程度,降低血清CRP水平(P<0.01);参芪复方组PI3-KP85amRNA表达水平低于模型组,但无统计学意义;与模型组比较,参芪复方组能明显降低腹主动脉血管壁AktmRNA表达水平(P<0.01)。结论参芪复方可有效防治糖尿病大血管病变的发生发展,其机制可能与抑制糖尿病GK大鼠主动脉血管壁AktmRNA表达量,抑制PI3-K/Akt信号通路有关。     

Spatial relationship of phosphorylated epidermal growth factor receptor and activated AKT in head and neck squamous cell carcinoma

Background

Overexpression of EGFR correlates with decreased survival after radiotherapy in head and neck squamous cell carcinoma (HNSCC). However, the contribution of the activated form, pEGFR, and its downstream signaling (PI3-K/AKT) pathway is not clear yet.

Methods

Fifty-eight patients with HNSCC were included in the study. pEGFR, pAKT, hypoxia, and vessels were visualized using immunohistochemistry. Fractions (defined as the tumor area positive for the respective markers relative to the total tumor area) were calculated by automated image analysis and related to clinical outcome.

Results

Both pEGFR (median 0.6%, range 0-34%) and pAKT (median 1.8%, range 0-16%) expression differed between tumors. Also, a large variation in hypoxia was found (median pimonidazole fraction 3.9% 0-20%). A significant correlation between pEGFR and pAKT (r_s 0.44, p = 0.004) was seen, however, analysis revealed that this was not always based on spatial coexpression. Low pAKT expression was associated with increased risk of regional recurrence (p < 0.05, log-rank) and distant metastasis (p = 0.04).

Conclusion

The correlation between expression of pEGFR and pAKT is indicative of activation of the PI3-K/AKT pathway through phosphorylation of EGFR. Since not all tumors show coexpression to the same extent, other factors must be involved in the activation of this pathway as well.     

糖原合酶激酶-3β信号分子在心肌肥厚中的作用

Glycogen synthase kinase-3β (GSK-3β) is a serine/threonine protein kinase, which takes part not only in glycogen metabolism, but also in cell proliferation, differentiation and apoptosis. GSK-3β is inhibited by growth factors and hypertrophic stimuli through phosphorylation of its N-terminal end serine (Ser9) residue. It is also activated by phosphorylation of its tyrosine (Tyr216) residue. GSK-3β is profoundly inactivated in mice with hypertrophic cardiomyopathy (HCM) and plays a secondary role in myosin heavy chain mutation. However, the role of GSK-3β in HCM was controversial. Recent studies have demonstrated that the activation of GSK-3β inhibits the myocardial hypertrophy, and is regulated by Wnt/Frizzld and PI3-K/Akt signaling pathways. This article introduces the molecular role of glycogen synthase kinase-3β signaling in myocardial hypertrophy and the different pathways on the activity of glycogen synthase kinase-3β (GSK-3β)     

柳州市0～5岁儿童睡眠状况调查

目的:了解柳州市市区0～5岁儿童睡眠状况,为制定相关干预措施提供科学依据。方法:2009年7～12月在柳州市4城区8街道按系统抽样法抽取8个街道中1408名0～5岁儿童进行睡眠状况的问卷调查。结果:0～5岁儿童睡眠障碍发生率35.04%,其中入睡困难7.96%、打鼾3.29%、入睡过早3.14%、磨牙3.06%、用口呼吸2.98%、夜醒2.90%。儿童每天总睡眠时间和白天睡眠时间随年龄增长逐渐缩短,夜间睡眠时间逐渐延长,8月龄夜间持续睡眠形成。睡眠昼夜节律于5月龄开始形成。和国内《儿童保健学》及尼氏儿科学比较,柳州市儿童在3岁前的各年龄段睡眠时间均减少1h左右。结论:目前柳州市0～5岁儿童睡眠障碍的发生率较高,应该引起儿童保健工作者和家长的关注。     

雾化吸入氟化碳对脂多糖性肺损伤大鼠肺内AQP-1及钠钾ATP酶活性的影响

目的观察雾化吸入氟化碳（perfluorocarbon,PFC）对急性肺损伤（acute lung injury,ALI）大鼠肺水肿、肺内水通道蛋白-1（AQP-1）及钠钾ATP酶活性的影响。方法大鼠腹腔注射脂多糖（lipopolysaccharide,LPS）建立ALI模型并雾化吸入PFC进行干预。在LPS注射后6h观察PFC对ALI大鼠动脉血气、肺损伤评分、肺湿干质量比值、肺泡通透指数及钠钾ATP酶活性等的影响,并采用western-blot观察肺内AQP-1表达的变化。结果LPS性肺损伤以肺水肿为主要表现之一。雾化吸入PFC可以缓解LPS诱导ALI后的低氧血症,降低ALI大鼠的肺损伤评分、肺湿干质量比值、肺泡通透指数,同时增加肺组织钠钾ATP酶活性及AQP-1的表达。结论雾化吸入PFC减轻LPS性肺损伤大鼠肺水肿,上调肺损伤期间钠钾ATP酶活性与AQP-1表达。     

Endogenous Endophthalmitis Caused by ST66-K2 Hypervirulent Klebsiella pneumoniae,United States

We describe a case of endogenous endophthalmitis caused by sequence type 66-K2 hypervirulent Klebsiella pneumoniae in a diabetic patient with no travel history outside the United States. Genomic analysis showed the pathogen has remained highly conserved, retaining >98% genetic similarity to the original strain described in Indonesia in 1935.     

Differential sensitivities of glioblastoma cell lines towards metabolic and signaling pathway inhibitions

In glioblastoma multiforme (GBM), the activation of the phosphatidylinositol 3-kinase (PI3-K) pathway is known to promote aerobic glycolysis. The relative sensitivity of GBM towards PI3-K and metabolic inhibitors was examined in a panel of human GBM lines. We observed differential sensitivities towards oligomycin, an ATP synthase inhibitor that suppresses oxidative phosphorylation (OXPHOS). GBMs that were sensitive to oligomycin have greater intrinsic oxygen consumption. They also failed to undergo adaptive glycolytic switches in response to oligomycin, as reflected in the failure to activate AMPKα. On the other hand, GBM lines that were less sensitive to oligomycin could be rendered non-viable when simultaneously treated with the glycolysis inhibitor, 2-Deoxyglucose (2DG). Furthermore, inhibiting either PI3-K pathway or glycolysis was effective in suppressing cell migration. Inhibiting OXPHOS alone did not have any significant effects on cell motility. However, both oligomycin and 2DG acted synergistically in suppressing cell migration. We conclude that while there was less synergy by the combined inhibition of PI3-K and glycolysis, the simultaneous targeting of glycolysis and OXPHOS is highly effective in blocking GBM tumorigenic phenotypes.     

三甲基氯化锡对脉络丛钠-钾-ATP酶活性的影响

目的研究三甲基氯化锡(trimethyltin chloride,TMT)对大鼠脉络丛上皮细胞钠-钾-ATP酶(NKA)活性的影响。方法取SPF级SD雌性大鼠,TMT 10mg/kg腹腔注射染毒,染毒后1、24、36、48、72 h处死,分别测定血钾、脉络丛NKA活性、脑脊液(CSF)电解质和葡萄糖(GLU)浓度,并在光镜下观察脉络丛上皮细胞形态。结果染毒动物出现低血钾,并伴有神经损害症状。染毒动物脉络丛NKA的活性显著下降,与血钾浓度变化一致。染毒24、36 h动物CSF中GLU升高,而染毒48、72 h动物CSF中钾显著下降。光镜下未发现脉络丛上皮细胞形态异常。结论 TMT可抑制脉络丛上皮NKA的活性,引起CSF电解质失衡,这可能是TMT引起中枢神经系统损伤的机制。