摘要：Cancer is the most common cause of human mortality and has created an unbridgeable health gap due to its unrestrained aberrant proliferation,rapid growth,metastasis,and high *** two-dimensional cell culture and animal models for tumor diagnostic and therapeutic studies have extremely low clinical translation rates due to their intrinsic *** tumor models are therefore required for cancer *** human three-dimensional(3D)cancer models stand out for their ability to better replicate the spatial organization,cellular resources,and microenvironmental features(e.g.,hypoxia,necrosis,and delayed proliferation)of actual human ***,the fabrication of these models can be achieved by an emerging technology known as 3D bioprinting,which allows for the fabrication of living structures by precisely regulating the spatial distribution of cells,biomolecules,and matrix *** aim of this paper is to review the current technologies and bioinks associated with 3D bioprinted cancer models for glioma,breast,liver,intestinal,cervical,ovarian,and neuroblastoma,as well as,advances in the applications of 3D bioprinted-based tumor models in the fields of tumor microenvironment,tumor vascularization,tumor stem cells,tumor resistance and therapeutic drug screening,tumorimmunotherapy,and precision medicine.

摘要：本研究采用简单的两步法合成了由非晶态硫化钴和碳纳米管结合形成的异质结CNT-a-CoS_(x)催化剂.与晶态CoS_(x)和碳纳米管形成的晶态CNT-c-CoS_(x)异质结催化剂相比,非晶态CNT-a-CoS_(x)具有丰富的活性位点、优异的电子输运特性和大的电化学活性面积等结构特性,因而在酸性电解质中表现出更高的电催化氢析出性能.达到10 m A cm^(-2)的阴极电流密度时,CNT-a-CoS_(x)所需的过电位仅为76 m V.更值得注意的是,经过60,000 s的电化学耐久性测试,未观察到明显的电催化性能下降.这一简单的原位构建异质结催化剂的策略为设计和合成活性高、稳定性好的非晶异质结电催化剂提供了技术支持.

摘要：肝星状细胞(HSCs)的活化是肝纤维化病程进展中的核心环节。肝纤维化是一个可逆的病理过程,去除病因后,肝纤维化可以通过活化的HSCs凋亡和失活发生逆转。我们前期研究发现,蛋白酪氨酸磷酸酶1B(PTP1B)在肝纤维化进展期和逆转恢复期,可分别促进HSC活化和抑制aHSCs失活。但其在肝纤维化逆转期,对活化的HSCs凋亡的作用尚不明确。为了探究PTP1B对aHSCs凋亡的影响,本实验构建了小鼠肝纤维化及逆转模型;体外培养了大鼠肝星状细胞系HSC-T6, TGF-β1刺激活化后给予TRAIL诱导其凋亡以模拟肝纤维化逆转期aH SC凋亡过程。结果显示, PTP1B在肝纤维化肝组织中表达上调,而在纤维化自发恢复后表达降低。PTP1B在活化的HSC-T6中表达上调,在凋亡的aH SCs中表达下降。此外, PTP1B抑制了TRAIL的肝纤维化缓解效应,表现为过表达PTP1B后, TRAIL无法降低α-平滑肌肌动蛋白(α-SMA)及胶原蛋白的表达。同时,过表达PTP1B可以抑制TRAIL诱导的细胞凋亡,减少凋亡细胞的数量,降低凋亡蛋白的表达及活性。研究表明, PTP1B可以通过影响aH SCs的凋亡参与肝纤维化的逆转。

摘要：目的调查相关营养评估指标与卒中后抑郁(poststroke depression,PSD)的关系,分析营养指标预测老年缺血性脑卒中患者发生PSD的表现,为护理人员早期识别PSD高危患者,优化脑卒中管理,改善预后提供参考依据。方法于2022年9月至2023年5月在深圳市1所医院神经内科选取239例老年缺血性脑卒中患者为研究对象。采用自行设计的问卷,收集患者一般人口学资料及疾病相关信息;采用白蛋白、微型营养评定简表(Mini Nutritional Assessment Short Form,MNA-SF)、老年营养风险指数(Geriatric Nutrition Risk Index,GNRI)评估患者的营养状况;采用医院焦虑抑郁量表的抑郁分量表(Hospital Anxiety and Depression Scale-Depression,HADS-D)评估卒中后抑郁情况。采用二元逻辑回归分析,分析卒中后抑郁相关影响因素,并采用受试者工作特征曲线分析方法比较营养指标的表现。结果老年缺血性脑卒中患者平均年龄为71.10±7.41岁,男性占66.5%(159/239),PSD发生率为32.6%(78/239)。不同营养指标的低值组PSD的发生率显著大于高值组,差异均具有统计学意义(P<0.05)。二元逻辑回归分析表明白蛋白(OR,0.681;95%CI,0.508~0.913,P=0.010)、GNRI(OR,1.238;95%CI,1.034~1.483,P=0.020)、MNA-SF(OR,0.708;95%CI,0.614~0.815,P<0.001)是影响PSD的因素(P<0.05)。白蛋白、GNRI和MNA-SF 3个指标联合预测老年缺血性脑卒中患者PSD的ROC曲线下面积最大,有较高的区分度(AUC,0.738;敏感度为75.6%,特异度为60.9%)。结论由白蛋白、GNRI、MNASF联合组成的营养评价指标可作为预测老年缺血性脑卒中营养不良患者发生PSD风险的辅助工具。需要护理人员在更多样化的患者群体中进行进一步的验证,以证明预测的准确性。

摘要：Objective： HER-2 plays an important role in the development and progression of ovarian carcinoma. A number of monoclonal antibodies （MAbs） and engineered antibody fragments （such as scFvs） against the subdomain II or IV of HER-2 extracellular domain （ECD） have been developed. We investigated the effect of chA21, an engineered anti-HER-2 antibody that bind primarily to subdomain I, on ovarian carcinoma cell invasion in vitro, and explored its possible mechanisms. Methods： Growth inhibition of SK-OV-3 cells was assessed using a Methyl thiazolyl tetrazolium （MTT） assay. The invasion ability of SK-OV-3 was determined by a Transwell invasion assay. The expression of matrix metalloproteinase-2 （MMP-2） and its tissue inhibitors （TIMP-2） was detected by immunocytochemical staining, and the expression of p38 and the phosphorylation of p38 were assayed by both immunocytochemistry and Western blot. Results： After treatment with chA21, the invasion of human ovarian cancer SK-OV-3 cells was inhibited in dose- and time-dependent manners. Simultaneously the expression of p38, phospho-p38, MMP-2 and the MMP-2/TIMP-2 ratio decreased, while TIMP-2 expression increased. Additionally, the decrease in phospho-p38 was much greater than that of p38. Conclusion： chA21 may inhibit SK-OV-3 cell invasion via the signal transduction pathway involving MMP-2, TIMP-2, p38 and the activation of p38MAPK.