自噬对肿瘤细胞能量代谢调控的研究进展

目的总结近年来自噬参与肿瘤细胞能量代谢关系的最新研究进展。方法主要根据Pub Med检索相关资料,就近年来关于自噬对肿瘤细胞能量代谢调控机理以及对肿瘤生物学效应影响的最新研究进展进行综述。结果自噬能够通过对肿瘤细胞葡萄糖摄取、糖酵解途径、氧化磷酸化以及脂代谢和氨基酸代谢进行调控,从而使肿瘤的生物学行为发生改变。结论自噬对肿瘤能量代谢的调控为肿瘤在应激条件下的存活机制提供了理论依据。加深自噬对肿瘤能量代谢的调控机制以及对肿瘤生物学行为影响的研究有助于开发新的、更有效的个性化的抗癌疗法。就自噬对肿瘤能量代谢研究进展来看,我们必须揭示清楚的是自噬对肿瘤能量代谢调控是否与癌基因、抑癌基因、信号通路等其他因素有关,以及对不同类型肿瘤生物学行为产生何种影响。     

三基序蛋白23在肿瘤进展中的作用及机制

三基序蛋白23(TRIM23)是TRIM家族中的一员, 其编码的蛋白具有E3泛素连接酶及GTP酶双重活性, 广泛参与细胞凋亡、自噬、免疫、炎症和肿瘤等多种病理生理过程。TRIM23在多种肿瘤中表达失调, 发挥癌基因的作用, 促进肿瘤进展, 并与患者的不良预后相关。本文主要就TRIM23在肿瘤发生发展中的作用及机制作一综述。     

自噬在肿瘤治疗中的研究进展

自噬是广泛存在于真核细胞内的一种溶酶体依赖性的降解途径,细胞质内形成空泡为其特征.近年来研究发现,肿瘤细胞面对自身新陈代谢或外部人为干预诱导的应激反应时,自噬表达升高并对细胞有保护作用,这可能有助于发现新的肿瘤治疗方法.本文对自噬与肿瘤发生发展的关系及其在肿瘤治疗中的作用进行综述.     

微RNA调控自噬研究进展

近年自噬与微RNA（miRNA）概念备受关注,涉及真核细胞基因表达、发育分化、凋亡、应激等多方面调控.自噬与微RNA广泛参与免疫防御、肿瘤抑制等多种生理和病理过程,成为细胞生物学研究热点.该文就微RNA与自噬调控相关分子机制研究进展作一综述.     

细胞自噬在肿瘤中的作用

自噬为一种细胞的自我消耗过程,其具有潜在的抗肿瘤生物学活性,亦与肿瘤耐药有关。该文从自噬的调节机制入手,综述自噬参与肿瘤发生的机制,自噬在肿瘤治疗中的作用及应用,以期为自噬在临床上的应用提供依据。     

长链非编码RNA调控自噬以影响肿瘤耐药的研究进展

目的总结长链非编码RNA(LncRNA)调控自噬以影响肿瘤耐药的研究进展。方法查阅国内外相关文献,就LncRNA调控自噬以影响肿瘤耐药的最新研究进展进行综述。结果耐药是抗肿瘤治疗过程中普遍存在的问题,自噬作为重要的维持细胞稳态的机制,在肿瘤耐药过程中发挥了重要的作用。LncRNA的调控异常可促成肿瘤的发生和发展,也可以通过促进或者抑制自噬而介导肿瘤细胞对抗肿瘤药物产生耐药。结论 LncRNA可以正向或者负向介导肿瘤自噬,而自噬对于肿瘤耐药是一把"双刃剑"。LncRNA可能通过调控自噬来改善肿瘤对药物的耐药性。     

细胞自噬及其在肾脏疾病中的作用

自噬（autophagy）是保持细胞内物质合成与分解代谢平衡,维持细胞器更新的重要生物学过程.近十年来随着自噬相关基因和相关标志蛋白的发现以及检测手段的进步,自噬的研究不断取得新的突破.细胞自噬不仅在细胞分化、生长、发育、老化等生理过程中有重要作用,在应激和疾病中,如内质网（ER）应激、氧化应激和自由氧离子（ROS）产生、神经元退行性疾病、微生物感染、肿瘤、肾病中同样起了重要作用.     

自噬及其在胃癌中的研究进展

目的总结自噬及其在胃癌中的研究进展。方法检索并筛选近年来国内外发表的有关自噬与胃癌关系的文献并分别对自噬的特点、分子标志、调控因素及其在胃癌中的意义和作用进行综述。结果自噬既可促进细胞的死亡,也可延长肿瘤形成中癌细胞的存活。调控自噬的药物(包括中药)在肿瘤治疗中具有广阔的应用前景,但基于自噬调控的抗肿瘤治疗效果仍取决于细胞内自噬的实际水平。结论目前对胃癌自噬现象的了解仍然知之甚少,阐明自噬现象的分子机理并通过合理调控自噬来杀伤癌细胞仍然需要更为深入的实验研究。     

MicroRNA与细胞自噬调控

细胞自噬是进化过程中高度保守的物质降解再循环过程,是细胞将异常蛋白质、受损细胞器转运至溶酶体降解再利用的活动。自噬过程受到精密的调控。自噬功能障碍与神经退行性疾病、心血管疾病、肿瘤、骨代谢疾病、衰老等的发生有关。MicroRNA是一类对基因进行转录后修饰的非编码单链小RNA。越来越多的证据表明,MicroRNA可以通过调控自噬相关基因及其调节因子来影响自噬水平,是治疗自噬功能障碍所引发疾病的潜在靶点。本文对有关MicroRNA参与自噬调控的最新动态进行综述。     

细胞凋亡和自噬在椎间盘退变中的研究进展

细胞凋亡和自噬是细胞程序性死亡的主要方式.细胞凋亡是细胞在一定条件下出现胞浆皱缩、核浓集,染色质和核结构蛋白断裂,磷脂酰丝氨酸外翻,从而促进巨噬细胞吞噬的过程[1].细胞自噬是细胞的亚细胞膜结构发生动态的形态学改变,并通过溶酶体介导蛋白质和细胞器降解的过程,主要包括底物诱导自噬前体的形成、自噬体形成、自噬体与溶酶体融合和自噬体内容物被降解等过程[2].细胞凋亡和自噬一方面在多种组织和器官发育过程和维持组织稳态方面发挥着重要作用,另一方面其异常与许多疾病(包括肿瘤、自身免疫性疾病和退行性疾病等)的发生、发展有密切关系[1-2].椎间盘退变作为一种典型的退行性疾病,已有越来越多的研究表明其与椎间盘细胞凋亡和自噬的异常相关,现就近年来国内外的相关研究作一综述.     

P物质在诱导肉芽组织成纤维细胞增殖中的作用

目的　探讨感觉神经肽P物质 (substanceP ,SP)对离体培养的肉芽组织成纤维细胞的促增殖作用及其对碱性成纤维细胞生长因子 (basicfibroblastgrowthfactor,bFGF)基因表达的调控作用。　方法　采用MTT法测定SP对原代培养的肉芽组织成纤维细胞的促增殖作用 ;采用RT PCR方法检测SP对成纤维细胞bFGF基因表达的调控作用 ,观察时间及剂量 效应关系。　结果　 10 -9～ 10 -5mol/L的SP在体外对原代培养的肉芽组织成纤维细胞均具有明显的促增殖作用 (P <0 0 1) ,且具有明显的剂量依赖性 (r=0 5 94 ,P <0 0 1) ,bFGF抗体能部分抑制这一作用。在作用后 3、6hSP可诱导成纤维细胞bFGFmRNA的表达 ,在 10 -9～ 10 -5mol/L范围内均可以显著促进成纤维细胞bFGFmRNA表达 ,在 10 -7mol/L达到峰值 (P <0 0 1)。　结论　SP对肉芽组织成纤维细胞具有明显的促增殖作用 ,这种作用与其诱导内源性bFGF基因表达有关     

热诱导调控序列的合成及其热诱导特性的研究

目的 探讨合成热诱导性的HSP70启动子调控序列,并鉴定加热条件下诱导其下游报告基因表达的特性。方法 利用PCR方法,以肝癌细胞株HepG2基因组为模板,体外合成热休克蛋白70（HSP70）启动子序列。利用双酶切法构建HSP70启动子调控的含EGFP报告基因的真核表达载体pcDNA-HSP70-EGFP。以脂质体为载体,体外转染肝癌细胞株HepG2,在不同的温度下（37℃、39℃、41℃、43℃、45℃）加热不同时间（0、15、30、45、60min）后,利用流式细胞术检测报告基因EGFP表达强度,从而判定温度及时间对HSP70启动子热诱导活性的影响。结果 合成的HSP70启动子序列测序结果与GeneBank 中AL671762所提供序列完全一致。低温加热后EGFP在HepG2细胞中的表达强度不同程度增强,在43℃/30 min 时最为明显,为未加热组的3.3倍。结论 成功合成可热诱导的HSP70启动子序列;HSP70启动子在低温加热下能明显增强其下游外源基因的表达,为进一步研究肿瘤热疗-基因治疗提供了实验基础。     

Reconstruction of hematopoietic function in irradiated mice promoted by polysaccharide peptide

Objective:To study the effect of polysaccharide peptide (PSP) on the reconstruction of the hematopoietic function in mice irradiated by lethal dose.Methods:The characteristics of proliferation of colony forming unit-granulocyte macrophage(CFU-GM) and colony forming unit-spleen(CFU-S) were measured after continuous injection of PSP in mice for seven days with different doses.Results:Injection of 25 mg/kg PSP in mice could promote and increase CFU-GM proliferation and cell mitosis,markedly enhance survival ratio,survival time and CFU-S.Conclusions:PSP has significant regulative effects on the reconstruction of the hematopoietic and the immunologic functions in mice irradiated by lethal dose.     

Modification of a model for cerebral ischemia in the cat: a new method to occlude the middle cerebral artery

A modified method of occluding the middle cerebral artery (MCA) by inserting a tiny copper wire into the lumen of the vessel to make a model for cerebral ischemia in the cat is described. Of 22 rats, 4 were controls and the remaining 18 were divided into two groups. Bipolar electrocoagulation was used in 9 cats and copper wire insertion was used in the other 9 to occlude the MCA through a transorbital approach. Two cats died after surgery and were excluded from this study. Of the 16 cats in two experimental groups, 13 of 14 showed hemiplegia and the other 2 were killed under anesthesia. Typical ischemic changes can be seen in the territory of the occluded MCA. Increased water content and decreased amplitude of somatosensory evoked potentials can be found in the ischemic hemisphere. Histochemical fluorescence study demonstrated that the sympathetic nerve fibers normally existing on the MCA can be completely destroyed by electrocoagulation but may remain intact with the copper wire method. This new method may have less influence on the vascular regulative function of the autonomic nervous system and be more similar to the pathological changes of cerebral infarction in man. We think our method can be useful for further research in cerebral ischemic disease and the regulative effects of the nervous system on brain vessels.     

Molecular biology studies of bladder cancer

The mechanisms that control the biological behaviour of urothelial cancer are complex, and many regulative interactions are involved. So far, few aspects of these control mechanisms have been recognized and characterized. A precondition for better understanding is knowledge the interaction of this factors. Some markers (e.g., chromosomal aberrations, EGFR expression) are correlated with progression of tumour. Whether they are the cause or the result of the aggressive behaviour of growth remains unknown. Only a few markers, especially in flow cytometry, will have any benefit in clinical routine. Whether it is possible to find a marker with prognostic value remains uncertain.     

Osteoid induction

Osteoinduction is a biological principle. The implantation of tissue with inductive properties results in the proliferation and differentiation of undifferentiated cells to cartilage and bone. This process, which is similar to a cascade-type mechanism, is controlled by a series of humoral and local growth factors. It was possible to isolate a number of macromolecular substances with osteoinductive, mitogenic, or chemotactic properties specifically from the extracellular bone matrix. A deeper understanding of the regulative mechanisms as well as the greater availability of growth factors may lead to new therapeutic approaches in bone surgery.     

氧应激与肝再生的关系研究进展

肝脏再生是一个涉及多因素、多步骤的复杂而又精确的调控过程,其中氧应激作用在此过程中起重要的作用。笔者就氧应激与肝再生相关的概念、氧应激对肝脏的损害、氧应激与肝再生的关系、氧应激在肝再生中的作用机制及抗氧剂对肝再生的影响进行综述。     

早期肠内营养对烧伤后高代谢反应调节作用的研究

目的 观察早期肠内营养对烧伤高代谢反应的调节作用。方法 通过３０例烧伤患者用间接测热法监测静息能量消耗（ＲＥＥ）,监测血浆激素、脂类调节因子、细胞因子水平,并结合临床疗效和氮平衡变化来评价早期肠内营养的作用。结果 早期肠内营养（ＥＥＮ）组较延迟肠内营养（ＤＥＮ）组ＲＥＥ显著下降（Ｐ＜０.０５－０.０１）,升高的时间缩短（Ｐ＜０.０５）;ＥＥＮ组非蛋白呼吸商（ＮＰＲＱ）较ＤＥＮ组更接近生理状态,负氮平衡时间缩短。伤后第４天ＥＥＮ组血浆去甲肾上腺素（ＮＥ）、胰高糖素（ＧＬＵＣＡＧＯＮ）、前列腺素Ｅ２（ＰＧＥ２）、血栓素Ｂ２（ＴＸＢ２）、低于ＤＥＮ组（Ｐ＜０.０５）;伤后８－１２d肿瘤坏死因子α（ＴＮＦ－α）、白细胞介素－６（ＩＬ－６）显著低于ＤＥＮ组（Ｐ＜０.０５－０.０１）,胰岛素水平呈相反变化。结论 严重烧伤后尽早开始肠内营养对高代谢反应有重要的调节作用。     

Legal aspects of medical errors

Healing people and medical care are together highly organized technological system with significant expert, ethical and legal regulative. Taking medical care is very sensitive area and it interfears deep into one's integrity, so the law is necessary in this area as a regulator. The aim of work is to show medical errors from legal aspects and clinical practice. Errors, negligent conduct during the medical treatment and bad results of medical treatment are categories that can easily be switched or can sublime themselves into the same thing. That is why correct differentiation of medical errors and viewing every way of medical errors appearance is necessary.     

Regulative effect of P38MAPK on release of TNF

Objective: To evaluate activation of P38 mitogen-activatedprotein kinase (P38MAPK) in alveolar macrophage (AM), release of TNFα and NO from cells, and their relationship following lipopolysacchride (LPS) stimulation.Methods: AM was isolated from branch alveolar lavage fluid (BALF). The activation of P38MAPK was assayed by Westernblot. SB203580, a specific inhibitor of P38MAPK, was used with gradient concentration to evaluate the regulative effect of P38MAPK on the release of TNFα and NO from AM.Results: P38MAPK was activated by LPS (100 ng/ml) with peak activation at 30 minutes. The activation of P38MAPK was inhibited by SB203580. The secretion of TNFα and NO stimulated with LPS increased (P<0.01) and was inhibited by SB203580 significantly.Conclusions: The results indicate that P38MAPK is involved in the secreting process of TNFα and NO following LPS stimulation. P38MAPK may be an important site for controlling the secretion of both inflammatory mediators during lung inflammatory disorders.