1.Hemorrhgic and thromboembolic complications during warfarin anticoagulation therapy
Aijun HOU ; Juntang XU ; Jihong GUO
Chinese Journal of Practical Internal Medicine 2001;0(02):-
Objective To study the incidence of and identity risk factors for hemorrhage and thromboembolism during long-term warfarin therapy.Methods All patients were studied in the People's Hospital of Peking University Anticoagulant Clinic from 2001-04 to 2003-11,in whom a course of warfarin therapy intended to last for more than 4 weeks.All bleeding and thromboembolism events were classified as minor or serious or fatal and life-threatening.Incidences of adverse events were analyzed statistically.Results A total of 128 patients were enrolled in the investigation,the median age of the study group was 67 years(ranged 25 to 83).There were 41 bleeding events occurring in 34 patients,and 5 events of thromboembolism.Age and hepatocirrhosis were significantly associated with bleeding complications(P=0.040 and P=0.014).Conclusion Hemorrhage is the major side effect of warfarin;age and hepatocirrhosis are significantly associated with bleeding complications.
2.Construction of cDNA library of the treated Changliver cell and quality analysis
Juntang LIN ; Congrui WANG ; Huiyong ZHANG ; Yuchang LI ; Cunshuan XU
Journal of Xinxiang Medical College 2004;21(1):1-4
Objective To construct cDNA library of the treated Changliver cell by switching mechanism at 5′ end of RNA transcript (SMART) technique and analyze its quality.Methods cDNA of Changliver cell was aquired with reverse transcription polymerase chain reaction (RT-PCR) and long-distance PCR (LD-PCR),then the cDNA library was constructed with SMART cDNA library construction kit.Results Through testing,the high quality cDNA library containing full length cDNA of Changliver cell had been constructed.The titer of the amplified cDNA library was 4.5 × 1010 pfu*ml-1 and the average exogenous inserts of the recombinants was 1.5 kb.Conclusion These results suggest that the Changliver cell cDNA library has a high quality and lays a solid foundation for researching on Changliver cell and screening
3.Research progress of asynchronous brain-computer interfaces based on alpha control technology
Lijuan SHI ; Liuyang XU ; Xinqi HE ; Yun ZHAO ; Juntang LIN ; Yi YU
International Journal of Biomedical Engineering 2017;40(1):62-64,后插1
Brain-computerinterface(BCI) is a kind of direct channel for information communication and control established between the human brain and computer or other electronic equipment.BCI is a novel information communication system which does not depend on the conventional brain information pathways.The asynchronous brain-computer interface technology is based on alpha wave control,and can automatically switch system mode between working and idle and select the larger EEG signal associated with motion imagination.In this paper,the basic knowledge of BCI and alpha wave-based asynchronous BCI technology were introduced.The key technology and application prospect of the novel alpha wave-based asynchronous BCI technology were summarized,and the status and existing problems were analyzed.
4.MANF brakes TLR4 signaling by competitively binding S100A8 with S100A9 to regulate macrophage phenotypes in hepatic fibrosis.
Chao HOU ; Dong WANG ; Mingxia ZHAO ; Petek BALLAR ; Xinru ZHANG ; Qiong MEI ; Wei WANG ; Xiang LI ; Qiang SHENG ; Jun LIU ; Chuansheng WEI ; Yujun SHEN ; Yi YANG ; Peng WANG ; Juntang SHAO ; Sa XU ; Fuyan WANG ; Yang SUN ; Yuxian SHEN
Acta Pharmaceutica Sinica B 2023;13(10):4234-4252
The mesencephalic astrocyte-derived neurotrophic factor (MANF) has been recently identified as a neurotrophic factor, but its role in hepatic fibrosis is unknown. Here, we found that MANF was upregulated in the fibrotic liver tissues of the patients with chronic liver diseases and of mice treated with CCl4. MANF deficiency in either hepatocytes or hepatic mono-macrophages, particularly in hepatic mono-macrophages, clearly exacerbated hepatic fibrosis. Myeloid-specific MANF knockout increased the population of hepatic Ly6Chigh macrophages and promoted HSCs activation. Furthermore, MANF-sufficient macrophages (from WT mice) transfusion ameliorated CCl4-induced hepatic fibrosis in myeloid cells-specific MANF knockout (MKO) mice. Mechanistically, MANF interacted with S100A8 to competitively block S100A8/A9 heterodimer formation and inhibited S100A8/A9-mediated TLR4-NF-κB signal activation. Pharmacologically, systemic administration of recombinant human MANF significantly alleviated CCl4-induced hepatic fibrosis in both WT and hepatocytes-specific MANF knockout (HKO) mice. This study reveals a mechanism by which MANF targets S100A8/A9-TLR4 as a "brake" on the upstream of NF-κB pathway, which exerts an impact on macrophage differentiation and shed light on hepatic fibrosis treatment.