背景与目的:甲状腺乳头状癌(papillary thyroid carcinoma,PTC)和桥本甲状腺炎(Hashimoto’s thyroiditis,HT)的发病率均呈上升趋势,两者之间的关系已成为目前研究的热点。探讨PTC和HT之间的关系。方法:回顾性分析2014—2015年期间在中国科学院大学附属肿瘤医院头颈肿瘤外科行甲状腺癌手术治疗的首诊患者306例,术后病理学检查均明确诊断为PTC,其中术后病理学确诊伴发HT者42例,比较伴发HT与未伴发HT患者的临床病理学特征。结果:PTC患者女性发病年龄高于男性(46.2岁 vs 41.9岁)。相较于与未伴发HT的PTC患者,伴发HT的患者中女性比例更高(93% vs77%),中央区淋巴结数目较多[(5.0±3.4)枚 vs (2.5±2.7)枚],术前促甲状腺激素(thyroid-stimulating hormone,TSH)水平较高[(3.28±1.91)μU/mL vs (2.12±1.29)μU/mL],术前抗甲状腺过氧化物酶抗体(thyroid peroxidaseantibody,TPOAb)阳性率较高(55% vs 14%),术前甲状腺球蛋白抗体(thyroglobulin antibodies,TgAb)阳性率较高(69% vs 13%)。发生中央区淋巴结转移的患者中,中央区淋巴结转移数目与中央区淋巴结总数显著相关(Pearson相关系数=0.582)。多因素logistic回归分析发现,男性、低龄、被膜侵犯是PTC患者中央区淋巴结转移的独立危险因素。结论:伴发HT对PTC患者的预后无显著影响。伴发HT的PTC患者TSH水平显著偏高,提示HT可能是PTC发病风险因素之一。中央区淋巴结转移数目与中央区淋巴结总数相关,推测PTC淋巴结转移可能与淋巴结炎症反应相关。 相似文献
This meta-analysis examined whether early decompressive craniectomy (DC) can improve control of intracranial pressure (ICP) and mortality in patients with traumatic brain injury (TBI).Medline, Cochrane, EMBASE, and Google Scholar databases were searched until May 14, 2015, using the following terms: traumatic brain injury, refractory intracranial hypertension, high intracranial pressure, craniectomy, standard care, and medical management. Randomized controlled trials in which patients with TBI received DC and non-DC medical treatments were included.Of the 84 articles identified, 8 studies were selected for review, with 3 randomized controlled trials s having a total of 256 patients (123 DCs, 133 non-DCs) included in the meta-analysis. Patients receiving DC had a significantly greater reduction of ICP and shorter hospital stay. They also seemed to have lower odds of death than patients receiving only medical management, but the P value did not reach significance (pooled odds ratio 0.531, 95% confidence interval 0.209–1.350, Z = 1.95, P = 0.183) with respect to the effect on overall mortality; a separate analysis of 3 retrospective studies yielded a similar result.Whereas DC might effectively reduce ICP and shorten hospital stay in patients with TBI, its effect in decreasing mortality has not reached statistical significance. 相似文献
Aim of the study: Parkinson’s disease (PD) is a neurodegenerative disorder. It is caused by the degeneration of dopaminergic neurons and the dopamine (DA) deletion in the substantia nigra pars compacta (SNpc). Morphine elevates the level of dopamine in the mesolimbic dopamine system and plays a role in alleviating PD symptoms. However, the molecular mechanism is still unclear. The aim of the study is to investigate the mechanism on morphine alleviating PD symptoms.
Materials and methods: The viability of PC12 cells was measured by using MTT assay. The expressions of tyrosine hydroxylase (TH), thioredoxin-1 (Trx-1), CyclinD1 and Cyclin-dependent kinase5 (Cdk5) were detected by Western Blot.
Results: In present study, we found that morphine increased the cell viability in PC12 cells. 1-methyl-4-phenylpyridi-nium (MPP+) reduced the cell viability and TH expression, which were reversed by morphine. MPP+ decreased the expressions of Trx-1, CyclinD1, Cdk5, which were restored by morphine. Moreover, the role of morphine in restoring the expressions of Trx-1, CyclinD1 and Cdk5 decreased by MPP+ was abolished by LY294002, phosphatidylinositol-3-kinase (PI3K)/Akt inhibitor.
Conclusions: These results suggest that morphine reverses effects induced by MPP þ through activating PI3K/Akt pathway. 相似文献