18F-FDG PET/CT对非小细胞肺癌区域淋巴结诊断的假阴性与假阳性研究

目的探讨18^F-FDG PET／CT在检测非小细胞肺癌（NSCLC）区域淋巴结中出现假阴性和假阳性的因素。方法随机选择手术治疗的NSCLC患者48例，术前1周内行18^F—FDG PET／CT检查，同期行CT增强扫描，术后根据病理检查结果分析PET／CT诊断NSCLC区域淋巴结转移的假阴性与假阳性因素。结果48例患者共切除区域淋巴结313枚，转移淋巴结51枚，PET／CT结果7枚假阴性。8枚假阳性，阳性预测值和阴性预测值分别为85％，97％，高于CT（57％，94％；P=0．002，0．045）。3枚假阴性淋巴结内的癌灶较小；2枚淋巴结短径约为0．4mm，小于PET／CT的空间分辨率；2枚紧邻原发灶的淋巴结，图像无法区分而视为原发灶。8枚假阳性淋巴结为患者在原发病灶基础上并发不同程度的肺部疾病和淋巴结炎症，使其糖代谢率增高。结论假阳性出于（1）淋巴结的短径小于PET／CT的空间分辨率；（2）淋巴结内的小癌灶糖代谢率较低；（3）紧邻原发灶的淋巴结与原发灶无法区分。原发肿瘤合并肺部疾病是导致PET／CT出现假阳性的重要原因。     

Gastro-duodenal digestion products of the major peanut allergen Ara h 1 retain an allergenic potential

BACKGROUND: The process of gastro-duodenal digestion may play a role in determining the allergenic properties of food proteins. The sensitizing and allergenic potential of digestion products of highly degraded allergens, such as the major peanut allergen Ara h 1, is currently under debate. We evaluated the effect of in vitro gastro-duodenal digestion of Ara h 1 on T cell reactivity and basophil histamine release. METHODS: An in vitro model of gastro-duodenal digestion was used to investigate changes in the allergenic properties of Ara h 1 using in vitro assays monitoring T cell reactivity (proliferation, cytokine production) and histamine release of basophils from peanut allergic individuals. The digestion process was monitored using an SDS-PAGE gel. RESULTS: In vitro gastric digestion led to rapid degradation of Ara h 1 into small fragments M(r) L5600. Gastric digestion did not affect the ability of Ara h 1 to stimulate cellular proliferation. Gastro-duodenal digestion significantly reduced its ability to stimulate clonal expansion (P<0,05; Wilxocon's signed rank test). The Th-2 type cytokine polarization of T cells from peanut allergic donors (IFN-gamma/IL-13 ratio and IFN-gamma/IL-4 ratio of CFSE(low) CD4(+) T cells) remained unchanged regardless of the level of digestion. Histamine release of basophils from peanut allergic individuals was induced to the same extent by native Ara h 1 and its digestion products. CONCLUSION: Gastro-duodenal digestion fragments of Ara h 1 retain T cell stimulatory and IgE-binding and cross-linking properties of the intact protein.     

Highly resolved in vivo 1H NMR spectroscopy of the mouse brain at 9.4 T.

An efficient shim system and an optimized localization sequence were used to measure in vivo 1H NMR spectra from cerebral cortex, hippocampus, striatum, and cerebellum of C57BL/6 mice at 9.4 T. The combination of automatic first- and second-order shimming (FASTMAP) with strong custom-designed second-order shim coils (shim strength up to 0.04 mT/cm2) was crucial to achieve high spectral resolution (water line width of 11-14 Hz). Requirements for second-order shim strengths to compensate field inhomogeneities in the mouse brain at 9.4 T were assessed. The achieved spectral quality (resolution, S/N, water suppression, localization performance) allowed reliable quantification of 16 brain metabolites (LCModel analysis) from 5-10-microL brain volumes. Significant regional differences (up to 2-fold, P < 0.05) were found for all quantified metabolites but Asp, Glc, and Gln. In contrast, 1H NMR spectra measured from the striatum of C57BL/6, CBA, and CBA/BL6 mice revealed only small (<13%, P < 0.05) interstrain differences in Gln, Glu, Ins, Lac, NAAG, and PE. It is concluded that 1H NMR spectroscopy at 9.4 T can provide precise biochemical information from distinct regions of the mouse brain noninvasively that can be used for monitoring of disease progression and treatment as well as phenotyping in transgenic mice models.     

放疗化疗联合治疗局部晚期非小细胞肺癌43例

目的 探讨以顺铂为主的化疗方案加放疗对局部晚期非小细胞肺癌的疗效。方法 86例局部晚期非小细胞肺癌患随机分为治疗组及对照组各43例，放疗方案以CAP、EP、MVP或MOP，每人至少化疗两个周期，化疗后10～14天放射治疗，放疗采用^60Co外照射。结果 治疗组有效率83．7％，中位生存期14．5个月，对照组有效率67．4％，中位生存期10个月，两组不良反应为骨髓抑制、胃肠道反应。结论 以顺铂为主的化疗方案加放疗治疗局部晚期非小细胞肺癌的疗效较高，可提高肿瘤的局部控制率和延长生存期。     

氟对体外培养人牙乳头间充质细胞合成I型胶原的影响

目的:明确氟对人牙乳头细胞合成 I型胶原的影响。 方法:对人牙乳头细胞进行体外培养 ,分别给予0 .0、0 .2× 10 - 6、1.0× 10 - 6、5 .0× 10 - 6、2 5 .0× 10 - 6 g/ L 氟处理 ,采用免疫细胞化学方法染色 ,图象分析氟对细胞合成 I型胶原的影响。 结果:I型胶原在对照组和 4种氟浓度处理组细胞表达均为阳性。图象分析结果表明 ,4种氟浓度对体外培养的人牙乳头细胞合成 I型胶原量与对照组相比差异无统计学意义 (P>0 .0 5 )。结论:过量氟对牙本质基质 型胶原的影响可能不是通过影响成牙本质细胞内合成实现的     

用COEP方案治疗小细胞未分化肺癌的近期疗效

采用 COEP(CTX、VCR、VP—16、PDN)联合化疗方案治疗小细胞未分化肺癌50例,获 CR 5例(10%)、PR 28例(56%)、RR 33例(66%)。其中初治37例获 CR 2例(5.4%)PR 27例(73%)、RR 29例(78.4%);复治13例获 CR 3例(23.1%)、PR 1例(7.7%)、RR 4例(30.8%),疗效比较满意。     

Reelin expression is upregulated following ocular tissue injury

Purpose Reelin is important in the guidance of neuronal stem cells in the central nervous system during normal development. We wished to determine whether reelin is expressed in the retina and cornea after injury. Methods Mice underwent laceration of their retina as well as corneal epithelial debridement. The mice were sacrificed at 3 days, and eyes were fixed and stained for reelin expression and reelin messenger ribonucleic acid (mRNA). Results In normal eyes, reelin was expressed only at very low levels in the ganglion cell layer of the retina and the endothelial cell layer of the cornea. In injured eyes, there was marked expression in reelin immunoreactivity in the retina and cornea. Reelin gene expression was seen in the retina and cornea. Conclusions Reelin is expressed during normal retinogenesis. This study shows that reelin is also upregulated following injury to the retina and cornea. The expression of reelin following injury suggests that reelin may play an important role in regulating stem cell trafficking in neuronal and nonneuronal tissues following injury similar to its role in normal organogenesis. For consideration of publication in Graefe’s Archive for Clinical and Experimental Ophthalmology.     

Morphological and biochemical correlates of chemical induced injury in the lung

We have reviewed some of the factors which contribute to lung damage by various toxicants. These include disposition of the chemical, its metabolism, individual cell type susceptibility and the potential for the tissue to repair. We have discussed the use of biochemical parameters to measure the functional activity of individual cell types in order to predict the damage to specific cell types and concluded that careful morphological analysis of lung tissue is likely to provide a more sensitive and informative measure of specific cell type injury. However, in order to investigate the mechanism of toxicity of pulmonary toxicants it is essential to establish the primary biochemical event that leads to cell damage and morphological change. The importance of separating the relevant biochemical change(s) from the cascade of biochemical events associated with dead and dying cells and the reparative response of the lung is emphasised.This report results from a discussion sponsored and organised by the Advisory Subgroup in Toxicology (AST) of the European Science Foundation's Standing Committee for the European Medical Research Councils and held at the Medical Research Council Toxicology Unit, Carshalton, U. K. Those taking part were: W. N. Aldridge (AST; as above); J. Bignon (Unit for Research in Renal and Pulmonary Pathology, University of Paris, Creteil, France); P. H. Burri (Section of Developmental Biology, Institute of Anatomy, University of Berne, Switzerland); G. M. Cohen (as above); D. Dinsdale (MRC Toxicology Unit, Carshalton U. K.); P. Hedqvist (Dept. of Physiology, Karolinska Institute, Stockholm, Sweden); D. Henschler (AST; Dept. of Toxicology and Pharmacology, University of Wurzburg, FDR); G. J. Laurent (Biochemistry Unit, Cardiothoracic Institute, University of London, London, U. K.); R. Lauwerys (AST Industrial and Medical Toxicology Unit, University of Louvain, Brussels, Belgium); F. Lembeck (AST; Dept. for Experimental and Clinical Pharmacology, University of Graz, Austria); N. Lery (AST; Poison Control Centre, Lyon, France); P. Moldeus (Dept. of Forensic Medicine, Karolinska Institute, Stockholm, Sweden); B. Nemery (MRC Toxicology Unit, Carshalton, U. K.); A. Saria (Dept. for Experimental and Clinical Pharmacology, University of Graz, Austria); L. L. Smith (as above);B. Terracini (AST; Dept. of Pathology and Cancer Epidemiology, University of Turin, Italy)     

神经干细胞移植延缓失神经肌萎的作用机制

Objective To study the effect and mechanism of transplanting spinal fetal neural stem cells (NSCs) into the peripheral nerve for delaying muscle denervation atrophy. Methods Spinal. fetal NSCs were separated from spinal cord of enceinte 10 to 12 days SD rats, cultured and purified. After three passages, the formed NSC spheres were blew into single cell suspension ( 106/μl×5 μl) and transplanted into the distal part of the transected tibial nerve. 5 μl of cell culture medium was injected into the distal tibial nerve in the control group. Three and 5 months after the transplantation, the distal part of the tibial nerve and the triceps suraes were harvested and identified with specific markers, by means of indirect immunofluorescent staining to evaluate survival and differentiation of transplanted NSCs in the nerve, and to observe the neuromuscular junctions.Results Compare to the control group, atrophy of the triceps suraes muscle was less severe 3 and 5 months after NSCs transplantation. Postsynaptic membrane was also better preserved in NSCs transplanted group. Five months after NSCs transplantation, new synapses (neuromuscular junction) formed in the denervated muscle.Conclusion NSCs transplantation can delay atrophy denervated muscles. NSCs transplantation can not only maintain the structure of postsynaptic membrane, but also form new synapse with the denervated muscle.