新生牛皮胶原蛋白海绵的制备及其体外细胞相容性

目的:采用新生牛皮提取胶原蛋白、制备生物医用胶原蛋白海绵,观察其生物学活性与细胞相容性。方法:实验于2006-05/2007-02在西北民族大学生命科学与工程学院生物工程与技术国家民委重点实验室完成。实验方法:①取出生24h内宰杀的新生尕里巴牛犊皮制备胶原蛋白海绵。②将新生牛皮胶原蛋白海绵与黑裘皮羔羊肾F3代成纤维细胞混悬液共培养,分别设胶原海绵材料组、阴性对照组(生理盐水)、阳性对照组(橡胶塞浸提液)。实验评估:①应用倒置相差显微镜观察细胞形态。②培养20,35d对细胞与胶原蛋白海绵共培养物进行AO染色观察细胞在胶原海绵中的增殖情况。③培养65d后制石蜡切片,行苏木精-伊红染色观察细胞在胶原海绵中的生长情况。结果:①细胞形态观察结果:阳性对照组细胞培养24h细胞圆缩,不贴壁,3d后全部死亡。胶原海绵材料组与阴性对照组细胞形态均正常,细胞贴壁生长良好。随着培养时间的延长,海绵孔隙逐渐变小,细胞数量增加,形态变小,海绵外观从柔软、混浊变得挺拔、透明。②细胞在胶原海绵中的增殖情况:吖啶橙-AO染色显示培养20,35d胶原海绵-羔羊肾成纤维细胞共培养物中有大量细胞存在,并且在胶原蛋白空隙中有大量细胞成团簇状生长。③细胞在胶原海绵中的生长情况:苏木精-伊红染色显示有大量蓝色细胞核和新生的红色胶原纤维。结论:制备的新生牛皮胶原蛋白海绵对岷县黑裘皮羔羊肾成纤维细胞有良好的生物相容性,无细胞毒性。     

基于Linux操作系统嵌入式心电记录仪的设计

介绍了一种基于ARM9和Linux操作系统的心电记录仪。该记录仪以32位低功耗ARM9微处理器S3C2410X为核心,在其上移植了Linux操作系统,利用轻量级的图形用户界面支持系统MiniGUI进行软件界面开发,实现了心电信号的实时采集显示、心率计算、心律失常分析并利用GPRS进行心律失常报警等功能。为了检验系统的性能,使用心电信号模拟发生器(MPS450多参数模拟器)产生各种类型的心电信号,用该记录仪进行采集分析,记录仪分析获得的心率值与模拟发生器产生的心率值基本相同,当模拟发生器产生异常心电时,记录仪通过GPRS发出报警信息,同时在主界面上显示心律失常类型。实验结果表明,该记录仪能实时采集显示心电波形,当发生心动过速、心动过缓、心律不齐、漏搏、停搏时,能通过GPRS进行实时报警,实现了心电信号的无线远程实时监护。     

Concepts of body constitution,health and sub-health from traditional Chinese medicine perspective

This paper described and discussed the important literature and ideas about the concepts, types and measurement of body constitution, in terms of healthy, sub-healthy and disease status. In view of traditional Chinese medicine, ‘‘healthy” state is a status of relative balance of Yin and Yang to keep our bodily homeostasis. If there are significant physical and/or psychological stressors, such as loss of a beloved one and failure in study or work, the body can no longer keep its own bodily condition balanced and subsequently enter a state of ‘‘sub-health” (sub-optimal health). ‘‘unhealthy” body constitution such as ‘‘Dampness-heat”, ‘‘Cold-dampness” and ‘‘Heat- or Cold- dryness” with a subnormal body temperature and humidity and clinical manifestations such as insomnia, malaise and overweight will be presented. Immediate, appropriate strategies such as modification of life-style and seeking medical treatment can prevent evolution of an illness. Otherwise, the body will enter a disease status with a ‘‘pathological” body constitution of ‘‘Yin or Yang deficiency’’, ‘‘Blood-stasis” and/or ‘‘Phlegm-dampness”. To be complimentary with health promotion and disease prevention in Western medicine, understanding about an individual’s body constitution, together with its determinants (e.g., healthy eating and lifestyle behaviors), can contribute to a more proactive, holistic and individualized healthcare.     

Symptom clusters and quality of life among patients with advanced heart failure

Objectives To identify symptom clusters among patients with advanced heart failure (HF) and the independent relationships with their quality of life (QoL). Methods This is the secondary data analysis of a cross-sectional study which interviewed 119 patients with advanced HF in the geriatric unit of a regional hospital in Hong Kong. The symptom profile and QoL were assessed by using the Edmonton Symptom Assessment Scale (ESAS) and the McGill QoL Questionnaire. Exploratory factor analysis was used to identify the symptom clusters. Hierarchical regression analysis was used to examine the independent relationships with their QoL, after adjusting the effects of age, gender, and comorbidities. Results The patients were at an advanced age (82.9 ± 6.5 years). Three distinct symptom clusters were identified: they were the distress cluster (including shortness of breath, anxiety, and depression), the decondition cluster (fatigue, drowsiness, nausea, and reduced appetite), and the discomfort cluster (pain, and sense of generalized discomfort). These three symptom clusters accounted for 63.25% of variance of the patients’ symptom experience. The small to moderate correlations between these symptom clusters indicated that they were rather independent of one another. After adjusting the age, gender and comorbidities, the distress (beta = ?0.635, P < 0.001), the decondition (beta = -0.148, P = 0.01), and the discomfort (beta = -0.258, P < 0.001) symptom clusters independently predicted their QoL. Conclusions This study identified the distinctive symptom clusters among patients with advanced HF. The results shed light on the need to develop palliative care interventions for optimizing the symptom control for this life-limiting disease.     

腹腔鏡下子宫切除术46例

1 临床资料腹腔鏡下子宫次全切除(laparoscopic surgery on hyesterectomy, LSH)患者46例,年龄38～56岁. 诊断(B超、CT)子宫肌瘤37例,宫血9例,肌瘤均<12 cm. 手术取截石位,头低30°,采取口腔明视静脉复合麻醉. 气腹形成后,采用3～4 cm切口,下腹部左、右侧分别切口,位置取髂前上棘内上方2 cm处,用直径0.5 cm的穿刺针穿刺,置操作钳,于脐孔处用直径1 cm的穿刺针穿刺,经穿刺孔放置腹腔镜,在脐与耻骨结节连线中点处穿刺另一操作孔.     

飞行人员花粉症快速免疫治疗68例

1 临床资料现役飞行人员花粉症患者94例,男,年龄24～50岁,平均飞行时间1320(300～2200) h. 出现以打喷嚏、流涕、鼻塞等典型花粉症表现. 通过变应原皮肤试验对患者进行各种变应原测定. 标准变应原由北京协和医院变态反应科提供.     

Retinoic acid-resistant HL-60 cells exclusively contain mutant retinoic acid receptor-alpha

Sequence analysis of the retinoic acid receptor-alpha (RAR alpha) gene from a subline of HL-60 cells (RA-res) stably resistant to all-trans retinoic acid (RA) disclosed a single-base change in codon number 411, the same C to T transition previously reported in an independently selected HL-60 RA resistant clone by Robertson et al (Blood 80:1885, 1992). This mutation eliminates a FokI restriction endonuclease site. Using primers framing this mutation in exon 9 of the RAR alpha gene, we showed that polymerase chain reaction products amplified from either mRNA or genomic DNA templates from the RA-res subline were completely resistant to FokI digestion whereas those from wild-type (wt) HL-60 cells could be digested to completion. The lack of a normal allele in the RA-res cells was confirmed by mixing experiments and hybridization analyses. Southern blot analysis of DNA from the RA-res and wt cells versus control placental DNA indicated that the RAR alpha gene is not haploid. The independent isolation of the same RAR alpha mutation in different laboratories suggests either that the mutation exits in a small subpopulation in the wt line or that this is a mutational "hot spot." Furthermore, the results indicate that if a dominant negative mode of resistance is involved in the RA-res subline, this must involve interference with the function of heterologous receptor proteins such as the retinoid X receptors. The lack of any normal RAR alpha in this subline may facilitate studies of the mode of action of retinoids.     

Lipopolysaccharide enhances CD11b/CD18 function but inhibits neutrophil aggregation

Human neutrophils are primed in the presence of complexes of lipopolysaccharide (LPS) with its serum binding protein (LBP) in a manner dependent on CD14. Cellular consequences of priming include increased responsiveness, the upregulation of surface proteins including the adhesive integrin CD11b/CD18 (Mac-1), the increased binding of certain ligands to CD11b/CD18, and the concurrent shedding of the L-selectin homing receptor. Because expression of both CD11b/CD18 and L-selectin is obligatory for formyl peptide-stimulated neutrophil aggregation in vitro (Simon et al, Blood 82:1097, 1993), we have examined the consequences of bacterial endotoxin on the expression of neutrophil adhesive molecules. We observed that the exposure of neutrophils to LPS/LBP, while enhancing the surface numbers and adhesive function of CD11b/CD18 for latex particles, did not induce aggregation. In contrast, as the LPS/LBP concentration increased (ED50 = 30 ng/mL LPS/LBP), the ability of neutrophils to aggregate decreased in parallel with the shedding of L-selectin. Moreover, when L-selectin adhesive activity was blocked by treatment with Fab fragments of Dreg- 200, aggregation was inhibited to an extent roughly proportional to the available L-selection. Blocking of LPS/LBP with CD14-specific monoclonal antibodies suppressed L-selectin shedding and preserved formyl peptide-stimulated aggregation. Taken together, the data suggest that inhibition of neutrophil aggregation by LPS/LBP is related to the expression of L-selectin via CD14 rather than LPS inhibition of CD11b/CD18 function during cellular stimulation.     

Platelet adhesion to collagen type IV under flow conditions

Collagen type IV is a sheet-forming collagen and a major constituent of the vessel wall. To find out which conditions are important for platelet adhesion to collagen type IV, we performed perfusion studies with anticoagulated blood in parallel plate perfusion chambers. The role of divalent cations was investigated by using plasmas with variable concentrations of Mg2+ and Ca2+ ions. When Mg2+ concentration was decreased from 2.00 mmol/L to 0.25 mmol/L at a fixed Ca2+ concentration of 1.25 mmol/L, platelet coverage on the collagen type IV surface decreased from 22.8% +/- 1.8% (n = 4) to 4.6% +/- 0.6% (n = 4) at a shear rate of 1,600 s-1. Also, platelet aggregate formation on collagen type IV was strongly impaired. A monoclonal antibody against the glycoprotein (Gp) Ib receptor and von Willebrand factor (vWF)- depleted plasma reduced the platelet coverage to collagen type IV to, respectively, 10% and 45% of the control value. Electron microscopy showed that vWF was only present between platelets and between the platelet and the collagen type IV surface, but did not bind elsewhere to collagen type IV. These data indicate that collagen type IV is a reactive collagen for platelets. Differences in physiologic plasma magnesium concentrations may in part explain the differences in platelet reactivity to collagen type IV between individuals, and perhaps contribute to differences in the risk for thrombosis.