导水叶上浮无法下落的缺陷分析及处理

水轮发电机组活动导水叶上浮严重,不进行处理将直接威胁到顶盖抗磨环的寿命,直接关系着活动导水叶的操作灵活性,直接影响到端面密封的效果,甚至导致活动导水叶漏水量过大无法正常停机。本文从导水叶上浮产生的原因为切入点,分析各部可能产生的问题为导向,通过一步一步核实,根据分解过程一步一步处理,对活动导水叶上浮无法下落的问题及产生的后果进行分析及处理,最终查出根源并彻底处理,保证了机组安全平稳运行。此次问题的圆满解决,给国内外同类电厂提供了良好的改造依据和参考示例。

HPLC-ELSD国产流动相试剂的降噪音方法

目的:建立一种降低HPLC-ELSD国产流动相试剂(甲醇、乙腈、二氯甲烷等)噪音的方法。方法:将流动相试剂置蒸馏装置中进行常压蒸馏、水浴加热,水温控制在高出被蒸馏试剂沸点5-20℃,再将馏出液经有机滤膜过滤、超声波脱气。结果:经本法处理后的国产流动相试剂ELSD噪音得到明显降低,达到正常检测的要求。结论:该方法简单、有效、可明显降低HPLC-ELSD国产流动相试剂的噪音。

168例结直肠腺瘤性息肉内镜治疗后并发症及病理分析

目的评估并了解内镜下摘除结直肠腺瘤性息肉(colorectal adenomatous polyps,CAP)的安全性及术后病理情况。方法收集2017年3月至2019年3月收治的168例CAP住院患者的临床资料。按年龄段将其分为3组:青年组(≤34岁,n=26)、中年组(35~59岁,n=101)及老年组(≥60岁,n=41),分析3组的术后并发症、息肉部位及病理类型。结果168例患者均在内镜下成功摘除息肉。17例出现出血(术中出血14例,术后迟发性出血3例)、占10.1%(17/168),均在内镜下钛夹或电凝止血成功;穿孔2例、占1.2%(2/168),原因主要是因息肉过大及切除过深;其他2组未见出血、穿孔发生,3组均未发生感染;3组并发症比较差异无统计学意义(P>0.05)。息肉发生部位:左半结肠明显多于右半结肠,位于直肠61例(36.3%,61/168)的发生率高于其他部位(P<0.05)。病理分型:青年组均为管状腺瘤;中年组管状腺瘤84例,占83.2%(84/168);老年组绒毛状腺瘤11例、占26.8%(11/168),腺瘤出现局部癌变2例、占4.9%(2/168)。老年组混合性腺瘤、绒毛状腺瘤、高级别瘤变及局部癌变比例高于其他2组(P<0.05)。结论内镜下切除CAP效果确切,术后并发症较低,病理以管状腺瘤为主,随着年龄的增长,混合性腺瘤及绒毛状腺瘤的发生比例逐渐增高。

事务块认证机制与并行存储结构

采用有向无环图结构的区块链共识机制能并行执行交易,但效率与稳定性较差。因此一些共识机制采用联盟链的方式处理交易。本文设计并提出基于有向无环图的并行存储结构,通过并行存储结构实现事务块认证机制(TBCM)的共识机制,由此TBCM共识机制能有效提升联盟链整体对大量交易的并行处理能力。TBCM中采用联盟链的方式组织节点,验证节点组验证网络中生成的交易块,采用并行存储结构的网络中的同步用户不必处理整个网络的交易负载,由验证节点组并行处理网络中的区块。由此结构设计的共识机制使联盟链系统具备并行处理事务的能力,以此提高交易的实时性。TBCM拥有并行性实时交易的优势,能实现更高的稳定性和交易确认效率。

片仔癀胶囊治疗转移性结肠癌随机双盲对照试验研究

目的评价片仔癀胶囊对转移性结肠癌患者的临床疗效与安全性。方法采用随机双盲安慰剂对照研究方法,将患者按2:1的比例分配至试验组(79例)和对照组(38例),分别给予片仔癀胶囊和安慰剂,每次2粒,每日3次,连续治疗28天为1个疗程,以疾病出现进展为干预终点。检测患者肿瘤标志物(CEA、CA199)、血常规(RBC、WBC、NEU、PLT)及肝肾功能(ALT、AST、γ-GGT、TBIL、BUN、SCr),计算两组无进展生存期(PFS),观察两组患者不良事件(AE)。结果与本组治疗前比较,对照组治疗2个疗程后CA199降低(P<0.01),试验组治疗2个疗程后CEA和CA199降低(P<0.01)。与对照组同期比较,试验组治疗2个疗程后CA199升高(P<0.05)。使用片仔癀胶囊和用药周期≥3个疗程为保护因素(P<0.01,P<0.05)。片仔癀胶囊可提高患者1年无进展生存率(P=0.011)。结论服用片仔癀胶囊3个疗程以上,可降低患者肿瘤标志物CA199,提高PFS,且不增加AE。

Box-Behnken响应面法优选牛至中百里香酚与香芹酚的提取工艺

目的采用Box-Behnken响应面法优选牛至中百里香酚与香芹酚的提取工艺。方法在单因素实验的基础上,以百里香酚与香芹酚提取率之和为评价指标,采用Box-Behnken设计法考察乙醇浓度、液固比和药材粒度对提取率的影响。结果最佳的提取工艺参数为:乙醇浓度体积分数80%,液固比13∶1(mL/g),药材粒度为过40目筛,最高提取率为694.80μg·g-1,与预测值的偏差较小。结论所优选的提取方法操作简便、成本低、预测性良好,可为牛至中百里香酚与香芹酚的规模化大生产提供参考。

基于网络药理学探讨精制保和颗粒抑制大肠癌生长的作用机制

目的:探讨精制保和颗粒(RBG)对大肠癌作用的分子机制。方法:采用网络药理学技术分析RBG治疗大肠癌关键成分及靶标,并通过体外实验进一步研究RBG对大肠癌细胞HCT-116和HCT-8生长抑制的作用机制。结果:利用相关数据库及拓扑分析共筛选出22个潜在活性成分和217个潜在靶点,靶点富集分析发现与大肠癌等多种肿瘤和多条肿瘤相关通路有关。体外研究发现,RBG能明显抑制HCT-116和HCT-8细胞活力、集落形成数量和诱导细胞凋亡,并能显著下调Bcl-2和上调Bax蛋白表达,促进Caspase-3和Caspase-9活化,同时显著抑制AKT信号通路的活化。结论:RBG具有多成分、多靶点和多途径的作用特点,可通过诱导细胞凋亡抑制大肠癌细胞的生长,且抑制AKT信号通路的活化可能是其重要的作用机制。

Huoxin Pill(活心丸)Attenuates Cardiac Fibrosis by Suppressing TGF-β1/Smad2/3 Pathway in Isoproterenol-Induced Heart Failure Rats

Objective:To evaluate the effects of Huoxin Pill(活心丸,HXP)on cardiac fibrosis and heart failure(HF)in isoproterenol(ISO)-induced HF rats.Methods:Thirty Wistar rats were randomly divided into 5 groups including control,HF,isosorbide mononitrate(ISMN),HXP low(HXP-L),and HXP high(HXP-H)groups(n=6 for each group)according to the complete randomization method.Rats were pretreated with ISMN(5 mg/kg daily),low concentration of HXP(10 mg/kg daily)or high concentration of HXP(30 mg/kg daily)or equal volume of saline by intragastric administration for 1 week,followed by intraperitoneal injection of ISO(10 mg/kg,14 days),and continually intragastric administrated with above medicines or saline for additional 6 weeks.The effects of HXP treatment on the cardiac function,heart weight index(HWI),pathological changes,and collagen content were further assessed.Moreover,the role of HXP on activation of transforming growth factor-β1(TGF-β1)/Smads pathway was further explored using immunohistochemistry(IHC)and Westernblot assay.Results:HXP treatment significantly alleviated the decrease of ejection fraction(EF)and fractional shortening(FS),while decreased the elevation of left ventricular end-systolic volume(LVESV)in ISO-induced HF rats(P<0.05).Moreover,HXP treatment obviously attenuated the increase of HWI and serum level of creatine kinase MB(CK-MB,P<0.05),as well as pathological changes in ISO-induced HF rats.Further determination indicated that HXP treatment alleviated the elevation of collagenⅠand collagenⅢprotein expression in cardiac tissues of ISO-induced HF rats.Furthermore,HXP treatment significantly down-regulated the increase of TGF-β1 and p-Smad2/3 protein expression in cardiac tissues of HF rats(P<0.05),while did not affect the expression of total Smad2/3.Conclusions:HXP attenuated heart failure and cardiac fibrosis in ISO-induced HF rats by suppression of TGF-β1/Smad2/3 pathway.

Bear Bile Powder Inhibits Growth of Hepatocellular Carcinoma via Suppressing STAT3 Signaling Pathway in Mice

Objective: To evaluate the inhibitory effect of bear bile powder(BBP) on hepatocellular carcinoma(HCC) growth in vivo and investigate the underlying mechanisms. Methods: A HCC xenograft mouse model was developed by producing with huh7 cells. After 5 days following xenograft implantation, ten HCC xenograft mice were given intra-gastric administration with 10 mg/(kg·d) dose of BBP or saline for 3 weeks. Tumor growth in HCC xenograft mice was evaluated by measuring the tumor weight and volume. Cell apoptosis, proliferation or tumor angiogenesis were examined via immunohistochemical(IHC) staining for transferase-mediated deoxyuridine triphosphate-biotin nick end labeling(TUNEL), proliferating cell nuclear antigen(PCNA) or cluster of differentiation 31(CD31), respectively. Phosphorylation of signal transducer and activator of transcription 3(STAT3) were determined by Western blot. The m RNA and protein expressions of Bcl-2, Bax, Cyclin D1 and Cyclin-dependent kinase 4(CDK4) in HCC tumor tissues were respectively determined by reverse transcription polymerase chain reaction(RT-PCR) and Western blot. The protein expression of vascular endothelial growth factor A(VEGF-A) in tumor tissues was examined by IHC staining. Results: BBP treatment led to a significant decrease on tumor volume and tumor weight in HCC mice(P<0.05) and had no effect on the change of body weight. In addition, BBP profoundly promoted cell apoptosis, inhibited cell proliferation and intratumoral microvessel density in HCC tumor tissues(P<0.05). Moreover, BBP treatment remarkably suppressed the STAT3 phosphorylation and modulated the expression of critical target genes including Bcl-2, Bax, Cyclin D1, CDK4 and VEGF-A in HCC mice. Conclusion: BBP exerts its anti-cancer activities via suppressing STAT3 signaling pathway and affecting multiple intracellular targets.

Qingxuan Jiangya Decoction(清眩降压汤) Prevents Blood Pressure Elevation and Ameliorates Vascular Structural Remodeling via Modulating TGF-β 1/Smad Pathway in Spontaneously Hypertensive Rats

Objective:To elevate the effects of Qingxuan Jiangya Decoction(清眩降压汤,QXJYD)on hypertension and vascular structural remodeling(VSR)in spontaneously hypertensive rats(SHRs),and investigate the underlying mechanisms.Methods:SHRs(n=8)were given intra-gastric administration with 60 mg/kg of QXJYD or saline,daily for 8 weeks,while rats in SHR-control(n=8)and WKY(n=8)groups were received equal volumes of saline solution.Systolic blood pressures(SBP),diastolic blood pressures(DBP)and mean blood pressures(MBP)were measured once a week.The levels of angiotensinⅡ(AngⅡ),endothelin 1(ET-1)and plasma renin activity(PRA)were tested by enzyme-linked immunosorbent assay(ELISA)and radioimmunoassay,respectively.The effect of QXJYD on VSR was determined by examining the media thickness and the ex vivo contractility of thoracic aortic.The proliferation and fibrosis of vascular smooth muscle cells(VSMCs)were examined via immunohistochemical(IHC)staining for proliferating cell nuclear antigen(PCNA),collagen Ⅰ and collagen Ⅲ,respectively.The mRNA and protein expressions of transforming growth factor β1(TGF-β1),Smad3 and phosphorylation of Smad3 in thoracic aorta tissues were determined by real-time polymerase chain reaction(PCR)and Western blot assay,respectively.Results:QXJYD treatment led to a significant decrease of the elevation of blood pressure in SHRs and reduced the levels of AngⅡ,ET-1 and PRA in the serum(P<0.05).In addition,QXJYD treatment remarkably ameliorated VSR and vascular function in SHRs.Moreover,QXJYD inhibited VSMC proliferation and fibrosis by suppressing the expression of PCNA,collagen Ⅰ and collagen Ⅲ in thoracic aortic.Furthermore,QXJYD inhibited the expression of TGF-β1,Smad3 and the phosphorylation of Smad3,respectively(P<0.05).Conclusion:QXJYD reversed VSR by inhibiting VSMC proliferation and collagen deposition via regulation of TGF-β1/Smad signaling pathway,which may,in part,illuminate its anti-hypertensive activities.

寒凝血瘀成因及病理

寒邪属于六淫之一,具有凝滞、收引的特性,若寒邪侵袭血脉,或损伤阳气或阳虚寒自内生,易导致血脉挛缩,气血运行不畅,则凝聚成瘀。与其他类型的血瘀不同,因寒致瘀、寒凝血瘀,与季节或天气剧变关系密切,多具有慢性和反复发作的特征。寒凝血瘀在疾病论治中,从古至今备受重视。

Shexiang Tongxin Dropping Pill（麝香通心滴丸）Protects against Na2S2O4-Induced Hypoxia-Reoxygenation Injury in H9c2 Cells

Objectives: To investigate the protective effects of Shexiang Tongxin Dropping Pill(麝香通心滴丸,STP) on Na2S2O4-induced hypoxia-reoxygenation injury in cardiomyoblast H9c2 cells. Methods: The cell viability and levels of mRNA and protein expression in H9c2 cells were determined following Na2S2O4-induced hypoxia using Hoechst staining, annexin V/propidium iodide(PI) flow cytometry, real-time polymerase chain reaction and Western blot analysis. Results: STP pretreatment signi?cantly increased the viability and inhibited aberrant morphological changes in H9c2 cardiomyoblast cells induced by Na2S2O4 treatment(P<0.05). In addition, STP pretreatment attenuated Na2S2O4-induced hypoxic damage, down-regulated the expression of pro-apoptotic Bax,and up-regulated the expression of anti-apoptotic Bcl-2 in H9c2 cells(P<0.05). Conclusions: STP was strongly cardioprotective in hypoxia-reoxygenation injury by preventing hypoxic damage and inhibiting cellular apoptosis.These results further support the use of STP as an effective drug for the treatment of ischemic heart disease.

维持性血液透析患者透析中低血压的影响因素及证候特征

目的探讨维持性血液透析患者透析过程中发生低血压的影响因素及证候特征。方法选取2021年4月-2021年6月于费森尤斯连锁透析中心行维持性血液透析的患者210例,根据透析期间是否发生低血压分为观察组(有低血压者42例)和对照组(无低血压者168例)进行横断面研究。分析2组患者性别、年龄、BMI、是否合并糖尿病或冠心病、血流量、平均透析间期体重增长率、超滤率、透析前血红蛋白、血清白蛋白水平、血尿素、PTH、肾素的差异性。并采用多因素Logistic回归分析透析中低血压的独立影响因素。同时进行四诊合参,采用中医证候调查表,对观察组患者的中医证候特征进行总结分析。结果维持性血液透析患者透析过程中发生低血压的独立危险因素为年龄、冠心病、贫血。血液透析低血压患者在中医证型分布上以脾肾阳虚,脾肾气虚、湿热证、血瘀证为主。结论维持性血液透析过程中应对高龄、合并糖尿病冠心病、贫血以及中医证型为脾肾阳虚,脾肾气虚、湿热证、血瘀证的患者加强监测,采用相关预防措施,降低低血压发生率。

Pharmacodynamic Mechanism of Kuanxiong Aerosol for Vasodilation and Improvement of Myocardial Ischemia

Objective: To explore the effect of Kuanxiong Aerosol(KXA)on isoproterenol(ISO)-induced myocardial injury in rat models.Methods: Totally 24 rats were radomly divided into control,ISO,KXA low-dose and high-dose groups according to the randomized block design method,and were administered by intragastric administration for 10 consecutive days,and on the 9th and 10th days,rats were injected with ISO for 2 consecutive days to construct an acute myocardial ischemia model to evaluate the improvement of myocardial ischemia by KXA.In addition,the diastolic effect of KXA on rat thoracic aorta and its regulation of ion channels were tested by in vitro vascular tension test.The influence of KXA on the expression of calcium-CaM-dependent protein kinase Ⅱ(CaMK Ⅱ)/extracellular regulated protein kinases(ERK)signaling pathway has also been tested.Results: KXA significantly reduced the ISO-induced increase in ST-segment,interventricular septal thickness,cardiac mass index and cardiac tissue pathological changes in rats.Moreover,the relaxation of isolated thoracic arterial rings that had been precontracted using norepinephrine(NE)or potassium chloride(KCl)was increased after KXA treatment in an endothelium-independent manner,and was attenuated by preincubation with verapamil,but not with tetraethylammonium chloride,4-aminopyridine,glibenclamide,or barium chloride.KXA pretreatment attenuated vasoconstriction induced by CaCl_(2)in Ca^(2+)-free solutions containing K^(+) or NE.In addition,KXA pretreatment inhibited accumulation of Ca^(2+)in A7r5 cells mediated by KCl and NE and significantly decreased p-CaMK Ⅱ and p-ERK levels.Conclusion: KXA may inhibit influx and release of calcium and activate the CaMK Ⅱ/ERK signaling pathway to produce vasodilatory effects,thereby improving myocardial injury.

Scutellaria barbata D.Don Inhibits Colorectal Cancer Growth via Suppression of Wnt/β-Catenin Signaling Pathway

Objective： To investigate the effect of the ethanol extract of Scutellaria barbata D. Don（EESB） on colorectal cancer（CRC） growth and Wnt/β-catenin signaling pathway in vivo and in vitro. Methods： In vivoexperiment, CRC xenograft mouse model was constructed with injection of HT-29 cells. Following xenograft implantation, twenty mice were randomly divided into EESB-treated group（n=10） and control group（n=10） by a random number table, and were given with intra-gastric administration of 2 g/kg EESB or saline, 5 days a week for 16 days, respectively. At the end of experiment, tumors were removed and weighed by electronic scales. The proliferation biomarker Ki-67 of tumor was evaluated by immunohistochemistry（IHC） assay. In vitro study, HT-29 cells were treated with 0, 0.5, 1.5, 2.5 mg/m L EESB for 24 h. At the end of the treatment, the viability and survival of HT-29 cells were determined by methylthiazolyldiphenyl-tetrazolium bromide（MTT） assay and colony formation assay, respectively. The m RNA expression of c-Myc, Survivin and adenomatous polyposis coli（APC） was examined by reverse transcription-polymerase chain reaction（RT-PCR） both in tumor tissues of CRC xenograft mice and HT-29 cells. Protein expression of c-Myc, Survivin, APC, and β-catenin as well as β-catenin phosphorylation level were evaluated by IHC assay or Western blotting. Results： EESB significantly reduced tumor weight in CRC xenografts mice, compared with the control group（P〈0.05）. IHC assay showed that EESB significantly inhibited protein expression of Ki-67 in tumor tissues（P〈0.05）. MTT assay showed that EESB significantly reduced HT-29 cell viability in a dose-dependent manner（P〈0.05）. Colony formation assay showed that EESB dose-dependently decreased the survival of HT-29 cells（P〈0.05）. In addition, RT-PCR assay showed that EESB decreased the m RNA expression of c-Myc and Survivin and increased APC expression, both in tumor tissues of CRC xenograft mice and HT-29 cells（P〈0.05）. IHC assay or Western blotting showed that EESB decreased protein expression of β-catenin, c-Myc and Survivin, as well as increased APC expression and β-catenin phosphorylation in tumor tissues or HT-29 cells（P〈0.05）. Conclusions： EESB significantly reduced tumor growth in CRC xenografts mice, and inhibited the viability and survival of HT-29 cells. EESB could suppress the activation of the Wnt/β-catenin pathway, which might be one of the mechanisms whereby Scutellaria barbata D. Don exerts its anticancer activity.

Therapeutic Effects of Different Animal Bile Powders on Lipid Metabolism Disorders and Their Composition Analysis

Objective: To compare the therapeutic effect of different animal bile powders on lipid metabolism disorders induced by high-fat diet in rats, and analyze the bioactive components of each animal bile powder. Methods: Sixty Sprague-Dawley rats were randomly divided into 6 groups(n=10): normal diet control group, high-fat diet model group, high-fat diet groups orally treated with bear, pig, cow and chicken bile powders, respectively. Serum biochemical markers from the abdominal aorta in each group were analyzed. Changes in the body weight and liver weight were recorded. Pathohistological changes in the livers were examined. High performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry was used to determine the composition of bioactive components in each animal bile powder. Results: Treatment with different types of animal bile powders had different inhibitory effects on high-fat diet-induced increase of body weight and/or liver weight in rats, most notably in bear and pig bile powders(P<0.05). High-fat diet induced lipid metabolism disorder in rats, which could be reversed by treatment with all kinds of bile powders. Bear bile and chicken bile showed the most potent therapeutic effect against lipid metabolism disorder. Cow and bear bile effectively alleviated high-fat diet induced liver enlargement and discoloration, hepatocyte swelling, infiltration of inflammatory cells and formation of lipid vacuoles. Bioactive component analysis revealed that there were significant differences in the relative content of taurocholic acid, taurodeoxycholic acid and ursodeoxycholic acid among different types of animal bile. Interestingly, a unique component with molecular weight of 496.2738 Da, whose function has not yet been reported, was identified only in bear bile powder. Conclusions: Different animal bile powders had varying therapeutic effect against lipid metabolism disorders induced by high-fat diet, and bear bile powder demonstrated the most effective benefits. Bioactive compositions were different in different types of animal bile with a novel compound identified only in bear bile powder.

Pien Tze Huang(片仔癀) Overcomes Doxorubicin Resistance and Inhibits Epithelial-Mesenchymal Transition in MCF-7/ADR Cells

Objective: To evaluate the effect of Pien Tze Huang (片仔癀, PZH) on breast cancer chemo resistance and related epithelial-mesenchymal transition (EMT) and investigate the underlying mechanisms. Methods: 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was used to determine the cell viability. Adriamycin (ADR) staining observed by fluorescence microscope was performed to detect the accumulation of ADR. Transwell assay was used to analyze the cell migration and invasion. Western-blot was performed to detect the protein expression of related genes. Results: MCF-7/ADR cells were resistant to ADR treatment, and PZH treatment inhibited the viability of MCF-7/ADR cells in a dose-dependent manner. PZH treatment also increased the intercellular accumulation of ADR and down-regulated the expression of ABCG2 and ABCB1 in MCF-7/ADR cells (P<0.05). In addition, PZH treatment inhibited EMT, migration and invasion of MCF-7/ADR cells (P<0.05). Moreover, PZH suppressed activation of transforming growth factor β 1 (TGF-β) signaling in MCF-7/ADR cells (P<0.05). Conclusion: PZH treatment can effectively overcome chemoresistance via down-regulating ABCG2, ABCB1 and inhibit EMT in ADR resistant human breast cancer cells via suppression of the TGF-β 1 pathway.