Screening of human anti-TNF-alpha scFv from large phage library

AIM: To clone human anti-TNF-alpha scFv from large phage antibody library. METHODS: Panning of large phage library against TNF-alpha was conducted to select specific antibodies. The antigen binding activity and DNA sequence were determined and analyzed by ELISA, restriction enzyme map. RESULTS: After 4 rounds of panning, 62 positive clones were obtained and 27 clones had specific binding ability to TNF-alpha. DNA fingerprinting of the 27 clones showed 7 different stripes indicated 7 different positive clones. 5 of the 7 clones expressed soluble anti-TNF-alpha activity. DNA sequence analysis showed that the variable regions of these scFvs belonged to different subgroups. CONCLUSION: Human TNF-alpha scFv have been successfully obtained from large phage antibody library.     

The critical role of ocular-infiltrating macrophages in the development of choroidal neovascularization

Choroidal neovascularization (CNV) is directly related to visual loss in some eye diseases, such as age-related macular degeneration. Although several human histological studies have suggested the participation of macrophages in CNV formation, the precise mechanisms are still not fully understood. In this study, we elucidated the role of ocular-infiltrating macrophages in experimental CNV using CCR2 knockout (KO) mice, wild-type mice, and C57BL/6 (B6) mice. CCR2 is the receptor of monocyte chemoattractant protein-1, and the number of infiltrating macrophage and the area of CNV were significantly reduced in CCR2 KO mice. Enriched ocular-infiltrating macrophages from B6 mice actually showed angiogenic ability in a dorsal air sac assay. Moreover, their expression of class II, CD40, B7-1 and B7-2 molecules, and the mRNA for potential angiogenic factors, such as vascular endothelial growth factor, basic fibroblast growth factor, and tumor necrosis factor alpha, was also observed. Collectively, we conclude that ocular-infiltrating macrophages play an important role in CNV generation.     

单侧外周伤害性刺激诱发大鼠脊髓中转录因子CREB的双侧磷酸化(英文)

c AMP反应成分结合蛋白 (c AMP response elem ent-binding protein,CREB)是一种转录因子 ,它在磷酸化之后可调节靶基因的转录。 CREB在 13 3位置的丝氨酸的磷酸化 ,与脊髓中伤害性传入的处理有关 ,本文作者等用特殊抗体对此进行了免疫细胞化学研究。在正常大鼠 ,虽然几乎所有脊髓神经元的核中都可见 CREB的轻度着色 ,但磷酸化的 CREB仅见于双侧腰段脊髓的 ～ 层 (75± 15 vs60± 18)和 层 (9± 3 )。用福尔马林注射引起一侧后脚掌出现炎症时 ,可在双侧腰段脊髓看到磷酸化CREB细胞核的快速 (小于 5 min)和节段性的显著增多 ;它们主要分布在双侧背角表层 ～ 层 (2 5 4± 2 0 vs 2 62± 2 3 )、 层(115± 13 )和双侧 ～ 层 (3 46± 2 0 vs3 2 8± 2 6) ;而在对照和炎症组大鼠的胸段脊髓中均未见磷酸化 CREB的增加。在注射CFA诱发一侧炎症或切断一侧坐骨神经的实验组大鼠 ,也可看到至少延续到第三天的强而双侧性的 CREB的磷酸化。这种由一侧后肢伤害性传入引致腰段脊髓中镜像式双侧 CREB磷酸化的出现 ,与一般看到的损伤传入只在同侧脊髓背角引起某些神经化学改变的结果不同 ,可能是人神经损伤后或在实验动物中出现对侧镜像式疼痛过敏现象的基础     

盲人智能探路手杖的研究

本文介绍了盲人智能探路手杖的研究.该系统由单片机控制,采用两只超声波传感器的探测模式,对盲人行进路上的路况进行探测和分析,并针对不同的路况发出相应的提示信息,以达到辅助盲人安全行走的目的.     

妊娠合并登革热35例临床分析

目的 探讨登革热对妊娠的影响。方法 对35例妊娠合并登革热进行回顾性分析。结果 35例患有27例出现不正常分娩及产后大出血,有22例出现流产、死胎、早产及畸胎。结论 妊娠合并登革热在妊娠早期可出现流产或死胎,中期可引起早产,晚期可出现产后大出血。     

A retrospective study of neck rejuvenation using a noninsulated microneedle radiofrequency in Chinese subjects

Lasers in Medical Science - Large-scale long-term retrospective study of noninsulated microneedle radiofrequency treatment on neck rejuvenation is lacking. We conducted a 3-year retrospective...     

Microiontophoresis of cocaine, desipramine, sulpiride, methysergide, and naloxone in habenula and parafasciculus

The effects of microiontophoretically applied cocaine, desipramine (DES), sulpiride (SUL), methysergide (METH), and naloxone (NAL) on the responses of physiologically identified single neurons in the habenula (Hab) and parafasciculus thalami nucleus (PF) were examined in rats. Three cell types were identified in both nuclei on the basis of the responses obtained following noxious stimulation that were classified as "nociceptive-on," "nociceptive-off," and "nonnociceptive" cells. Administration of cocaine generally resulted in a decrease in the firing rate of nociceptive-on and nonnociceptive neurons in both Hab and PF. In contrast, cocaine generally induced an excitation in the baseline firing of the nociceptive-off cells. Cocaine application concomitant with noxious stimulation prevented the evoked responses of the nociceptive-on and the nociceptive-off cells. DES, when applied alone, was found to induce excitation in neuronal discharge of all three cell types in both sites. Combined application of cocaine with DES resulted in no observable change in discharge frequency for the nociceptive-on and nonnociceptive cells, while inducing an additive excitatory effect on the nociceptive-off cells. SUL, in contrast, induced no observable effect on baseline firing when given alone, yet consistently antagonized cocaine-induced effects on all three cell types. Finally, METH and NAL induced no effects on baseline firing or cocaine-induced modifications in neuronal discharge frequency.     

Determination of trace selenium in human body by anodic stripping voltammetry at gold-disc electrode

Summary For determination of trace Se we used high-pressure wet digester to pretreat the specimens obtained from the human body. This method is very effective in preventing loss of Se by volatilization which often occurs in the sample pretreatment. We studied the method of using anodic stripping voltammetry at gold-disc electrode to measure the trace Se present in the human body and found it to be the optimal procedure. The detection limitation was about 2x10⁻⁸ g/L, the recovery rate of Se about 96.6±6,7 % , and the coefficient of variation CV = 7.0%.     

氯丙嗪预处理对冷保存肝脏缺血性损伤的影响

目的：本实验旨在探讨利用氯丙嗪预处理供体,观察对冷保存过程中供体肝脏缺血性损伤的保护作用及其作用机制。方法：切取大鼠肝脏在0℃Euro-Collins液中冷保存,每隔2小时切取肝脏标本测定GSH,ATP含量。结果：实验结果表明,随着肝脏冷保存时间的延长,对照组肝组织内的GSH及ATP含量迅速下降。实验组肝组织内的GSH和ATP含量下降速度明显缓慢。结论：本文认为,氯丙嗪预处理供体有改善肝组织在冷保存过程中的缺血性损伤作用。其主要作用机制可能是由于氯丙嗪作为Ca^ 通道的阻滞剂,降低肝细胞胞浆内Ca^ 浓度,减少ATP的消耗和氧自由基的生成,维持肝组织内GSH和ATP的含量,从而减轻了肝脏在冷保存过程中的缺血性损伤。     

Novel stop-gain RNF170 variation detected in a Chinese family with adolescent-onset hereditary spastic paraplegia

Hereditary spastic paraplegia (HSP) is a heterogeneous group of inherited neurodegenerative disease characterized by progressive lower limb spasticity. Recent studies revealed that biallelic variants in RNF170 gene cause autosomal recessive complicated HSP with infancy onset. Here, we report an adolescent-onset HSP patient from a consanguineous Chinese family, with lower extremity stiffness, spastic gait, and unstable straight-line walking as the main manifestations. Whole-exome sequencing identifies a novel RNF170 mutation c.190C>T (p.R64*), which co-segregates with the disease in this pedigree. Functional analysis, including quantitative real-time PCR (RT-qPCR) and Western blot, indicates that both the mRNA and protein levels of mutant RNF170 are significantly reduced, which confirms the loss-of-function mechanism. Our study expands the spectrum of RNF170-associated HSP, while the RNF170 protein-involved degradation of the inositol 1,4,5-trisphosphate receptor in neurodegenerative motor neuron disorders deserves further investigation.