上调FBP1表达对胃癌细胞生长的抑制作用

目的探讨上调果糖-1,6-二磷酸酶1(fructose-1,6-bisphosphatase 1,FBP1)表达对胃癌细胞增殖、凋亡的影响及其机制。方法以实时定量PCR和Western blotting检测胃癌BGC-823、SGC-7901细胞中FBP1 mRNA和蛋白的表达;将培养的BGC-823细胞随机分为对照组(未转染)、阴性组(转染pc DNA3.1质粒)和实验组(转染pc DNA3.1-Flag-FBP1质粒),以实时定量PCR检测FBP1 mRNA表达,MTT法检测细胞增殖,流式细胞仪检测细胞凋亡,Western blotting检测FBP1、Cyclin D1、c-Myc和Cleaved caspase-3蛋白表达。结果与正常胃黏膜上皮GES-1细胞相比,胃癌BGC-823、SGC-7901细胞中FBP1蛋白及mRNA的相对表达水平均显著降低,且BGC-823细胞较SGC-7901细胞下降更为明显;转染后,与对照组相比,实验组细胞中FBP1蛋白及mRNA、细胞的增殖能力和Cyclin D1、c-Myc蛋白表达水平均显著降低,细胞凋亡能力和Cleaved caspase-3蛋白表达水平均显著升高,差异有统计学意义(P0.05);阴性组与对照组比较,差异无统计学意义(P0.05)。结论 FBP1在胃癌细胞中低表达,上调其表达能够抑制细胞增殖并诱导细胞凋亡,其作用机制可能与上调Cleaved caspase-3蛋白和下调Cyclin D1、c-Myc蛋白表达有关。     

重组质粒pcDNA3.1/SurP/Trail联合吉西他滨诱导胰腺癌细胞凋亡的实验研究

目的研究重组质粒pc DNA3.1/Sur P/Trail联合吉西他滨诱导胰腺癌细胞凋亡的能力。方法将人胰腺癌细胞株SW1990分为4组,第1组转染重组质粒联合吉西他滨(联合组),第2组单纯转染重组质粒(重组质粒组),第3组单纯加入吉西他滨(吉西他滨组),第4组未加任何处理(空白对照组)。通过Western blotting检测各组细胞中Trail蛋白表达的情况,并用流式细胞仪检测SW1990胰腺癌细胞凋亡率。结果 (1)重组质粒组、联合组均有Trail蛋白表达,吉西他滨组、空白对照组则无Trail蛋白表达;(2)联合组SW1990细胞凋亡率显著高于其他各组(P0.05);重组质粒组和吉西他滨组SW1990细胞凋亡率显著高于空白对照组(P0.05);重组质粒组与吉西他滨组比较,差异无统计学意义(P0.05)。结论重组质粒pc DNA3.1/Sur P/Trail与吉西他滨联可显著提高SW1990胰腺癌细胞的凋亡率。     

WWOX基因过表达对人胃癌细胞增殖、凋亡能力的影响及机制研究

目的探究含有WW结构域的氧化还原酶基因(WWOX)mRNA在胃癌中的表达量及过表达WWOX对人胃癌SGC7901细胞增殖、凋亡能力的影响及作用机制。方法使用实时荧光定量PCR(qRT-PCR)检测WWOX mRNA在胃癌组织和癌旁组织中的表达量;利用脂质体LipofectamineTM2000将重组质粒pc DNA3.0-WWOX、空载体pc DNA3.0-NC转入人胃癌SGC7901细胞中,未转染细胞为空白组,蛋白质印迹法(Western blotting)检测WWOX蛋白表达量;绘制转染后人胃癌SGC7901细胞增殖状况;流式细胞术检测SGC7901细胞凋亡率;Western blotting检测转染后细胞周期蛋白D1(Cyclin D1)和生存素(Survivn)蛋白的表达量。结果 WWOX mRNA在胃癌组织中的表达量显著低于癌旁组织(P0.05);pc DNA3.0-WWOX组WWOX蛋白的表达量显著高于pc DNA3.0-NC组和空白组(P0.05);绘制细胞生长曲线发现,WWOX基因能抑制胃癌SGC7901细胞的增殖;流式细胞术检测结果显示,pc DNA3.0-WWOX组细胞的凋亡率显著高于pc DNA3.0-NC组和空白组(P0.05);pc DNA3.0-WWOX组细胞Cyclin D1蛋白的表达显著低于pc DNA3.0-NC组和空白组(P0.05),而Survivn蛋白显著高于pc DNA3.0-NC组和空白组(P0.05)。结论 WWOX mRNA在胃癌中的表达量低于癌旁组织;过表达WWOX可通过降低Cyclin D1蛋白、增加Survivn蛋白抑制胃癌SGC7901细胞的增殖,并促进其凋亡。     

PUMA基因转染对胰腺癌细胞生长的影响

目的 探讨PUMA基因转染抑制胰腺肿瘤生长的体内外效果.方法 利用脂质体转染法将表达PUMA的质粒转染导入胰腺癌细胞株PC-3中,G418筛选出阳性克隆,Western和RT-PCR法检测PUMA转染后PC-3 PUMA的表达,流式细胞仪检测转染后细胞凋亡率;分别将转染PUMA的PC-3细胞(实验组)和未转染的PC-3细胞移植到裸鼠体内,比较裸鼠移植肿瘤的大小和重量以及PUMA表达.结果 PUMA表达质粒转染的PC-3细胞(PC-3/PUMA)稳定表达PUMA,其细胞凋亡率为(5.50 ± 0.90)%,明显高于未转染组的(1.073 ± 0.248)%和空载体转染组的(1.08 ± 0.35)%(P ＜0.05);裸鼠接种4周后PC-3/PUMA细胞成瘤率为70%,PC-3细胞和空载体PC-3细胞成瘤率为100%(P ＞ 0.05),PC-3/PUMA细胞形成的肿瘤体积比PC-3细胞和空载体PC-3细胞明显减小(P ＜0.05),并且形成的肿瘤组织中PUMA高表达.结论 胰腺癌细胞中缺失PUMA基因表达,PUMA转染胰腺癌细胞后表达PUMA,并能促进细胞凋亡.     

p15~(INK4B)基因对人胰腺癌细胞系BxPC3增殖的影响

目的 探讨p15~(INK4B)(p15)基因转染对人胰腺癌细胞系BxPC3细胞增殖的影响.方法 采用脂质体将pCDNA3.1(+)-p15质粒及阴性对照pCDNA3.1(+)-neo质粒转染BxPC3细胞,以亲本细胞作为对照组.应用RT-PCR检测细胞p15 mRNA表达;Western blotting检测细胞p15蛋白表达;MTT法检测细胞增殖;透射电镜观察细胞超微结构变化;流式细胞仪检测细胞周期和凋亡率.结果 p15转染组细胞恢复p15 mRNA和蛋白表达.培养第2天生长被抑制,至第7天,生长抑制率达47.9%.G_0/G_1期细胞占(61.56±3.96)%,显著高于空质粒转染组的(47.44±6.35)%和对照组的(49.22±7.23)%(P<0.05).出现明显的G,凋亡峰,细胞凋亡率为(5.27±1.04)%,显著高于空质粒转染组的(0.11±0.06)%和对照组的(0.09±0.07)%(P<0.05).透射电镜观察到p15转染组发生细胞凋亡.结论 体外p15基因转染可以抑制人胰腺癌细胞系BxPC3细胞增殖,并能诱导其凋亡.     

血管紧张素转换酶2对人胰腺癌细胞BxPC3体外增殖及成瘤性的效应研究

目的探讨血管紧张素转换酶2(ACE2)基因对人胰腺癌细胞BxPC3在体外的增殖及成瘤性的影响及其初步机制。方法通过脂质体转染法建立稳定过表达ACE2基因的胰腺癌BxPC3细胞株。设实验组(转染ACE2质粒组,BxPC3/ACE2)、阴性对照组(转染GFP对照质粒组,BxPC3/GFP)及空白对照组(未转染组,BxPC3),Western blotting法验证转染后各组细胞ACE2蛋白的表达;MTT法检测细胞增殖变化,克隆形成实验检测细胞在体外的成瘤性;流式细胞仪和Caspase-3蛋白检测观察各组细胞凋亡情况。结果 ACE2表达质粒转染胰腺癌细胞BxPC3后,BxPC3中ACE2蛋白表达明显上调。在48 h、72 h时间点,BxPC3/ACE2细胞的增殖能力下降,与阴性对照组及空白对照组相比,差异有统计学意义(P0.05)。克隆形成实验显示,BxPC3/ACE2组的细胞克隆与两对照组相比,不仅数目少(P0.05),且克隆体积也相对较小。流式细胞计数检测,从撤除血清后的24 h开始,实验组细胞凋亡率明显增加,与两对照组相比差异有统计学意义(P0.05);Caspase-3蛋白印迹发现典型凋亡特征片段。结论 ACE2基因可通过促进胰腺癌细胞BxPC3的凋亡,进而抑制其在体外的增殖及成瘤能力。     

PUMA基因转染对胰腺癌细胞生长的影响

目的探讨PUMA基因转染抑制胰腺肿瘤生长的体内外效果。方法利用脂质体转染法将表达PUMA的质粒转染导入胰腺癌细胞株PC-3中,G418筛选出阳性克隆,Western和RT-PCR法检测PUMA转染后PC-3PUMA的表达,流式细胞仪检测转染后细胞凋亡率;分别将转染PUMA的PC-3细胞(实验组)和未转染的PC-3细胞移植到裸鼠体内,比较裸鼠移植肿瘤的大小和重量以及PUMA表达。结果PUMA表达质粒转染的PC-3细胞(PC-3/PUMA)稳定表达PUMA,其细胞凋亡率为(5.50±0.90)%,明显高于未转染组的(1.073±0.248)%和空载体转染组的(1.08±0.35)%(P<0.05);裸鼠接种4周后PC-3/PUMA细胞成瘤率为70%,PC-3细胞和空载体PC-3细胞成瘤率为100%(P>0.05),PC-3/PUMA细胞形成的肿瘤体积比PC-3细胞和空载体PC-3细胞明显减小(P<0.05),并且形成的肿瘤组织中PUMA高表达。结论胰腺癌细胞中缺失PUMA基因表达,PUMA转染胰腺癌细胞后表达PUMA,并能促进细胞凋亡。     

血管紧张素转化酶Ⅱ对吉西他滨治疗胰腺癌细胞株敏感性的影响

目的探讨血管紧张素转化酶Ⅱ（ACE2）在胰腺癌细胞化学治疗中的作用。方法构建质粒,通过脂质体转染技术将质粒DNA转入胰腺癌细胞株SW1990并建立稳定高表达ACE2的胰腺癌细胞克隆。设实验组（转染ACE2表达质粒）、阴性对照组（转染GFP对照质粒）及未转染组,Western印迹法检测转染后各组细胞ACE2蛋白的表达。采用化学治疗药物吉西他滨作用不同处理组细胞,应用MTT法检测细胞增殖变化,流式细胞仪和TUNEL法检测细胞的凋亡变化。结果50μmol／L吉西他滨干预细胞24h后,实验组、阴性对照组和未转染组的细胞增殖抑制率分别为（51．2±4．8）％、（24．2±3．3）％和（21．3±2．6）％,3组间差异有统计学意义（P〈0．05）;流式细胞计数检测实验组细胞凋亡较阴性对照组及未转染组明显增加[（31．2±3．8）％、（17．64±2．3）％、（15．9±1．7）％,P〈0．05],TUNEL标记分析发现典型凋亡特征。结论稳定高表达ACE2基因可明显增强SW1990对吉西他滨的治疗敏感性,两者联合应用在胰腺癌治疗中具有潜在的价值。     

14-3-3γ对异丙肾上腺素诱导大鼠心肌损伤的保护作用

目的研究14-3-3γ在异丙肾上腺素(Iso)诱导的大鼠心肌损伤中的保护作用。方法构建pc DNA3.1~(-1)4-3-3γ重组载体,使用pc DNA3.1~(-1)4-3-3γ或pc DNA3.1对体外培养的H9c2(2~(-1))细胞进行转染。实验分为四组:pc DNA3.1~(-1)4-3-3γ+Iso损伤组,pc DNA3.1+Iso损伤组,Iso损伤组及空白对照组(未经任何处理细胞组)。Western印迹检测心肌细胞中14-3-3γ的表达情况;MTT法检测心肌细胞增长率;取培养液检测各组细胞丙二醛(MDA)含量变化和超氧化物歧化酶(SOD)活性变化;流式细胞法检测重组质粒转染对心肌细胞凋亡的影响。结果 Iso损伤使心肌细胞的MDA含量显著增加、SOD活性降低、细胞增长率降低、细胞凋亡增加,转染pc DNA3.1~(-1)4-3-3γ重组质粒后再进行Iso损伤,则MDA含量显著减少、SOD活性增高、细胞增长率增高、细胞凋亡减少(P0.05)。结论 14-3-3γ对Iso诱导的大鼠心肌细胞损伤有明显的对抗和保护作用。     

HOXD10基因转染对人胃癌耐药SGC7901/VCR细胞增殖、凋亡及侵袭能力的影响

目的研究HOXD10基因转染人胃癌耐药细胞系SGC7901/VCR后表达情况及对细胞增殖、凋亡、侵袭能力的影响。方法将HOXD10基因表达质粒(pc DNA3.1-EGFP-HOXD10)转染至SGC7901/VCR中,利用Real-time PCR和Western blotting检测HOXD10基因转染后表达效果;MTT方法、平板单克隆实验、流式细胞术、Transwell方法分别检测HOXD10基因转染对细胞增殖、单克隆形成、细胞周期、凋亡、侵袭能力的影响;并用Western blotting检测HOXD10基因转染对肿瘤侵袭性相关因子MMP-2蛋白表达的影响。结果 HOXD10基因转染至人胃癌SGC7901/VCR细胞后其基因和蛋白表达水平均显著上升(P0.05),能够抑制SGC7901/VCR细胞增殖、单克隆形成、细胞周期,并提高顺铂作用下细胞凋亡率(P0.05),同时显著抑制细胞侵袭能力和MMP-2蛋白的表达(P0.05)。结论 HOXD10基因转染人胃癌耐药细胞系SGC7901/VCR后能够高表达,进而抑制细胞增殖、单克隆形成、细胞周期和侵袭能力并提高顺铂下细胞凋亡率,而其抑制细胞侵袭能力可能与MMP-2表达减少有关。     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

治疗高血压药物的经济学评价

重视高血压治疗中的经济学评价,对利用我国有限的卫生资源来遏制高血压对人民群众的危害有着重要的现实意义。药物经济学对于药物治疗的成本和治疗的结果给予同样的关注。因为治疗高血压的费用,不仅涉及药物价格,还包括患者的危险水平,降压疗效和对临床终点事件的影响,以及治疗的依从性和安全性。因此药物经济学更强调整体成本和价-效比。低危病人,若非药价低廉,治疗的价-效比不够理想。而在高危的患者,价-效比越小越经济而不是药费越便宜越好。