Objective:To study the clinicopathological features of mixed epithelial and stromal tumor of the kidney(MESTK). Methods:Clinical and pathological characteristics of one case of MESTK was stu-died. Results:A case of MESTK which uncommonly occurred in a 16-year old adolescent male presented with dysuria and a large mass in the right renal region without a history of estrogen/progestogen treatment and/or obesity or urogenital surgery. Radiology revealed a large cystic/solid mass within the right kidney. Grossly, it was well demarcated and had a solid and cystic appearance on sectioning. Microscopically, the tumor was composed of a mixture of stromal and epithelial components. The epithelial component was composed of flat to columnar cells forming glands or tubules. The stromal components essentially consisted of bland, loosely packed spindle cells in an edematous and myxoid background. In some areas, there were smooth muscle cells forming bands and fascicles but no ovarian-type stroma was present. Immunohistochemical staining revealed that the epithelial components were positive for AE1/AE3 and focally positive for estrogen receptor(ER),progesterone receptor(PR), CD10 and Vimentin, whereas the stromal components were positive for ER, PR, Desmin and smooth muscle actin(SMA). Both epithelial and stromal components were negative for HMB-45, S-100,?-inhibin and WT-T. Five months after resection, the patient was well without evidence of recurrence. Conclusion:MESTK occurred in a pubertal male, as in the current case, supports the hypothesis that proliferation of remnants of the primitive mesenchyme in the kidney in situation of sex-steroid abnormity may play an important role in the pathogenesis of male MESTK.

BACKGROUND: Adipose-derived mesenchymal stem cells (ADMSCs) can improve the liver function of rats with liver failure, which illustrates the important research value in the field of tissue engineering and cell transplantation.OBJECTIVE: To evaluate the therapeutic potential of human ADMSCs in heart failure rats and to discuss the possible biological mechanisms involved.METHODS: Heart failure rats were randomized into model and ADMSCs groups, which were given normal saline or DAPI-labeled human ADMSCs (3.0×106) via the tail vein. At 1, 3, 7 days after transplantation, we detected the biochemical indexes for liver function in rats. At 3 days after transplantation, the serum levels of cytokines, such as tumor necrosis factor α and interleukin-10, were detected, the histomorphological changes in the liver were observed by hematoxylin-eosin staining, and the protein expression of proliferating cell nuclear antigen was detected by western blot. RESULTS AND CONCLUSION: We found that human ADMSCs could migrate to the liver and lung tissues in rats after the transplantation via the tail vein. At 1 and 3 days after transplantation, the levels of serum alanine aminotransferase and aspartate aminotransferase were significantly reduced in the ADMSCs group as compared with the model group (P< 0.05); furthermore, the secretion of tumor necrosis factor α and interleukin-10 was significantly suppressed at 3 days after cell transplantation (P < 0.05). The results of hematoxylin-eosin staining indicated a significant improvement in liver degeneration and necrosis. The expression of proliferating cell nuclear antigen protein in the ADMSCs group was significantly up-regulated compared with the model group. To conclude, human ADMSCs can inhibit the inflammatory reaction and up-regulate the expression of proliferating cell nuclear antigen, to promote the regeneration of liver cells and he recovery of liver function.

BACKGROUND:Recent studies have shown that adipose-derivedmesenchymal stem cells (ADMSCs) not only have multilineage differentiation potential, but also exert an important role in blood sugar balance and hormone production.OBJECTIVE:To observe the differentiation potential of human ADMSCs (hADMSCs) into functional islet-like cells and the therapeutic effect of hADMSCs transplantation in diabetic rats.METHODS:PDX-1 gene was transfected into hADMSCs by adenovirus. Cell differentiation and insulin secretion were identified and detected by dithizone staining and ELISA, respectively. Twenty male Sprague-Dawley rats were randomly divided into control group (n=4), diabetes group (n=8) and transplantation group (n=8). Rats in the latter two groups were subjected to making diabetic models by 65 mg/kg streptozotocin injection. Afterwards, rats in the transplantation group were given PDX-1 transfected ADMSCs via the tail vein.RESULTS AND CONCLUSION:At 15 days after transfection, the number of insulin positive cells and insulin secretion were both increased significantly (P < 0.05). Fasting glucose levels in the transplantation group decreased significantly (P < 0.05), while the body weight increased significantly (P < 0.05). In the diabetic group, the fasting glucose level still maintained at a high level, and the body weight of rats was significantly decreased. These results implicated that PDX-1 gene could induce hADMSCs differentiating into functional islet-like cells. PDX-1 transfected ADMSCs transplantation is effective in treating diabetic rats, but the mechanism needs further study.

Purpose To investigate the clinicopathologic characteristics of colorectal metastatic tumors. Methods Cases which were clinically diagnosed as metastatic tumors to the colorectum were retrieved from the data base of the Department of Pathology, Peking U-niversity Third Hospital. The clinicopathologic features were studied and immunohistochemical stains were performed on some of the ca-ses for differential diagnosis. Results Fifty three cases which showed intestinal wall involvement were studied. In 43. 4% (23/53) of them, only serosa/subserosa was involved and mucosal involvement was observed in 37. 7% (20/53) of the cases. Sigmoid colon and rectum were the most frequently involved intestinal segments (24/53, 45. 3%). Female reproductive system was the most common ori-gin of the metastatic tumors (33/53, 62. 3%), followed by the digestive system (15/53, 28. 3%). The most common histological type was ovarian serous carcinoma (22/53, 41. 5%). 96. 2% (51/53) of the metastatic tumors were centrally located at the serosa/subserosa or the muscular propria and prominent lymphovascular invasion was observed in 26. 4% (14/53) of the cases. In cases with mucosal involvement, 35% ( 7/20 ) had foci that were lack of desmoplastic reaction, 20% ( 4/20 ) exhibited in-situ growth and/or paradoxical maturation of tumor cells which led to misdiagnosis in 2 of the 17 pre-operative biopsies. Conclusions Metastatic carcino-ma in the colorectum can be highly informed by predominantly involving the serosa/subserosa or muscular propria and prominent lym-phovascular invasion. In-situ growth and paradoxical maturation of tumor cells in the mucosa are diagnostic pitfalls in pre-operative co-lonic biopsy and should be aware in practice.

Beijing ; Humans ; Internship and Residency ; Pathology, Clinical ; education

Colorectal Neoplasms ; genetics ; Humans ; Mass Screening ; Microsatellite Instability

Objective To observe the therapeutic effect of Qingxiang Concentrated Pill (QCP) on mammary gland hyperplasia (MGH) in rats. Methods Injection of estradiol were given to establish rat models of MGH and QCP was given QCP at the same time. Pathologic changes of mammary gland in rats were observed under light microscope. Changes of breast diameter, mammary gland volume and weight were measured; serum sex hormones levels, SOD activity and MDA content were also estimated. Results QCP could decrease the increased breast diameter, mammary gland volume and weight, reduce the numbers of mammary gland lobules and mammary acini and the diameter of acinar cavities. It could also decrease eatradiol level and MDA content in serum, inhibit the decrease of the coefficient of thymus and increase the serum progesterone level. Conclusion QCP can regulate sex hormone levels, inhibit lipid peroxidation and relieve the pathologic changes of mammary gland in MGH rats.

In mammalian retina,Müller cells are dominating macroglial cells and span the entire retina.These cells perform a variety of physiological roles to maitain the normal function of retina.However,Müller cells become ‘reactivity'in response to every pathological changes in the retina.Reactive Müller cells play an important role in retinal damage and repair.Reactive gliosis is a complex process that is considered to represent a cellular response to protect the retina from further damage and to promote its repair following pathological insult in the early stage of retina injury.Reactive Müller cells protect the tissue and preserve tissue function by releasing neurotrophic factors,and may contribute to retinal regeneration by generating neural progenitor.However,continued proliferation of Müller cells can also lead to cell dysfunction and damage of photoreceptors and neurons.What's more,Müller cell gliosis may result in the formation of glial scars,which can inhibit retinal remodeling and reprograming of the injured retina.A better understanding of the role and mechanism of Müller cells in retinopathy is essential for the efficient therapeutic strategies of retina diseases.

Objective: To investigate the expression of co-stimulatory molecule CD86 and inducible costimulator(ICOS) in the intestinal mucosa of Crohn disease (CD) and to exlpore its pathologic significance. Methods: Expression of co-stimulator CD86 and ICOS was examined by immunohistoehemistry on paraffin embedded tissue from patients with CD (30 cases) and normal controls (20 cases). The subsets of lamina propria mononuclear cells (LPMC) were also analysed via immunostaining for CD4, CD8 and CD20. Results: Increased amount of CD86 or ICOS positive LPMC was observed in the lesional area of CD when compared with the essentially normal area of CD and normal controls (q = 9. 23 ,P ＜0. 01 and q =5. 46 ,P＜0. 01). In addition, the expression of CD86 or ICOS was higher in intestinal epithelium of CD than that in normal controls (H = 24. 93, P＜0. 01 and H = 4. 66, P＜0. 01 ) , whereas no significant difference was seen between the diseased and the essentially normal area of CD. The amount of CD4 or CD8 positive lymphocytes in lamina propria, epithelium and small vascular walls was also significantly increased in CD than that in normal controls (P＜0. 05 or P＜0. 01). Conclusion: Increased amount of CD86 or ICOS positive LPMC and enterocytes in CD suggests that co-stimulatory molecules may play a role in the pathogenesis of CD. The enterocytes may act as non-specific antigen presenting cells in the process of cellular immunity activation in CD.

ObjectiveTo investigate the expression of miR-155 in whole blood of patients with breast cancer and explore the possibility of miR-155 in whole blood as a marker of beast cancer. Methods65 cases (breast cancer:47 cases, non-breast cancer:18 cases) in Thyroid and Breast Surgery Department of No.1 People's Hospital of Huai'an from Dec 2010 to Apr 2011 were enrolled according to the selected criteria.Two milliliters anticoagulant blood were sampled to isolate total RNA.The expression level of miR-155 in whole blood was measured by real-time quantitative polymerase chain reaction (real-time qPCR)analysis.The relationship between the expression level of miR-155 in whole blood and the clinical pathological fearutres was analyzed.ResultsThe expression level of miR-155 in breast cancer patients was up-regulated compared with that in non-breast cancer patients(P ＜ 0.05).The expression level of miR-155 in patients with positive lymph nodes was up-regulated compared with that in patients with negative lymph nodes( P ＜ 0.05).The expression level of miR-155 in stage Ⅲ breast cancer was up-regulated compared with that in stage Ⅰ & Ⅱ breast cancer( P ＜ 0.05 ).The expression level of miR-155 in patients with positive ER and PR was down-regulated compared with that in patients with negative ER and PR breast cancer.Conclusion The study demonstrates that the expression of miR-155 in whole blood is related to clinical pathological features of patients with breast cancer and can be used as a potential marker of breast cancer.