0.05),but there were the significant difference of prognosis in point and sheet bleeding groups,internal carotid artery system group with hemorrhage,multiple site bleeding group compared with that of cerebral infarction group(all P0.05).Conclusion The correlation factors of impact on HT after cerebral infarction mainly have the volume of blood and bleeding part.

Objective To investigate the dedifferentiation of epidermal cells into their progenitor stem cells induced by basic fibroblasts growth factors(bFGF) in vitro.Methods HEKa cells obtained from Cascade were found flattening and formation of cell-to-cell contacts after 6 to 7 passages,which resembled differentiated epidermal cells in vivo.To examine the effect of growth factors on the cell proliferative alterations,bFGF(100 ng/ml) was added into the culture medium for different periods(6,12,24,48,or 72 h),then the cell proliferation was measured by MTT assay.Phenotypic changes and the cell-fate determination of HEKa cells after bFGF treatment were detected by immunocytochemical assays,flow cytometry and RT-PCR analysis.HEK cells with no intervention treatment were used as a control.Results MTT assay proved that the optimal culture condition to induce the dedifferentiation of epidermal cells into their progenitors was to culture HEKa cells for 36 to 48 h when the addition of bFGF was 100 ng/ml.After treatment with bFGF for 48 h,clusters of round-shaped cells appeared around differentiated epidermal cells,and expanded progressively thereafter.These cells were smaller in shape and with larger nuclear/cytoplasm ratio,and had not only clonogenicity but also ability to form a cutaneous ridge-like structure.Immunohistochemical staining revealed that the expression levels of ?1 integrin,CK19 and CK14 were up-regulated,while the expression of CK10 was significant down-regulated after bFGF treatment.Flow cytometry indicated that there were more CK19-positive and CK14-positive cells in the treatment group than in the control(74.77% vs 15.74%,and 87.14% vs 67.26%respectively),but much lesser CK10-positive cells(4.56% vs 98.56%).Additionally,the mRNA expression levels of ?1 integrin,CK19 and CK14 were up-regulated after bFGF treatment,but that of CK10 was down-regulated.Conclusion bFGF can reverse the differentiated process of epidermal cells and induce them to produce immature,stem-like cells,which can proliferate and be used in the wound repair and regeneration of skin tissues.

Bone Marrow Cells ; metabolism ; DNA-Activated Protein Kinase ; genetics ; metabolism ; Humans ; Leukemia ; genetics ; Nuclear Proteins ; genetics ; metabolism ; PTEN Phosphohydrolase ; genetics ; metabolism ; RNA, Messenger ; Telomerase ; genetics ; metabolism

Objective To evaluate whether Ly294002,suppressing phosphatidylinositol 3 kinase (PI3K)/AKT survival signaling pathway,can change the sensitivity of breast cancer cells to radiotherapy. Methods Breast cancer cultured MCF7 cells treated with:radiation alone;Ly294002;or the combination of radiation and Ly294002.The inhibition of PI3K/AKT by Ly294002 was confirmed by Western blot.Clo- nogenic assay was used quantitatively to measure the mitotic cell death,and caspase-3 assay was used to e- valuate apoptosis.Results 1.Ly29400 could partially inhibit phosphorylated AKT but not radiation,the combination of both could enhance the inhibition of phosphorylated AKT,2.Timing of exposing cells to Ly294002 had some impact on clonogenic survival by radiation,one hour pre-radiation and 10 days post-ra- diation exposing to Ly294002 could maximally sensitize the cells to irradiation,3.Ly29400 combined with radiation could synergistically enhance mitotic death and apoptosis of MCF7 cells,with SER of SF_4 and D_0, being equal to 1.25 and 1.42.Conclusions PI3K/AKT pathway may be a potential target for enhancing the response of breast cancer cells to radiotherapy.

Objective To investigate the expression of pSTAT5 in 7 pancreatic carcinoma cell lines,and the change of expression of pSTAT5 in pancreatic carcinoma cells SW1990 after growth hormone (GH) treatment, and explore its molecular mechanism. Methods Human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, AsPc, P3, PANC1) were cultured in vitro, and Western blotting was used to detect the expression of pSTAT5 in these cell lines. SW1990 in exponential growth phase was collected and nude Balb/c mice were inoculated with SW1990 cells. When tumors became palpable after inoculation, mice (normal saline group). 1 h, 2 h and 24 h after the last dose of GH treatment, the mice were sacrificed.Western blotting was used to detect the expression of pSTAT5 in SW1990 and inoculation tumor cells after GH injection. Results Positive expression of pSTAT5 was observed in all human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, Aspc, P3, PANC1). 5 minutes after GH (50 ng/ml) stimulation, the expression of pSTAT5 in SW1990 was 0.57 ±0.05, which was significantly increased; and it reached 0.64 ±0.04 at 10 minutes, then decreased to 0.39 ±0.03 at 15 minutes, however, it remained higher than that in the control group at 1 h (0.33 ± 0.02 vs 0.25 ± 0.06), and its expression at 2 h was 0.26 ± 0.03 and returned to the normal level. The expression of pSTAT5 in xenograft was not significantly changed. Conclusions GH could rapidly up-regulate the expression of pSTAT5 in SW1990 but the effect lasted for a relatively short period. GH had no significant effect on the expression of pSTAT5 in xenograft.

Objective To study the impact of exogenous growth hormone (GH) on the levels of insulin-like growth factor-Ⅰ and -Ⅱ (IGF-Ⅰ, -Ⅱ) of the pancreatic cancer tissue and the small intestine mucosa of the host. Methods In situ hybridization was performed on pancreatic cancer cell lines (SW-1990) and inoculation tumor of the host to determine the location of the mRNA transcript encoding IGF R-Ⅰ,-Ⅱ. Athymic nude Balb/c mice were inoculated with SW-1990 cells. After inoculated tumors have become palpable, animals were randomized to receive GH (4 mg/kg once daily for 2 weeks) versus saline control. After the animals were killed at time point, tissues (tumor and small intestine) were rapidly incised for subsequent immune blotting analysis. Results Strong IGF R-Ⅰ,-Ⅱ mRNA hybridization signal could be detected in pancreatic cancer cell. There was no statistically significant difference between the level of IGF-Ⅰ, Ⅱ in the tumor of the GH and NS groups after 1 hours of GH injection (P>0.05). GH augmented the expression of IGF-Ⅰ(1 h : 0.33±0.05, P<0.05 ; 2 h : 0.34±0.04, P<0.05 ; 6 h:0.34±0.05, P<0.05), -Ⅱ(1 h : 0.36±0.05, P<0.05) in the small intestine mucosa of the host. Conclusions The expression of IGF-Ⅰ, Ⅱ in the small intestine mucosa of the host was elevated by GH, but not in the inoculation tumor in vivo. The discrepancy of GH-IGF pathway between inoculation tumor and small intestine of the host may help to explain the phenomena that GH doesn't accelerate growth of pancreatic tumor in vivo.

Objective To investigate the effect of GH on proliferation of pancreatic cancer cells and observe the features of IGF-IGFBP3 pathway in the host after GH administration. Methods Pancreatic cancer cells (SW-1990,PANC-1 and P3) during exponential growth stage were harvested and cultured in medium containing growth hormone (50 ng/ml). After 24, 48 and 72 hours, cells were counted using a Coulter Counter. Thirty-five Athymic nude Balb/c mice were inoculated with SW-1990cells. When tumors became palpable after inoculation, animals were randomized to receive GH points (1 h, 2 h, 6 h, 24 after the last injection), plasma samples were gathered for subsequent ELISA determination and liver was rapidly incised for immune blotting analysis. Results The results revealed that GH stimulated cell growth in vitro. GH elevated levels of IGF-Ⅰ , Ⅱ at the 1st , 2nd , 6th hour after the last injection. GH augmented the expression of IGFBP3 in the liver of the host in vivo (1 h, 2 h, 6 h, 24 h, respectively). Conclusion Such proteins as IGF- Ⅰ and Ⅱ might be associated with mechanism of last effect of GH on tumor host. The up-regulation of IGFBP3 by GH administration in the host may help to explain the phenomena that GH doesn't accelerate growth of pancreatic tumor in vivo.

Objective To investigate the value of 18 F-fluorodeoxyglucose FDG) positron emission tomography (PET)-computed tomography (CT) in predicting the progression-free survival (PFS)and overall survival (OS) of patients with esophageal squamous cell carcinoma (ESCC) after threedimensional (3D) radiotherapy.Methods A retrospective analysis was performed on 98 ESCC patients,who underwent FDG PET-CT before 3D radiotherapy from 2004 to 2010,to investigate their 1-,3-,and 5-year PFS and OS rates.The relationship of maximum standard uptake value (SUVmax),mean SUV (SUVmean),metabolic target volume (MTV),length of primary tumor on PET-CT before radiotherapy,and number of tumors on PET with PFS and OS were analyzed.The SUVs and clinical data were analysed by independent samples t-test or Hotelling T2 test; the Kaplan-Meier method was used for calculating PFS and OS rates,and the Logrank test was used for survival difference analysis;the prognostic factors were analysed using the Cox proportional hazard model.Results The follow-up rate was 100％ ;56 patients were followed up for at least 3 years,and 27 for at 5 years.The SUVmax SUVmean and MTV of primary tumor,length of primary tumor on PET-CT before radiotherapy,and number of tumors on PET were correlated with PFS and OS (x2 =8.99-41.82,all P ＜ 0.01).The Cox regression analysis showed that PFS could be well predicted based on SUVmean (x2 =4.41,P =0.036,RR =1.398) and number of tumors on PET (x2 =6.79,P =0.009,RR =3.650) and that OS could be well predicted based on number of tumors on PET (x2 =5.03,P =0.025,RR =3.740).Conclusions When estimating the long-term response to precise radiotherapy in patients with ESCC,SUV mean and number of tumors on PET may be used to predict PFS,and number of tumors on PET may be used to predict OS.

Objective To analyze the causes of inappropriate discharge of implantable cardioverter defibrillator (ICD) in elderly patients and to discuss the corresponding solutions.Methods Totally 95 elderly patients with ICD were collected.They were followed up and the inappropriate ICD discharges were recorded and analyzed.Results All patients were followed up for 235 times/year totally.There were 16 patients with inappropriate ICD discharges.The causes of inappropriate ICD discharges included ventricular oversensing in 7 patients (43.7％),supraventricular tachycardia misclassified into ventricular tachycardia in 4 patients (25.0％),electrode fracture in 2 patients (12.5％),and electromyogram (EMG) interference,electromagnetic interference and electrode fracture with EMG interference in 1 patients respectively (6.3％ each).11 inappropriate ICD discharges were reduced and avoided by reprogrammed and noninvasive treatment in 16 patients.1 patient with the underdetected ventricular fibrillation after reprogramming and the problem was solved by external defibrillation.The other 5 patients got better by the invasive treatment.Conclusions Different causes account for inappropriate discharges in patients with ICD.Reprogramming the corresponding parameters in different ICD can reduce or avoid inappropriate discharges without affecting the sensitivity of ICD.

To analyze complications of hyperbar ic treatment and the management of these complications． Methods: There are 129 cases treated with huperbaria, 125 were severe head injury, 2 were brain infarction, one was carbon monoxide toxication and an other was anesthesia accident． These complications were analyzed． Results: There were 7 of 129 cases suffered with headache and vertigo, one of them was dead． Conclusion: Severe h ead injury patients treated with hyperbaria must be careful, cease the huperbaric treatmen t immediately whenever patients feel discomfort．