Diagnostic accuracy of Raman spectroscopy for prostate cancer: a systematic review and meta-analysis

BackgroundAlthough various studies have been conducted to demonstrate the possibility of Raman spectroscopy (RS) as a diagnostic tool for prostate cancer (PC), it is difficult to use it in the real clinical area because of imitations in various research processes. Therefore, we did a systematic review and meta-analysis about the accuracy in diagnostic use of RS for PC.MethodsA literature search was done using PubMed, Embase, and Cochrane library databases in March 2019 to analyze the accuracy of RS for diagnosis of PC. The accuracy of RS for diagnosis of PC was evaluated by means of pooled sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and summary receiver operating characteristic (SROC).ResultsFive studies were included for qualitative analysis by screening the remaining articles according to the inclusion and exclusion criteria by means of a systematic review. The pooled sensitivity and specificity of RS were 0.89 (95% CI: 0.87–0.91) and 0.91 (95% CI: 0.89–0.93), respectively. The overall PLR and NLR were 9.12 (95% CI: 4.15–20.08) and 0.14 (95% CI: 0.07–0.29), respectively. The DOR of RS demonstrated high accuracy (73.32; 95% CI: 18.43–291.73). The area under the curves (AUCs) of SROC curves was 0.93.ConclusionsRS is an optical diagnostic method with high potential for diagnosis and grading of PC and has advantages of real-time and convenient use. In order to consider real-time use of RS in an actual clinical setting, more studies for standardization and generalization of RS performance and analytical method must be conducted.     

Effect of Semax peptide on survival of cultured rat pheochromocytoma cells during oxidative stress

We studied the effects of Semax (antiinsulin peptide with neuroprotective effect) on the survival of cultured rat pheochromocytoma cell after oxidative stress induced by short-term incubation with hydrogen peroxide. Studies with fluorescent dyes propidium iodide and Hoechst 33258 showed that cell incubation with hydrogen peroxide led to the formation of damaged cells with characteristic signs of necrosis. Semax dose-dependently reduced the number of cells damaged by oxidative stress. The efficiency of Semax depended on the time of its addition to the culture medium. The results suggest that the neuroprotective effect of Semax in ischemic stroke can be due to its capacity to protect neurons from damage caused by oxidative stress.     

EGb对MPP^＋诱导的PC12细胞凋亡的影响

目的 观察EGb对MPP^ 诱导的PC12细胞凋亡的细胞。方法 MPP^ 诱导PC12细胞凋亡,AO／EB染色,荧光显微镜下观察凋亡细胞。结果 EGb50、100μg/ml在6h、12h、24h可抑制细胞凋亡,而EGb25μg/ml则无效。结论 EGb在6h、12h、24h时呈剂量依赖性降低细胞凋亡率,提示EGb有可能通过抑制DA能神经元凋亡而相对增加DA含量。     

多巴胺诱导PC12细胞凋亡的免疫组织化学及超微结构分析

目的 研究帕金森病（PD）多巴胺能神经元的死亡机制,方法在免疫组织化学基础上,采用流式细胞仪,电泳及电镜技术观察不同浓度多巴胺（DA）诱导大鼠嗜铬细胞瘤PC12细胞凋亡的超微结构及生化改变。结果 适当浓度DA可诱导PC12细胞凋亡,早期表现为线粒体结构及功能的改变并有抗凋亡蛋白bcl-2的达,后期电镜下可见亡特征性核结构改变及典型的DNA阶梯状电泳带,结论 细胞凋亡参与了PD的病变过程,线粒体在早期细胞凋亡中起着重要的调节作用。     

少突胶质细胞对PC12细胞JAK2基因表达的影响及其意义

目的 探讨少突胶质细胞对PC12细胞JAK2基因表达的影响及其意义。方法 用分离培养的少突胶质细胞及其细胞碎片分别作用于培养的PC12细胞,于不同作用时相点在观察PC12细胞突起变化的同时检测PC12细胞内JAK2mRNA的表达JAK2蛋白的磷酸化。结果 在给予少突胶质细胞及其细胞碎片处理后10min,JAK2 mRNA表达较对照组有显著增高（P＜0．05）,但处理12h后,其表达虽较处理10min及4h有显著下降,但仍显著高于对照组（P＜0．05）。对照组JAK2蛋白的活性较低,但少突胶质细胞及其细胞碎片加入后,JAK2蛋白很快便被磷酸化而激活,到处理后12h,激活的蛋白呈较处理10min有显著下降,但仍显著高于正常对照组（P＜0．05）。少突胶质细胞及其细胞碎片对其影响差别不显著（P＞0．05）。结论 少突胶质细胞作用于PC12细胞时可调节PC12细胞JAK2的表达与激活,这种表达与激活在一定程度上可能介导少突胶质细胞对PC12细胞突起生长的影响。     

牛坐骨神经中神经再生抑制物的分离与鉴定

目的 在周围神经内寻找与中枢神经内轴突生长抑制因子有相同生物学活性的神经再生抑制物。方法 取新生小牛坐骨神经提取液经ＳｅｐｈａｃｒｙｌＳ－１００凝胶柱层析,得洗脱峰,再将各峰成分用不同分子的滤管超滤分别得到６组不同Ｍｒ的粗提液,将各组分加入到体外培养的ＰＣ１２细胞中观察细胞生长情况,并检测细胞活性。细胞活力检测指标是ＭＴＴ法细胞活性检测和细胞总蛋白含量测定。结果 有抑制活性的物质主要集中在Ｍｒ〈１     

NM-Win: A Personal Computer-Based Microsoft® Windows™ Front-End to NONMEM IV

A Microsoft Windows-based front-end, NM-Win, has been written to provide a more user-friendly environment to do nonlinear mixed effect modeling with the NONMEM program. NM-Win utilizes an object-oriented interface design which allows users to view and edit control, PRED, and/or data files using Windows Notepad. In addition, calls made to the Microsoft FORTRAN compiler and linker which generate the final NONMEN executable are performed simply by clicking the Run NONMEN button. During the executive step, iterations can be viewed in a window to check the progress of the run. Errors encountered while NONMEN or NM-TRAN is running are brought to a window for ease in debugging. Advanced options allow the user the flexibility of compiling user-written PRED files and creating linker response files. While the PC platform is not optimal for large data set or complex models, it does permit easier debugging and offers multitasking while Windows is running.     

头颈部恶性肿瘤累及颈动脉的治疗(附3例报告)

报告３例头颈部恶性肿瘤颈部转移累及颈动脉,术中保留预动脉,术后４～６ｄ颈动脉破裂大出血。分析原因为伤口感染和颈动脉已被肿瘤浸润所致,提示受肿瘤侵犯的颈动脉不宜保留。     

Ultrastructural confirmation of neuronal protection by melatonin against the neurotoxin 6-hydroxydopamine cell damage

6-Hydroxydopamine (6-OHDA) is a neurotoxin used in the induction of experimental Parkinson's disease in both animals and cultured neuronal cells. Biochemical and molecular approaches showed previously that low doses of 6-OHDA induced apoptosis in PC12 cells, while high doses of this neurotoxin induced necrosis. Melatonin has been shown to protect against the neuronal programmed cell death induced by 6-OHDA, although it was not able to prevent the massive necrotic cellular death occurring after the addition of high doses of the neurotoxin. In the present work, we demonstrate by ultrastructural analysis that although low doses of 6-OHDA induced apoptosis in PC12 cells, it also damaged the non-apoptotic cells, morphologically corresponding this damage to incipient and reversible necrotic lesions. When the doses of the neurotoxin increase, there are still apoptotic cells, although most of the cells show necrotic irreversible lesions. We also found that melatonin partially prevents the incipient necrotic lesions caused by low doses of 6-OHDA. The fact that melatonin was shown in previous work to prevent apoptosis caused by low doses of 6-OHDA, but not necrosis induced by high doses of the neurotoxin, seemed to indicate that this agent is only able to protect against apoptosis. However, our present results, melatonin preventing also the incipient necrotic neuronal lesions, suggest that this hormone may provide a general protection against cell death, suggesting that higher doses should be tried in order to prevent the necrotic cell death induced by high doses of the neurotoxin.     

脱位晶状体摘出联合后房型人工晶状体缝线固定术

目的　探讨晶状体脱位手术摘出联合Ⅰ期后房型人工晶状体缝线固定的临床疗效。方法　对１５眼脱位晶状体,其中Ｍａｒｆａｎ 综合征２ 眼、钝挫性晶状体脱位７ 眼、确诊为单纯性晶状体脱位３ 眼、白内障囊外摘出术中晶状体脱入玻璃体内３ 眼进行晶状体摘出联合后房型人工晶状体缝线固定术。结果　术后视力在０．１ 以上者１３ 眼（８６．７％ ）,０．５ 以上者９眼（６０％ ）;主要手术并发症：前房少量出血、高眼压、虹膜炎性反应、玻璃体腔内出血,术后１～２ｗ ｋ 均得到控制。结论　此术式是一种安全有效、视力恢复满意的治疗方法,可获得好的临床效果。