中医氧分压传感针的研制

一种针型氧分压（Ｐｏ＿２）传感器，外形、体积与传统中医针灸针相同（Φ０．３３ｍｍ）。其线性范围为０．０５～２０ＫＰａ，响应时间小于２ｍｉｎ，分辨率为０．１ＫＰａ，测量误差小于０．２ＫＰａ。在体内准确、快速、方便地测定被测对象的氧分压值，具有耐提插捻转的优点。     

手术治疗急性重型颅脑损伤患者的意义及其脑组织氧分压变化

目的探求手术治疗重型颅脑损伤患者脑组织氧分压（PbtO2）变化的临床意义。方法对42例急性重型脑损伤患者（均在全麻下急诊行血肿清除术和/或去骨瓣减压术）,并且符合GCS≤8分,术前以及术后行PbtO2持续监测,同时行血电解质、动脉血氧分压（PaO2）、动脉血二氧化碳分压（PcaO2）测定;分析PbtO2变化的临床意义。结果预后良好及预后不良组经过手术的干预,8、24、48、72h后PbtO2均明显升高,与术前相比差异有统计学意义（P〈0.05）;而在预后死亡组中,术后8、24、48hPbtO2与术前相比差异均无统计学意义（P〉0.05）。没有发生与插入监测电极相关的并发症。结论脑组织氧分压测定是一种安全、灵敏、可靠的局部脑组织氧监测方法,可反映出重型脑损伤后的脑组织缺血缺氧情况,对临床治疗具有重要的指导作用。持续脑组织氧分压监测可判断重型脑外伤患者预后。     

高血压微循环与体循环动力学临床研究系列(下)——Ⅷ.高血压病人经皮测氧的临床观察

选择高血压病人、不同年龄正常人各30例进行Transcutaneous pressure-oxygen(TcPO_2)测定,结果发现正常青年组TcPO_2明显高于正常老年组,而高血压病人TcPO_2显著低于相同年龄正常组。结果提示:随着年龄增大,微血管将出现退行性改变,而高血压病人则出现微循环灌注障碍,两者均影响组织O_2的交换。     

电化学对提高PBS和人血浆氧分压的研究

采用电化学处理的方法，对人血浆及ＰＢＳ（磷酸盐缓冲盐水）进行了提高氧分压的基础实验研究。结果显示：电化学处理对人血浆和ＰＢＳ的氧分压有明显的增强作用。统计学处理结果具有非常显著性差异（Ｐ＜０．００１），对进一步研究放射治疗增敏具有实际意义。     

脑组织氧分压监测技术的研究与应用进展

脑组织氧分压 (brain tissue oxygen partial pressure,Pbti O2 )技术是进入 90年代后逐渐成熟起来的脑氧代谢监测方法 ,与传统的脑氧监测方法相比具有微创、安全、准确的特点。应用这一技术可以对病人进行术中及术后的长期、动态监测 ,有助于正确判断脑血流量、颅内压、脑灌注压之间的关系 ,早期判断预后。但脑组织氧分压监测所获得的信息尚需结合其他监测手段获得的数据加以综合分析 ,才能得出准确结论     

低氧环境对人类胚胎体外受精发育潜能和临床结局的影响

目的探讨不同氧分压环境下（20％02＆5％O2）体外受精一胚胎移植中胚胎发育潜能与临床结局关系。方法选择2012年9月至2012年11月年在郑大三附院生殖医学中心行助孕治疗的280个周期,分别为IVF（n=200）,ICSI（n=80）。随机分组：研究组（5％氧分压）和对照组（20％氧分压）,对比两组间正常受精率、卵裂率、优质胚胎率、生化妊娠率、临床妊娠率和着床率。结果实验组与对照组正常受精率、卵裂率、优质胚胎率、生化妊娠率、临床妊娠率和着床率无统计学差异。结论人类早期胚胎在低氧环境下进行体外培养是有利的,可以获得更好结局。     

脑组织氧分压监测技术的研究与应用进展

脑组织氧分压（brain tissue oxygen partial pressure,PbtiO2) 技术是进入90年代后逐渐成熟起来的脑氧代谢监测方法,与传统的脑氧监测方法相比具有微创,安全,准确的特点,应用这一技术可以对病人进行术中及术后的长期,动态监测,有助于正确判断脑血流量,颅内压,脑灌注压之间的关系,早期判断预后,但脑组织氧分压监测所获得的信息尚需结合其他监测手段获得的数据加以综合分析,才能得出准确结论。     

中医肺气虚的循环呼吸动力学机理

气体的输运是中医气血运行的重要方面，本文通过对呼吸－循环系统的分析建立了一个描述气体在体内运行的血流动力学模型。通过对模型的分析研究我们发现心肺系统的参数异常改变会引起细胞代谢活动的外环境－组织液的氧分压的降低，进而导致各种肺气虚症状的出现，本模型可以定量解释肺气虚的一些生理学现象，并可以将临床关于肺气虚研究的各种发现结合起来，说明将组织液氧分压作为衡量肺气虚的指标是符合中、西医理论的，这为临床肺气虚证的研究新的方法与途径。     

心绞痛、心肌梗塞病人的经皮氧分压和二氧化碳分压监测

目的研究冠心病心绞痛、心肌梗塞病人的经皮氧分压（ＰｔｃＯ２）和二氧化碳分压（ＰｔｃＣＯ２）的改变。方法采用经皮组织氧分压监测仪对３１例临床上确诊为心绞痛、心肌梗塞病人及２０例健康人分别测定前臂内侧的ＰｔｃＯ２、ＰｔｃＣＯ２值。结果测得心绞痛、心肌梗塞组 ＰｔｃＯ２、ＰｔｃＣＯ；值分别为 ５９． ８５±１０． ４０ｍｍＨｇ、 ５７． ２０± ６． ０９ｍｍＨｇ，健康组为 ７６． ８０± ７． ５８、５３． ３２±１０．８１ｍｍＨｇ。结论冠心病心绞痛、心肌梗塞病人的ＰｔｃＯ２值明显低于正常人（Ｐ＜０．００１），而ＰｔｃＯ２虽较健康组高，但无显著性差异。ＰｔｃＯ２、ＰｔｃＯ２可作为冠心病、心绞痛、心肌梗塞病人的外周微循环改变的监测指标。     

标度律对单细胞生物和肿瘤生长的影响研究

目的:研究标度律对单细胞生物和肿瘤生长的影响。方法:基于单细胞模型,引入标度律研究单细胞生物生长中氧分压及氧代谢情况;用结合了扩散原理的多细胞肿瘤球体模型来研究标度律刻画的肿瘤生长。结果:研究给出了单细胞生物的氧分压分布及其代谢速率与半径关系,引入标度律得到的单细胞生物的生长结果与实验较符合;引入标度律得到了多细胞球体肿瘤不同区域内的氧分压分布,并给出了肿瘤的氧气消耗速率函数,扩散速率函数以及氧气消耗速率,扩散速率与肿瘤半径的关系。结论:引入标度律所得的单细胞生物的代谢速率及生长结果与实验较符合,标度律对单细胞生物生长的影响很明显。区别于前人研究肿瘤,对多细胞球体肿瘤的生长引入标度律得到的肿瘤单位体积氧消耗速率Q与半径的关系及肿瘤中氧分压的分布也和实验较一致,说明标度律对肿瘤生长的影响也很明显,但相对前者,肿瘤是个更复杂的体系,要完整而准确地描述整个肿瘤生长需要考虑更多的影响因子。     

DEVELOPMENT OF SENSOR NEEDLES FORCHINESE TRADITIONAL MEDICINE

Development of sensor needles for chinese traditional medicine is a long term re-search project in our university. Now, temperature. PH, PO_2 and potential sensor needles havebeen developed. These new elements are derived from the combination between a sensor and an ac-tuator. The design principle, functional materials, fabrication technic, calibration method and clin-ical application of these needles are reported in this paper.     

ASPP2对P53家族的调控及其在肿瘤治疗中的意义

P53凋亡激活蛋白2(apoptosis stimulating proteins of P53 2,ASPP2)作为P53家族共同转录激活辅因子能和p53野生型、p63和p73结合,并促进其对下游促凋亡靶基因的转录,促进细胞凋亡.研究表明ASPP2参与细胞生长,凋亡以及损伤应激等一系列的生理反应,对研究肿瘤发生和治疗具有重要意义.     

流感病毒膜蛋白M2e应用研究进展

流行性感冒是一种传染性较高的急性呼吸道疾病,极大地威胁了人类健康.由于流感病毒易发生变异,致目前的防治措施不能及时有效地应对,使防治效果严重降低.流感病毒膜蛋白M2e(extracellular domain of the M2 protein)高度保守,是流感病毒的通用性作用靶点,基于M2e的免疫预防措施可提供广谱的保护作用.M2e疫苗及M2e抗体已成功在动物模型中发挥抗流感作用,临床应用则报道较少,因而研究M2e对于流感病毒的防治具有重要意义.     

过氧化氢酶在衰老和疾病调控中的作用机制

H_2O_2是细胞正常代谢的产物,调节多种生理和生化过程。它通常处在一种相对稳定的动态平衡中,有许多与H_2O_2有关的酶参与和维持,其中过氧化氢酶是细胞内H_2O_2的重要清除剂,许多研究证实它的变化将导致H_2O_2的动态失衡,使细胞内发生一系列相应的反应,表现出特殊的形态特征。文章综述了过氧化氢酶在衰老和疾病发生方面的作用机制。     

Inhibition of cyclooxygenase-2 suppresses the invasiveness of oral squamous cell carcinoma cell lines via down-regulation of matrix metalloproteinase-2 production and activation

Increased cyclooxygenase (COX-2) expression in tumors is known to be correlated with tumor invasion, angiogenesis, resistance to apoptosis, and suppression of host immunity. We previously reported that the invasiveness of human oral squamous cell carcinoma (OSCC) cell lines NA and HSC-4 was suppressed by treatment with either NS-398, a selective COX-2 inhibitor, or COX-2 antisense oligonucleotide (AS). In the present study, to explore the effects of COX-2 inhibition on the interaction between cancer cells and fibroblasts, we examined the effects of these anti-COX-2 reagents on the expression of matrix metalloproteinases (MMPs) in fibroblast cell lines WI-38 and MRC-5. Western blotting and enzyme-linked immunosorbent assay revealed that NS-398 and COX-2 AS down-regulated the expression and secretion of MMP-2 and the tissue inhibitor of matrix metalloproteinase-2 (TIMP-2) in human fibroblast cell lines. Furthermore, invasion activity of OSCC cells was down-regulated by the addition of culture supernatant from fibroblasts treated with anti-COX-2 reagents in a Matrigel^® invasion assay. These results suggest that selective COX-2 inhibition suppresses the invasion activity of OSCC cells via down-regulation of an MMP-2-activating mechanism involving TIMP-2 and production of the MMP-2 protein by an interaction between cancer cells and stromal fibroblasts. Genetic or pharmacological inhibition of COX-2 may therefore be a beneficial strategy in the treatment of OSCC.     

The contribution of founder mutations to early-onset breast cancer in French-Canadian women

In an ethnically‐homogeneous population, it is valuable to identify founder mutations in cancer‐predisposing genes. Founder mutations have been found in four breast‐cancer‐predisposing genes in French‐Canadian breast cancer families. The frequencies of the mutant alleles have been measured neither in a large series of unselected breast cancer patients from Quebec, nor in healthy controls. These estimates are necessary to measure their contribution to the hereditary burden of breast cancer in Quebec and to help develop genetic screening policies which are appropriate for the province. We studied 564 French‐Canadian women with early‐onset invasive breast cancer who were treated at a single Montreal hospital. Patients had been diagnosed at age 50 or less, and were ascertained between 2004 and 2008. We screened all 564 patients for nine founder mutations: four in BRCA1, three in BRCA2 and one each in PALB2 and CHEK2. We also studied 6433 DNA samples from newborn infants from the Quebec City area to estimate the frequency of the nine variant alleles in the French‐Canadian population. We identified a mutation in 36 of the 564 breast cancer cases (6.4%) and in 35 of 6443 controls (0.5%). In the breast cancer patients, the majority of mutations were in BRCA2 (54%). However, in the general population (newborn infants), the majority of mutations were in CHEK2 (54%). The odds ratio for breast cancer to age 50, given a BRCA1 mutation, was 10.1 (95% CI: 3.7–28) and given a BRCA2 mutation was 29.5 (95% CI: 12.9–67). The odds ratio for breast cancer to age 50, given a CHEK2 mutation, was 3.6 (95% CI: 1.4–9.1). One‐half of the women with a mutation had a first‐ or second‐degree relative diagnosed with breast or ovarian cancer. Thus, it can be concluded that a predisposing mutation in BRCA1, BRCA2, CHEK2 or PALB2 is present in approximately 6% of French‐Canadian women with early‐onset breast cancer. It is reasonable to offer screening for founder mutations to all French‐Canadian women with breast cancer before age 50. The frequency of these mutations in the general population (0.5%) is too low to advocate population‐based screening.     

COX-2抑制剂在乳腺癌药物治疗中的研究进展

环氧化酶-2(COX-2)在乳腺癌细胞中过度表达,影响乳腺癌的发生、发展和预后,可作为预防和治疗的靶分子。选择性COX-2抑制剂可联合化疗、内分泌治疗及生物治疗等,作为肿瘤治疗的辅助药物应用于临床,为乳腺癌的治疗提供一种新的途径。     

Inhibitory role of peroxiredoxin 2 in LRRK2 kinase activity induced cellular pathogenesis

Parkinson's disease (PD) is a major neurodegenerative disease. One of the known genetic contributors to PD pathogenesis is leucine-rich repeat kinase 2 (LRRK2) whose mutations with elevated kinase activity could lead to both familial and sporadic PD. However, how the pathogenic kinase activity of LRRK2 is regulated remains largely unclear. Here we report that peroxiredoxin 2 (Prx2) was identified as a novel interacting protein to LRRK2 with preferential expression in dopaminergic neurons over other Prx proteins. We also confirmed that Prx2 interacted with LRRK2 through its COR domain and its overexpression significantly decreased the kinase activity of mutant LRRK2. Functionally, overexpressed Prx2 rescued the transfected cells from LRRK2 mutant induced apoptotic processes. Importantly, overexpressed Prx2 reversed the altered subcellular distribution of cation-independent mannose 6-phosphate receptor (CI-M6PR) induced by PD-mutant LRRK2. Our results suggest that, by interacting with LRRK2, Prx2 may play an inhibitory role in the LRRK2 mediated cellular toxicity in PD by inhibiting its kinase activity.     

Involvement of PGE2 and PGDH but not COX-2 in thrombin-induced cortical neuron apoptosis

The pathways that contribute to thrombin-induced neuron death have been incompletely defined. Induction of cyclooxygenase 2 (COX-2), the enzyme that catalyzes the first step in prostaglandin synthesis, promotes neuronal injury. PGE2, a downstream product of COX-2 metabolism, is neurotoxic in vitro and in vivo, and is thought to be the bioactive mediator responsible for COX-2 neurotoxicity. The objective of this study is to determine the ability of thrombin to affect PGE2 metabolism in cultured neurons. The data show that in thrombin-induced apoptosis of cultured neurons, PGE2 release increases when COX-2 is absent, and is regulated by prostaglandin dehydrogenase (PGDH), a key enzyme that degrades PGE2. NS398, a COX-2 specific inhibitor, protects neurons against thrombin toxicity, by inducing active PGDH. These data implicate PGDH in thrombin-mediated neuronal cell death.     

Prevalence and genetic characterization of canine parvoviruses in Korea

The prevalence of canine parvovirus (CPV) variants in dog was investigated in a total of 51 fecal samples submitted over a 2-year period (2005–2007) in Korea. The CPV VP2 gene was amplified and sequenced from the fecal samples, and the results indicated that of the 51 samples, 49 samples belong to the CPV-2a family, 1 to CPV-2b, and the remaining 1 to CPV-2a variant. The VP2 gene of 20 isolates was sequenced and phylogenetic analysis was conducted. With one exception, all of the isolates were closely related to a Taiwanese isolate (CPV T37) and they formed geographical patterns of VP2 gene nucleotide sequences. Our finding showed that CPV-2a was the predominant type and CPV-2b and CPV-2a variant also existed in Korea. Using the hemagglutination inhibition (HI) and the neutralization (Nt) test, the animals inoculated with CPV-2 developed low antibody titers against the CPV-2 variants in laboratory animal was also identified. Nucleotide sequence data reported is available in the GenBank database under the accession No. EF599096, EF599097, EF599098.