Objective To compare the body weight,height,head circumference of premature babies fed by different ways,and to analyze the advantages and disadvantages.Methods 260 premature infants were selected as the research subjects,according to random number table,they were divided into four groups.Group A:premature infant formula feeding,80 cases;Group B:pure breast feeding group,60 cases;Group C:normal full term formula feeding,60 cases;Group D:premature infant formula mixed breast feeding,60 cases.All children were fed at the first 12 to 24h after birth.The body weight,height,head circumference and catch up full term time were evaluation index. Results After correct gestational age 40 weeks,group B children'weight,height,head circumference were higher than other groups,group C was the lowest levels,the difference was statistically significant (F =3.563,P <0.05).Correct gestational age 1,3,6 months later,group A children'weight,height and head circumference index were higher than other feeding group,the level of group D was the second,the lowest level was group C,the differences were statistically significant (F =3.011,2.853,2.779,all P <0.05).In 6 months,group A,38.8% (31 /80),was the fastest one to reach the full term infant,the difference was statistically significant (χ2 =29.149,P <0.05).At other time,the pur-suing number of group A was bigger,but there was no statistically significant difference.Conclusion For premature babies,preterm infant formula milk powder or premature infant formula and milk feeding way is better than that of pure breast feeding and normal full term milk powder,which can guarantee the children's nutrition demand,shorten the time of pursuing full term infant,promote baby's health.

Objective To observe the clinical manifestation and the mode of RET proto-oncogene mutation in a pedigree of mutiple endocrine neoplasia type 2A (MEN2A). Methods Genomic DNA was extracted from the peripheral blood lymphocytes in 18 family members including 3 patients, then PCR was performed to amplify seven exons of the RET proto-oncogene, i. e. exon 8,10,11,13-16. The PCR products were directly sequenced to identify the RET mutation and then sequenced after subcloning to identify their heterozygosity. Results The male proband suffered from pheochromocytoma and medullary thyroid carcinoma since the age of 30; while his sibling sister was ill with pheochromocytoma, and his brother with medullary thyroid carcinoma. A novel heterozygous mutation, 1893-1895delCGA, was detected in exon 11 of the RET proto-oncogene in the 3 patients and the other 2 family members. Conclusion A novel heterozygous mutation of RET proto-oncogene, 1893-1895delCGA, seems to be the disease-causing mutation in the studied MEN2A family.

[Abstract] Objective: To investigate he effect of tetracycline- (Tet-on) mediated livin RNA interference on growth of lung carcinoma xenegrafts, and find a better regulatory way to interfere the development on lung cancer. Methods: livin shRNA lentiviral vectors were constructed; and the lung cancerA549 cells were subcutaneously injected into right upper back of nude mice to establish xenegraft model. The livin shRNAlentiviral vectors were injected into xenografts to interfere the expression of livin, then tetracycline was injected intraperitoneally for the induction. The suppressive effect of Tet-on mediated livin RNA interference efficiency was investigated and lung cancer xenograft development was observed. Results: After the induction with Tet-on, livin gene expression was significantly inhibited by livin shRNAcompared with the control group and Tet-on-NC group; the xenograft volume in Tet-on- livin shRNAgroup was significantly smaller than that in control group and Tet-on-NC group ([5.31±0.86]g vs [8.22±0.63]g and [7.17±0.54] g, P<0.05). Moreover, little body toxicity was observed and no nude mice died in this study. Conclusion: The Tet-on mediated livin shRNA could suppress the growth of lung cancer development with good targeting and controllable characteristics, which might provide a potent tool for treating lung cancer with livin protein as target.