Biochemistry and molecular biology is one of the most important professional basic courses for students in medical universities.Constructing scientific teaching quality control system for biochemistry and molecular biology is essential for improving its teaching quality.This paper discussed on some principles needed to be followed in constructing the teaching quality control system for biochemistry and molecular biology in medical universities and elucidated the three leveled frame of this system including university,college and department.This paper also illuminated on the main contents,implementation,organization system,evaluation system and incentive measures of this teaching quality control system.

Objective To study the dynamic changes of the activities of superoxide dismutase (SOD), amylase (AM) and alkaline phosphatase (ALP) and of the contents of epithelium growth factors (EGF) and insulin growth factors (IGF-1) in human colostrum (lactation 1-7 days postpartum). Methods A total of 118 samples of human colostrum were taken from 20 healthy women postpartum. The activities of SOD, AM and ALP in human colostrum were determined by methods of pyrogallol autoxidation, colorimetry of iodine-starch and pyrocatechol phosphate respectively. EGF and IGF-1 contents in human colostrum were measured by radioimmunoassay. Results The SOD activity of human colostrum increased slightly during lactation 1-4 days postpartum, from (18.7?2.2) kU/L to (22.5?2.9) kU/L, then it tended to decrease, being (11.2?2.1) kU/L on the 7th day. The SOD activities in lactation 1-5 days postpartum were significantly higher than that on day 7 ( P

Objective : To investigate the effects of milk derived pentapeptide prolin⁃glycine⁃proline⁃isoleucine⁃pro⁃ line ( PGPIP) on chronic alcoholic liver injury in mice and its related molecular mechanism . Methods : Forty C57BL/6 mice were randomly divided into control group , model group , glutathione(GSH) group , PGPIPN group .The mice model of chronic alcoholic fatty liver was established by 10 d ad libitum oral feeding with the Lieber⁃DeCarli(LD) ethanol liquid diet plus one binge . Drug intervention was given at the same time . Based on the reported RNA sequencing data in gene expression omnibus (GEO) database , the differential expression of liver endoplasmic reticulum stress⁃related genes was analyzed by cluster heat map . Liver hematoxylin⁃eosin (HE) staining was used to analyze the pathological effects of each treatment group on alcoholic liver injury in mice . Oiled Red O staining was used to analyze the effects of each treatment group on the accumulation of liver lipid droplets in mice . Transtransduction protein expression was detected by Western blot . Results : The pathological examination of PGPIP group was similar to that of Control group , and the liver injury of mice was significantly reduced . The accumulation of lipid droplets in the liver of mice in the model group was manifested as mixed lipid droplets of different sizes , and PGPIP treatment significantly reduced the accumulation of liver lipid droplets induced by alcohol . PGPIP had significant effects on the PERK⁃eIF2α⁃ATF4 pathway and the expression of transcriptional activator 6 ( ATF6 ), Cleaved Caspase 3 protein . Conclusion Pentapeptide PGPIP can alleviate chronic alcoholic fatty liver and liver injury in mice . The mechanism may be attributed to reducing the accumulation of lipid droplets in hepatocytes , en⁃ doplasmic reticulum stress , and hepatocyte apoptosis .

Objective : To investing ate the milk-derived hexapeptide PGPIPN and its truncated pentapeptide PGPIP to alleviate chronic alcoholic liver injury in mice and its associated molecular mechanisms． Methods : Sixty Kun- ming mice were randomly divided into control group，model group，GSH group，PGPIPN group，and truncated pen- tapeptide PGPIP group．The model of chronic alcoholic liver injury in mice was established by gavage with gradient alcohol． Drug intervention was given at the same time for 12 weeks． Liver HE staining was used to analyze the pathological effects of each treatment group on alcoholic liver injury in mice．Primary mouse hepatocytes and human normal hepatocyte line L-02 were isolated and cultured in vitro．The appropriate PGPIPN induction concentrations of both cells were determined by WST-1 method． L-02 cells were induced at different times． The expression of FoxO3a and phosphorylated FoxO3a protein were detected by Western blot to determine the appropriate induction time．The subcellular localization of FoxO3a in L-02 cells was detected by cellular immunofluorescence．The mR- NA changes of FoxO3a and MnSOD genes in primary hepatocytes and L-02 cells of mice in different treatment groups were detected by qRT-PCR. Results : The pathological examination of PGPIPN group and PGPIP group was similar to that of GSH group，and the liver injury of mice was significantly reduced．Medium and high concentra- tions of PGPIPN were respectively selected to induce mouse primary hepatocytes and L-02 cells．At 16 hours，the expression of FoxO3a protein in L-02 cells increased significantly．FoxO3a protein was mainly expressed in the nu- cleus．In addition，mRNA levels in both types of cells increased significantly after induction with the corresponding dose of PGPIPN． Conclusion PGPIPN and truncated pentapeptide PGPIP can reduce chronic alcoholic liver injury in mice．The mechanism may be to reduce alcohol-induced oxidative stress through FoxO3a-MnSOD signaling path- way.

Objective : The CRISPR / dCas9-SAM system was used to explore genes related to the proliferation of gastric cancer cells AGS，and their role in the occurrence and development of gastric cancer was analyzed． Methods : sgRNA was designed for genes with differential expression between gastric cancer and normal gastric tissue， and a lentiviral library was obtained after packaging was constructed．The AGS cells at different time points after the library was infected with AGS cells were used as the screening pressure，and the AGS cells at three time points on days 0，7 and 14 were collected．High-throughput sequencing analyzed sgRNA enrichment in AGS cells at dif- ferent time points after infection to obtain differential genes related to AGS cell proliferation. Results : Bioinformat- ics showed that compared with the 0 d group，42 and 45 negative screening differential genes and 59 and 40 posi- tive screening differential genes were obtained in the 7 d group and 14 d group，respectively．Among them，the 7 d group and the 14 d group had 11 genes in the negative screening and the positive screening． Conclusion In this study，11 genes inhibiting the proliferation of AGS cells were screened，of which 5 were protein-coding genes and 6 were long non-coding RNA ( lncRNA ) genes． 11 candidate genes that promoted AGS cell proliferation were screened，of which 3 were protein-coding genes and 8 were lncRNA genes．It laid a foundation for further function- al verification and comprehensive analysis of the occurrence and development process of gastric cancer.