口腔扁平苔藓浸润细胞免疫组化分析

为探讨免疫应答在扁平苔藓发病过程中的作用及相互关系，本研究中应用ABC技术，用T3、T4、T8、IgG单抗及S－100蛋白标记病损已浸润细胞。结果表明：病损区以细胞免疫为主，淋巴细胞数量与上皮钉突的增殖程度呈正相关；病损区中郎罕氏细胞明显偏高；基底膜区损害与T细胞数量呈正相关；IgG阳性细胞散在分布于病损区，其阳性物质在基底膜区沉积。提示该疾病以细胞免疫为主，同时有体液免疫应答的参与。     

熔附条件对牙科复合树脂中SP1 SiO_2表面结构及形态的影响

目的:研究熔附温度和熔附时间对多微孔纳米二氧化硅粒子(SP1 SiO2)表面结构及形态的影响。方法:将SP1SiO2以250℃/h的升温速度分别升至500、650、800、950、1100℃,并分别保持10、30min和3h制作试样,进行表面结构及形态测试。结果:随烧结温度的增高和时间的延长,SP1 SiO2颗粒表面的Si-OH键特征峰值逐渐减弱,条件为950℃、10min和30min,650℃、3h时完全消失;随着熔附温度的升高和熔附时间的延长颗粒增大、粒度分布变窄。结论:熔附温度和熔附时间影响SP1 SiO2颗粒表面的Si-OH含量和颗粒大小、粒度分布。     

Miniature specimens for fracture toughness evaluation of dental resin composites

Objective

Millimeter-scale (“miniature”) specimens enable in-situ evaluation of mechanical properties of engineering materials at reduced cost. Here three such specimens for measuring fracture toughness (K_C) are developed and implemented to new dental materials. The latter include concurrent methacrylate-based and new ether-based resin composites designed to reduce polymerization stress and enhance service life in restored teeth.

A comparison of enamelin and amelogenin expression in developing mouse molars

Amelogenin and enamelin are structural proteins in the enamel matrix of developing teeth. The temporal and spatial patterns of enamelin expression in developing mouse molars have not been characterized, while controversy remains with respect to amelogenin expression by odontoblasts and cementoblasts. Here we report the results of in situ hybridization analyses of amelogenin and enamelin expression in mouse molars from postnatal days 1, 2, 3, 7, 9, 14, and 21. Amelogenin and enamelin mRNA in maxillary first molars was first observed in pre-ameloblasts on the cusp slopes at day 2. The onsets of amelogenin and enamelin expression were approximately synchronous with the initial accumulation of predentin matrix. Both proteins were expressed by ameloblasts throughout the secretory, transition, and early maturation stages. Enamelin expression terminated in maturation stage ameloblasts on day 9, while amelogenin expression is still detected in maturation stage ameloblasts on day 14. No amelogenin expression was observed in day 21 mouse molars. Amelogenin and enamelin RNA messages were restricted to ameloblasts. No expression was observed in pulp, bone, or along the developing root. We conclude that amelogenin and enamelin are enamel-specific and do not directly participate in the formation of dentin or cementum in developing mouse molars.     

术中 X-线定位在神经内镜切除甲介型蝶窦垂体瘤手术中的应用简

目的探讨术中x-线定位在经神经内镜下甲介型蝶窦垂体瘤手术的应用。方法回顾性分析6例甲介型蝶窦垂体瘤病人的临床资料,均采用神经内镜下垂体瘤切除结合术中X-线定位方法。结果术中X-线定位准确4例;2例发生纵向偏差,均纠正。肿瘤全切除5例,次全切除1例。术后激素水平正常,视力视野改善。出现暂时性尿崩1例,治疗后痊愈。无脑脊液鼻漏、垂体功能低下、蝶窦炎发生,无死亡病例。6例病人随访3年,均无复发。结论神经内镜技术结合术中X-线定位是一种治疗甲介型蝶窦垂体瘤的安全、有效方法。     

Expression Characteristics of KAI1 and Vascular Endothelial Growth Factor and Their Diagnostic Value for Hepatocellular Carcinoma

Background/Aims

We tried to investigate the expression characteristics of KAI1, a suppressor of wide-spectrum tumor metastasis, and vascular endothelial growth factor (VEGF), the most common angiogenesis factor, and then to analyze their diagnostic value for hepatocellular carcinoma (HCC).

Methods

The protein and mRNA expression levels of KAI1 or VEGF in HCC tissues and in self-controlled para-carcinoma tissues were analyzed by Western blot and real-time polymerase chain reaction, respectively. Serum levels of KAI1 and VEGF in the patients with HCC, benign liver disease or in healthy controls were quantitatively detected by enzyme-linked immunosorbent assay.

Results

The expression level of KAI1 was downregulated, while the expression level of VEGF was upregulated in the tissues or serum of the patients with HCC. The expression level of serum KAI1 in HCC patients was correlated with TNM staging, intrahepatic metastasis, lymph node or peritoneal metastasis, and portal vein thrombus. In addition to the factors that were correlated with KAI1 expression, VEGF expression was also closely related to the α-fetoprotein level of the patients. The area under the receiver operating characteristic curve for the diagnosis of HCC was 0.907 for KAI1 and 0.779 for VEGF. The sensitivity of serum KAI1 levels in the diagnosis of HCC was 86.96%; the accuracy was 83.06%, while the sensitivity, the accuracy and the negative predictive value were improved to 91.86%, 84.68%, and 78.79% according to the combined detection of KAI1 and VEGF, respectively.

Conclusions

A combined detection of KAI1 and VEGF may greatly improve the efficiency of diagnosis and form a reliable panel of diagnostic markers for HCC.     

Presumed Mycobacteriosis in Laboratory Zebra Finch (Taeniopygia guttata)

Husbandry staff noticed a research-naïve, young-adult, female finch tossing its head back intermittently. A second finch exhibiting similar signs was reported a few days later. Postmortem necropsy and histopathology with hematoxylin and eosin and acid-fast staining on the first finch revealed the presence of acid-fast organisms in several organs. After presumptive diagnosis of mycobacteriosis, all remaining finches housed in the same room as the first underwent necropsy and histology. Three additional finches were positive for Mycobacterium-like acid-fast organisms. Incidental findings of megabacteriosis were noted histopathologically on 2 other finches.Abbreviation: MAC, Mycobacterium avium complexMycobacteriosis has a worldwide distribution and is found often in free-living birds, poultry, and wild birds. Several natural cases of mycobacteriosis have occurred in pet birds, including canaries (Spinus cucullatus), Eurasian goldfinches (Carduelis carduelis), and Zebra finches (Taeniopygia guttata).⁶ Reports regarding cases of mycobacteriosis in the laboratory animal research setting are scarce. The most common agents of avian mycobacteriosis are Mycobacterium avium intracellulare, one of the group of bacteria known as Mycobacterium avium complex (MAC), and Mycobacterium genavense, a known cause of mycobacteriosis in birds and mammals.^1,5,9-11 In addition, immunocompromised humans can be infected with MAC.^3,6,10 Mycobacteria are saprophytic, aerobic, and common in soil and the environment. These organisms can be transmitted by ingestion of soil or cage litter contaminated by fecal matter from infected birds.^1,2 The most common clinical signs in affected birds are depression, lethargy, and feather erection or fluffing, as are typical for most sick birds.^9,11 Neurologic signs, if they occur, can include imbalance and the inability to walk or fly normally.⁹     

Serum levels of sclerostin,Dickkopf-1, and secreted frizzled-related protein-4 are not changed in individuals with high bone mass causing mutations in LRP5

Summary

We compared circulating levels of Wnt inhibitors among patients with high bone mass mutations in LRP5, unaffected kindred, and unrelated normal controls. Inhibitors were unchanged in affected and unaffected kindred. We saw no meaningful differences between controls and affected individuals. LRP5 signaling may not influence circulating levels of these inhibitors.

Introduction

It is thought that gain-of-function mutations in LRP5 result in high bone mass syndromes because these allelic variants confer resistance to the actions of endogenous inhibitors of Wnt signaling. We therefore attempted to determine if circulating levels of Wnt inhibitors are altered in patients with gain-of-function mutations in LRP5.

Methods

This is a cross-sectional study in a university research center. Serum was collected from consented volunteers known to have either the G171V or N198S gain-of-function mutations in LRP5, kindred members affected with either mutation, unrelated kindred, and unrelated normal age-matched controls. BMD was provided or measured on site.

Results

There were no significant differences found in the serum levels of sclerostin (SOST), Dickkopf-1 (Dkk-1), or secreted frizzled-related protein-4 (SFRP-4) in affected vs. unaffected individuals from different kindreds or when compared to age-matched unrelated normal individuals. Mean serum SOST values in affected and unaffected kindred members and unrelated normal controls were 52.7?±?6.1, 36.5?±?9.6, and 54.8?±?5.4, respectively. For Dkk-1, the values were 25.9?±?3.4, 25.7?±?3.0, and 17.3?±?2.3 and for SFRP-4, 38.1?±?2.3, 39.8?±?3.6, and 28.5?±?1.7. Serum levels of RANKL and osteoprotegerin (OPG) were not different in the three groups.

Conclusions

Circulating levels of endogenous Wnt inhibitors do not change in patients with gain-of-function mutations in LRP5 including Dkk1, which is suppressed by Wnt signaling. It may be that circulating levels of Wnt inhibitors do not reflect changes in target tissues. It is also possible that other mechanisms besides or in addition to resistance in Wnt inhibitors explains the skeletal effects of these mutations.