Suerm monoamine oxidasa isoenzymes (MAOi) were determined in 105 cases of liver disea ses and 49 normal controls.MAOi were separated into 3 bands (I. Ⅱ.Ⅲ) by polyacrylamide gel elcctrophoresis. The results revealed that MAOi Ⅲ% was increased in chronic liver diseases, especially in liver cirrhosis. Our findings suggest that serum MAOi determination is more sensitive than serum albumin, MAO, ChE, and ADA determinationsin in the early diagnosis of liver cirrhosis

Clinical tutor system is a unique exploration and practice with characteristics of our school,which has been carried out in the process of clinical course learning and clinical practice among eight-year-program clinical majors.Through analyzing and summarizing the implementation among 2005 and 2006 grade students,we found that the clinical tutor played an active role in cultivating students' clinical thoughts and personal ethics and in improving clinical ability and scientific ability.However,some problem were existed in tutors themselves-specialized major,busy,unclear cultivation objective,etc.Therefore,further improvement of the system was needed in order to better meet the needs of the eight-year-program medical talent training and to provide related references.

BACKGROUND:The etiology of anterior cruciate ligament injury remains unclear yet, and some researchers have pointed that interior and exterior factors both contribute to anterior cruciate ligament injury;additionally, the genetic factor interior factors stand out. Collagen genes COL1A1, COL5A1, and COL12A1 are reported to be associated with anterior cruciate ligament injury in Caucasian populations. OBJECTIVE:To investigate the association of polymorphisms of COL1A1, COL5A1 and COL12A1 genes with anterior cruciate ligament injury in Chinese Han population . METHODS:105 patients with anterior cruciate ligament injury were enrolled and 110 patients without history of anterior cruciate ligament injury were as controlls. The first intron rs1800012 in COL1A1, rs127722 and rs13946 in the 3'-UTR region of COL5A1 gene, rs970547 and rs240736 in the 65 and 29 regions of COL12A1 extron were detected and classified by restriction fragment length polymorphism and genetic sequencing technology. RESULTS AND CONCLUSION:rs1800012, rs12722 and rs13946 genotypes, phenotypes and haplotypes in COL1A1 and COL5A1 genes showed no significant differences between groups. rs970547 and rs240736 genotypes as well as phenotypes and haplotypes in COL12A1 also showed no significant differences between groups. However, there was a significant difference in rs970547 gene frequence in male patients between groups. In conclusion, the Sp1 binding site of COL1A1 rs1800012 is not the susceptibility locus of anterior cruciate ligament injury in Chinese Han population. COL5A1 genes rs12722 and rs13946 in COL5A1 are not closely related to anterior cruciate ligament injury. COL12A1 rs970547 and rs240736 have a certain association with anterior cruciate ligament injury in Chinese men. Male individuals with COL12A1 rs970547 A allelicgene and AA genotype are likely to be susceptible to anterior cruciate ligament injury in Chinese Han population.

The last two decades have witnessed a paradigm shift from cytotoxic drugs to targeted therapy in medical oncology and pharmaceutical innovation. Inspired by breakthroughs in molecular and cellular biology, a number of novel synthesized chemical compounds and recombinant antibodies have been developed to selectively target oncogenic signaling pathways in a broad array of tumor types. Although targeted therapeutic agents show impressive clinical efficacy and minimized adverse effects compared with traditional treatments, the challenging drug-resistant issue has also emerged to limit their benefits to cancer patients. In this regard, we aim to improve targeted therapy by presenting a systematic framework regarding the drug resistance mechanisms and alternative approaches to re-sensitize cancer cells/tissues therapeutically.
Antineoplastic Agents ; Drug Resistance, Neoplasm ; Humans ; Neoplasms ; Signal Transduction

BACKGROUND:Neuregulin 1 has been shown to be characterized in cell proliferation,differentiation,and vascular growth.Human amniotic mesenchymal stem cells are important seed cells in the field of tissue engineering,and have been shown to be involved in tissue repair and regeneration. OBJECTIVE:To construct human amniotic mesenchymal stem cells overexpressing neuregulin 1 and investigate their proliferation and migration abilities,as well as their effects on wound healing. METHODS:(1)Human amniotic mesenchymal stem cells were in vitro isolated and cultured and identified.(2)A lentivirus overexpressing neuregulin 1 was constructed.Human amniotic mesenchymal stem cells were divided into empty group,neuregulin 1 group,and control group,and transfected with empty lentivirus and lentivirus overexpressing neuregulin 1,or not transfected,respectively.(3)Edu assay was used to detect the proliferation ability of the cells of each group,and Transwell assay was used to detect the migration ability of the cells.(4)The C57 BL/6 mouse trauma models were constructed and randomly divided into control group,empty group,neuregulin 1 group,with 8 mice in each group.Human amniotic mesenchymal stem cells transfected with empty lentivirus or lentivirus overexpressing neuregulin-1 were uniformly injected with 1 mL at multiple local wound sites.The control group was injected with an equal amount of saline.(5)The healing of the trauma was observed at 1,7,and 14 days after model establishment.Histological changes of the healing of the trauma were observed by hematoxylin-eosin staining.The expression of CD31 on the trauma was observed by immunohistochemistry. RESULTS AND CONCLUSION:(1)Human amniotic mesenchymal stem cells overexpressing neuregulin-1 were successfully constructed.The mRNA and protein expression of intracellular neuregulin 1 was significantly up-regulated compared with the empty group(P<0.05).(2)The overexpression of neuregulin 1 promoted the migratory ability(P<0.01)and proliferative ability of human amniotic mesenchymal stem cells(P<0.05).(3)Human amniotic mesenchymal stem cells overexpressing neuregulin 1 promoted wound healing in mice(P<0.05)and wound angiogenesis(P<0.05).The results showed that overexpression of neuregulin 1 resulted in an increase in the proliferative and migratory capacities of human amniotic mesenchymal stem cells,significantly promoting wound healing and angiogenesis.

【Objective】 To investigate the protection of astragaloside IV from high glucose induced podocyte injury and mitochondrial dysfunction and its molecular mechanisms. 【Methods】 The model of podocyte injury induced by high glucose (30 mmol/L glucose) was established, and the model cells were treated with low, medium and high doses of astragaloside IV respectively; cell activity was detected by CCK-8. Apoptosis was detected by TUNEL staining. Mitochondrial membrane potential was detected by JC-1 fluorescence probe. ATP content was detected by the kit. The expression levels of apoptosis and podocyte injury related proteins and Notch pathway related proteins were detected by Western blotting. 【Results】 Compared with the control group, cell activity was decreased, apoptosis level was increased (P<0.05), anti-apoptotic protein (Bcl2) expression was decreased, and apoptosis protein (Bax, cleaved-caspase 9, cleaved-caspase 3) expressions were increased (all P<0.05) in HG group. Compared with HG group, HG+AS-IV improved cell activity and apoptosis level induced by high glucose (P<0.05), increased expression of anti-apoptotic protein (Bcl2), and decreased expressions of apoptotic protein (Bax, cleaved-caspase 9, and cleaved-caspase 3) (all P<0.05). Compared with the control group, mitochondrial dysfunction occurred in HG group, JC-1 monomer content increased, and ATP content decreased (all P<0.05). Compared with HG group, HG+AS-IV improved mitochondrial dysfunction, increased JC-1 polymer content and ATP content (P<0.05). In addition, compared with the control group, the expression of Notch pathway-related protein was decreased in HG group (P<0.05). Compared with HG group, Notch pathway-related protein expression was increased in HG+AS-IV group (all P<0.05). Molecular docking results showed that AS-IV could bind Notch1. 【Conclusion】 Astragaloside IV can improve podocyte injury and mitochondrial dysfunction induced by high glucose, possibly by inhibiting Notch pathway activation.