Background and purpose:Parotid gland is rich in fat and has obvious contrast with bone and muscle in CT image.The preoperative examination of CT could help to evaluate the scale of tumor invasion and the relationship between tumor and normal tissues so that the proper therapy could be properly designed.The purpose of this study was to evaluate the roles of computer tomography(CT)in differential diagnosis of benign and malignant parotid tumors and to improve the diagnostic accuracy.Methods:CT images of 17 patients with benign parotid tumors and 15 patients with malignant parotid tumors proved by pathology were analyzed retrospectively.All patients underwent CT contrast-enhanced examination preoperatively.Images of all patients were retrospectively reviewed by two experienced radiologists in the diagnosis of head and neck tumors.Results:14 of 17 cases of benign tumors had round shapes and 9 of 15 cases of malignant tumors exhibited lobular or irregular masses(P

Purpose:To investigate the values of three newer contrast enhanced MRI sequences including gadolinium-enhanced FLAIR MRI(CE FLAIR), dynamic contrast-enhanced MRI (DCE MRI) and perfusion- weighted MRI(PWI) by comparing their advantages and disadvantages respectively in the diagnosis of intracranial tumors. Methods:43 patients with intracranial tumors underwent DCE MRI, CE FLAIR and PWI respectively. The gadolinium-enhanced FLAIR, dynamic enhanced MR and perfusion-weighted MR images were evaluated independently by two radiologists for the number of examinations with one or more enhancing lesions, the number and location of enhancing lesions per examination, the detectability for different lesions in different locations, size and extent of the lesions. Results:Perfusion-weighted MR images showed poor quality and could not give a diagnosis in 5 of 43 cases because of heavy susceptibility artifacts. There were 47 lesions in the 38 cases. However, 41 lesions were found on CE FLAIR MR images and 42 on DCE MRI and 45 on PWI. 3 lesions(2 located in the subcortical area and 1 in paraventricle) were only revealed on the CE FLAIR images. 4 lesions in the basal ganglia area were only found on dynamic enhanced images. 7 lesions in the cerebral hemisphere were only found on perfusion-weighted images. So there were significant differences in revealing lesions of different locations with the three MR modalities(P

Objective To observe whether bone marrow mesenchymal stem cells (MSCs) can promote the repair of IgA nephropathy and to explore its possible mechanism. Methods Sprague-Dawley rats were randomly divided into three groups which were MSCs injection group, normal saline(NS) infusion group and healthy control group. IgA nephropathy model was established by the improving method with BSA +SEB +CCl4 in former two groups. MSCs of SD rats were continuously cultured in vitro and identified with specific surface antigens by flow cytometry and osteogenic and adipogenic differentiation. MSCs were labeled with bromodeoxyuridine (BrdU) in vitro before transplanted. At 1st and 4th week after MSCs injection, the changes of body weight, urine protein, renal function, histopathology and IgA immunofluorescence were observed. MCP-1, TGF-β1 in urine were detected by ELISA. The expression of MCP-1, TGF-β1 in kidney were examined by RT-PCR. The cytokines and BrdU labeled MSCs were detected by immunohistochemistry to observe the disposition in kidney. Results At the end of the first week of MSCs transplantation, MSCs group urine protein (36.86±4.78) mg/24 h, serum creatinine (53.50±6.28) μmol/L, and the NS group urine protein (66.98±5.86) mg/24 h, serum creatinine (82.50±8.36) μmol/L, the differences between two groups were significant (P<0.05). At the same time, the content of MCP-1, TGF-β1 in urine and expression in renal tissue of MSCs group were obviously less than those of NS group (P <0.05). At the end of the 4th week, the body weight, histopatholngy, IgA immunofluorescence of MSCs group were remarkably improved as compared with those of NS group. The content of MCP-1, TGF-β1 in urine and expression in renal tissue, and renal pathological change in MSCs group had no significant differences as compared with those of healthy control group. As the time passed, the disposition of BrdU-labeled MSCs in kidney was taper. Conclusions MSCs injection contributes to renal repair in rat IgA nephropathy. The mechanism may partly depend on adjusting the excretion of cytokines in renal microenvironment and/or other functions rather than completely depend on their differentiation to renal cells.

AIM: To observe the growthinhibiting cell cycle-modifying and apoptosis-inducing effects of satraplatin on human ovarian carcinoma cell line A2780, and to explore its possible mechanism. METHODS: The effect of satraplatin on A2780 cells proliferation was determined using MTT, and the change in cell cycle was analyzed using PI staining. Morphologic change was visualized by fluorescence and electron microscopy. AnnexinV-FITC/PI staining multiparameter flow cytometry and immuno- histochemical TUNEL assay were used to detect apoptotic cells. The activity of caspase-3 and the effect of pan-caspase inhibitor on cell viability were measured as well. RESULTS: The growthinhibiting and apoptosis-inducing effects of satraplatin were dose-dependent and similar to those of cisplatin. Satraplatin mainly caused A2780 cell accumulation in S phase accompanied by minor accumulation in G2/M phase. Cells treated with satraplatin exhibited typical morphology of apoptosis. Satraplatin-induced increase in caspase-3 activity of A2780 cells was concentration-dependent. The viability of A2780 cells was affected by pan-caspase inhibitor z-VAD-fmk in a dose-dependent manner under certain concentration of z-VAD-fmk. CONCLUSION: Satraplatin-induced apoptosis in A2780 in vitro was observed. Caspase-dependent and independent pathways were involved in apoptosis induced by satraplatin, and the latter included caspase-3 dependent and non-caspase-3 dependent pathways.

The combined teaching method of case-based learning and W2 H2 thinking-type learning was used in the comparative morphology experiment teaching.The teaching method can further strengthen the reform of the compar-ative morphology experiment teaching, and improve the quality of practice teaching.

0.05). Four lesions were only revealed on CE FLAIR whereas 7 lesions were only found on postcontrast T_1WI. Enhancing lesions located in cerebral hemisphere or the forth ventricle was revealed much more on T_1WI than that on CE FLAIR. However, postcontrast fast FLAIR images may be useful in detecting superficial abnormalities and those located in sulcus or lateral ventricle. The enhancement degree of enhanced T_1WI was much more intense than that of CE FLAIR(P0.05) and statistical significance in GWC, CNR and CER(P

Through the addition of discussion course associated with judicial expertise during the pre medical education, integration of true and typical forensic pathological cases into basic medical theory and experimental education, further addition of optional course of forensic medicine,and guiding the medical students applying the scientifically training projects about forensic pathology, students may improve their learning interesting and clinical thought, and are made early warning and increase the abilities of preventing and dealing with the suddenly medical tangles in the future, at the same time, the medical teachers also increase their professional levels and teaching qualities.These benefit the growing up of high quality medical doctors, decrease and even prevent the happening of medical tangles.

Objective To explore the significance of MYCN gene amplification in children with neuroblastic tumors(NT).Methods The clinicopathological data of 154 cases with NT were reviewed,including general data, classification of pathology,clinical stage and prognosis.MYCN gene amplification was detected by fluorescence in situ hybridization(FISH) and its relationship between pathological characteristics and prognostic significance was analyzed.Results There was 154 cases of NT aged 1 day to 11 years,with a mean age of 26.1 months,and the median age of 20.5 months.Male and female ratio was 1.48 : 1.00.According to International Neuroblastoma Staging System (INSS) ,20 cases were of stage Ⅰ (13.0％) ,23 cases of stage Ⅱ (14.9％) ,43 cases of stage Ⅲ (27.9％) ,64 cases of stage Ⅳ(41.6％) and 4 cases of Ⅳs (2.6％).There were 72 cases(46.8％) with favorable histology,and 82 cases(53.2％) with unfavorable histology.MYCN amplification was found in 20 cases (13.0％) and the signal ratio of MYCN and chromosome 2 (CEP2) was 4.08-43.29.One hundred and thirty-four cases of MYCN non-amplification included MYCN gain in 91 cases(68.0％) ,MYCN negative in 43 cases(32.0％).MYCN expression showed the significant differences in ages, neuroblastoma type, international neuroblastoma pathology classification (INPC), mitosis karyorrhexis index (MKI), and clinical stages (all P ＜ 0.05).No significant difference was found in gender(P ＞ 0.05).Of 20 MYCN amplification cases,4 cases (20.0％) survived and 16 cases (80.0％) died,and the overall survival rate was 20.0％ (4/20 cases) ,with survival time was (17.10 ± 2.24) months;of 134 MYCN non-amplification cases,96 cases (71.6％) survived and 38 cases (28.4％) died, with survival time of (28.71 ± 1.28)months.Survival analysis showed the cases with MYCN amplification had worse prognosis (x2 =19.596, P ＜ 0.05).Conclusions Patients with MYCN amplification had poorer prognosis and lower incidence of MYCN amplification of pediatric NT was found in China.

Purpose To investigate the histopathological features of cystic lung diseases ( CLD) , and to discuss the timing of clinical interventions. Methods HE and immunohistochemical staining were performed and reviewed in 125 cases of CLD. Results 125 ca-ses of CLD aged from birth to 11 years and 6 month, with an average age of 23. 0 months, median age 15 months, of which 60 cases were less than 1 year (48. 0%). 75 cases were male and 50 cases female, with male to female ratio of 1. 5 ∶ 1. Grossly, 50 cases showed single or multiple cysts with the size 0. 5 ~8. 0 cm in diameter, which did not communicate with bronchial cavity. 18 cases showed honeycomb cysts with the diameter of 0. 1~2. 0 cm. 26 cases were solid lesions without visible cysts. 21 cases were observed lung abscess with thick and rough wall and pus inside. 7 cases of emphysema showed microcysts with crepitation. 2 cases were identi-fied cystic and solid masses, with fish-fresh like cut surface. Histopathologically, 94 cases (75. 2%) were related to congenital bron-chopulmonary dysplasia in 125 cases of CLD, in which there were 59 patients (47. 2%) of congenial pulmonary airway malformation (CPAM), including 29 cases of type 1 (49. 2%), 18 cases of type 2 (30. 5%), and 12 cases of type 4 (20. 3%), there were 26 ca-ses (20. 8%) of pulmonary sequestration, including 15 cases of intralobar type (57. 7%) and 11 of extralobar cases (42. 3%), 5 ca-ses were complicated with CPAM type 2, 8 cases were bronchial cyst (6. 4%) and 1 case of enteric cyst (0. 8%). Acquired lesions were detected in 31 cases (24. 8%), including 21 cases of infected lung abscess, 1 case of fungal abscess. 7 cases of emphysema, and 3 cases of pleuralpulmonary blastoma (typeⅠ1 case and typeⅡ2 cases). Conclusion Pediatric CLD is characterized as com-plexed categories. The prognosis depends on correct pathological diagnosis, combined with imaging evaluation and appropriate timing of surgery.

AIM: To observe the relationship between aortic atherosclerosis plaque formation and telomerase activation in vascular smooth muscle cells (VSMC). METHODS:Iliac artery atherosclerosis plaque from 20 renal failure patients and five cases of normal iliac arteries were obtained and confirmed by histological examination. The endothelial cells and the connective tissue on surface were lightly scraped and removed. Telomerase activity of the residual tissue was detected by telomeric repeat sequence amplification protocol. RESULTS:Five cases of normal iliac arteries showed negative telomerase activity. Eight of 20 cases athorosclerosis plaque showed positive telomerase activity, the other 12 cases showed negative telomerase activity. CONCLUSION: Telomerase activation may play a certain role in VSMC proliferation and atherosclerosis formation.