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| 1 | Exosomes as therapeutic drug carriers and delivery vehicles across biological membranes:current perspectives and future challenges显示文摘Exosomes are small intracellular membrane-based vesicles with different compositions that are involved in several biological and pathological processes. The exploitation of exosomes as drug delivery vehicles offers important advantages compared to other nanoparticulate drug delivery systems such as liposomes and polymeric nanoparticles; exosomes are non-immunogenic in nature due to similar composition as body's own cells. In this article, the origin and structure of exosomes as well as their biological functions are outlined. We will then focus on specific applications of exosomes as drug delivery systems in pharmaceutical drug development. An overview of the advantages and challenges faced when using exosomes as a pharmaceutical drug delivery vehicles will also be discussed. | Dinh Ha Ningning Yang Venkatareddy Nadithe | 2016 | Acta Pharmaceutica Sinica B2016，6，4： | 104 |
| 2 | Autophagy and multidrug resistance in cancer显示文摘Multidrug resistance(MDR) occurs frequently after long-term chemotherapy, resulting in refractory cancer and tumor recurrence.Therefore, combatting MDR is an important issue. Autophagy, a self-degradative system, universally arises during the treatment of sensitive and MDR cancer. Autophagy can be a double-edged sword for MDR tumors: it participates in the development of MDR and protects cancer cells from chemotherapeutics but can also kill MDR cancer cells in which apoptosis pathways are inactive. Autophagy induced by anticancer drugs could also activate apoptosis signaling pathways in MDR cells, facilitating MDR reversal. Therefore, research on the regulation of autophagy to combat MDR is expanding and is becoming increasingly important. We summarize advanced studies of autophagy in MDR tumors, including the variable role of autophagy in MDR cancer cells. | Ying-Jie Li Yu-He Lei Nan Yao Chen-Ran Wang Nan Hu Wen-Cai Ye Dong-Mei Zhang Zhe-Sheng Chen | 2017 | Chinese Journal of Cancer2017，36，8： | 54 |
| 3 | 利奈唑胺抗结核作用的研究及其最新进展显示文摘 | 唐神结 肖和平 | 2010 | 中华临床医师杂志(电子版)2010，4，1： | 48 |
| 4 | Standard triple therapy for Helicobacter pylori infection in China: A meta-analysis显示文摘AIM:To assess the efficacy and safety of standard triple therapy compared with other pre-existing and new therapies in China.METHODS:Literature searches were conducted in the following databases:PubMed,EMBASE,the Cochrane Central Register of Controlled Trials,the VIP database,the China National Knowledge Infrastructure database,and the Chinese Biomedical Database.A meta-analysis of all randomized controlled trials(RCTs)comparing standard triple therapy for the eradication of Helicobacter pylori with pre-existing and new therapies in China was performed using Comprehensive Meta-Analysis 2.0.There were 49 studies that met our criteria and the qualities of these studies were assessed using the Jadad scale.The Mantel-Haenszel method was used for pooling dichotomous data.We also conducted subgroupanalyses according to age,duration of treatment and drug type.Sensitivity analyses and a cumulative metaanalysis were also performed with CMA 2.0.Publication bias was evaluated using Egger’s test,Begg’s test or a funnel plot.RESULTS:A total of 49 RCTs including 8332 patients were assessed.This meta-analysis showed that standard triple therapy with proton pump inhibitors(PPIs),amoxicillin(AMO)and clarithromycin(CLA)was inferior to sequential therapy[relative risk(RR)=0.863;95%confidence interval(CI):0.824-0.904],but was not superior to quadruple therapy(RR=1.073;95%CI:0.849-1.357)or other triple therapies(RR=1.01;95%CI:0.936-1.089).The meta-analysis also suggested that standard triple therapy is slightly more effective than dual therapy(RR=1.14;95%CI:0.99-1.31).However,the differences were not statistically significant.We removed the only trial with a regimen lasting14 d by sensitivity analysis and found that 7-d standard triple therapy was superior to 7-d dual therapy(RR=1.222;95%CI:1.021-1.461).Moreover,a sub-analysis based on the duration of quadruple therapy indicated that the 7-d and 10-d standard triple therapies were inferior to sequential therapy(RR=0.790;95%CI:0.718-0.868;RR=0.917;95%CI:0.839-1.002,respectively).Additionally,there were no significant differences in cure rate or adverse events among standard triple therapy,quadruple therapy,and other triple therapies(RR=0.940;95%CI:0.825-1.072;RR=1.081;95%CI:0.848-1.378,respectively).Standard triple therapy had a higher occurrence of side effects than sequential therapy(RR=1.283;95%CI:1.066-1.544).CONCLUSION:The eradication rates with a standard triple therapy consisting of PPI,AMO,and CLA are suboptimal in China,and new treatment agents need to be developed. | Ben Wang Zhi-Fa Lv You-Hua Wang Hui Wang Xiao-Qun Liu Yong Xie Xiao-Jiang Zhou | 2014 | World Journal of Gastroenterology2014，20，40： | 46 |
| 5 | 耐药结核病的流行和监测显示文摘20世纪抗结核病药物相继问世,使结核病的治愈成为可能,但随之出现了结核分枝杆菌的耐药性。染色体自发突变导致对某种抗结核病药物耐药的发生频率为10^-6~10^18,由于不同药物耐药的突变位点不同,同时使用3种抗结核药的同时耐药频率为10^-18-10^20。因此,联用3种有效的抗结核药物时,发生抗结核药物耐药的概率极少。从这一点出发,可以认为耐药的发生是结核分枝杆菌基因突变被人为放大的结果。不合理的用药、治疗管理不善、药物供应不足和质量不佳以及间断用药等,刺激结核分枝杆菌发生耐药性,即获得性耐药(acquired drug resistance);随后,耐药结核分枝杆菌在人群中传播,发生耐药结核分枝杆菌感染,即原发耐药(primary drug resistance);耐多药结核病(MDR-TB)是指至少同时对异烟肼和利福平耐药的结核病。 | 端木宏谨 | 2006 | 中华结核和呼吸杂志2006，29，8： | 37 |
| 6 | ATC/DDD系统的建立及其在药物利用研究中的应用显示文摘 | 张文双 杨永弘 | 2009 | 临床药物治疗杂志2009，7，1： | 38 |
| 7 | 严重耐多药结核病的研究进展显示文摘近年来,严重耐多药结核病(extensively drug resistant tuberculosis,XDR-TB)的流行与传播使本已严峻的全球结核病防治形势变得更为紧迫,引起了各国结核病防治工作者的极大关注。XDR—TB的发生与发展暴露了世界结核病控制措施的薄弱和不足,也给全球公共卫生带来了前所未有的挑战。世界各国结核病防治专家正在寻找XDR—TB产生的原因,认识其对人类的危害,并探讨控制其发生与发展的可能对策。笔者在此将目前XDR—TB的研究进展综述如下。 | 唐神结 肖和平 | 2009 | 中华结核和呼吸杂志2009，32，5： | 39 |
| 8 | Androgen receptor: structure, role in prostate cancer and drug discovery显示文摘Androgens and androgen receptors (AR) play a pivotal role in expression of the male phenotype. Several diseases, such as androgen insensitivity syndrome (AIS) and prostate cancer, are associated with alterations in AR functions. Indeed, androgen blockade by drugs that prevent the production of androgens and/or block the action of the AR inhibits prostate cancer growth. However, resistance to these drugs often occurs after 2-3 years as the patients develop castration-resistant prostate cancer (CRPC). In CRPC, a functional AR remains a key regulator. Early studies focused on the functional domains of the AR and its crucial role in the pathology. The elucidation of the structures of the AR DNA binding domain (DBD) and ligand binding domain (LBD) provides a new framework for understanding the functions of this receptor and leads to the development of rational drug design for the treatment of prostate cancer. An overview of androgen receptor structure and activity, its actions in prostate cancer, and how structural information and high-throughput screening have been or can be used for drug discovery are provided herein. | MH Eileen TAN Jun LI H Eric XU Karsten MELCHER Eu-leong YONG | 2015 | Acta Pharmacologica Sinica2015，36，1： | 39 |
| 9 | Role of autophagy in tumorigenesis,metastasis,targeted therapy and drug resistance of hepatocellular carcinoma显示文摘Autophagy is a 'self-degradative' process and is involved in the maintenance of cellular homeostasis and the control of cellular components by facilitating the clearance or turnover of long-lived or misfolded proteins, protein aggregates, and damaged organelles. Autophagy plays a dual role in cancer, including in tumor progression and tumor promotion, suggesting that autophagy acts as a double-edged sword in cancer cells. Liver cancer is one of the greatest leading causes of cancer death worldwide due to its high recurrence rate and poor prognosis. Especially in China, liver cancer has become one of the most common cancers due to the high infection rate of hepatitis virus. In primary liver cancer, hepatocellular carcinoma (HCC) is the most common type. Considering the perniciousness and complexity of HCC, it is essential to elucidate the function of autophagy in HCC. In this review, we summarize the physiological function of autophagy in cancer, analyze the role of autophagy in tumorigenesis and metastasis, discuss the therapeutic strategies targeting autophagy and the mechanisms of drug-resistance in HCC, and provide potential methods to circumvent resistance and combined anticancer strategies for HCC patients. | Fang Huang Bing-Rong Wang Yi-Gang Wang | 2018 | World Journal of Gastroenterology2018，24，41： | 37 |
| 10 | Effect of cholecystokinin on cytokines during endotoxic shock in rats显示文摘AIM To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in lipopolysaccharide (LPS)-induced endotoxic shock (ES) rats.``METHODS The changes of blood pressure were observed using physiological record instrument in four groups of rats: LPS (8 mg. kg-1, iv) induced ES; CCK-8 (40 μg.kg- 1 iv) pretreatment 10 min before LPS (8 mg. kg- 1);CCK-8 (40 μg.kg-1, iv) or normal saline (control) groups.Differences in tissue and circulating specificity of the proinflammatory cytokines (TNF-a, IL-l3 and IL-6) were assayed with ELISA kits.``RESULTS CCK-8 reversed LPS-induced decrease of mean artery blood pressure (MABP) in rats. Compared with control, LPS elevated the serum level of IL-6 significantly (3567_-687 ng.L-1 vs 128_+22 ng.L-1, P<0.01), while contents of TNF-a and IL- lβ elevated significantly (277 _± 86ng.L-1 vs not detectable and 43 ± 9 ng.L-1 vs notdetectable, P<0.01) but less extent than IL-6, CCK-8significantly inhibited the LPS-induced increase in serum TNF-a, IL-lβ and IL-6. LPS elevated spleen and lung content of IL-Iβ significantly (5184 ± 85 ng.L-1 vs 1047 ±21 ng.L-1 and 4050 ± 614 ng.L-1 vs not detectable,P<0,01). while levels of TNF-a and IL-6 also rosesignificantly but in less extent than IL-lβ. CCK-8 inhibited the LPS-induced increase of the cytokines in spleen and lung. in the heart, CCK-8 significantly inhibited LPS.induced increase of TNF-a (864 ± 123 ng. L-1 in CCK-8 +LPS group vs 1599_-227 ng-L-1 in LPS group, P<0.01),and IL-lβ (282 ± 93 ng-L-1 in CCK-8 + LPS group vs 621 ±145 ng.L-1 in LPS group, P<0.01).``CONCLUSION CCK-8 reverses ES, which may be relatedto its inhibitory effect on the overproduction of cytokines. | Yi-Ling Ling~1 Ai-Hong Meng~1 Xiao-Yun Zhao~1 Bao-En Shan~2 Jun-Lan Zhang~1 Xiao-Peng Zhang~3 1 Department of Pathophysiology,Hebei Medical University,Shijiazhuang 050017,Hebei Province,China2 Research Center of Fourth Hospital,Hebei Medical University,Shijiazhuang 050000,Hebei Province,China3 Department of Chest Surgery of Hebei Provincial People’s Hospital,Shijiazhuang 050000,Hebei Province,China | 2001 | World Journal of Gastroenterology2001，7，5： | 31 |
| 11 | 耐多药结核病化疗研究的新进展显示文摘耐多药结核病(multidrug—resistant tuberculosis,MDR—TB)的流行与传播给全球公共卫生所带来的影响已逐步显现,MDR—TB的防治形势也变得越来越复杂。近年来,广泛耐药结核病(extensively drug resistant tuberculosis,XDR—TB)的出现使得全球结核病控制工作雪上加霜。因此,研究优化的MDR—TB化疗方案,以提高MDR—TB的治愈率,阻断其向更为难治的XDR—TB发生与发展迫在眉睫。最近,国外有关MDR-TB治疗的研究较为深入,其中不乏值得我们借鉴的经验与精髓,仔细拜读,颇有收益,愿与广大同道分享。 | 唐神结 肖和平 张青 | 2009 | 中华结核和呼吸杂志2009，32，8： | 32 |
| 12 | Mechanisms of drug resistance in colon cancer and its therapeutic strategies显示文摘Drug resistance develops in nearly all patients with colon cancer, leading to a decrease in the therapeutic efficacies of anticancer agents. This review provides an up-to-date summary on over-expression of ATPbinding cassette(ABC) transporters and evasion of apoptosis, two representatives of transport-based and non-transport-based mechanisms of drug resistance, as well as their therapeutic strategies. Different ABC transporters were found to be up-regulated in colon cancer, which can facilitate the efflux of anticancer drugs out of cancer cells and decrease their therapeutic effects. Inhibition of ABC transporters by suppressing their protein expressions or co-administration of modulators has been proven as an effective approach to sensitize drug-resistant cancer cells to anticancer drugs in vitro. On the other hand, evasion of apoptosis observed in drug-resistant cancers also results in drug resistance to anticancer agents, especially to apoptosis inducers. Restoration of apoptotic signals by BH3 mimetics or epidermal growth factor receptor inhibitors and inhibition of cancer cell growth by alternative cell death pathways, such as autophagy, are effective means to treat such resistant cancer types. Given that the drug resistance mechanisms are different among colon cancer patients and may change even in a single patient at different stages, personalized and specific combination therapy is proposed to be more effective and safer for the reversal of drug resistance in clinics. | Tao Hu Zhen Li Chun-Ying Gao Chi Hin Cho | 2016 | World Journal of Gastroenterology2016，22，30： | 29 |
| 13 | Insulin resistance and chronic liver disease显示文摘Increased insulin resistance is frequently associated with chronic liver disease and is a pathophysiological feature of hepatogenous diabetes.Distinctive factors including hepatic parenchymal cell damage,portalsystemic shunting and hepatitis C virus are responsible for the development of hepatogenous insulin resistance/diabetes.Although it remains unclear whether insulin secretion from pancreatic beta cells is impaired as it is in type 2 diabetes,retinopathic and cardiovascular risk is low and major causes of death in cirrhotic patients with diabetes are liver failure,hepatocellular carcinoma and gastrointestinal hemorrhage.Hemoglobin A1c is an inaccurate marker for the assessment and management of hepatogenous diabetes.Moreover,exogenous insulin or sulfonylureas may be harmful because these agents may promote hepatocarcinogenesis.Thus,pathogenesis,cause of death,assessment and therapeutic strategy for hepatogenous insulin resistance/diabetes differ from those for lifestyle-related type 2 diabetes.In this article,we review features of insulin resistance in relationship to chronic liver disease.We also discuss the impact of anti-diabetic agents on interferon treatment and hepatocarcinogenesis. | Takumi Kawaguchi Eitaro Taniguchi Minoru Itou Masahiro Sakata Shuji Sumie Michio Sata | 2011 | World Journal of Hepatology2011，3，5： | 25 |
| 14 | Red blood cell membrane-camouflaged nanoparticles: a novel drug delivery system for antitumor application显示文摘Erythrocytes(red blood cells, RBCs) are the most abundant circulating cells in the blood and have been widely used in drug delivery systems(DDS) because of their features of biocompatibility,biodegradability, and long circulating half-life. Accordingly, a 'camouflage' comprised of erythrocyte membranes renders nanoparticles as a platform that combines the advantages of native erythrocyte membranes with those of nanomaterials. Following injection into the blood of animal models, the coated nanoparticles imitate RBCs and interact with the surroundings to achieve long-term circulation. In this review, the biomimetic platform of erythrocyte membrane-coated nano-cores is described with regard to various aspects, with particular focus placed on the coating mechanism, preparation methods, verification methods, and the latest anti-tumor applications. Finally, further functional modifications of the erythrocyte membranes and attempts to fuse the surface properties of multiple cell membranes are discussed,providing a foundation to stimulate extensive research into multifunctional nano-biomimetic systems. | Qing Xia Yongtai Zhang Zhe Li Xuefeng Hou Nianping Feng | 2019 | Acta Pharmaceutica Sinica B2019，9，4： | 26 |
| 15 | Mechanisms of resistance to sorafenib and the corresponding strategies in hepatocellular carcinoma显示文摘Sorafenib, the unique drug as first-line treatment for advanced hepatocellular carcinoma (HCC), has opened a window of hope after searching for effective agents to combat HCC for decades. However, the overall outcomes are far from satisfactory. One of the explanations is the genetic heterogeneity of HCC, which has led to identifying predictive biomarkers for primary resistance to sorafenib, and then applying the concept of personalized medicine, or seeking therapeutic strategies such as combining sorafenib with other anticancer agents. Some of the combinations have demonstrated a better effectiveness than sorafenib alone, with good tolerance. The acquired resistance to sorafenib has also drawn attention. As a multikinase inhibitor, sorafenib targets several cellular signaling pathways but simultaneously or sequentially the addiction switches and compensatory pathways are activated. Several mechanisms are involved in the acquired resistance to sorafenib, such as crosstalks involving PI3K/Akt and JAK-STAT pathways, hypoxia-inducible pathways, epithelial-mesenchymal transition, etc . Based on the investigated mechanisms,some other molecular targeted drugs have been applied as second-line treatment for treat HCC after the failure of sorafenib therapy and more are under evaluation in clinical trials. However, the exact mechanisms accounting for sorafenib resistance remains unclear. Further investigation on the crosstalk and relationship of associated pathways will better our understanding of the mechanisms and help to find effective strategies for overcoming sorafenib resistance in HCC. | Bo Zhai Xue-Ying Sun | 2013 | World Journal of Hepatology2013，5，7： | 24 |
| 16 | Suppression of P-gp induced multiple drug resistance in a drug resistant gastric cancer cell line by overexpression of Fas显示文摘AIM To observe the drug sensitizing effect andrelated mechanisms of fas gene transduction onhuman drug-resistant gastric cancer cellSGC7901/VCR(resistant to Vincristine).METHODS The cell cycle alteration wasobserved by FACS.The sensitivity of gastriccancer cells to apoptosis was determined by invitro apoptosis assay.The drug sensitization ofcells to several anti-tumor drugs was observedby MTT assay.Immunochemical method wasused to show expression of P-gp and Topo Ⅱ ingastric cancer cells.RESULTS Comparing to SGC7901 and pBK-SGC7901/VCR,fas-SGC7901/VCR showeddecreasing G2 cells and increasing S cells,theG2 phase fraction of pBK-SGC7901/VCR wasabout 3.0 times that of fas-SGC7901/VCR,but Sphase fraction of fas-SGC7901/VCR was about1.9 times that of pBK-SGC7901/VCR,indicatingS phase arrest of fas-SGC7901/VCR.FACS alsosuggested apoptosis of fas-SGC7901/VCR,fas-SGC7901/VCR was more sensitive to apoptosisinducing agent VM-26 than pBK-SGC7901/VCR.MTT assay showed increased sensitization offas-SGC7901/VCR to DDP,MMC and 5-FU,butsame sensitization to VCR according to pBK-SGC7901/VCR.SGC7901,pBK-SGC7901/ VCRand fas-SGC7901/VCR had positively stainedTopo Ⅱ equally.P-gp staining in pBK- SGC7901/VCR was stronger than in SG07901,but there was little staining of P-gp in fas.SGC7901/VCR.CONCLUSION fas gene transduction couldreverse the MDR of human drug-resistant gastriccancer cell SGC7901/VCR to a degree,possiblybecause of higher sensitization to apoptosis anddecreased expression of P-gp. | Yin F Shi YQ Zhao WP Xiao B Miao JY Fan DM | 2000 | World Journal of Gastroenterology2000，6，5： | 24 |
| 17 | Transduction of Fas gene or Bcl-2 antisense RNA sensitizes cultured drug resistant gastric cancer cells to chemotherapeutic drugs显示文摘INTRODUCTIONChemotherapyisoneofthemajormethodsintumortreatment,butitoftendoesnotworkduetomultidrugresistance(MDR).Recentstudi... | XIAO Bing, SHI Yong Quan, ZHAO Yan Qiu, YOU Han, WANG Zuo You, LIU Xian Ling, YIN Fang, QIAO Tai Dong and FAN Dai Ming | 1998 | World Journal of Gastroenterology1998，4，5： | 24 |
| 18 | Molecular biology and the diagnosis and treatment of liver diseases显示文摘MolecularbiologyandthediagnosisandtreatmentofliverdiseasesHowardJ.Worman,FengLin,NaotoMamiyaandPaulJ.MustacchiaSubjectheading... | Howard J. Worman, Feng Lin, Naoto Mamiya and Paul J. Mustacchia | 1998 | World Journal of Gastroenterology1998，4，3： | 24 |
| 19 | Theranostic nanoparticles with tumor-specific enzyme-triggered size reduction and drug release to perform photothermal therapy for breast cancer treatment显示文摘Although progress has been indeed made by nanomedicines, their efficacies for cancer treatment remain low, consequently leading to failures in translation to clinic. To improve the drug delivery efficiency,nanoparticles need to change size so as to fully utilize the enhanced permeability and retention(EPR) effect of solid tumor, which is the golden principle of nanoparticles used for cancer treatment. Herein, we employed cationic small-sized red emission bovine serum albumin(BSA) protected gold nanocluster(Au NC@CBSA,21.06 nm) to both load indocyanine green(ICG) and act as imaging probe to realize theranostic. Then Au NC@CBSA-ICG was fabricated with negatively charged hyaluronic acid(HA) to form Au NC@CBSAICG@HA, which was about 200 nm to easily retain at tumor site and could be degraded by tumor-specific hyaluronidase into small nanoparticles for deep tumor penetration. The HA shell also endowed Au NC@CBSA-ICG@HA with actively targeting ability and hyaluronidase-dependent drug release. Furthermore, the quenching and recovery of fluorescence revealed the interaction between ICG and carrier, which was essential for the investigation of pharmacokinetic profiles. No matter in vitro or in vivo, Au NC@CBSAICG@HA showed markedly anti-tumor effect, and could suppress 95.0% of tumor growth on mice breast cancer model. All results demonstrated Au NC@CBSA-ICG@HA was potential for breast cancer therapy. | Rui Liu Chuan Hu Yuanyuan Yang Jingqing Zhang Huile Gao | 2019 | Acta Pharmaceutica Sinica B2019，9，2： | 24 |
| 20 | Effect of clinician-patient communication on compliance with flupentixol-melitracen in functional dyspepsia patients显示文摘AIM: To explore whether clinician-patient communication affects adherence to psychoactive drugs in functional dyspepsia(FD) patients with psychological symptoms. METHODS: A total of 262 FD patients with psychological symptoms were randomly assigned to four groups. The patients in Groups 1-3 were given flupentixol-melitracen(FM) plus omeprazole treatment. Those in Group 1 received explanations of both the psychological and gastrointestinal(GI) mechanisms of the generation of FD symptoms and the effects of FM. In Group 2, only the psychological mechanisms were emphasized. The patients in Group 3 were not given an explanation for the prescription of FM. Those in Group 4 were given omeprazole alone. The primary endpoints of this study were compliance rate and compliance index to FM in Groups 1-3. Survival analyses were also conducted. The secondary end points were dyspepsia and psychological symptom improvement in Groups 1-4. The correlations between the compliance indices and the reductions in dyspepsia and psychological symptom scores were also evaluated in Groups 1-3.RESULTS: After 8 wk of treatment, the compliance rates were 67.7% in Group 1, 42.4% in Group 2 and 47.7% in Group 3(Group 1 vs Group 2, P = 0.006; Group 1 vs Group 3, P = 0.033). The compliance index(Group 1 vs Group 2, P = 0.002; Group 1 vs Group 3, P = 0.024) with the FM regimen was significantly higher in Group 1 than in Groups 2 and 3. The survival analysis revealed that the patients in Group 1 exhibited a significantlyhigher compliance rate than Groups 2 and 3(Group 1 vs Group 2, P = 0.002; Group 1 vs Group 3, P = 0.018). The improvement in dyspepsia(Group 1 vs Group 2, P < 0.05; Group 1 vs Group 3, P < 0.05; Group 1 vs Group 4, P < 0.01) and psychological symptom scores(anxiety: Group 1 vs Group 2, P < 0.01; Group 1 vs Group 3, P < 0.05; Group 1 vs Group 4, P < 0.01; depression: Group 1 vs Group 2, P < 0.01; Group 1 vs Group 3, P < 0.01; Group 1 vs Group 4, P < 0.01) in Group 1 were greater than those in Groups 2-4. The compliance indices were positively correlated with the reduction in symptom scores in Groups 1-3. CONCLUSION: Appropriate clinician-patient communication regarding the reasons for prescribing psychoactive drugs that emphasizes both the psychological and GI mechanisms might improve adherence to FM in patients with FD. | Xiu-Juan Yan Wen-Ting Li Xin Chen Er-Man Wang Qing Liu Hong-Yi Qiu Zhi-Jun Cao Sheng-Liang Chen | 2015 | World Journal of Gastroenterology2015，21，15： | 23 |
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