物理震动排石临床疗效分析

目的分析物理震动排石治疗尿路结石的疗效。方法对2014年2月至2014年7月在我院采用物理震动排石单独治疗或联合外科手术处理肾结石、输尿管结石患者进行回顾性分析,评价及总结疗效。结果 80例患者排石次数1~4次,术后1个月输尿管上段结石排出率33.3%,结石排净率22.2%;术后1个月输尿管下段结石排出率16.7%,结石排净率50.0%;术后1个月肾上盏结石排出率40.0%,结石排净率23.3%;术后1个月肾中盏结石排出率27.7%,结石排净率38.8%;术后1个月肾下盏结石排出率60.0%,结石排净率20.0%。物理震动排石联合软镜钬激光碎石术术后1个月结石排出率52.1%,结石排净率39.1%。7例结石合并肾绞痛患者予物理震动排石后疼痛症状明显缓解。结论物理震动排石作为无创治疗结石的手段之一,对输尿管下段结石、软镜术后排石有较好的效果,同时体外物理震动排石能缓解结石引起的疼痛。     

震动伤犬血清皮质醇、胃泌素含量研究

目的:观察震动伤犬血清COR和GAS含量的变化特点,对震动伤犬的伤情分类、临床诊断和临床治疗方案的确定提供依据。方法:在试验时,分别在距爆炸中心地平面0m、100m、200m、300m处设四个点,选择当地家犬34只,采用自由位和右卧位布放在上述四个点。使用放射免疫分析,在爆炸前、后对动物血清中的COR和GAS进行分析。结果:爆后24h犬血清COR和GAS含量即开始下降,爆后第9d和爆后第17d犬血清COR含量仍明显低于爆前值。结论:动物受到震动伤时血清COR水平下降。检测血清COR含量可作为震动伤的辅助诊断手段之一。     

一种智能膝关节假肢模型的阻尼参数优化方法

目的 为了提高智能膝关节假肢的穿戴调试效率及行走的步态对称性，提出了一种利用假肢模型对膝关节假肢的阻尼参数进行优化的方法。方法 首先利用多杆刚体系统对智能膝关节假肢构建由膝关节、连杆及阻尼器组成的假肢模型。选择5例测试对象，其中男性3例，女性2例；年龄29～55岁，平均年龄44.20岁（标准差10.45岁）；身高1.52～1.78 m，平均身高1.650 m（标准差0.098 m）；体质量55～75 kg，平均体质量63.60 kg（标准差8.59 kg）；大腿长0.37～0.44 m，平均大腿长0.404 m（标准差0.027 m）；小腿长0.43～0.51 m，平均小腿长0.470 m（标准差0.029 m）；步幅0.56～0.66 m，平均步幅0.610 m（标准差0.038 m）。将不同步速（0.8 m/s、1.2 m/s、1.6 m/s）的健肢侧膝关节角度及足底反力信息导入该模型，结合S.S.Rao Mechanical Vibration的二阶振动理论，以假肢模型与健肢之间的膝关节角度最小均方根误差为优化目标，对阻尼参数（ωd,ζ）进行优化求解。结果 通过对5例测试对象的步...     

震动伤引起的家犬外周血淋巴细胞凋亡及其机制

应用免疫细胞化学和酶细胞化学技术，观察了震动伤引起的家犬外周血淋巴细胞凋亡，Ｔ淋巴细胞数的变化及其发生机制。结果表明，实验所用２００、１００和８０三种垂直加速度值（Ｇ）在致伤后不同时间，均可引起淋巴细胞的凋亡，其凋亡率随Ｇ值增加而增大；观察伤后不同时间细胞凋亡的变化，发现在伤后３ｄ其凋亡率达到峰值，约为伤前的５～８倍；而外周血Ｔ淋巴细胞数在伤后明显降低，与凋亡呈现出相反的变化趋势；还发现伤后３ｄ与凋亡相关的ｐ５３和Ｂａｘ蛋白阳性率分别为伤前值的２．３和１．８倍，二者在诱发淋巴细胞凋亡中可能起着重要作用。     

震动伤犬血清CG、ALT含量测定

目的 观察震动伤犬血清甘胆酸(CG)和丙氨酸氨基转移酶(ALT)含量变化特点,对震动伤的伤情分类、临床诊断和治疗方案的确定提供依据.方法 在地下模拟爆炸炸现场获取震动伤动物模型.方法是分别在距爆炸心地平面0m、100m、200m、300m处设四个点,选择当地家犬34只,采用自由位和右卧位布放在上述四上个点.对爆炸炸前、后动物血清中的CG和ALT含量进行配对分析.结果 检查发现,爆炸后10小时开始,血清CG和ALT含量即明显升高(1116.8±1181.2nmol/L和66.8±49.5U/L,P＜0.01.),至爆炸后17d血清CG尚未完全恢复(773.2± 408.1nmol/L,P＜0.01.).结论 实验动物受震动伤时,血清CG和ALT水平异常升高.提示在临床诊断、治疗震动伤伤员时,除常规检测血清ALT外,血清CG含量测定是反应肝脏损伤和修复程度的敏感指标.特别是在治疗后期,血清ALT已经恢复正常时,CG含量测定可为临床治疗效果的评价提供可靠依据.     

现代吸脂技术采集脂肪混合物在脂肪干细胞制备领域中的应用

背景：目前用于整容的吸脂术发展很快,但为了脂肪干细胞应用而进行的综合吸脂术研究和比较尚未见报道。 目的：对比目前各种类型脂肪抽取技术的特点以及对基质血管层、脂肪细胞、脂肪干细胞的数量和存活率等指标的影响,评价出细胞活性高、适合进行脂肪干细胞制备、储存及临床科学研究的吸脂技术。 方法：作者分别采用检索关键词“adipose-derived stem cells,ADSCs, liposuction,SAL,UAL,PAL,WAL”和“脂肪干细胞、脂肪抽取术、负压吸脂术、超声辅助吸脂术、震动辅助吸脂术、水动力辅助吸脂术”检索了PubMed数据库、中国知网全文期刊数据库和美国NIH 临床试验数据库,排除与研究目的无关和内容重复者,保留50篇文献进行进一步分析。 结果与结论：目前可应用于脂肪间充质干细胞采集的现代吸脂技术主要有负压吸脂、超声辅助吸脂、震动辅助吸脂、水动力辅助吸脂。其中负压吸脂、超声辅助吸脂技术、水动力辅助吸脂技术3类技术采集的脂肪混合物中可以分离出脂肪干细胞且具有较高的活性,可以用作自体细胞辅助移植技术和再生疗法。这4类技术虽然各有特点,有必要进一步研究这些吸脂技术获得的脂肪干细胞的活性、遗传性状稳定性、分化能力等系统性对比数据,为未来的再生医学工程提供更准确完善的支持。中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程全文链接：     

投入:工作倦怠研究的新视角

目的 对工作投入的相关研究进行综述.方法 文献整理法.结果 投入是雇员持续的、积极的情感激活状态,其特征为活力、奉献和专注;国外关于投入的测量方法主要有两种;倦怠和投入是可以相互区分的两个心理学概念.结论 投入是倦怠未来研究的新方向,应当对工作投入问题加以关注.     

耳廓软骨膜炎1例

1 临床资料患者女,19岁.主因"左耳水肿红斑3 d"于2007年10月9日来空军总医院门诊就诊.患者3 d前无明显诱因自觉左耳烧灼、痒痛,次日晨耳前上部位突然高度水肿、胀痛难忍,自服"扑尔敏"、外用"肤轻松",症状不能缓解,为进一步治疗来我院就诊.患者病程中无发热,精神饮食睡眠均正常.既往及家族史无特殊.体格检查;系统检查未见异常.皮肤科检查:左耳廓前部红肿,触之坚硬,压痛明显,表面无破溃、渗出糜烂,耳垂正常.     

疣状皮肤结核1例

1 临床资料患者, 女性, 11岁.右膝斑块7年就诊.7年前无诱因患者右膝部出现豆粒大小红色丘疹, 圆形, 边界清楚, 表面无鳞屑, 无水疱、 大疱, 无出血、渗出、溃破, 自觉微痒, 当时未介意.此后皮损渐增至鸡蛋大小, 偶感瘙痒, 无其他任何不适, 按"湿疹"在多家医院诊治, 皮损从未消退.     

应用Microsoft Excel软件进行《组织学与胚胎学》考卷组织的体会

考试是教学活动中的一个重要环节,目前考试成绩仍然是衡量教学质量最常用的指标,而考卷的质量直接影响到学生的考试成绩。为了更好地组织出符合教学大纲要求,既能涵盖《组织学与胚胎学》主要内容,又能够有一定区分度的试卷,我们将Microsoft Excel软件应用到其中,具体体会报道如下。     

线粒体DNA损伤与细胞凋亡

细胞核DNA（nuclear DNA,nDNA）损伤后诱导细胞凋亡的信号转导途径已经逐渐清晰,而线粒体DNA（mitochondrial DNA,mtDNA）损伤与细胞凋亡之间的关系尚有待进一步明确.目前已有研究结果表明：mtDNA断裂、缺失或功能缺陷能够显著影响细胞凋亡发生率;线粒体缺失细胞（p0细胞）同其亲代细胞相比,对多种凋亡诱导因素的反应存在显著差异;ROS的产生并非mtDNA损伤诱导凋亡的必要条件,mtDNA损伤断裂本身可能启动了凋亡的级联反应.但mtDNA的损伤,在细胞凋亡的信号转导途径具体扮演何种角色,还有待深入研究.     

Oxidative damage and age-related functional declines

Most organisms experience progressive declines in physiological function as they age. Since this senescence of function is thought to underlie the decrease in quality of life in addition to the increase in susceptibility to disease and death associated with aging, identifying the mechanisms involved would be highly beneficial. One of the leading mechanistic theories for aging is the oxidative damage hypothesis. A number of studies in a variety of species support a strong link between oxidative damage and life span determination. The role of oxidative damage in functional senescence has also been investigated, albeit not as comprehensively. Here, we review these investigations. Several studies show that the age-related loss of a number of functions is associated with an accrual of oxidative damage in the tissues mediating those functions. Additionally, treatments that increase the accumulation of oxidative damage with age frequently exacerbate functional losses. Moreover, treatments that reduce the accumulation of oxidative damage often attenuate or delay the loss of function associated with aging. These data provide the foundation for a link between oxidative damage and functional senescence, thereby supporting the oxidative damage hypothesis of aging within the context of age-related functional decline.     

DNA damage in bronchial epithelial and mesothelial cells with and without associated crocidolite asbestos fibers

Mesothelioma is induced almost exclusively by exposure to asbestos fibers. We have investigated whether the induction of DNA damage in human bronchial epithelial BEAS 2B cells and human mesothelial MeT 5A cells by crocidolite asbestos (2 microg/cm2) requires the presence of asbestos fibers in the cells. DNA damage was measured microscopically by the Comet assay, and the presence of fibers in the same cells was assessed using bright-field illumination. After treatment times of 6-72 hr, damage levels were, on the average, two times higher in cells with fibers than in cells without fibers. It was further found that DNA damage decreased with time in BEAS 2B cells both with and without fibers. No decrease in damage with time was seen in MeT 5A cells, suggesting that these mesothelial cells repair the initial damage poorly, lack induction of protective systems, or constantly produce high levels of damaging species. Our results indicate that crocidolite-treated human mesothelial MeT 5A and bronchial epithelial BEAS 2B cells show an elevated level of DNA damage if they contain a fiber. In comparison with epithelial BEAS 2B cells, mesothelial MeT 5A cells have more DNA damage after the crocidolite treatment and the damage is more persistent.     

Structural muscle damage and muscle strength after incremental number of isometric and forced lengthening contractions

Summary Exercise-induced muscle damage is characterized by histological changes, like Z-line streaming, inflammatory response and decreased muscle function reflected in a prolonged decline in maximal isometric muscle strength after eccentric work. It is assumed that force decrement is mainly related to the amount of structural damage. However, the relationship between number of eccentric contractions, magnitude of structural damage and force decrement is not very well documented. Therefore we studied the effect of an increasing number of both isometric and eccentric (forced lengthening) contractions on histological parameters of muscle damage and maximal isometric force in an experimental in situ rat model. Tibialis anterior muscles of male Wistar rats were subjected to an increasing number of either isometric or eccentric contractions and were examined for histological markers of muscle damage. The present study shows that muscle damage increases progressively with the number of forced lengthening contractions. Maximal isometric torque was found to decline after both types of exercise. However, the decline after forced lengthening exercise was more pronounced. Only a weak relationship between percentage of histological muscle damage and isometric torque after forced lengthening contractions was found. The findings of the present study suggest that the decline in muscle force after eccentric exercise may partly be attributed to other factors than structural damage.     

The impact of DNA damage, genetic mutation and cellular responses on cancer prevention, longevity and aging: observations in humans and mice

Over the past 5 years, data collected from the mouse suggest that pathways important for either preventing or resolving DNA damage are longevity assurance mechanisms whose critical overall function is somatic cell maintenance, a necessary part of cancer prevention. These pathways include those that reduce DNA damage levels caused by exogenous sources, replication errors and by-products of cellular respiration. Unresolved DNA damage leads to permanent mutations in the genetic code that may be oncogenic. Therefore, pathways that resolve DNA damage are important anti-cancer mechanisms. As an important line of defense, there are a variety of pathways that repair DNA damage. In addition, there are anti-cancer pathways that respond to DNA damage by either preventing cellular replication or inducing cell death. Genes in these pathways, termed longevity assurance genes (LAG), code for proteins that reduce cancer incidence and as a result assures a sufficiently long health span needed for reproduction. Data from mouse models, many that were originally designed to study cancer, are showing that a potential consequence of DNA damage and responses to DNA damage is aging; these models support the hypothesis that at least some aspects of normal aging are the consequence of anticancer mechanisms designed to deal with damaged DNA.     

The relationship between cement fatigue damage and implant surface finish in proximal femoral prostheses

The majority of cemented femoral hip replacements fail as a consequence of loosening. One design feature that may affect loosening rates is implant surface finish. To determine whether or not surface finish effects fatigue damage accumulation in a bone cement mantle, we developed an experimental model of the implanted proximal femur that allows visualisation of damage growth in the cement layer. Five matt surface and five polished surface stems were tested. Pre-load damage and damage after two million cycles was measured. Levels of pre-load (shrinkage) damage were the same for both matt and polished stems; furthermore damage for matt vs. polished stems was not significantly different after two million cycles. This was due to the large variability in damage accumulation rates. Finite element analysis showed that the stress is higher for the polished (assumed debonded) stem, and therefore we must conclude that either the magnitude of the stress increase is not enough to appreciably increase the damage accumulation rate or, alternatively, the polished stem does not debond immediately from the cement. Significantly (P=0.05) more damage was initiated in the lateral cement compared to the medial cement for both kinds of surface finish. It was concluded that, despite the higher cement stresses with debonded stems, polished prostheses do not provoke the damage accumulation failure scenario.     

Analysis of UV-induced damage and repair in young and senescent human dermal fibroblasts using the comet assay

A major cause of ageing is thought to be the accumulation of damage to macromolecules. Accumulation to DNA damage in cells therefore presupposes that aged cells are unable to repair this damage. We have used the in vitro model of cellular ageing to test the idea that senescent cells are deficient in some aspect of DNA repair. Using the alkaline single cell gel electrophoresis assay (comet assay), we have determined the responses of young and senescent human dermal fibroblasts to DNA damage caused by exposure to UVC light. At low doses of UVC, senescent cells generate smaller comets than young cells whilst at medium doses the situation is reversed. At high doses, young and senescent cells respond similarly to one another. Time course experiments revealing repair of DNA damage show that senescent cells generate larger comets than young cells at early stages of repair suggesting that either senescent cells bear more damage per genome than do young cells or that senescent cells are more efficient at excising bulky adducts from DNA. Cells maintained in low levels of serum irrespective of age are less able to repair DNA damage compared with cells maintained in high levels of serum, and furthermore young and senescent cells maintained in high levels of serum are equally able to repair DNA damage. Our data, therefore, reveal both age-dependent and age-independent responses to UV-induced DNA damage. Use of the comet assay highlights the heterogeneity of cellular responses to genotoxic stress.     

Oxidative damage and platelet activation as new predictors of mobility disability and mortality in elders

Mobility disability is an early phase of the disablement process in older adults, and represents a major risk factor for physical disability and mortality. Pathophysiological mechanisms responsible for the onset of mobility limitation are still largely unknown. Oxidative damage, responsible for the disruption of the equilibrium of biological systems by damaging major constituent molecules, might play an important role in the pathway leading to major health-related events. It has been suggested the existence of a vicious cycle involving oxidative damage, platelet activation, and inflammation as promoter of pathophysiological changes occurring with aging. This hypothesis is based on the following observations: (a) oxidative damage is associated with diseases and clinical conditions potentially leading to disability and mortality; (b) oxidative damage is associated with platelet activation, and a vicious cycle involving oxidative damage, platelet activation, and inflammation has been demonstrated in several metabolic disorders potentially leading to mobility disability; (c) the age-related physical decline may be associated to the oxidative damage due to the excess of free radicals; (d) antioxidant defense and behavioral factors (e.g., physical activity, dietary restriction, smoking cessation) play an important role in the reduction of oxidative damage levels and are associated with improved physical performance and muscle strength.     

Flies,worms and the Free Radical Theory of ageing

Drosophila and Caenorhabditis elegans have provided the largest body of evidence addressing the Free Radical Theory of ageing, however the evidence has not been unequivocally supportive. Oxidative damage to DNA is probably not a major contributor, damage to lipids is assuming greater importance and damage to proteins probably the source of pathology. On balance the evidence does not support a primary role of oxidative damage in ageing in C. elegans, perhaps because of its particular energy metabolic and stress resistance profile. Evidence is more numerous, varied and consistent and hence more compelling for Drosophila, although not conclusive. However there is good evidence for a role of oxidative damage in later life pathology. Future work should: 1/ make more use of protein oxidative damage measurements; 2/ use inducible transgenic systems or pharmacotherapy to ensure genetic equivalence of controls and avoid confounding effects during development; 3/ to try to delay ageing, target interventions which reduce and/or repair protein oxidative damage.     

Cellular dynamics and modulation of WRN protein is DNA damage specific

The human premature aging protein Werner (WRN), deficient in Werner syndrome (WS), is localized mainly to the nucleolus in many cell types. DNA damage or replication arrest causes WRN to redistribute from the nucleolus to the nucleoplasm into discrete foci. In this study, we have investigated DNA damage specific cellular redistribution of WRN. In response to agents causing DNA double strand breaks or DNA base damage, WRN is re-distributed from the nucleolus to the nucleoplasm in a reversible manner. However, after ultraviolet (UV) irradiation such redistribution of WRN is largely absent. We also show that WRN is associated with the insoluble protein fraction of cells after exposure to various kinds of DNA damage but not after UV irradiation. Further, we have studied the DNA damage specific post-translational modulation of WRN. Our results show that WRN is acetylated after mytomycin C or methyl methane-sulfonate treatment, but not after UV irradiation. Also, DNA damage specific phosphorylation of WRN is absent in UV irradiated cells. Inhibition of phosphorylation fails to restore WRN localization. Thus, our results suggest that the dynamics of WRN protein trafficking is DNA damage specific and is related to its post-translational modulation. The results also indicate a preferred role of WRN in recombination and base excision repair rather than nucleotide excision repair.