Objective The anti tumor and anti metastasis effects of angiocytotoxic therapy (TNP 470/Gemcitabine) were investigated using a model of human pancreatic carcinoma by surgical orthotopic implantation (SOI). Methods The SOI model was developed by suturing small pieces of SW1990 tumors into the tail of pancreas in nude mice. Twenty four male mice were randomly divided into control group, G100 group receiving 100 mg/kg Gemcitabine intraperitoneally injection on days 0,3,6 and 9 after transplantation, and T30 group receiving 30 mg/kg TNP 470 subcutaneous injection on alternate days for 8 weeks. Another thirty two male mice were randomly divided into control group, T15 group, G50 group and combination group (TNP 470 30 mg/kg+ Gemcitabine 50 mg/kg). Animals were sacrificed ten weeks after transplantation. Results G100 group had a significant inhibitory effect on tumor growth of pancreatic carcinoma compared to T30 group, while the metastasis of tumor was significantly inhibited by T30 group compared to G100 group. Neither G100 group nor T30 group showed a significant improvement on survival rate. T15 group and G50 group alone had no significant inhibitory effect on the tumor growth and its metastasis. Mean while a significant anti tumor, anti metastatic effect and a significant improvement on the survival rate were observed in combination group. The inhibitory effect of G50 group was enhanced by 2 times with T30, and 2/8 of the tumors bearing animals were cured by the combination therapy. The level of microvessel density in T30 group was significantly lower than that in T15 group and control group ( P

Objective To explore the role of CD95 system in chemotherapeutic sensitivity of pancreatic cancer cells, in an attempt to enhance the efficacy of chemotherapy by transfection CD95 gene, and to provide the evidence for the immunological treatment of pancreatic cancer. Methods CD95 gene was transfected into the pancreatic cancer cell line SW1990 by lipofectamine. The transfected cells were selected by G418. CD95 expressions of the transfected cells were detected by Northern blot and Western blot. MTT assay was used to analyze the response of the transfected cells to 5 fluorouracil, adriamycin (ADM), gemcitabine and in combination with anti CD95 monoclonal antibody (mAb). The drug induced apoptosis of transfected cells was measured by flow cytometry. Results The transfected pancreatic cancer cell SW1990 could overexpress CD95 stably. The CD95 mRNA and protein expressions were significantly increased in the transfected cells than in the controls. Anti CD95 mAb could inhibit the growth of the transfected cells. In addition, transfected cells were more sensitive to clinically relevant concentrations of chemotherapeutic drugs than non transfected cells. Anti CD95 mAb addition could enhance the cytotoxic effect of chemotherapeutic drugs. Drug induced apoptosis in ADM treated transfected cells more pronounced than in non transfected cells. Conclusions CD95 transfection could increase the sensitivity of pancreatic cancer cell SW1990 to, and partly reverse the resistance to, chemotherapeutic drugs. The combination of chemotherapeutic drugs with anti CD95 mAb showed a synergistic cytotoxicity to pancreatic cancer cells.

AIM: The current study was designed to construct eukaryotic expression vector containing NK4 gene and transfect it into human pancreatic cancer cell lines.METHODS: The recombinant of pcDNA3/hNK4 was digested by restriction enzyme, the NK4 gene was cloned into a high effective eukaryotic expressing plasmid which contains CMV2 immediate early gene promoter and then transiently introduced into the pancreatic cancer cell line SW1990 by lipofectamine and clonal cell lines that secrete high levels of NK4 protein were isolated.The expression of NK4 was observed by RT-PCR and Western blot, in vitro the vascular endothelial cell proliferation inhibiting activity of NK4 was examined by 3-[4,5-dimethylthiazolzyl]-2,5-diphenyl tetrazolium bromide(MTT) method. RESULTS: A specific expression of NK4 gene mRNA by lipofectamine-mediated transfer exhibited only in SW1990/NK4 cells,Western blot analysis demonstrated that there was positive expression of NK4 protein(50 kD).The NK4 inhibited proliferation of the vascular endothelial cells in vitro. CONCLUSION: The recombinant of pRC/CMV2-hNK4 is a high effective expressing eukaryotic vector.The bio-engineering product of the NK4 is an angiogenesis inhibitor and may play an important role in the gene therapy for tumor.

BACKGROUND: Our team has built finite element dynamic bone models of different parts, but how to ensure the model’s precision and effectiveness, there still needs further study.OBJECTIVE: To provide accurate biomechanics model of Digital Human. METHODS: The CT data of Virtual Chinese Human --the male No.1 (VCH-M1) were imported into the MIMICS13.1 software authorized by the Materialise Company, and then the outcome document was entered into the ABAQUS6.7 software to perform finite element analysis. The result was observed and then the effectiveness of the models was tested. RESULTS AND CONCLUSION: The “.lis” document was chosen in the finite element analysis software ABAQUS6.7. Three dimension models of cervicalt were acquired. The model has 10 465 panel points and 52 752 units. It is verified that this model is effective. Results confirmed that the biomechanics model of Digital Human can be calculated for meeting the revolutionary requirement of the future digital medical science.

AIM: To investigate the expression of MAT1 protein in pancreatic cancers and the relationship between MAT1 and clinicopathological features of pancreatic cancers. METHODS: 94 surgical specimens, including 70 pancreatic cancers, 10 pancreatic benign tumors, 14 chronic pancreatitis and 10 autopsy normal pancreas tissues, were analyzed immunohistochemically, and then MAT1 expression and clinicopathological features were compared. RESULTS: MAT1 was expressed mainly in the cancer cells,and also in the fibroblasts, where it was localized within the cytoplasm and nuclear envelope. MAT1 expression was found in 75.7% (53/70) of the cancers, but not detected or weakly expressed in control tissues. There was a significant difference in expression of MAT1 among the above four tissues (P

AIM: To observe the different changes of neuroendocrine systems between the state of sport fatigue and poverty of movement. METHODS: 60 male Wistar rats were randomly divided into three groups: normal control group, sport fatigue model group and poverty of movement model group (20 rats in each group). The sport fatigue model was established by the method of combining basal diet and loaded swimming during 2 weeks, whereas the method of restricted activities was used to establish the poverty of movement model with total experimental time of 10 weeks. By the end of experiment, the climbing pole time was determined. The contents of hypothalamus thyrotropin releasing hormone (TRH), and serum norepinephrine (NE) and epinephrine (E) in rats with different treatments were determined by ELISA. In addition, the changes of hypothalamus corticotropin release hormone (CRH), pituitary adrenocorticotropic hormone (ACTH) and thyroid stimulating hormone (TSH), and serum corticosterone (CORT), triiodothyronine (T_3), tetraiodothyronine (T_4) were determined by radioimmunoassay to evaluate the functions of adrenergic nerve-adrenomedullin system, hypothalamo-pituitary-adrenal (HPA) axis and hypothalamo-pituitary-thyroid (HPT) axis. RESULTS: Compared to control group, the climbing pole time of the animals was obviously decreased in two model group. The adrenergic nerve-adrenomedullin system and HPA axis were inhibited in sport fatigue model rats, but HPT axis was unchanged. Interestingly, the HPA axis was hyperfunctional and HPT axis was inhibited in poverty of movement model rats. However, no change in the adrenergic nerve-adrenomedullin system was observed. CONCLUSION: Sport fatigue and poverty of movement all affect neuroendocrine system and lead to the adjustment mechanism imbalance, but the target and tendency are different.

Objective To observe the changes of rotation behavior and tyrosine hydroxylase immunopositive neurons and investigate how Mrh-aFGF affects them in substantia nigra of Parkinson disease rats. Methods After building a rat model of Parkinson disease by injecting 6-OHDA into substantia nigra and ventral tegmental area,we used Mrh-aFGF to intervene rats by lateral ventricle injection to observe how behavior of rats induced by apomorphine and tyrosine hydroxylase immunopositive neurons in substantia nigra of rats changes,then quantitatively analyzed the change of tyrosine hydroxylase immunopositive neurons. Results Rotation behavior was not found in control group,otherwise,actuation time was shorted,time length was prolonged,and average velocity of rotation was accelerated in Parkinson disease rats(P

AIM: To elucidate the pattern of 5-fluorocytosine(5-FC) induced apoptosis and its role in gene therapy for human pancreatic cancer. METHODS: The human pancreatic cancer SW1990 cells(CEA-producing) were infected with recombinant adenoviruses(Adex1CEA-prCD or Adex1CEA-prZ).Cytosine deaminase(CD) expression was examind by western blot. Apoptosis induced by 5-FC in human pancreatic cancer SW1990 cells genetically modified to express cytosine deaminase was investigated by applying electron microscopy, DNA electrophoresis and flow cytometry analysis techniques. RESULTS: The SW1990 cells infected with Adex1 CEA-prCD were treated with 5-FC at 100 ?mol?L -1 for 48 h, cell apoptosis occurred. Typical apoptosis morphological feature appeared and DNA ladder could be demonstrated on DNA electrophoresis. Apoptosis peak was also showed by flow cytometry. Apoptotic cells accounted for 34.6% of the cell population. Cells in G 1, S and G 2/M phase of cell cycle were 64%, 11% and 7%, respectively. CONCLUSION: The apoptosis induced by 5-FC may be a primary mechanism in CD gene therapy for pancreatic cancer.

ObjectiveTo observe the effect of modified Tianwang Buxindan （MTBD） on the skin of sleep-deprived （SD） mice and investigate its mechanism. MethodSixty 2-month-old female Kunming mice were randomly divided into a blank group， a model group， a vitamin C （VC， 0.08 g·kg^-1）， and MTBD low-， medium-， and high-dose groups （6.5， 12.5， 25 g·kg^-1）. Except for the blank group， the other groups were subjected to SD mouse model induction （using multiple platform water environment method for 18 hours of sleep deprivation daily from 15：00 to next day 9：00）， continuously for 14 days， and caffeine （CAF， 7.5 mg·kg^-1） was injected intraperitoneally from the 2nd week onwards， continuously for 7 days. While modeling， the blank group and the model group were administered with normal saline （0.01 mL·g^-1）， and the other groups received corresponding drugs for treatment. On the day of the experiment， general observations were recorded （such as body weight， spirit， fur， and skin）. After sampling， skin tissue pathological changes were observed under an optical microscope using hematoxylin-eosin （HE） and Masson staining methods. Skin thickness and skin moisture content were measured. Biochemical assay kits were used to detect skin hydroxyproline （HYP） content， skin and serum superoxide dismutase （SOD） activity， and malondialdehyde （MDA） content. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum interleukin （IL）-6， tumor necrosis factor （TNF）-α， and IL-1β levels in mice. Western blot was used to detect skin tissue type Ⅰ collagen （ColⅠ）， type Ⅲ collagen （ColⅢ）， phosphatidylinositol 3-kinase （PI3K）， phosphorylated （p）-PI3K， protein kinase B （Akt）， p-Akt， nuclear factor E₂-related factor 2 （Nrf2）， heme oxygenase （HO）-1， and nuclear factor （NF）-κB protein expression. ResultCompared with the blank group， the model group showed varying degrees of changes. In general， signs of aging such as reduced body weight （P<0.01）， listlessness， dull fur color， and formation of wrinkles on the skin appeared. Tissue specimen testing revealed skin thinning， flattening of the dermoepidermal junction （DEJ）， and reduced collagen fibers under the optical microscope. Skin thickness and moisture content decreased， skin tissue HYP content significantly decreased （P<0.01）， skin and serum SOD activity significantly decreased （P<0.01）， and MDA content significantly increased （P<0.01）. Serum IL-6， TNF-α， and IL-1β levels significantly increased （P<0.01）. Skin ColⅠ， ColⅢ， p-PI3K/PI3K， p-Akt/Akt， Nrf2， and HO-1 protein expression significantly decreased （P<0.05， P<0.01）， and NF-κB expression increased （P<0.01）. Compared with the model group， the VC group and the MTBD low-dose group showed increased skin moisture content， HYP content， SOD activity， and ColⅠ， ColⅢ， p-PI3K/PI3K protein expression （P<0.05， P<0.01）， and decreased serum MDA content （P<0.05）. In addition， a decrease in serum IL-6 and IL-1β levels was detected in the MTBD low-dose group （P<0.05）， while the above indicators in the MTBD medium- and high-dose groups improved （P<0.05， P<0.01）. ConclusionSleep deprivation accelerates the aging process of the skin in SD model mice. MTBD can improve this phenomenon， exerting anti-inflammatory and antioxidant effects， and its mechanism of action may be related to the activation of the PI3K/Akt/Nrf2 signaling pathway.

Transposition of simple or composite forearm island flaps with a radial vascular pedicle was performed in repairing tissue defects of the hand and reconstruction of the thumb in 16 patients. It was found to be easy to operate and no suturing of blood vessels was necessary. The postoperative swelling was less marked. The flap was good in texture and sensation after the operation. The overall result wassatisfactory. Anatomic-physiological situdy was also carried out. 16 patients have been operated on, including 2 thumb reconstructions, with satisfactoryresults.