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目的 研究18β-甘草次酸哌嗪衍生物D34、D35对SMMC-7721细胞增殖的的抑制作用及对凋亡的影响。方法 用18β-甘草次酸哌嗪衍生物D34、D35以不同浓度、不同时间段处理SMMC-7721细胞,显微镜下观察其对肝癌SMMC-7721细胞形态结构的影响;MTT法检测18β-甘草次酸哌嗪衍生物D34、D35对SMMC-7721细胞的增殖抑制率;Hoechst-33258细胞凋亡染色试剂盒检测细胞凋亡情况;Annexin V-FITC/PI双染法检测细胞凋亡率。结果MTT检测结果表明,18β-甘草次酸哌嗪衍生物D34、D35能够抑制肝癌SMMC-7721细胞增殖,且呈浓度依赖性（P〈0.05）;流式细胞仪检测细胞凋亡率,D35为26.71%、D34为36.95%。结论 18β-甘草次酸哌嗪衍生物D34、D35对SMMC-7721细胞有增殖抑制作用和促凋亡作用,且优于18β-甘草次酸（GA）。

替吉奥胶囊是一种氟尿嘧啶衍生物口服抗癌剂，临床应用时耐受性较好，用于胃癌、乳腺癌、非小细胞肺癌（nonsmall celll ungcancer,NSCLC）等多种恶性肿瘤的治疗。其主要剂量限制性毒性反应是骨髓抑制，肺损伤相对罕见，临床上仅有少数病例报道。

胶质纤维酸性蛋白glial fibrillary acidic protein （GFAP）结蛋白desmin （Des）结核菌素纯蛋白衍生物purified protein derivative of tuberculin（PPD）

A high performance liquid chromatographic (HPLC) method for the determination of formaldehyde, acetaldehyde and propionaldehyde in packed drinking water was developed. Aldehydes were derivatized with 0.5 mL DNPH (2,4-dinitrophenylhydrazine) reagent and 0.1 mL 2 M perchloride at 55°C in 60 minutes, then adsorbed in C18 glass cartridge (was performed), eluted with 5 mL acetonitrile ,and finally determined by HPLC. Formaldehyde, acetaldehyde and propionaldehyde-DNPH-derivatives were seperated on a Cosmosil 5C18-MS column by using acetonitrile/D.I. water (55/45, v/v) as a mobile phase, and detected with UV 360 nm. Recovery studies were performed by fortifying D.I. water with formaldehyde, acetaldehyde and propionaldehyde at various concentrations from 2 to 200 ppb. Recovery rates were in the range of 84.4 – 103.2%, 90.2 – 122.1% and 60.8 – 100.4%. The detection limits for all three aldehydes were 1 ppb. Sixty-three packed drinking water samples collected from various markets were analyzed. These results were well

目的：探讨有机锗多酸衍生物对S180肿瘤细胞DNA合成的抑制作用。方法：用^3H-TdR掺入法检测有机锗多酸衍生物在体外对S180肿瘤细胞DNA合成的抑制作用，观察不同剂量有机锗多酸衍生物对S180实体瘤的抑制作用和对免疫器官的影响。结果：体外实验表明，有机锗多酸衍生物对S180细胞的生长具有明显的抑制作用，而且浓度越高，抑制作用越强。体内实验也表明，有机锗多酸衍生物对S180实体瘤的生长具有抑制作用，而且剂量越大，抑制作用越强，且有机锗多酸衍生可防止荷瘤鼠脾脏重量的下降。结论：有机锗多酸衍生物可抑制肿瘤细胞生长，并存在剂量依赖关系。

Patulin hemisuccinate (P-HS) was synthesized and conjugated to bovineserum albumin (BSA) as the hapten-protein conjugation for immunization.Polyclonal antibodies were obtained from the antiascites of six immunized mice.Titers and specificity were determined using an indirect ELISA. The resultsindicated that three of the six mice were better immunized and that theantibodies acted strongly against patulin-hemisuccinate-BSA. Slight ELISAresponses of the antibodies against patulin alone showed the potential fordeveloping monoclonal antibodies.

It has been widely recognized that inflammation, particularly chronic inflammation, can increase the risk of cancer and that the simultaneous treatment of inflammation and cancer may produce excellent therapeutic effects. Berberine, an alkaloid isolated from Rhizoma coptidis, has broad applications, particularly as an antibacterial agent in the clinic with a long history. Over the past decade, many reports have demonstrated that this natural product and its derivatives have high activity against both cancer and inflammation In this review, we sqmmarize the advances in studing berberine and its derivatives as anti-inflammatory and anti-tumor agents in the digestive system; we also discuss their structure-activity relationship. These data should be useful for the development of this natural product as novel anticancer drugs with anti-inflammation activity.

Mitocbondrial fusion is a highly coordinated process that mixes and unifies the mitochondrial compartment for normal mitochondrial functions and mitochondrial DNA inheritance. Dysregulated mitochondrial fusion causes mitochondrial fragmentation, abnormal mitochondrial physiology and inheritance, and has been causally linked with a number of neuronal diseases. Here, we identified a diterpenoid derivative 15-oxospiramilactone （$3） that potently induced mitochondrial fusion to restore the mitochondrial network and oxidative respiration in cells that are deficient in either Mfnl or Mfn2. A mitochondria-localized deubiquitinase USP30 is a target of $3. The inhibition of USP30 by $3 leads to an increase of non-degradative ubiquitination of Mfnl/2, which enhances Mfnl and Mfn2 activity and promotes mitochondrial fusion. Thus, through the use of an inhibitor of USP30, our study uncovers an unconventional function of non-degradative ubiquitination of Mfns in promoting mitochondrial fusion.

Endocardial fibroelastosis （EFE） refers to the thickening of the ventricular endocardium as a result of de novo deposition of subendocardial fibrous tissue layers during neonatal heart development. The origin of EFE fibroblasts is proposed to be postnatal endocardial cells that undergo an aberrant endothelial-to-mesenchymal transition （End- MT）. Genetic lineage tracing of endocardial cells with the inducible endocardial Cre line Npr3-CreER and the endo- thelial cell tracing line Cdh5-CreER on an EFE-like model did not reveal any contribution of neonatal endocardial cells to fibroblasts in the EFE-like tissues. Instead, lineage tracing of embryonic epicardium by Wtl-CreER suggested that epicardium-derived mesenchymal cells （MCs） served as the major source of EFE fibroblasts. By labeling MCs using Sox9-CreER, we confirmed that MCs of the embryonic heart expand and contribute to the majority of neonatal EFE fibroblasts. During this pathological process, TGFp signaling, the key mediator of fibroblasts activation, was highly upregulated in the EFE-like tissues. Targeting TGFp signaling by administration of its antagonist bone mor- phogenetic protein 7 effectively reduced fibroblast accumulation and tissue fibrosis in the EFE-like model. Our study provides genetic evidence that excessive fibroblasts in the EFE-like tissues mainly originate from the epicardium-de- rived MCs through epicardial to mesenchymal transition （EpiMT）. These EpiMT-derived fibroblasts within the EFE- like tissues could serve as a potential therapeutic target.