异常增生的

Abstract］ objective to study the pathological features and histopathological type and differential diagnosis of hepatic focal nodular hyperplasia.methods the clinicopathological characteristics of 40 cases of fnh were studied.all were evaluted by use of paraffin embedded sections and he staining before light microcope observation.results there were 28 females and 12 males fnh patients whose age were from 16 to 62 years（median 41.3）,all alpha-fetoprotein was negative and had no hepatitis history.25 cases were classic type showed characteristic central stellate fibrotic scar,composed of fibrous connestive tissue and tortuous blood vessels.8 cases were telangiectic type,the left were mixed type and adenomatoid type.conclusion fnh is a reactive proliferation of hepatic cells to local blood vessel anomalies,it is not realy a tumor.its differential diagnosis includes hepatic adenomatous hyperplasia nodule,hepatic anaplasia nodular hyperplasia,fibrolamellar hepatocellular carcinoma and hepatocellular adenoma.

目的 探讨肝局灶性结节性增生的病理形态特点、组织分型及鉴别诊断。方法分析40例肝局灶性结节性增生的临床资料，并采用石蜡包埋he染色光镜下观察其组织学特点。结果 40例肝局灶性结节性增生患者中，女28例，男12例，年龄18~62岁，平均年龄41.3岁，所有病例术前均无肝炎病史，甲胎蛋白阴性，组织学上25例为经典型，有特征性的中央纤维瘢痕，由纤维结缔组织及扭曲血管组成。8例为毛细血管扩张型，其余为混合型及腺瘤样增生型。结论肝结节性增生是一种肝细胞对局部血管的异常反应性增生，并非真性肿瘤，主要与肝腺瘤样增生性结节、肝间变性结节状增生、肝纤维板层癌及肝细胞腺瘤鉴别。

Objective To study the origin and progress of myelodysplastic syndrome with hypoplasia.

目的 探讨低增生骨髓增生异常综合征的由来和发展。

The protein is a key cause of the over-production of the white blood cells that characterizes this form of CML.

这种蛋白质是白细胞异常增生的主要原因，而白细胞异常增生是慢性粒细胞白血病的一种表现。

The positive expressions of TGF-β 1 and α-SMA were measured with immunohistochemical method.

主要的病理改变是肝内细胞外基质的异常增生与沉淀。

Results: CK18 was not detected in normal and abnormal oral tissue sections. But in normal nonkeratinized mucosa, CK19 was detected in the basal cell layer dispersively. In epithelial dysplasia, CK19 was detected in the suprabasal cell layer and the number of CK19-positive cell layers was correlated with the dysplasia degree of epithelia. Furthermore, CK19 was detected in oral squamous cell carcinoma, especially in the poor-differentiated cancer cells.

结果：正常和异常的口腔粘膜均未检测到CK18；CK19可表达于正常非角化上皮的基底层细胞、异常增生上皮的基底上层细胞及口腔鳞状细胞癌中，阳性细胞数与上皮的异常增生程度及鳞癌的分化程度相关。

Methods 85 normal, hyperplastic, dysplastic and malignant oral epithelia were studied by immunohistochemistry.

用SP免疫组织化学染色法检查85例正常、单纯及异常增生的口腔上皮和口腔鳞癌中CD44v3和CD44v6的表达。

Objective:To establish a stable human dysplastic oral keritinocytes culture system in vitro and to offer a cell model for oral pre-cancer research.

目的 ：建立稳定的人口腔黏膜异常增生细胞(DysplasticOralKeratinocyte ，DOK )体外培养体系，为口腔癌前病变体外细胞模型的建立提供基础。

hemophagocytic syndrome is an abnormal systemic proliferation of histocyte lineage mediated by tc cells. it is confirmed that t cell receptor γ or β gene monoclonal rearrangements are present in some patients.

噬血细胞综合征是t细胞介导的组织细胞异常增生，部分病例已证实tcrγ或β基因的单克隆重排。

P16 gene is composed of two intervening sequences and three exons , and encodes p16 protein , which is the inhibiter of CDK4 and CDK6 . They can together prevent phosphorylation deactivation of pRB , and make the cell cycle blocked in G1 stage. P16 gene promoter region has a great of CpG islands , which can be methylated when some adverse factor appears , and so the genetic transcription of p16 can be inhibited , which leads to gene silencing, cell paraplasm, and tumor generate.

抑癌基因p16编码蛋白P16 ，是细胞周期蛋白CDK4和CDK6抑制剂，它阻止pRB磷酸化失活，使细胞周期阻滞于G1期。P16基因启动子区域富含CpG岛，当受到各种有害因素影响时，容易发生甲基化，从而抑制P16基因转录，导致基因沉默，细胞异常增生，导致肿瘤的发生[5]。

Methods The clinical characteristics and experimental data of 24 patients with MDS-RA and 59 cases with CAA were analysed.

比较24例骨髓异常增生综合征难治性贫血与59例慢性再生障碍性贫血的临床特点和实验室资料。

In the United States, chronic alcoholism and hepatitis C are the most common ones.

在美国，慢性酒精中毒，肝炎是最常见的。

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