专家综述

嵌合基因与恶性肿瘤的研究进展

Advances in the study of chimeric genes in malignant tumors

:1-10
 
嵌合基因是指由两个或多个原本不连续的基因片段重组而成的新基因,它们可以通过基因组重排、转录诱导等机制产生。嵌合基因在正常生理和发育过程中具有重要的功能和调控作用。嵌合基因可以改变原有基因的表达水平、编码蛋白质的结构和功能、信号通路的激活和抑制等,从而促进肿瘤细胞的增殖、侵袭、转移和耐药性。近年来,随着高通量测序技术的发展和应用,越来越多的嵌合基因被发现和鉴定,它们在不同类型的肿瘤中具有不同的表达模式和功能作用,为肿瘤的分子诊断、预后评估和靶向治疗提供了新的机会和挑战。本文旨在对嵌合基因产生的机制、检测方法和在肿瘤中的功能和应用等方面进行综述,为进一步认识嵌合基因在肿瘤进展中的功能机制及其精准化治疗提供参考。
Chimeric genes refer to novel genes formed by the recombination of two or more originally non-contiguous gene fragments through mechanisms like genomic rearrangement and transcriptional induction.They play important roles in physiological and developmental regulation.Chimeric genes can alter the expression,structure and function of original genes,modulate signaling pathway activation and inhibition,and thereby promote tumor cell proliferation,invasion,metastasis and drug resistance.In recent years,with the development and application of high-throughput sequencing technologies,increasing numbers of chimeric genes have been discovered and identified.They demonstrate different expression patterns and functional roles in various tumor types,providing new opportunities and challenges for molecular diagnosis,prognostic assessment and targeted therapy of cancers.This review summarizes the mechanisms of chimeric gene formation,detection methods and their functions and applications in tumors,to provide insights into the functional mechanisms of chimeric genes in tumor progression and their implications for precision treatment.
专家综述

纳米载体药物用于缓解慢性肾脏病纤维化的研究进展

Recent advances in nanomedicines for alleviating chronic kidney disease fibrosis

:1-10
 
慢性肾脏病是一类具有高发病率、高死亡率的慢性疾病群。临床上一般采用血液透析和肾脏移植治疗终末期的慢性肾脏病。研究表明,小分子药物或核酸类药物在慢性肾脏病治疗中极具潜力,但是缺乏特异性导致肾脏纤维化治疗效果有限,亟需开发新的治疗策略。纳米载体因具有良好的理化性质,被广泛应用于生物医学领域。本文综述了近年来纳米载体递送小分子或核酸类药物在慢性肾脏病中的研究进展。
Chronic kidney disease (CKD) is a series of chronic disease groups associated with high morbidity and mortality. Hemodialysis and kidney transplantation are the only choices for end-stage renal disease. According to the literature report, it is shown that small molecule and nucleic acid drugs have great potential in CKD treatments with an unsatisfied therapeutic efficacy because of the lack of specific targeting. Thus, it is necessary to develop a new strategy. Nanocarriers have been widely used in biomedical fields due to their excellent physical and chemical properties. In this review, we have summarized the recent advances in applying functional nanocarriers to deliver the small molecules and nucleic acid drugs in the treatment of CKD.
专家综述

声学调控实体肿瘤理化微环境的机制与研究进展

:7-13
 
实体肿瘤物理和化学微环境异常阻碍了肿瘤与外界进行物质交换,降低了药物渗入肿瘤组织,是肿瘤对放化疗抵抗的重要原因。目前,已有多种针对肿瘤微环境各个组分的治疗方法,如使血管正常化、降低肿瘤间质液压、降解细胞外基质等,以达到增强药物等的渗出,从而增强肿瘤治疗效果。声学调控是改变肿瘤理化微环境的一种有效方法,本文对声学调控其中几个主要的机制和研究进展进行综述,以期为临床肿瘤治疗提供新思路。
综述

中医药治疗前列腺癌研究进展

Research progress of traditional Chinese medicine in the treatment of prostate cancer

:135-138
 
前列腺癌作为最常见的男性泌尿系统恶性肿瘤之一,目前常规治疗手段主要为手术、放化疗、内分泌治疗等,但后期并发症、治疗副作用等问题突出,且多转化为去势抵抗性前列腺癌,预后极差。既往研究已然证实,中医药在前列腺癌的治疗中可有效减少复发、减轻症状,提高患者生活质量。本文旨在总结近几年中医药对前列腺癌的研究,为往后的研究与临床治疗提供一些新的思路。
Prostate cancer(PCa) is one of the most common male urinary system malignancies.At present,conventional treatment methods are mainly surgery, radiotherapy and chemotherapy, endocrine therapy,etc.However, late complications, treatment side effects and other problems are prominent, and prostate cancer tends to develop as castration-resistant prostate cancer (CRPC), and the prognosis is very poor. Previous studies have confirmed that Chinese medicine can effectively reduce recurrence incidence, relieve symptoms and improve the quality of life of patients in the treatment of prostate cancer. This article summarizes the research of traditional Chinese medicine on prostate cancer in recent years, and provides some new ideas for future research and clinical treatment.
论著

糖尿病肾病患者肾功能恶化进展的危险因素

Risk factors of renal function deterioration in patients with diabetic nephropathy

:40-43
 
目的 探讨糖尿病肾病患者肾功能恶化的危险因素。 方法 采用回顾性队列研究分析山东省立第三医院2017年1月—2020年5月108例患者的临床数据。将病人分为糖尿病肾病肌酐翻倍组和不翻倍组,比较两组间临床数据的变化。结果 糖尿病肾病肌酐翻倍组的BUN、胱抑素C和ACR水平均高于肌酐不翻倍组;eGFR、CO2、ALB、HGB均低于肌酐不翻倍组,差异有统计学意义(P<0.05)。而UA、GLU、血脂、糖化血红蛋白,糖尿病和高血压病史差异无统计学意义(P>0.05)。相关分析表明血肌酐与BUN、eGFR、胱抑素C、ACR呈正相关;与ALB,HGB和CO2呈负相关。多元线性回归分析结果显示,eGFR,胱抑素C,ACR, ALB和HGB是糖尿病肾病肾功能恶化的影响因素(P<0.05)。结论 糖尿病肾病除检测肾功能的常规指标外,还可观察ACR、ALB和HGB水平的变化,对判断患者肾功能是否恶化有一定价值。
Objective To investigate the risk factors of renal function deterioration in patients with diabetic nephropathy. Methods Retrospective cohort study was used to analyze the clinical data of 108 patients from January 2017 to May 2020 in the Third Hospital of Shandong Province. Patients were divided into diabetic nephropathy creatinine doubling group and non-doubling group. The changes of clinical data in two groups were compared and the risk factors of renal function deterioration were analyzed. Results The levels of BUN、cystatin C and ACR in the creatinine doubling group were higher than those in the creatinine non-doubling group, and the levels of eGFR、CO2、ALB、 HGB were lower than those in the creatinine non-doubling group, the differences were statistically significant (P<0.05). However, there were no significant differences in the levels of UA, blood glucose, blood lipid, glycosylated hemoglobin, the history of diabetes and hypertension (P>0.05). The correlation analysis showed that serum creatinine was positively correlated with BUN、 eGFR、cystatin C and ACR and negatively correlated with CO2、ALB and HGB. The results of multiple regression analysis showed that eGFR、cystatin C、ACR、ALB and HGB were independent influencing factors of renal function deterioration(all P<0.05). Conclusion Diabetic nephropathy can not only notice the routine indexes of renal function, but also observe the changes of ACR、ALB and HGB levels, which has certain value for awareing the renal function deterioration in patients.
论著

替罗非班联合丁苯酞治疗进展性脑梗死的疗效分析

Analysis of the clinical effect of triofiban combined with butylphthalide in the patients with progressive cerebral infarction

:76-79
 
目的 探讨替罗非班联合丁苯酞应用于进展性脑梗死的疗效与安全性。方法 选取2016年1月—2018年1月广州医科大学附属第三医院神经内科收治的进展性脑梗死患者98例。对照组采用硫酸氢氯吡格雷加阿司匹林(双抗)治疗,观察组采用替罗非班(静脉治疗48 h)联合丁苯酞序贯双抗治疗。结果 替罗非班联合丁苯酞序贯双抗治疗组的神经功能缺损(NIHSS)评分、日常生活能力评定量表(Barthel指数)、改良 Rankin 量表评分优于对照组,血浆凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)与凝血酶时间(TT)水平高于对照组,两组有差异。两组患者药物不良反应发生率无差异。结论 替罗非班联合丁苯酞序贯双抗治疗可明显改善进展性脑梗死的神经功能,为时间窗外的进展性脑梗死提供了治疗方法,疗效显著。
Objective To observe the effect and safety of triofiban combined with butylphthalide in treatment of progressive cerebral infarction. Methods A total of 98 patients with progressive cerebral infarction in the department of neurology from January 2016 to January 2018.The control group was treated with clopidogrel hydrogen sulfate plus aspirin(dual antiplatelet). The observer group was treated with Tirofiban(48 h intravenous treatment) combined with butylphthalide on the basis of the treatment of the control group. Results The score of National Institutes of Health Stroke、 Barthel Index and mRS in the triofiban combined with butylphthalide group were better than that of the control group. There were statistical differences between the two groups. PT,APTT and TT were higher than that in the control group .There was no significant difference in drug adverse reactions between the two groups. Conclusion Triofiban combined with butylphthalide may improve the neurologic function of progressive cerebral infarction and provide treatment for progressive cerebral infarction outside the time window.
综述

瘦素对高血压肾损害相关机制的研究进展

Advances in research on the mechanism of leptin on hypertensive renal damage

:110-113
 
瘦素(leptin)是由控制各种生理过程的脂肪组织合成和分泌的一类激素,通过作用于靶细胞膜上的瘦素受体并经信号传导在各器官和系统中发挥一系列生物学效应。肾脏是高血压常见的靶器官之一。相关研究表明,瘦素在高血压肾损害中发挥作用,其机制可能与氧化应激及其炎症反应有关。本文以瘦素对高血压肾损害及其相关机制作一综述,并探讨瘦素对高血压肾损害发病机制研究进展。
Leptin which is a kind of synthesis and secretion of hormone that participates in various physiological processes is the role of the leptin receptor on the target cell membrane and the signal transduction through a series of biological effects in different organs and systems. Kidney is one of the common target organs of hypertension, and related research shows that leptin plays a role in hypertensive kidney damage, whose mechanism may be related to oxidative stress and its inflammatory reaction. The paper reviewed leptin on renal damage in hypertension and its related mechanisms, to explore the leptin on renal pathogenesis of hypertension research progress.
综述

尼可地尔在急性心肌梗死中的研究进展

Advancement in the study of nicorandil in acute myocardial infarction

:105-109
 
尼可地尔是一种ATP敏感型钾离子通道开放剂,同时兼有类硝酸酯作用,具有舒张冠脉和外周血管及通过缺血预适应对心脏起保护作用等双重功效,主要用于抗心绞痛的治疗。介于尼可地尔这种特殊结构及其作用机制能否降低急性心肌梗死患者PCI术后无复流的发生率及改善临床预后,目前临床研究仍在探索中。现就尼可地尔的作用机制、模拟的药物预适应作用、及综合作用与急性心肌梗死的关系做一综述,评估尼可地尔作为辅助药物在AMI行介入治疗中的作用及临床预后,指导临床用药。
Nicorandil is an ATP-sensitive potassium (K-ATP) channel opener, meanwhile has an effect like nitrate, has dual actions including coronary and peripheral vasodilatation and cardioprotective effects through ischemic preconditioning, mainly for the treatment of anti-angina. Whether the specific structure of nicorandil and its mechanism can reduce the incidence of no-reflow in patients with acute myocardial infarction (AMI) after PCI and improve the clinical prognosis, the current clinical research is still under investigation. We will expound mechanisms of nicorandil, drug preconditioning and its comprehensive effect. The role of nicorandil in the interventional therapy of AMI was reviewed to guide clinical medication.
综述

miRNAs在肝细胞肝癌发展过程中的研究进展

Research progess of miRNAs in hepatocellular carcinoma

:123-126
 
肝细胞肝癌(HCC)是世界上最常见的肿瘤之一,其病因及确切的分子机制尚不完全清楚,目前认为其发病是多因素、多步骤的复杂过程,且预后较差。miRNAs在调控细胞的周期变化中起到重要的作用,它具有较高的组织特异性,在肿瘤发生中起到关键作用,从而有潜力作为肝癌的诊断和分类的新生物标志物,以及预测患者预后的工具。本文就近年来miRNAs在肝细胞肝癌方面的研究进展做一综述。
综述

青蒿素类药物的抗疟机制及耐药性产生研究进展

Advances in the synthesis and antimalarial study of artemisinin and its heteroatomic derivatives

:119-122
 
青蒿素类药物作为抗疟特效药,其特殊分子骨架和过氧基在抗疟中起着关键作用。通过损伤虫体的器膜、诱导蛋白变性、抑制ATP 蛋白6(Pf ATP6)活性等方式杀灭疟原虫。恶性疟原虫基因序列的突变和长期不规范用药均会使其产生耐药性。本文依据文献报道,对世界关于青蒿素类药物抗疟机制、耐药性的产生原因作一综述。
Artemisinin is an effective anti-malaria drug, It's special molecular framework and peroxy group play a key role in antimalarial. Plasmodium falciparum was killed by the inducing cytoplasmic organelledamage protein denaturation, inhibiting ATP6 activity. Mutations in the genetic sequence of plasmodium falciparum and long-time using drugs without rule will develop drug resistance. This article is based on the literature, do a review of the world's causes for the resistance of artemisinin to antimalarial mechanisms.
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