Objective To explore early clinical diagnosis of infant with cerebral palsy(CP). Methods Early diagnosis of cerebral palsy information abroad was referenced. DDST scale screening, newborn NBAS inspection stan-dards, VOJTA postural reflex and the nervous system reflective were used to evaluate the cerebral palsy. Results 90 cases CP of which 63 eases spastie. Xu mobile hand-foot-15 cases, 12 cases of mixed type. Conclusion Standardized,quantitative indicators,only workable and easy to use.

Objective To study on preparation and encapsulation of Curcumin liposomes. Method Liposome was prepared by five kinds of methods, determining the encapsulation efficiency by Visible Spectrophotomery on 424 nm. Result The envelopment ratio of Curcumin liposome made by the method of ethanol injection was 73.5%. Conclusion The preparation process of ethanol injection is simple and apt to control. The new form of prepared drug can improve bioavailability of Curcumin.

Objective: To obtain the optimum prescription of the rhubarb lactobacillin dispersible tablets.Methods: The kind and amount of the excipient were investigated by using the disintegrating time to establish the optimum prescription and preparation process.Results: The tablets were prepared by compressing moist granulation with the PVPP and CMS-Na as the disintegrant,MCC as diluent,sodium alginate as sweller,magnesium stearate as lubricant and 80% alcohol as adhesive agent.The preparation complied with the requirement of Pharmacopeia of the People's Republic of China(2005edition).Conclusion: This prescription of the tablet is reasonable and the preparation process is feasible.

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.

ObjectiveTo explore the feasibility, safety and clinical value of laparoscopic Rouxen-Y cystojejunostomy in the treatment of pancreatic pseudocyst. Method Four patients with pancreatic pseudocyst received totally laparoscopic pancreatic pseudocystojejunostomy. The data on intraoperative bleeding, operative time, postoperative time to get out of bed, time of first flatus/bowel motion, complication and duration of hospital stay were collected and analyzed retrospectively. ResultsAll operations were carried out successfully with laparoscopic surgery. The mean operative time was 90 min. The average intraoperative blood loss was 40 ml. The mean postoperative time to get out of bed was 1.5 d, and the mean time of first flatus/bowel motion was 2. 3 d. All patients recovered smoothly without any pancreatic fistula. The average hospital stay was 7 days. Fever, pancreatitis,adhesive intestinal obstruction and other complications did not occur. ConclusionsTotally laparoscopic Roux-en-Y pancreatic pseudocystojejunostomy was an efficacious, safe, and minimally invasive procedure.

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.

AIM: To construct a recombinant hEGF-hbFGF(78-154aa)fusion protein, which not only has the heparin-binding ability, but also promotes the growth of the cells, and to express the fusion protein in E. coli expression system with high expression level.METHODS: hEGF gene was joined with 231 bp fragment coding hbFGF(78-154aa) and expressed in E. coli. The fusion protein was purified using affinity chromatography of heparin-Hyper D and analyzed with western blot. The pI value and the biological activity were both assayed.RESULTS: The fusion protein was expressed in a high expression level of about 30% of the total cell protein, as estimated by SDS-PAGE. Western analysis results showed that the antigenicity of fusion protein was similar to hEGF. Fusion protein could not only bind heparin but also promote the growth of 3T3 cell. The pI value of fusion protein was 5.2.CONCLUSION: The recombinant hEGF-hbFGF(78-154aa) fusion protein possessed the characteristics of both hEGF and hbFGF. This new-designed protein would become a good object for the research on the relationship between the structure and the function of the growth factor.

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 analyze the current prevalence status of gynecological diseases on female workers in an automobile manufacturing company. METHODS: By judgment sampling,382 female workers who exposed to occupational hazard factors were selected as exposure group and 367 female executive staffs without exposure to those factors were selected as control group. Among the three subgroups of the exposure group,the prevalence rate of vaginitis,pelvic inflammatory disease,cervicitis,annex cysts,ovarian cysts and uterine fibroid in these two groups were analyzed. RESULTS: The prevalence rate of vaginitis and uterine fibroid in exposure group was higher than that of control group(24. 9% vs20. 7%,20. 4% vs 9. 8%,P < 0. 05). Among the three subgroups of the exposure group,the prevalence rate of vaginitis in welding subgroup was the highest(35. 4%,P < 0. 017); the prevalence rate of annex cysts in coating subgroup was the highest among all subgroups(11. 4%,P < 0. 017); the prevalence rate of uterine fibroid in assembly subgroup was the highest(28. 1%,P < 0. 017). The prevalence rate of uterine fibroid in exposure group presented an increasing tendency with the increase of age(P < 0. 05). The prevalence rate of cervicitis,annex cysts and uterine fibroid in exposure group presented an increasing tendency with the increase of seniority(P < 0. 05). CONCLUSION: The prevalence rate of gynecological diseases in female workers who exposed to occupational hazard factors in an automobile manufacturing company was significantly higher than general population. The prevalence rate of gynecological diseases among different types of female workers was significantly different. Disparity of gynecological diseases prevalence of female workers might due to differences in occupational hazard factors exposure.

BACKGROUNDThe human FHIT gene at chromosome 3p14.2 is a tumor suppressor gene, and its abnormality in structure and function is related to carcinogenesis and progression of lung cancer. It is postulated that FHIT and NIT1 likewise collaborate in biochemical or cellular pathway in mammalian cells, but their molecular mechanisms in lung cancer cell are still unknown. The aim of this study is to construct procaryotic expression vector of human NIT1, providing a foundation to explore the expression of human NIT1 protein and to study the interaction of NIT1 and FHIT genes in lung cancer cell lines.

METHODSThe NIT1 cDNA was acquired by RT-PCR. EcoRI/NotI digested PCR product was directly cloned into procaryotic expression vector pET-32a.

RESULTSThe sequence of NIT1 cDNA clone exactly corresponded with the sequence of NIT1 cDNA in GenBank. The expectant fragments of DNA were obtained after recombinant procaryotic expression vector was digested by EcoRI and NotI.

CONCLUSIONSThe procaryotic expression vector of human NIT1 is successfully constructed by RT-PCR and direct clone. It provides an important basis to detect the expression of NIT1 protein and to further explore the relationship between NIT1 and FHIT genes in oncogenesis and development of human lung cancer.