Objective To establish human osteoblast-like cell lines TE85 model of neoplastic transformation for exploring molecular mechanism in canceration process of osteosarcoma.Methods HOS TE85 cells were treated by MNNG(initiated factor) and TPA(promotor).The malignancy of transformed cells was identified by observing the cell form,colony forming frequency on soft agar and tumorigenesis in nude mice.Results Continuous passage after induction of neoplastic transformation led to the formation of a few paramorph foci that exhibited an extensively random orientation.The agglomeration in experiment group was more than that in control group.As compared with that of negative control cells,colony formation efficiency of transformed cells in semisolid agar showed a significant increase and the transformed cells could form tumor subcutaneously in the nude mice.The tumors were a poorly differentiated osteosarcoma confirmed by histopathological examination.Conclusion Simulating the process of malignant transformation of human cells,we establish neoplastic transformation of human osteoblast-like cell lines TE85 model.

Metabotropic glutamate receptors (mGluRs) are a family of G protein coupled receptors linked to modulation of ion channel functions and multiple second messengers. These receptors are widely distributed throughout the basal ganglia (BG). Studies have demonstrated that these mGluRs subtypes located at various synapses in BG could modulate the release of dopamine and glutamate which correlates with brain area,the subtype selectivity and concentration of the ligands. Metab otropic glutamate receptors have been proposed as potentially new therapeutic targets for Parkinsons disease by providing a method of pharmacologically regulating neurotransmission in the BG.

Objective:To study the mechanism and clinical significance of the precordial ST segment deviations in acute inferiorwall myocardial infarction (AIMI) involving adjacent area. Methods: Characteristics of electrocardiogram were analyzed in118 patients with AIMI. Results: (1)The magnitude of ST segment elevation of inferior wall leads (Ⅱ, Ⅲ and aVF) wassignificantly negatively correlated with that of precordial leads (P＜0.01). (2)The changed magnitude of ST segment oflead V2 (0.63±1.82 mm) and V2/aVF ratio (0.84±1.61) in 16 cases associated with right ventricular infarction weresignificantly higher than those of only inferior wall myocardial infarction group (V2:0.35±1.65 mm,V2/aVF ratio:0.29±1.28)(P＞0.05 and P＞0.05). (3)The magnitude of ST segment fall of lead V2(-1.20±1.52 mm) and V2/aVFratio (-0.33±1.15) in 38 cases associated with lateral-posterior wall in farction were higher than those of only inferiorwall infarction group (P＜0.05). (4)If the cases associated with right ventricular and lateral-posterior wall infarction werenot included, the ST segment correlation coefficient between inferior and precordial leads would significantly increase inAIMI (r =-0.797, P＜0.01). Conclusion:The directions of ST segment deviations of precordial leads elevate in casesassociated with right ventricular infarction and fall in eases associated with lateral-posterior wall infarction in AIMI.

Purpose To study the value of the ultrasonic imaging in the diagnosis and differential diagnosis of benign and malignant breast tumor. Methods Color doppler ultrasound examination were conducted in 262 cases of patients with breast tumor. The mor-phology of the tumor, edge, envelope, internal echo, microcalcification, length and breadth ratio, axillary lymph node and blood-flow signals of color doppler in breast tumors were observed and these results were compared with the pathological observation postoperation. Results There were 314 tumors in all cases, the coincidence rate in the diagnosis of benign breast diseases with ultrasonic imaging and pathological diagnosis was 97. 3%, the misdiagnosis rate was 2. 7%. The coincidence rate in the diagnosis of breast malignant tumors with ultrasound imaging and pathological diagnosis was 92. 9%, the misdiagnosis rate was 7. 1%. There were statistically signif-icant differences between benign tumors and malignant tumors in the tumor shape, edge, echo, microcalcification, length and breadth ratio, axillary lymph node imaging characteristics (P<0. 01). Conclusion Ultrasound imaging can be more accurate diagnosis and i-dentification of benign and malignant breast tumors.

Purpose: To investigate the diagnosis, pathological characteristics and treatment of primary malignant lymphoma of the breast (PMLB). Methods: Clinical and pathological data of 16 cases of PMLB were analyzed retrospectively. Results: No case was correctly diagnosed before operation. All the 12 cases were operated and identified by pathology, in which total mastectomy, radical mastectomy and modified radical mastectomy were carried out in 5, 3 and 4 patients respectively. Moreover, all cases were combined with post-operative chemotherapy or radiotherapy. 10 cases were followed up 1 - 10 years. 4 cases who survived 22 months on the average died of the tumor spread and metastasis during follows-up, and the others are still alive. Especially, 1 case, recurring 2 times locally, has survived for 4. 5 years after reoperation. Conclusions: The final diagnosis of this disease depends on the pathological examination. The majority of PMLB is non-Hodgkins lymphoma ( NHL), and mostly of B cell origin and are mostly related to the mucosa-associated lymphoid tissue ( MALT). Total mastectomy or mastectomy plus axillary nodes dissection is the preferred method of operation and the adequate post-operative chemotherapy is very important.

Purpose:To investigate the clinical characteristics, diagnosis and treatment of accessory breast tumors.Methods:Clinical and pathological data of 16 cases of accessory breast tumors were analyzed retrospectively. Results:There were 5 cases of accessory breast fibroadenoma, 2 cases of intraductal papilloma, 9 cases of accessory breast carcinoma. Local mass resection and radical resection were carried out respectively. All these patients had post operative chemotherapy and radiotherapy. 13 cases (81.3%0 were followed up for 1—10 year. As to results, 3 cases died of metastasis in 2,2.5 and 4 years respectively after operation;one case, reoperated because of local recurrence, still survives (over 3 years):and the others recovered well.Conclusions:It is possible for benign or malignant tumor to occur in the accessory breast,and the manifestation of the accessory breast tumors is similar to that of the primary breast tumor. Operation is the first choice for all treatment benign tumor with local mass resection including the whole accessory breast while accessory breast carcinoma should be treated by radical dissection.

0.05). In hFOB, the expression of P53 was not detected, and that of P63 was weakly positive. The expression of P53 and P63 in HOS transformed by niekel sulfate were higher than that in normal HOS (P

Objective To analyse 35 cases with failure and malfunction hemodialysis access managed by interventional radiology. Methods 35 cases with failure and malfunction hemodialysis access were examined by angiography and treated by interventional management subseqently. 26 cases of thrombosis occlusilon were treated with thrombolytic therapy and 15 cases of malfunctioning hemodialysis access were done with PTA. Results The initial angiogram showed 9 patients with simple stenosis while 26 patients with thrombosis occlusion, with concurrent stenosis in 13 patients. The rate of immediate recanalization of thrombolysis was 88.4% (23/26). The PTA was successful in 12 cases, 7 of the 13 cases concurrent with stenosis and 8 cases with simple stenosis while the other 3 cases of the 15 cases confronted failure. Follow up was made in 6 patients concurrent with stenosis without further management and 3 patients failure to conduct PTA after thrombolytic therapy. Recanalization occurred in 7 cases within 1 month and then did in all the cases in 3 month. Conclusions Angiography and subsequent interventional management play a critical role in the diagnosis and treatment of failure and malfunction hemodialysis access.

Objective To explore the pathogenesis-related imprinted genes in osteosarcoma and investigate the role of imprinted genes expression in osteosarcoma pathogenesis.Methods The model of malignant transformed immortalized human osteoblastic cells was established and the malignant transformed cells were collected on day 40,55,70,90.The untreated cells passaged from the normal cells on day 90 served as control.After the total RNA extraction,the finally synthesized biotinylated cDNAs were hybridized to CapitalBio Genechip CAP-F0017.2 of the differentially expressed genes.Two genes were chosen at random to further confirm the array results using the SYBR Green real-time PCR in samples of control,day 40 and day 90. Results By an entrance limit of ≥2.0 or ≤0.5,ten imprinted genes which biological functions are mainly related with cell growth/maintenance and signaling transduction were detectable for notablely differential expression,including down-regulated genes of CD81,GRB10,NDN,MEST and up-regulated genes of H19,MKRN3,SLC22A1L,TSSC3,CDKN1C in the malignant transformation of immortalized human osteoblastic cells.The array results were further confirmed by the real-time RT-PCR.Conclusion Ten imprinted genes were detectable for notablely differential expression.Our results will promote our understanding of the molecular mechanisms of imprinted genes in the course of osteosarcoma pathogenesis.

AIM: To explore if metabotropic glutamate receptors (mGluRs) i nduces neuroprotection against 6-hydroxydopamine (6-OHDA) neurotoxicity in PC1 2 cells. METHODS: The alteration of the glutamate in extracellul ar fluid of PC12 cells was detected by high performance liquid chromatography (H PLC) with a fluorescent detector. The cytotoxic activity of PC12 cells was assay ed by means of MTT colorimetric method. RESULTS: 6-OHDA dose-d ependently increased glutamate release and decreased cell activity of PC12 cells , and the mGluRs ligands had no significant effect on that. CONCLUSION: The mGluR3 ligands has no protective effect on neurotoxicity of PC12 cel ls induced by 6-OHDA.