Influence of Qingdai Compound Capsule on the expression of c-myc in psoriatic keratinocytes) on the expression of c-myc in psoriatic keratinocytes

In this immunohistochemical study, the authors detected the expression of c-myc in keratinocytes (ECK) from 30 psoriatics before and after Qingdai Compound Capsule (QDCC) treatment and 12 normal subjects for control. The results showed that the ECK of patients before treatment was significantly higher than that in the normal control group, and its level was correlated with histopathological changes of affected skin. After treatment the ECK was normalized. It is believed that QDCC could decrease the ECK in psoriatics and this effect was probably mediated by inhibiting c-myc expression. This study provided an experimental evidence for the application of QDCC in treating psoriasis.     

医技人员血源性疾病感染情况调查

医务人员的医院内感染逐渐被人们所关注，其中血源性疾病的感染更应引起大家的重视。为了了解医务人员中医师、检验人员的医院感染发生情况，笔者对某中心医院的医师和检验人员的2002年度体检结果进行了统计分析，现报告如下。     

手助腹腔镜肝部分切除术治疗原发性肝癌

目的 探讨手助腹腔镜肝部分切除术治疗原发性肝癌的方法和应用价值。方法 经临床筛选的第Ⅱ、Ⅲ、Ⅵ段或边缘型的原发性肝癌6例，在腹腔镜辅助下．应用手助器、超声刀、切割器等特殊器械进行腹腔镜下肝癌切除术。结果 6例患者均成功完成手术，包括肝Ⅱ、Ⅲ段切除，Ⅵ段切除及非规则性肝段切除术，手术时间80～130min，术后住院6～9d，手术出血150～700ml，无中转开腹手术，无并发症。术后随访6～15个月，2例分别于手术后3和4个月肝内复发，其余4例随访至今无复发。结论 在经过临床选择的病例中，手助腹腔镜下作肝部分切除术治疗原发性肝癌是安全、可行的手术方式。     

磨损微粒诱导的局部生物学反应

人工髋关节置换失败的主要原因是假体的无菌性松动。研究表明 ,这和假体长期磨损产生的微粒作用于周围的巨噬细胞而诱发的生物学反应有关。磨损微粒激活假体周围组织细胞释放前炎症介质 ,诱导破骨细胞的活化和分化 ,引发假体周围的骨溶解。充分地认识这个过程 ,对减少人工关节无菌性松动 ,延长假体使用寿命具有重要意义。     

Hybrid tumours of the salivary glands. A report of two cases involving the palate and a review of the literature

Hybrid tumours are very rare salivary gland lesions composed of two or more different tumoural entities in a single neoplasm that arise within a definite topographical region. In most cases adenoid cystic carcinoma has been the predominant component in these lesions. In this study we describe two patients with hybrid tumours located in the palate, one in a 49-year-old woman and one in a 71-year-old man. The first case involved adenoid cystic carcinoma and mucoepidermoid carcinoma, and the patient in the second case exhibited adenoid cystic carcinoma and epithelial-myoepithelial carcinoma. Both patients were treated with surgery and radiotherapy, and there has been no evidence of recurrence after 13 and 36 months of follow-up, respectively. The recognition of the histologic component with the higher grade of malignancy in every case of hybrid tumour of the salivary glands is a necessary step to determine the biological behaviour and, consequently, to determine the proper therapeutic approach.     

Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.