Biochemistry and Molecular Biology are the cornerstone courses of talent training in the field of life science. Taking these course as an example, this study explored reconstructing the knowledge framework, developing teaching cases, sharing teaching resources, innovating teaching means and establishing ideological education patterns. Supported by the scientific research achievements with discipline characteristics and online teaching platform, this research explored and practiced an integrated curriculum reform mode. This mode is guided by scientific research and education, based on the course development, and driven by communication and cooperation. A shared space of "exchange, practice, openness and informatization" was developed to achieve free and independent integration of undergraduate and graduate teaching motivated by learning knowledge, resulting in an effective student training.
Humans ; Curriculum ; Students ; Learning ; Molecular Biology/education* ; Biochemistry/education*

Brain development requires a delicate balance between self-renewal and differentiation in neural stem cells (NSC), which rely on the precise regulation of gene expression. Ten-eleven translocation 2 (TET2) modulates gene expression by the hydroxymethylation of 5-methylcytosine in DNA as an important epigenetic factor and participates in the neuronal differentiation. Yet, the regulation of TET2 in the process of neuronal differentiation remains unknown. Here, the protein level of TET2 was reduced by the ubiquitin-proteasome pathway during NSC differentiation, in contrast to mRNA level. We identified that TET2 physically interacts with the core subunits of the glucose-induced degradation-deficient (GID) ubiquitin ligase complex, an evolutionarily conserved ubiquitin ligase complex and is ubiquitinated by itself. The protein levels of GID complex subunits increased reciprocally with TET2 level upon NSC differentiation. The silencing of the core subunits of the GID complex, including WDR26 and ARMC8, attenuated the ubiquitination and degradation of TET2, increased the global 5-hydroxymethylcytosine levels, and promoted the differentiation of the NSC. TET2 level increased in the brain of the Wdr26^+/- mice. Our results illustrated that the GID complex negatively regulates TET2 protein stability, further modulates NSC differentiation, and represents a novel regulatory mechanism involved in brain development.
Animals ; Mice ; DNA-Binding Proteins/genetics* ; Cell Differentiation ; Neural Stem Cells ; Translocation, Genetic ; Ubiquitins/genetics* ; Ligases/genetics*

Traditionally, liver cirrhosis has a bleeding tendency due to the reduction in blood coagulation factors, hyperfibrinolysis, thrombocytopenia, and increased portal hypertension. Some studies show that the patients with live cirrhosis are in a state of hypercoagulability and tend to develop venous thromboembolism, which greatly affects the patients′ prognosis. This article reviews the epidemiological features and risk factors of venous thromboembolism, as well as the significance of prevention of venous thromboembolism in patients with liver cirrhosis, so as to guide clinical practice.

Budd-Chiari syndrome (BCS) is characterized by the hepatic outflow obstruction from the small hepatic vein to the superior hepatic inferior vena cava. Portal vein thrombosis (PVT) refers to the development of thrombosis in the main portal vein, with or without thrombosis in the superior mesenteric or splenic vein. A large number of studies have shown that prothrombin (factor II, F2) G20210A mutation is related to BCS and PVT. F2 and its G20210A mutation are introduced, the effect of F2 G20210A mutation on thrombosis is reviewed, and the prevalence of F2 G20210A mutation in China is analyzed. An attempt is made to focus on the association of F2 G20210A mutation with PVT and BCS. It is believed that F2 G20210A mutation to some extent increases the risk for PVT and BCS. However, the prevalence of F2 G20210A mutation is extremely low in the Chinese population. Thus, this mutation may not be regarded as the cause of PVT and BCS in China.

ObjectiveTo systematically evaluate the efficacy of mirabilite umbilical compress in the treatment of ascites in liver cirrhosis. MethodsThe literature on the treatment of cirrhotic ascites with mirabilite umbilical compress was searched in CNKI, VIP, Wanfang Data, and PubMed databases. A meta-analysis was carried out using the random effect model. The continuous and categorical data were expressed as aas standard mean difference (SMD) and odds ratio (OR), respectively. ResultsA total of 11 randomized controlled trials were included. The mirabilite umbilical compress treatment group showed a significantly higher response rate of ascites (OR=3.19, P＜0.0001) and significantly reduced abdominal circumference (SMD=1.69, P＜0.0001) and body weight (SMD=2.77, P＜0.0001) compared with the control group. After mirabilite umbilical compress treatment, alanine transaminase level was significantly decreased (SMD=1.92, P=00009), albumin level was significantly increased (SMD=-1.78, P=0.0006), while aspartate aminotransferase and total bilirubin levels showed no significant changes (SMD=3.39, P=0.25). ConclusionMirabilite umbilical compress is effective in the treatment of ascites in liver cirrhosis, yet its efficacy in improving liver function remains uncertain.

Objective To investigate the location of receptor interacting protein 3( RIP3) in Necroptosis and its function in this signal passage, and explore the relationship between receptor interacting protein 1 ( RIP1 ) and RIP3 in nuclear translocation. Methods Primary cerebrocortical neurons were cultured for 12 days,then pre-treated with zVAD-fmk(20μ,mol/L) for half an hour to block apoptosis. ①Extracting nuclear and cytoplasmic protein after neurons were exposed to TNF for different time ,then protein levels of RIP3 were analyzed by western blot and immunofluorescence for qualitative observation;②In the following research,the neurons were treated with Nec-1 and shRlPl ,then the protein level of RIP1 and RIP3 with western blot were analyzed, cell viability were determined by measuring LDH levels. Results ①In signaling pathways of necroptosis, the protein level of RIP3 in cytoplasmic decreased gradually with prolonged TNF exposure, to the corresponding it rolled up in nucleus and a-chieved the peak in 12 hours of TNF treatment ( Cytoplasmic 0. 45 ± 0. 03 ,0. 41 ± 0. 02,0. 73 ± 0. 03 ,0. 90 ± 0.01,1.15 ±0.04,1.30 ±0.02,0.99 ±0.03,0.63 ±0. 03;Nucleus 0. 07 ±0.02,0. 26 ±0.02,0. 57 ±0. 02,0. 68 ± 0.02,0. 80 ± 0.01,0.92 ± 0.02,1.28 ± 0.03,0. 87 ± 0.02) (P < 0.01). ②Blocking the relationship between RIP1 and RIP3 with necrostatin-1 and shRIPl , nuclear translocation of RIP3 decreased and caused a great increase in cell viability( 1.00 ±0.05,0.39 ±0.03,0.50 ±0. 03) (P<0. 01). Conclusion RIP3 mainly locates in cy-tolymph of normal cells,it translocates into nucelus as necroptosis takes place. RIP1 function with RIP3 in nuclear translocation. Block nuclear translocation of RIP3 is a potential way to protect cells.

Objective To study the characteristic of 8 to 16-year-old children's short-term memory.Methods 157 subjects participated in this study (8,10,12,14 and 16 years old).All subjects completed the digit recall,word recall,spatial recall and position recall tests.Results Short-term memory spans increased with age (F(4,145)= 35.56,P<0.01) and peaked at 14 years old [ digit (8.83±1.31),word (4.79±0.68),spatial (5.90±0.77),position (5.42±1.28)].Conclusion The developmental trends of four tasks' memory span were similar.But the exact span-scores were different from what Pascual-Leone's model predicted.