Objective To measure 95% effective doses (ED95) of propofol and etomidate by using up-down intravenous administration method, and compare the potency ratio and the anesthesia duration of them. Methods Twenty eight male SD rats were divided into two groups randomly: the propofol group and the etomidate group. Loss of righting reflex was regarded as the judgment index of unconsciousness. The dose-response curve was made according to the formula of Y=Ymin+(Ymax-Ymin)/ [1+10log(ED50-X)× m]. Values of ED95 of propofol and etomidate were calculated, and the anesthesia duration periods after administration of the two equivalent dose drugs were measured respectively. Results The values of ED95 were 9 mg/kg and 1.5 mg/kg for propofol and etomidate. The ED95 ratio for propofol and etomidate was 6. There was a significant difference in anesthesia duration between propofol group (465.6±18.5)s and etomidate group (233.7±9.3)s (P<0.05). Conclusion The anesthesia duration of propofol is longer than that of etomidate, taking the ED95 as equivalent dose.

· AIM: To investigate the influence of TGF-β 2 antisense oligonucleotide(ASON) on the differentiation, proliferation of stromal fibroblast in corneal stroma injury.both eyes of 28 rabbits, the right eyes were served as experimental group, corneal incisions were sutured with 8-0 coated vicryl suture carrying TGF-β 2 ASON; the left eyes were served as control group, corneal incision were sutured with common 8-0 coated vicryl suture. Rabbits were killed at 4, 7, 14 and 28d after surgery, stromal fibroblasts were examined by immune histochemistry and electron microscopy.significantly reduced the numbers of cells expressingα -smooth muscle actin (α -SMA) and proliferating cell nuclear antigen (PCNA). The ultrastructure of fibroblast had no significant difference in two groups.differentiation and proliferation of stromal fibroblast in corneal injury. This will be a new method to adjust corneal wound repair.

This study developed a novel approach of targeting malignant glioma with pMAGE-A1(278-286)-specific cytotoxic T lymphocytes (CTLs) induced from the peripheral blood mononuclear cells of healthy donors by multiple stimulations with human leukocyte antigen (HLA)-A2-restricted pMAGE-A1(278-286) peptide-pulsed dentritic cells. Cytotoxic assays were performed by the colorimetric CytoTox 96 assay to analyze cytotoxic activity of the induced CTLs against various target cells. The induced CTLs showed approximately 45% specific lysis against T2pMAGE-A1(278-286) (pMAGE-A1(278-286) peptide pulsed T2 cells) and U251 (HLA-A2(+), MAGE-A1(+)) at an effector:target ratio of 40:1, and approximately 5% cytolysis against T2pHIV, A172 (HLA-A2(-), MAGE-A1(+)), K562 and T2 cells without being pulsed with peptide at any effector:target ratio. The specific killing activity of the induced CTLs against T2pMAGE-A1(278-286) and U251 was much more obvious than in any other control group (P<0.05). The cytotoxic activity against the T2pMAGE-A1(278-286) and U251 was significantly eliminated by anti-HLA class I mAb W6/32. These results suggest that pMAGE-A1(278-286) epitope may serve as a surrogate tumor antigen target of specific immunotherapy for treating HLA-A2 patients with malignant glioma.

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 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 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 investigate the clinical features of gynecological malignant tumor related multiple primary malignant neoplasms (MPMN).Methods Apply retrospective and comprehensive analysis to the clinical data of 30 patients with gynecological malignant tumor related MPMN.Results Synchronous MPMN were found in 9 patients.Their average age was 50.2 years old and their median age was 49 years old.The neoplasms were located at ovary,uterus,cervix,breast and intestine.Metachronous MPMN were found in 21 patients.Their average age was 57.7 and their median age was 57 years old.The median interval between the first and the second primary malignant neoplasm was 4.0 years.The neoplasms were located at breast,ovary,uterus,gastrointestinal tract,uterine cervix,lung etc.In 30 cases,26 of them were treated by surgical operation and further adjunctive treatment of chemotherapy and (or) radiotherapy was conducted as per the neoplasm staging and its pathological results.The rest 4 patients (first primary malignant neoplasms were excised from 3 of them and another one was not treated by surgical operation) received adjunctive treatment of chemotherapy and (or) radiotherapy.Followed ups,which varied from 6 to 60 months,were made to 29 patients and 20 out of the 29 were alive.5-year survival rate of patients with gynecological malignant tumor related MPMN was 47.8％,2-year survival rate was 73.9％,and 1-year survival rate was 88.6％.Conclusion Pay more attention to the patients with gynecological malignant tumor related MPMN,examine the high-risk patients with malignant tumor comprehensively,identify whether it is recurrence,metastasis or new growth of malignant neoplasm,and further ensure early diagnosis and proper treatment,avoiding misdiagnosis and missed diagnosis.

Objective:To explore the pathogenesis of multiple organ dysfunction syndrome(MODS)with respect to the bal- ance of Th1/Th2.Methods:Eighteen healthy male minipigs,weighing 22-30 kg,were randomly divided into two groups: MODS group and control group.Double-hit method including hemorrhagic shock and endotoxiemia was used to establish the porcine MODS model.The peripheral vein blood samples were collected at different time-points(before bloodletting,before en- dotoxin injection,1 h,24 h,48 h and 72 h after endotoxin injection)in the two groups.The spleen samples were collected after death of the animals.Plasma levels of IFN-?and IL-4 were detected by enzyme-linked immunosorbent assay(ELISA).Real- time PCR was used to detect the expression of IFN-?,IL-4,T-bet and GATA-3 mRNA(The latter 2 were the key transcription factors associated with Th1/Th2 response)in the spleen samples.Results:The plasma levels of IFN-?and IL-4 quickly reached the peak values 1 h after the endotoxin injection,then the level of IFN-?decreased quickly.The ratio of IFN-?/IL-4 was signifi- cantly lower than the baseline value 72 h after endotoxin injection(P=0.000).The ratio of IFN-?/IL-4 mRNA in MODS group was obviously lower than that in the control group(P=0.020);the ratio of T-bet/GATA-3 was also lower in MODS group (P=0.038).Conclusion:The shift from Th1 to Th2 occurs in the progress of MODS.

OBJECTIVETo evaluate the inhibitory effect of tumor suppressor PTEN on cell growth of endometrial carcinoma.

METHODSThe exogenous wild PTEN cDNA via an adenoviral vector (Ad-PTEN) was introduced into Ishikawa cells. The expression of PTEN protein was detected by Western blot. The growth of Ishikawa cells was evaluated by trypan blue exclusion method and MTT.

RESULTSThe expression of PTEN protein was induced on day 1, and greatly increasing on day 3 - 5 after Ad-PTEN infection. The expression of PTEN significantly inhibited the growth of Ishikawa cells, and also significantly inhibited the growth of Ishikawa cells induced by IGF-II.

CONCLUSIONAdenovirus-mediated introduction of exogenous PTEN into human endometrial carcinoma cells can induce growth suppression. PTEN gene may be a novel therapeutic agent for endometrial carcinoma.

Adenoviridae ; genetics ; Cell Proliferation ; Endometrial Neoplasms ; metabolism ; pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Insulin-Like Growth Factor II ; pharmacology ; PTEN Phosphohydrolase ; Phosphoric Monoester Hydrolases ; biosynthesis ; genetics ; physiology ; Recombination, Genetic ; Transfection ; Tumor Suppressor Proteins ; biosynthesis ; genetics ; physiology

OBJECTIVETo study the role of mast cells in the differential diagnosis of cellular leiomyoma and endometrial stromal sarcoma of uterus and its mechanism.

METHODSUsing SP immunohistochemical technique, the expression of proliferating cell nuclear antigen (PCNA) and mast cells in 25 cellular leiomyoma (CL) and 26 endometrial stromal sarcoma (ESS) of uterus were examined. The expression of estrogen receptor (ER) and CD44v3 in cellular leiomyoma was also studied.

RESULTSThe expression of PCNA was not significantly different from CL or ESS (P > 0.05), while mast cell count was statistically different between them (P < 0.01). Using a value of less than 7 mast cells per high power field was useful for the diagnosis of ESS, yielding 100% sensitivity and 92.0% specificity. There was a positive correlation between the mast cell count and CD44v3 in CL (r(s) = 0.589, P < 0.01), though no correlation was observed between mast cell count and PCNA or ER.

CONCLUSIONNumber of mast cells is valuable for the discrimination of CL from ESS in the uterus. The mechanism and the role of higher quantity of mast cells in CL need further study.

Adult ; Aged ; Female ; Humans ; Hyaluronan Receptors ; analysis ; Leiomyoma ; chemistry ; pathology ; Mast Cells ; pathology ; Middle Aged ; Proliferating Cell Nuclear Antigen ; analysis ; Receptors, Estrogen ; analysis ; Sarcoma, Endometrial Stromal ; chemistry ; pathology ; Uterine Neoplasms ; chemistry ; pathology