Bladder cancer represents a significant disease burden in men, as it is both highly common and a leading cause of cancer-related deaths. Despite advances in personalized therapies, patient outcomes continue to show considerable variability, and there is an urgent need to explore novel therapeutic targets for this disease. Ferroptosis has recently been implicated in chemotherapy response and proposed as a therapeutic target in various cancers; however, its regulatory mechanism in bladder cancer cells has not been fully elucidated. In this study, we analyzed public data from the GEO database and found that the transcription factor GLI2 was significantly upregulated in bladder cancer compared with normal bladder tissues. Functional assays revealed that GLI2 promotes malignant progression and represses ferroptosis in bladder cancer cells. Mechanistically, RNA sequencing and chromatin immunoprecipitation (ChIP) assays showed that GLI2 transcriptionally regulates the expression of peroxiredoxin 1 (PRDX1), a well-characterized ferroptosis-inhibiting gene. Additionally, rescue assay results indicated that PRDX1 mediates the role of GLI2 in ferroptosis repression and promotes malignant progression of bladder cancer. More importantly, inhibition of GLI2 via siRNA or a small-molecule inhibitor sensitized bladder cancer cells to both PRDX1 inhibitors and cisplatin. Together, these findings delineate a regulatory axis involving GLI2-PRDX1-mediated ferroptosis, provide mechanistic insights into its critical role in driving bladder cancer progression and chemosensitivity, and offer potential therapeutic targets for future clinical intervention.

Lung squamous cell carcinoma (LUSC) remains an aggressive malignancy with limited therapeutic options and poor prognosis. Recent studies have identified disulfidptosis as a novel form of metabolic stress-induced cell death, but its clinical implications in LUSC remain unexplored. This study investigates the prognostic value of disulfidptosis-related genes (DRGs) in LUSC. We analyzed transcriptomic data from TCGA-LUSC cohort and identified DRGs through intersection with established disulfidptosis-related gene sets. A protein-protein interaction (PPI) network was constructed, and univariate Cox regression was performed to select prognostic genes. A risk score model was developed using multivariate Cox regression. The model’s performance was evaluated using ROC curve and Kaplan-Meier analyses. Functional enrichment and immune microenvironment analyses were conducted to explore potential mechanisms. We identified 9 prognostic DRGs (FHOD1, ORC5, TRIR, ALKBH1, EPS8L2, MBLAC1, MYADM, HTRA2, and SRI) that significantly correlated with patient survival. The risk score model effectively stratified patients into high- and low-risk groups (P < 0.001), with C-index values of 0.78 at 1 year and 0.75 at 3 years. High-risk patients showed enriched cytokine-cytokine receptor interactions and immunosuppressive microenvironments, while low-risk patients exhibited activated metabolic pathways. Experimental validation confirmed ORC5’s oncogenic role in promoting proliferation and invasion. We established a novel 9-gene prognostic signature based on disulfidptosis-related genes that effectively predicts LUSC outcomes. These findings highlight the clinical relevance of disulfidptosis in LUSC and provide potential biomarkers for risk stratification and therapeutic targeting.

Ethnopharmacological relevance: Uncaria rhynchophylla (Miq.) Miq. ex Havil. is a plant species that is routinely devoted in traditional Chinese medicine to treat central nervous system disorders. Rhynchophylline (Rhy), a predominant alkaloid isolated from Uncaria rhynchophylla (Miq.) Miq. ex Havil., has been demonstrated to reverse methamphetamine-induced (METH-induced) conditioned place preference (CPP) effects in mice, rats and zebrafish. The precise mechanism is still poorly understood, thus further research is necessary. Aim of study: This study aimed to investigate the role of miRNAs in the inhibitory effect of Rhy on METH dependence. Materials and methods: A rat CPP paradigm and a PC12 cell addiction model were established. Microarray assays were used to screen and identify the candidate miRNA. Behavioral assessment, real-time PCR, dual-luciferase reporter assay, western blotting, stereotaxic injection of antagomir/agomir and cell transfection experiments were performed to elucidate the effect of the candidate miRNA and intervention mechanism of Rhy on METH dependence. Results: Rhy successfully reversed METH-induced CPP effect and the upregulated miR-181a-5p expression in METH-dependent rat hippocampus and PC12 cells. Moreover, suppression of miR-181a-5p by antagomir 181a reversed METH-induced CPP effect. Meanwhile, overexpression of miR-181a-5p by agomir 181a in combination with low-dose METH (0.5 mg/kg) elicited a significant CPP effect, which was blocked by Rhy through inhibiting miR-181a-5p. Finally, the result demonstrated that miR-181a-5p exerted its regulatory role by targeting gamma-aminobutyric acid A receptor alpha 1 (GABRA1) both in vivo and in vitro. Conclusion: This finding reveals that Rhy inhibits METH dependence via modulating the miR-181a-5p/GABRA1 axis, which may be a promising target for treatment of METH dependence.

BACKGROUND:Histone deacetylases (HDAC) contribute to oncogenic program, pointing to their inhibitors as a potential strategy against cancers. We, thus, studied the mechanism of HDAC inhibitor ITF2357 in resistance of mutant (mut)-KRAS non-small cell lung cancer (NSCLC) to pemetrexed (Pem).METHODS:We first determined the expression of NSCLC tumorigenesis-related HDAC2 and Rad51 in NSCLC tissues and cells. Next, we illustrated the effect of ITF2357 on the Pem resistance in wild type-KARS NSCLC cell line H1299, mut-KARS NSCLC cell line A549 and Pem-resistant mut-KARS cell line A549R in vitro and in xenografts of nude mice in vivo.RESULTS:Expression of HDAC2 and Rad51 was upregulated in NSCLC tissues and cells. Accordingly, it was revealed that ITF2357 downregulated HDAC2 expression to diminish the resistance of H1299, A549 and A549R cells to Pem. HDAC2 bound to miR-130a-3p to upregulate its target gene Rad51. The in vitro findings were reproduced in vivo, where ITF2357 inhibited the HDAC2/miR-130a-3p/Rad51 axis to reduce the resistance of mut-KRAS NSCLC to Pem.CONCLUSION:Taken together, HDAC inhibitor ITF2357 restores miR-130a-3p expression by inhibiting HDAC2, thereby repressing Rad51 and ultimately diminishing resistance of mut-KRAS NSCLC to Pem. Our findings suggested HDAC inhibitor ITF2357 as a promising adjuvant strategy to enhance the sensitivity of mut-KRAS NSCLC to Pem.

Background: Biochanin A is an excellent dietary isoflavone that has the concomitant function of both medicine and foodstuff. The attenuation function of biochanin A on blood-brain barrier (BBB) damage induced by cerebral ischemia-reperfusion remains unclear. Methods: C57BL/6 mice were subjected to 1 h middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion. The infarct volume of the brain was stained by TTC, while leakage of the brain was quantitatively stained by Evans blue, and the neurologic deficit score was measured. Microglial-induced morphologic changes were observed via immunofluorescence staining, and rolling and adhering leukocytes in venules were observed via two-photon imaging, while the inner fluorescein isothiocyanate-albumin of venules were compared with those of surrounding interstitial area through venular albumin leakage. Results: The attenuation effect of biochanin A on tight junction injury was compared in ischemia-reperfusion mice or conventional knockdown of leucine-rich α2-glycoprotein 1 (Lrg1) mice. Biochanin A could ameliorate BBB injury in mice with cerebral ischemia-reperfusion in a dose-dependent manner by strengthening the immunostaining volume of occludin, claudin-5, and zonula occludens-1. The amoeba morphologic changes of microglial combined with the elevated expression of Lrg1 could be relieved under the treatment of biochanin A. Biochanin A played a countervailing role on the rolling leukocytes in the vessel, while the leakage of blood vessels was reduced. Biochanin A diminished its functions to further improved attenuation for tight junction injury on conventional Lrg1-knockout mice, as well as the inhibition effects on TGF-β1, and the phosphorylation of suppressor of mothers against decapentaplegic 2 (Smad2)/Smad2 via western blot assay. Conclusion: Biochanin A could alleviate tight junction injury induced by cerebral ischemia-reperfusion and blocked the Lrg1/TGF-β/Smad2 pathway to modulate leukocyte migration patterns.

Background Chronic intermittent hypoxia (CIH) has been regarded as an important cause of atherosclerotic disease. In our study, we set out to investigate whether CIH regulated the high mobility group box 1/receptor for advanced glycation endproducts/NOD‐like receptor family pyrin domain‐containing 3 (HMGB1/RAGE/NLRP3) axis to affect the progression of atherosclerosis. Methods and Results Initially, peripheral blood samples were collected from patients with single obstructive sleep apnea, atherosclerosis complicated with obstructive sleep apnea, and healthy volunteers. In vitro cell experiments were conducted using human monocyte cell line THP‐1 and human umbilical vein endothelial cells to explore the role of HMGB1 in cell migration, apoptosis, adhesion, and transendothelial migration. In addition, a CIH‐induced atherosclerosis mouse model was established for further identifying the critical role of the HMGB1/RAGE/NLRP3 axis in atherosclerosis. Upregulated HMGB1 and RAGE were found in patients with atherosclerosis complicated with obstructive sleep apnea. CIH induction increased HMGB1 expression by inhibiting HMGB1 methylation, activating the RAGE/NLRP3 axis. After inhibition of the HMGB1/RAGE/NLRP3 axis, monocyte chemotaxis and adhesion were repressed, and macrophage‐derived foam cell formation was inhibited, accompanied by suppression of endothelial and foam cell apoptosis and inflammatory factor secretion. In vivo animal experiments also noted that the progression of atherosclerosis was prevented by inhibition of the HMGB1/RAGE/NLRP3 axis in CIH‐induced ApoE−/− mice. Conclusions Taken together, CIH induction can upregulate HMGB1 through inhibition of HMGB1 methylation, which activates the RAGE/NLRP3 axis to promote inflammatory factor secretion, thereby promoting the progression of atherosclerosis.

结合国内外发布的关于质量管理、风险管理、基于风险的质量管理等相关要求,依据现行版《药物临床试验质量管理规范》(GCP)的相关规定,以临床试验机构质量管理体系引入风险管理策略为切入点,通过对临床试验全过程中可能涉及的质量风险点进行识别、分析和评估,并提出针对不同风险等级制定相应的风险应对措施,充分发挥风险管理策略在临床试验机构质量管理中的作用,提高临床试验质量管理的效率,以期为其他医疗机构开展临床试验质量管理提供参考.

In recent years, receptor for advanced glycation end-products (RAGE) has been documented to induce liver fibrosis and inflammatory reaction. Further, microarray data analysis of this study predicted high expression of RAGE in non-alcoholic fatty liver disease (NAFLD). However, its specific mechanisms remain to be elucidated. Hence, this study is aimed at investigating the mechanistic insights of RAGE in chronic intermittent hypoxia (CIH)-induced NAFLD. ApoE knockout (ApoE −/− ) mice were exposed to CIH to induce NAFLD, and primary hepatocytes were also exposed to CIH to mimic in vitro setting. Accordingly, we found that RAGE and NF-κB were upregulated in the liver tissues of CIH-induced NAFLD mice and CIH-exposed hepatocytes. Depleted RAGE attenuated CIH-induced hepatocyte injury, lipid deposition, and inflammation. The relationship between RAGE and NF-κB was analyzed by in silico analysis and correlation analysis. It was demonstrated that knockdown of RAGE inhibited the NF-кB pathway, thus alleviating CIH-induced disorders in hepatocytes. Moreover, in vivo experiments also verified that depletion of RAGE alleviated CIH-induced NAFLD by inhibiting NF-кB pathway. Collectively, loss of RAGE blocked the NF-кB pathway to alleviate CIH-induced NAFLD, therefore, highlighting a potential hepatoprotective target for treating NAFLD.

目的:分析采用中医十层脉诊治新型冠状病毒肺炎的效果,总结采用中医十层脉诊治新型冠状病毒肺炎的临床思路.方法:南昌大学第一附属医院象湖院区为江西省重症新型冠状病毒肺炎患者定点收治医院,笔者将中医药介入治疗的4例患者主要分为4个证型:邪热壅肺证、肝胆郁热证、内闭外脱证及邪遏少阳证.此次研究从中选择各型典型治愈及好转案例,从舌脉及用药特点等方面予以分析,探讨中医十层脉诊治新型冠状病毒肺炎的效果.结果:采用中医十层脉诊治新型冠状病毒肺炎常见证型患者效果显著.结论:中医十层脉的肺、肝脉对新型冠状病毒肺炎患者的诊治具有一定指导意义.

目的 为临床试验机构规范管理试验用药品提供参考.方法 根据《药物临床试验质量管理规范》(GCP)的要求,建立符合我院实际情况的临床试验药房管理体系,药物管理员对试验用药品管理中出现的各种问题进行总结归纳,并积极解决工作中的各种问题.结果 与结论目前我院试验药房的管理模式符合本机构的实情,药物管理员在试验用药品管理中发挥着重要作用,通过分析并解决存在的问题,减少了工作中的各种差错,为临床试验结果科学、可靠提供了保障,并保障了受试者用药安全.

目的 探讨熊果酸(ursolic acid,UA)对肝细胞肝癌(hepatocellular carcinoma,HCC)细胞增殖、迁移与侵袭的作用及其机制.方法 采用0～80μmol/L UA处理HCC细胞系(BEL-7404、Huh7、SMMC-7721和HepG2)和正常肝细胞系(HL-7702和HHL-5),用CCK-8法筛选UA的剂量范围.用0～40μmol/L UA处理HepG2细胞48 h后,CCK-8法检测细胞活性;Transwell小室法检测细胞迁移与侵袭;RT-qPCR检测miR-148a-3p表达水平;免疫荧光染色法检测孕烷X受体(pregnane X receptor,PXR)表达水平.将miR-148a-3p inhibitor、sh-PXR或pcDNA-PXR转入HepG2细胞,再给予UA处理48 h后,检测细胞活性、迁移和侵袭情况.生物信息学和双荧光素酶活性法分析miR-148a-3p和PXR之间的关系.结果 在0～40μmol/L剂量范围内,UA对正常肝细胞系无毒但能抑制HCC细胞系活性.UA能剂量依赖性抑制HepG2细胞的细胞活性、迁移与侵袭,且伴随着升高miR-148a-3p的表达水平和降低PXR的表达水平.miR-148a-3p inhibitor转染能部分逆转UA对HepG2细胞的细胞活性、迁移与侵袭的抑制作用.沉默PXR具有UA类似的效果,而过表达PXR能消除UA的作用.PXR是miR-148a-3p的靶基因.结论 UA能通过调节miR-148a-3p/PXR轴抑制HCC细胞的增殖、迁移和侵袭.

本研究通过分析临床试验免费诊疗模式发展现状,结合临床试验现场核查对数据真实且可溯源的要求,设计了一种基于医院信息管理系统(HIS)的临床试验门诊免费诊疗信息模块.该模块可为受试者在HIS中开具临床试验免费医嘱和查询受试者在院临床试验史,具有操作简单、方便,不增加研究者工作量的优点,实现了全流程信息化监管和实时抓取医技部门开展临床试验检验检查的绩效数据,提高了研究者的积极性、医技人员的配合度和受试者的依从性.

Background: Mycobacterium tuberculosis (TB) is a pathogen that consequently leads to TB infection, which remains a significant global health concern. Programmed death 1 (PD-1)/programmed death-ligand 1 (PD-L1) signaling pathway is critical for terminating immune responses. The present study aimed to elucidate the regulatory role of the PD-1/PD-L1 signaling pathway in alveolar macrophages against Mycobacterium TB in mice. Methods: Specific pathogen free mice were initially prepared for Mycobacterium TB model establishment. The alveolar macrophages of the successfully modeled rats were evaluated to determine the levels of PD-1, PD-L1, AKT, mTOR, TNF-alpha, IL-2, IL-4, IL-6, IL-10, IL-17, IL-17A, and IFN-gamma. The surface makers of macrophages (CD11c, CD16, CD86, CD163, CD206, CX3CR-i and CSF-1R), level of ROS, apoptosis and cell cycle, were all assessed. Results: Elevated levels of PD -1 and PD -L1, decreased levels of AKT and mTOR, along with elevated levels of TNF-alpha, NF-kappa B, IL-17, IL-2, IL-6, IL-17A and IFN-gamma were identified in the alveolar macrophages infected with Mycobacterium TB, while an opposite trend was observed when PD-1/PD-L1 signaling pathway was inhibited. Additionally, elevated protein levels of CD11c, CD16 and CD86, as well as an increased rate of positive ROS and cell apoptosis, levels of Bax, and a diminished percentage of alveolar macrophages at the S and G2/M stages were detected in the event of Mycobacterium TB infection. A contrasting trend to the aforementioned findings was detected when the PD-1/PD-L1 signaling pathway was inhibited. Conclusion: Taken together, these results suggested that inhibition of the PD-1/PD-L1 signaling pathway enhanced the innate immune response of alveolar macrophages to Mycobacterium TB in mice.

目的 探讨人感染H7N9禽流感的临床特点及远期预后.方法 回顾性分析5例人感染H7N9禽流感患者的临床资料,并对5例患者随访1年.结果 5例患者中有4例为老年患者,4例合并基础疾病.入院时,5例患者的红细胞沉降率、C-反应蛋白、降钙素原、D二聚体、乳酸脱氢酶均升高;3例白细胞计数、2例淋巴细胞计数均下降,2例天冬氨酸氨基转移酶均升高,2例肌酸激酶及肌酸激酶同工酶均升高.以上血液学指标在随访时多数恢复正常.5例患者的胸部CT显示病灶范围均超过1叶,可见磨玻璃影、实变影,部分合并胸腔积液.6个月随访时,1例以实变为主的病灶明显吸收;4例均遗留有不同程度的肺间质改变(磨玻璃影、网格影、纤维条索影)及实性结节,这4例患者伴有肺弥散功能减低.5例患者经综合治疗,均康复出院.结论 临床医生要提高对H7N9禽流感的认识,并结合相关的血液学检测及影像学检查识别出病情的严重程度,加强对患者的监护管理及综合治疗,以降低病死率.老年合并基础疾病的患者在疾病恢复期的修复能力较差,可能会出现各器官系统功能的持续异常.

Numerous studies have investigated the association between ALDH2 gene rs671G>A polymorphism and various cancer type in Asians. However, the results remain inconclusive. We conducted a comprehensive meta-analysis including 63 articles with 66 studies containing 25,682 cases and 47,455 controls retrieved by searching PubMed and Embase electronic databases up to March 5, 2018. Pooled results indicated that ALDH2 gene rs671 polymorphism was significantly associated with the overall cancer risk in Asians (homozygous model: odds ratio [OR] =0.85, 95% confidence interval [CI]=0.72-0.99, P=.042; heterozygous model: OR=1.32, 95% CI=1.14-1.52, P<.001; recessive model: OR=0.73, 95% CI=0.60-0.88, P=.001; dominant model: OR=1.32, 95% CI=1.16-1.51, P<.001; and allele comparison model: OR=1.11, 95% CI=1.03-1.19, P=.004), especially in esophageal cancer and among the Chinese and the Japanese. Our results suggest that ALDH2 rs671 polymorphism is associated with the overall cancer risk in Asians. Well-designed prospective studies with more information about gene-environment interaction, such as drinking, should be conducted to validate our findings.

Long non-coding RNAs (lncRNAs) are a family of non-protein-coding RNAs, which have the ability to influence the chemo-resistance of lung adenocarcinoma (LAC). In this study, we explored the mechanism by which LINC00485 competitively binds to microRNA-195 (miR-195) in the regulation of the chemotherapy sensitivity in LAC by regulating checkpoint kinase 1 (CHEK1). Microarray analysis was used to screen out LAC related genes, and interaction between CHEK1 and miR-195, as well as that between miR-195 and LINC00485, was further confirmed by RNA-pull down and RIP. LINC00485 expression in LAC cells (A549 and H1299) was determined. The cells were then introduced with miR-195, anta-miR-195, LINC00485 or si-LINC00485 to identify the role of miR-195 and LINC00485 in LAC through evaluating the expression of CHEK1, CHEK1, Bax, Bcl-2, VEGF and HIF-1α in LAC cells by either RT-qPCR or Western blot analysis. After being treated with different concentration of cisplatin, cell proliferation, colony formation and apoptosis were assessed. LINC00485 acted as a competitive endogenous RNA against miR-195, and miR-195 directly targeted CHEK1. The expression of LINC00485 was higher in LAC cells. The down-regulation of LINC00485 or the up-regulation of miR-195 decreased the expression of CHEK1, Bcl-2, VEGF and HIF-1α, while also increasing the expression of Bax. Moreover, the over-expression of miR-195, or the silencing of LINC00485 enhanced the sensitivity of LAC cells to cisplatin, thereby promoting the apoptosis of LAC cells while suppressing the proliferation. LINC00485 competitively binds to miR-195 to elevate CHEK1 expression in LAC cells, suggesting that LINC00485 is a novel direction for therapeutic strategies of LAC.

Background/Aim: In recent years, the relationship between miR-200 expression and prognosis in lung cancer patients has been studied extensively. The miR-200 family plays a vital role in occurrence, development, metastasis, and drug resistance of lung cancer. Increasing evidence has shown that the miR-200 family is highly expressed in lung cancer and associated with poor prognosis. However, results have been inconclusive. Therefore, the aim of this study was to assess the association between miR-200 family expression and the clinicopathological and prognostic significance in patients with lung cancer via conducting a meta-analysis. Methods: A total of 9 different publications were searched from PubMed, Web of Science, Embase, and Cochrane library databases. Summary hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using random-effects/fixed-effects models. Results: A total of nine articles, consisting of 812 patients, were included in this meta-analysis. Pooling all eligible studies, this study found a shorter overall survival in patients with high expression of the miR-200 family (HR = 2.29, 95% CI: 1.10-4.73). Furthermore, subgroup analysis, based on area, demonstrated that a significant association was found between higher expression of the miR-200 family and poor overall survival (HR = 4.70, 95% CI: 1.5913.89) in the European population. However, there was no significant association between high expression of the miR-200 family and poor PFS (HR = 1.40, 95% CI: 0.21-9.25). In addition, this study failed to observe a correlation of increased miR-200 family expression with clinicopathological parameters, including age, sex, histology, tumor node metastasis (TNM) stage, lymph node metastasis, and tumor differentiation. Conclusion: High expression of the miR-200 family is significantly associated with poor clinical outcomes, particularly decreasing overall survival for European populations. Future studies should be performed to confirm the clinical utility of the miR-200 family in lung cancer.

Objective To analyzed the clinical characteristics and prognosis of patients with H7N9 avian influenza. Methods The baseline characteristics, clinical manifestations, treatments, laboratory and imaging findings were collected and analyzed for 20 patients with H7N9 avian influenza admitted to the First Affiliated Hospital of Nanchang University from December 2016 to March 2017. According to the final clinical outcome, the patients were divided into the death group and the survival group. Ten patients in the death group died, and 10 patients in the survival group were discharged. The data with normal distribution were analyzed by t test. The data with non?normal distribution were analyzed by Wilcoxon rank sum test. Results Of the 20 patients, 13 were males and 7 were females, aging 40-82 years, with a mean age of (60 ± 12) years. Twelve patients had a definite history of poultry exposure and 10 had chronic underlying diseases such as hypertension and diabetes. The clinical manifestations were mainly fever, cough, hemoptysis, respiratory distress, fatigue, etc. In the survival group, the platelet count was (167-315)×109/L,while it was (78-152)×109/L in the death group. The average white blood cell count was (7.78-11.52)×109/L and (9.91-15.93)×109/L in the survival and death groups respectively. The average value of lymphocyte count was (0.69-1.59)×109/L and (0.58-0.86)×109/L in the survival and death groups respectively. In the death group the glutamic?pyruvic transaminase (ALT) value was (14.0-352.0) U/L, the total bilirubin value was (6.9-34.5) μmol/L, the creatine kinase MB (CK?MB) was (16.0-162.0) U/L, the serum calcium value was (1.4-2.0) mmol/L, the C?reactive protein value was (33.1-414.0) mg/L, and the calcium reduction prime value was (0.6-100.0) μg/L. In the survival group,the ALT value was (25.0-181.0) U/L, the total bilirubin value was (4.8-25.9) μmol/L, the CK?MB value was (15.0-40.0) U/L, the serum calcium value was (1.9-2.4) mmol/L, the C-reaction protein value was (12.8-52.5) mg/L, and the procalcitonin value was (0.3-23.3) μg/L. Sixteen cases suffered severe pneumonia. Twelve patients received extracorporeal membrane oxygenation (ECMO), and 4 survived. The cause of death was mainly related to factors such as age, chronic underlying diseases and severity of illness. Conclusions Human infection with H7N9 avian influenza virus was highly pathogenic, and prone to progress into severe pneumonia, with a high mortality. Decreased platelet count was associated with mortality (t=4.07, P=0.001), predictive of patient outcome.

仿制药一致性评价推动着生物等效性试验的开展,生物等效性试验的风险日益突出.本文基于临床试验管理者的视角,对生物等效性试验实施过程中的机构组织管理、受试者管理、试验药物和生物样品管理风险现状及存在问题进行剖析,提出加强对机构管理者及研究者生物等效性试验专业知识和法规的培训、关注受试者招募合规性及试验期间管理的合理性、规范试验药物和生物样品的管理流程和记录等相应的风险管控措施和策略.

In this study, extractive electrospray ionization and mass spectrometry (EESI-MS) was used to evaluate whether volatile organic compounds (VOCs) in exhaled gases can serve as specific diagnostic markers of lung cancer. The patients with lung cancer were diagnosed by chest CT or chest X-ray exam and confirmed by histopathology and cytology. Patients with pulmonary infections were identified by imaging, pathological diagnosis, or improvement of symptoms after antiinflammatory treatment. The control group had no lung abnormalities in imaging. Exhaled gases were collected using a Tedlar sampling bag and were detected using electrospray ionization mass spectrometry. By combining statistical and analytical chemistry, characteristic volatile organic compounds were screened. The results show that butadiene, orotic acid, tetrahydrobiopterin, and N-phenylacetylglutamine in lung cancer patients are significantly different from those in the control and lung infection groups.