Objective It was designed to investigate the relationship between the productions of p16 and Rb genes expression and gastric carcinogenesis and evaluate the correlation between the expression of p16 and Rb genes in gastric carcinoma.Methods The expression of P16 and Rb proteins was examined in gastric carcinoma and precancerous lesion and normal gastric mucosa by streptavidin-peroxidase immunohistochemical method (S-P).Results The positive rates of P16 and Rb proteins expression showed as below: There were 96 25%(77/80) and 98 75%(79/80) in normal gastric mucosa, 92 00%(46/50) and 80 00%(40/50) in atypical hyperplasia gastric mucosa and 47 54%(58/122) and 59 84%(73/122) in gastric carcinoma respectively. The positive rates of P16 and Rb proteins expression in gastric carcinoma were significantly lower than that in normal gastric mucosa and atypical hyperplasia gastric mucosa (P

Objective To establish two-dimensional electrophoresis profiles with high resolution and reproducibility from human gastric carcinoma and paired normal gastric mucosa tissues and to analyse the differential expression proteins between the two types of the tissues. Methods The total proteins of gastric carcinoma and paired normal gastric mucosa tissues were seperated by immobilized pH gradient-based two-dimensional gel electrophoresis (2-DE).After silver staining, the differential expression proteins were analyzed by using Imaging Master 2D analysis software. Results ⑴Average protein spots were 1049?67, 1097?73 in gastric carcinoma and paired normal gastric mucosa respectively,the matched spots were 835?48, 953?56 in both the two types of tissues respectively, and the average matching rate was 79.6%, 86.7% respectively. ⑵A total of 769?45 protein spots were matched between the electrophoretic maps of 5 gastric carcinoma and paired normal gastric mucosa tissues. The 81 differential protein spots were identified between the two types of the tissues. 17 protein spots were expressed only in the gastric carcinoma and 24 protein spots were expressed only in the normal gastric mucosa. The expression levels of 26 protein spots in the gastric carcinoma were higher than those in the normal gastric mucosa, and the expression levels of 14 protein spots in the gastric carcinoma were lower than those in the normal gastric mucosa. Conclusion In this study, the well-resolved,reproducible 2-DE patterns of gastric carcinoma and paired normal gastric mucosa tissues were established and some differential proteins between the two types of tissues were found. These data will be helpful to further screen specific biomarkers of gastric carcinoma.

Objective To study the changes of serum protein spectrum in patients with systematic lupus erythematosus (SLE) in order to screen specific protein markers. Methods Serum samples from 72 patients with SLE and 85 age- and sex-matched controls were assessed using surface-enhanced laser desorp-tion/ionization time-of-flight mass spectrometry (SELDI-TOF-MS) with weak cation exchange (CM10) pro-rein chip. Forty samples from the patients and 50 control samples were randomly selected to serve as a pre-liminary training set; significantly different protein peaks were automatically chosen for the system training and development of a decision classification tree model. The validity of the model was then challenged with a blind test set (including another 32 samples from patients and 35 from human controls). Results A total of 73 effective protein peaks were detected within the mass/charge ratio (m/z) interval 2000 - 50000, among which, 15 protein peaks significantly differed between patients with SLE and controls (P < 0.01). Three pro-tein peaks with an m/z value of 4001, 6305 and 7356 were automatically chosen as a biomarker pattern in the training set that discriminated patients with SLE from controls with a sensitivity of 90.0% (36/40), speci-ficity of 92.0% (46/50) and accuracy rate of 91.1% (82/90). When the SELDI marker pattern was tested with the blinded test set, it yielded a sensitivity of 87.5% (28/32), specificity of 91.4% (32/35) and accuracy rate of 89.6% (60/67). Conclusions SELDI-TOF-MS protein chip could be used to screen serum protein for SLE, and the decision classification tree model with these biomarkers may favor the diagnosis of SLE.

Objective To improve the 2,3,5-triphenyl tetrazolium chloride (TTC) solution method for measuring the viability of Cistanche deserticola seeds and investigate the change in viability during storage at 5 ℃. Methods The effect of the testa,TTC concentration,sodium hypochlorite concentration (NaClO),and staining time were studied,and seed viability during storage at 5 ℃ was measured with the improved method. Results Seeds were kept for 48 h in 0.5% TTC solution at 40 ℃,and then for 2 h in 0.2% NaClO solution;Seed viability was measured under a stereomicroscope. Storing seeds of C. deserticola for 1 to 2 years at 5 ℃ had no significant effects on their viability. However,the percentage of seeds with high viability was increased with the extension of the storage time at 5 ℃. Conclusion A convenient and rapid method for measuring the viability of C. deserticola seeds is developed. Storing C. deserticola seeds at 5 ℃ could improve their viability

In vitro studies have established the prevalent theory that the mitochondrial kinase PINK1 protects neurodegeneration by removing damaged mitochondria in Parkinson's disease (PD). However, difficulty in detecting endogenous PINK1 protein in rodent brains and cell lines has prevented the rigorous investigation of the in vivo role of PINK1. Here we report that PINK1 kinase form is selectively expressed in the human and monkey brains. CRISPR/Cas9-mediated deficiency of PINK1 causes similar neurodegeneration in the brains of fetal and adult monkeys as well as cultured monkey neurons without affecting mitochondrial protein expression and morphology. Importantly, PINK1 mutations in the primate brain and human cells reduce protein phosphorylation that is important for neuronal function and survival. Our findings suggest that PINK1 kinase activity rather than its mitochondrial function is essential for the neuronal survival in the primate brains and that its kinase dysfunction could be involved in the pathogenesis of PD.