结直肠癌是人类第三大常见癌症，约占所有癌症的10%,也是癌症相关死亡的第二大原因。2020年全球约有190万新发病例和90万死亡病例 [1] 。近年来，随着经济发展以及生活方式和饮食的改变，中国结直肠癌的发病率和死亡率增加 [2] 。这给医疗系统带来了沉重的经济负担。因此，识别和评估新的生物标志物和治疗靶点迫在眉睫。目前，蛋白酶体26S非ATP酶调节亚基7（PSMD7）的表达及其在结直肠癌进展中的作用在很大程度上仍然未知。

目的 通过血浆蛋白质组液质联用分析寻找多发性硬化疾病中差异表达蛋白,寻找多发性硬化早期诊断相关的血浆标志物.方法 选取多发性硬化患者和健康对照人各9例,采用10标TMT标记技术进行血浆蛋白质组分析,筛选差异蛋白.结果 液质联用血浆蛋白质组差异分析共鉴定到52个差异蛋白质,其中上调27个,下调25个.差异蛋白质功能分析显示,这些蛋白与免疫系统、补体系统、急性期反应信号等通路相关.结论 在血浆蛋白质组中可以找到与多发性硬化相关的蛋白质,这些有可能成为其早期诊断的标志物.本研究为血浆蛋白质组学在多发性硬化诊断中的进一步应用奠定了基础.

唾液腺腺样囊性癌（salivary adenoid cystic carcinoma,SACC）又称涎腺腺样囊性癌作为常见的头颈部恶性肿瘤之一,是一种来源于润管储备细胞的上皮来源的高度恶性唾液腺肿瘤。典型的临床及生物学特征为生长缓慢,但局部侵润性强,高度嗜神经

目的:探讨骨碎补总黄酮对骨质疏松大鼠骨组织中骨硬化蛋白(SOST)表达的影响,阐明骨碎补总黄酮抗骨质疏松的作用机制.方法:将40只8月龄雌性大鼠分为正常对照组(每天灌胃生理盐水)、骨质疏松模型组(90 mg·kg-1·d-1维甲酸灌胃给药,持续14 d)、阳性药组(维甲酸灌胃14 d,同时以0.1 mg·kg-1·d-1皮下注射阿仑膦酸钠30 d)和骨碎补总黄酮组(维甲酸灌胃14 d,同时以58 mg·kg-1·d-1骨碎补总黄酮灌胃给药30 d),每组10只.采集各组大鼠静脉血,检测血清中钙、磷和碱性磷酸酶(ALP)水平,肝和肾功能指标,包括丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、肌酐(Crea)和尿素氮(BUN);取大鼠一侧股骨,采用HE染色观察骨组织病理形态表现;采用qRT-PCR法检测各组大鼠骨组织中SOST mRNA表达水平,Western blotting法检测大鼠骨组织中SOST蛋白表达水平.结果:与骨质疏松模型组比较,阳性药组大鼠血清中钙和磷水平明显降低(P<0.05或P<0.01),而骨碎补总黄酮组大鼠血清中钙水平明显升高(P<0.05);与阳性药组比较,骨碎补总黄酮组大鼠血清中钙、磷和ALP水平明显升高(P<0.05或P<0.01).与正常对照组比较,骨质疏松模型组、阳性药组和骨碎补总黄酮组大鼠血清中Crea水平明显降低(P<0.01);与骨质疏松模型组和阳性药组比较,骨碎补总黄酮组大鼠血清中Crea水平明显降低(P<0.01);各组大鼠血清中ALT、AST和BUN水平比较差异均无统计学意义(P>0.05).光镜下观察,骨质疏松模型组大鼠骨组织骨小梁稀疏、变薄和断裂;与骨质疏松模型组比较,阳性药组和骨碎补总黄酮组大鼠骨小梁明显变厚、断裂减少.与骨质疏松模型组比较,阳性药组和骨碎补总黄酮组大鼠骨组织中SOST mRNA表达水平均明显降低(P<0.01);阳性药组大鼠骨组织中SOST蛋白表达水平较正常对照组和骨质疏松模型组均明显降低(P<0.01),骨碎补总黄酮组大鼠SOST蛋白表达水平虽然较正常对照组和骨质疏松模型组低,但差异无统计学意义(P>0.05).结论:骨碎补总黄酮拮抗骨质疏松症的作用机制可能是通过抑制骨细胞合成SOST进而促进骨形成.

进入围绝经期的女性因卵巢功能的下降,随之雌激素水平逐渐减少,泌尿系统及生殖系统正常微生态菌群结构发生改变,使之成为发生泌尿系统感染的易发人群[1]。随着近年来广谱抗生素的大量应用,病原菌耐药性也随之增加[2]。因此本研究选取我院围绝经期伴泌尿系统感染患者,进行中段尿的细菌培养和鉴定,对分离出的173株病原菌的种类和耐药性进行分析,为临床医生对疾病的诊断和治

The antiresorptive agents still are the mainstay of osteoporosis treatment. This study aimed to investigate the efficacy of recombinant Lingzhi-8 (rLZ-8) on osteoclast in vitro and bone resorption in vivo. The rLZ-8 protein was derived from Ganoderma lucidum transformation and produced by a genetic system. Receptor activator of nuclear factor kappa-Β ligand induced RAW 264.7 cells to differentiate into osteoclastic cells in vitro. Cells were exposed to different doses of rLZ-8 for 7 days to measure differences of osteoclastic differentiation, apoptosis rate and gene expression. rLZ-8 was labeled with Alexa Fluor 568 to observe its intracellular distribution under super-resolution light microscopy. In addition, retinoic acid was administered to female rats for 14 days to develop osteopenia changes. Different doses of rLZ-8 were simultaneously administered to rats treated with retinoic acid to observe changes of bone mineral density, biochemical parameters and organ weight ratio. Results indicated that rLZ-8 regulated receptor activator of nuclear factor kappa-Β (RANK) - tumor necrosis factor receptor-associated factor 6 (TRAF6) - c-Jun N-terminal kinase (JNK) signaling pathway, by which rLZ-8 inhibited osteoclastic differentiation and promoted osteoclastic apoptosis. Through 3D-structured illumination microscopy, it was observed that rLZ-8 entered RAW264.7 cells and accumulated gradually into the cytoplasm but little into nucleus. Administration with rLZ-8 reversed loss of bone mass and improved ALP activity in osteoporotic rats. Low-to high-dose rLZ-8 treatments displayed little toxic effects on rat organs and did not seem to impact their overall health. All data suggested that rLZ-8 has possible action against osteoporosis.

To develop a rapid, dual-parameter, plate-based screening process to improve production and secretion rate of glucose oxidase simultaneously in Aspergillus niger.

目的测定vinculin在大肠癌及肾癌组织中的表达情况,探究其在大肠癌及肾癌发生发展中的意义。方法用二维液相色谱-质谱联用技术对20例DukesB期大肠癌患者的癌组织及癌旁组织、18例透明细胞肾癌患者的癌组织及癌旁组织中vinculin表达水平进行检测,并通过免疫印迹实验进一步验证。结果 vinculin在大肠癌组织中的表达水平低于其癌旁组织,相反,在肾癌组织中表达较其癌旁组织高。结论 vinculin在大肠癌及肾癌的发生发展中起一定作用。

泌尿系感染是医院感染中最常见的感染性疾病之一。其发病率仅次于最常见的上呼吸道感染,约占感染性疾病的20%]-30%[1。近年来,随着抗菌药物在临床治疗过程中的广泛应用,细菌对常用抗菌素的耐药性也在逐年升高[2],而细菌耐药是治疗泌尿系感染失败的主要原因。定期监测泌尿系感染的细菌分布及耐药性,指导临床合理选择治疗药物具有重要意义。为了解我院区患有泌尿系感染的患者常见病原菌分布及耐药状况,我们检测了自2015年2月份至2017年2月份就诊的泌尿系感染患者215例尿培养标本,对检测出的265株病原菌的种类以

成釉细胞瘤（AM）是一种牙源性上皮性肿瘤,约占牙源性肿瘤的60%以上,头颈部肿瘤的1%左右[1]。大多数肿瘤发生于颌骨内且多发生于下颌磨牙区,常导致颌骨膨大和面部变形[2]。虽属良性肿瘤但是其局部侵袭性和复发率较高。开窗减压术是一种保守的治疗方法,它可以减少囊腔内的压力,促进骨骼形成,迅速消除颌面畸形,有利于保存邻近结构

Objective To investigate the expression and significance of CNN1 in colorectal cancer and adjacent tis-sues.Methods Two-dimensional chromatography and mass spectrometry were used to detect the different proteins of colorectal cancer,in addition,the expression of diferential proteins were verified by Western blot.Results Forty-four differentially expressed proteins were detected in colorectal cancer based on the corresponding non-tumor normal tis-sues,and 23 of them were down-regulated,in which,CNN1 was one of the down regulated proteins.Conclusion The low expression of CNN1 has a relationship with a varity of cancers,including colorectal cancer,so CNN1 may play a role as a cancer suppressor.

BACKGROUND:The discovery of novel anticancer drugs is critical for the pharmaceutical research and development, and patient treatment. Repurposing existing drugs that may have unanticipated effects as potential candidates is one way to meet this important goal. Systematic investigation of efficient anticancer drugs could provide valuable insights into trends in the discovery of anticancer drugs, which may contribute to the systematic discovery of new anticancer drugs.RESULTS:In this study, we collected and analyzed 150 anticancer drugs approved by the US Food and Drug Administration (FDA). Based on drug mechanism of action, these agents are divided into two groups: 61 cytotoxic-based drugs and 89 target-based drugs. We found that in the recent years, the proportion of targeted agents tended to be increasing, and the targeted drugs tended to be delivered as signal drugs. For 89 target-based drugs, we collected 102 effect-mediating drug targets in the human genome and found that most targets located on the plasma membrane and most of them belonged to the enzyme, especially tyrosine kinase. From above 150 drugs, we built a drug-cancer network, which contained 183 nodes (150 drugs and 33 cancer types) and 248 drug-cancer associations. The network indicated that the cytotoxic drugs tended to be used to treat more cancer types than targeted drugs. From 89 targeted drugs, we built a cancer-drug-target network, which contained 214 nodes (23 cancer types, 89 drugs, and 102 targets) and 313 edges (118 drug-cancer associations and 195 drug-target associations). Starting from the network, we discovered 133 novel drug-cancer associations among 52 drugs and 16 cancer types by applying the common target-based approach. Most novel drug-cancer associations (116, 87%) are supported by at least one clinical trial study.CONCLUSIONS:In this study, we provided a comprehensive data source, including anticancer drugs and their targets and performed a detailed analysis in term of historical tendency and networks. Its application to identify novel drug-cancer associations demonstrated that the data collected in this study is promising to serve as a fundamental for anticancer drug repurposing and development.

BACKGROUND:Colorectal cancer (CRC) is one of the most common malignancies worldwide with poor prognosis. Studies have showed that abnormal microRNA (miRNA) expression can affect CRC pathogenesis and development through targeting critical genes in cellular system. However, it is unclear about which miRNAs play central roles in CRC's pathogenesis and how they interact with transcription factors (TFs) to regulate the cancer-related genes.RESULTS:To address this issue, we systematically explored the major regulation motifs, namely feed-forward loops (FFLs), that consist of miRNAs, TFs and CRC-related genes through the construction of a miRNA-TF regulatory network in CRC. First, we compiled CRC-related miRNAs, CRC-related genes, and human TFs from multiple data sources. Second, we identified 13,123 3-node FFLs including 25 miRNA-FFLs, 13,005 TF-FFLs and 93 composite-FFLs, and merged the 3-node FFLs to construct a CRC-related regulatory network. The network consists of three types of regulatory subnetworks (SNWs): miRNA-SNW, TF-SNW, and composite-SNW. To enhance the accuracy of the network, the results were filtered by using The Cancer Genome Atlas (TCGA) expression data in CRC, whereby we generated a core regulatory network consisting of 58 significant FFLs. We then applied a hub identification strategy to the significant FFLs and found 5 significant components, including two miRNAs (hsa-miR-25 and hsa-miR-31), two genes (ADAMTSL3 and AXIN1) and one TF (BRCA1). The follow up prognosis analysis indicated all of the 5 significant components having good prediction of overall survival of CRC patients.CONCLUSIONS:In summary, we generated a CRC-specific miRNA-TF regulatory network, which is helpful to understand the complex CRC regulatory mechanisms and guide clinical treatment. The discovered 5 regulators might have critical roles in CRC pathogenesis and warrant future investigation.

Objective To investigate the expression and significance of HSPD1 in renal cell carcinoma and adjacent normal tissues.Methods Two-dimensional chromatography and mass spectrometry method were applied to identifying the difference of HSPD1 expressed in renal cell carcinoma and adjacent normal tissues of 10 patients with renal cell car-cinoma.Results Identifications by mass spectrometer showed that HSPD1 expressed significantly lower in renal cell carcinoma than that in the tissue adjacent to carcinoma,and then confirmed the accuracy by western blot.Conclusion the decrease of HSPD1 expression may have a closely relationship with renal cell carcinoma.

目的探讨非肌肉肌球蛋白ⅡA在大肠癌癌组织中的表达及临床意义。方法采用免疫组织化学方法检测MYH9蛋白在90例大肠癌及相应癌旁组织中的表达,探讨MYH9在不同阶段大肠癌中表达及其与临床病理特征的相关性。结果 MYH9蛋白在大肠癌组织中阳性表达强度明显高于癌旁组织（P<0.05）。并且其表达水平与TNM分期、有无淋巴结转移及细胞分化程度显著相关（P<0.05）,而与患者的年龄、性别、肿瘤类别无关（P>0.05）。结论 MYH9在大肠癌中表达上调,并且与肿瘤恶性临床病理特征有关。

贫血是由多种原因引起外周血单位容积内血红蛋白浓度、红细胞计数及血细胞比容低于本地区、相同年龄和性别人群的参考值下限的一种症状[1],可以是原发于造血器官的疾病,也可能是某些系统疾病的表现。只有及时准确地找出贫血的病因,才能对症治疗。对贫血患者进行骨髓细胞学检查和铁染色是直接有效的诊断或鉴别诊断方法。现将本院1085例贫血待查患者的骨髓细胞学检查结果进行

Background Transcription Factors (TFs), essential for many cellular processes, generally work coordinately to induce transcriptional change in response to internal and external signals. Disrupted cooperation between TFs, leading to dysregulation of target genes, contributes to the pathogenesis of many diseases, including cancer. Although the aberrant activation of individual TFs and the functional effects have been widely studied, the perturbation of TF cooperativity in cancer has rarely been explored. Results We used TF co-expression as proxy as cooperativity and performed a large-scale study on disrupted TF cooperation across seven cancer types. While the connectivity of downstream effectors, like metabolic genes and TF targets, were more or similarly disrupted than/with non-TFs, the cooperativity of TFs (upstream regulators) were consistently less disturbed in all studied cancer types. Highly coordinated TFs in normal, however, generally lost that cooperation in cancer. Although different types of cancer shared very few TF pairs with highly disrupted cooperation, the cooperativity of interferon regulatory factors (IRF) was highly disrupted in six cancer types. Specifically, the cooperativity of IRF8 was highly perturbed in lung cancer, which was further validated by two independent lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) datasets. More interestingly, the cooperativity of IRF8 was markedly associated with tumor progression and even contributed to the patient survival independent of tumor stage. Conclusions Our findings underscore the far more important role of TF cooperativity in tumorigenesis than previously appreciated. Disrupted cooperation of TFs provides potential clinical utility as prognostic markers for predicting the patient survival.

Pancreatic cancer（PC）occurs when malignant cells develop in the part of the pancreas,a glandular organ behind the stomach.For 2015,there are about 40,560 people dead of pancreatic cancer（20,710 men and 19,850 women）in the US（Siegel et al.,2015）.Though PC accounts for about 3%of all cancers in the US,it can cause about 7%of cancer deaths.This is mainly because that the

Despite ongoing progress towards treating mental illness, there remain significant difficulties in selecting probable candidate drugs from the existing database. We describe an ontology — oriented approach aims to represent the nexus between genes, drugs, phenotypes, symptoms, and diseases from multiple information sources. Along with this approach, we report a case study in which we attempted to explore the candidate drugs that effective for both bipolar disorder and epilepsy. We constructed an ontology that incorporates the knowledge between the two diseases and performed semantic reasoning task on the ontology. The reasoning results suggested 48 candidate drugs that hold promise for a further breakthrough. The evaluation was performed and demonstrated the validity of the proposed ontology. The overarching goal of this research is to build a framework of ontology — based data integration underpinning psychiatric drug repurposing. This approach prioritizes the candidate drugs that have potential associations among genes, phenotypes and symptoms, and thus facilitates the data integration and drug repurposing in psychiatric disorders.