[Objective] To discuss Professor JI Wei's clinical experience in treating ankylosing spondylitis.[Methods] To expound Professor JI Wei's academic thoughts and clinical experience in ankylosing spondylitis from aspects of etiology,pathogenesis,and syndrome differentiation and treatment variation, summarizing the characteristics of her prescriptions and ways of treatment as well as exemplifying them. [Results] Professor JI Wei believes that the basic pathogenesis of this disease is kidney deficiency and governor vessel vacuity,with wind,coldness,dampness,heat,phlegm,and blood stasis obstructing channels and collaterals. In her opinion,the major task of the early- and middle-term of this disease is to dispel wind and eliminate dampness and to alleviate impediment and free the vessels,and that of the late-term is to supplement the kidney and reinforce the governor vessel and to transform phlegm and disperse blood stasis. When treating the disease,we should correlate all four examinations,differentiating carefully the primary from the secondary, paying attention to the unique use of aconitum,monkshood,triptolide and other toxic drugs,as well as the black snake,scorpion,centipede and other animal medicinals,and attaching importance to ankylosing spondylitis complicated with inflammatory bowel disease ,treatment of uveitis and syndrome. [Conclusion] Professor JI Wei's clinical experience in treating ankylosing spondylitis is effective and worthy of wide application.

Gastroenteropancreatic neuroencrine tumors (GEP-NETs) originate from the neuroendocrine cells of the digestive system.Over the past few years,the incidence has increased gradually.The clinical manifestations are diverse,and the related molecular mechanism is also more complex.Although there are more and more basic researches for GEP-NETs,the mechanism for carcinogenesis and metastasis has not been fully elucidated.This paper summarizes the latest progress on the development of GEP-NETs,and elaborates the new findings on tumor molecular mechanisms,mainly including the related receptors and its signaling pathways,gene mutations and epigenetic changes.

Enhancer of rudimentary homolog (ERH) is a small, highly conserved protein among eukaryotes. Since its discovery nearly 20 years ago, its molecular function has remained enigmatic. It has been implicated to play a role in transcriptional regulation and in cell cycle. We recently showed that ERH binds to the Sm complex and is required for the mRNA splicing of the mitotic motor protein CENP-E. Furthermore, cancer cells driven by mutations in the KRAS oncogene are particularly sensitive to RNAi-mediated suppression of ERH function, and ERH expression is inversely correlated with survival in colorectal cancer patients whose tumors harbor KRAS mutation. These recent findings indicate that ERH plays an important role in cell cycle through its mRNA splicing activity and is critically required for genomic stability and cancer cell survival.
Amino Acid Sequence ; Animals ; Cell Cycle ; Evolution, Molecular ; Humans ; Molecular Sequence Data ; Neoplasms ; metabolism ; RNA Splicing ; Transcription Factors ; chemistry ; metabolism ; Transcription, Genetic

Objective To compare the levels of thrombomodulin in acute cerebral infarction patients with different blood glucose levels.Methods Four hundred and eighty-nine patients with acute cerebral infarction were selected including 237 patients of non-diabetes (non-diabetes group),117 patients of diabetes and HbA1c ≤7.0％(diabetes controlled well group) and 135 patients of diabetes and HbA1c ＞7.0％ (diabetes controlled badly group).The level of thrombomodulin was assayed by enzyme-linked immunosorbent assay and compared among three groups.Results The level of thrombomodulin was (2.66 ± 1.20) μg/L in non-diabetes group,(2.80 ± 1.43) μg/L in diabetes controlled well group,(3.22 ±1.60) μ g/L in diabetes controlled badly group.There was the increasing of thrombomodulin among non-diabetes group,diabetes controlled well group and diabetes controlled badly group (P =0.030).There was difference between non-diabetes group and diabetes controlled badly group (P =0.008).Conclusion There is the increasing of thrombomodulin in patients with acute cerebral infarction when their blood glucose rising.

The pathophysiological mechanism of ischemic stroke is very complex.Many intracellular and extracellular factors play the important roles in it.Studies have shown that the expression of matrix metalloproteinase-9 (MMP-9) has the changes of quantity,time and space after stroke.These changes are closely associated with the occurrence and development of ischemic stroke.The experimental studies focusing on MMP-9 also have made corresponding effects.The in-depth study of the mechanism of action of MMP-9 is expected to provide a new approach for the diagnosis and treatment of ischemic stroke.

Insect antifreeze protein (AFP) has high antifreeze activity. Antifreeze proteins can be used in cryopreservation of biological tissues and cells. We expressed an antifreeze protein from the desert beetle Microdera punctipennis in yeast and determined the function of the protein at low temperatures. Yeast expression vector, pPIC9K-Mpafp698, was constructed and transformed into Pichia pastoris GS115. The expression of MpAFP698 was induced by methanol, and identified by tricine SDS-PAGE and Western blotting. Mpafp698 gene was inserted into the genome of the host yeast strain GS115, and correctly expressed. Hardly any yeast's own protein was secreted into the media. Cryoprotective experiments showed that MpAFP698 can significantly protect mouse liver as well as other mouse organs from cold damage compared with those in the control of Bovine serum albumin (BSA) addition. Besides, the hemolysis of blood cells protected by MpAFP698 at 4 degrees C was reduced and the survival rate of SF9 cells protected by MpAFP698 after freezing and thawing was increased compared to those of the control with BSA addition. Our results showed that MpAFP698 can be expressed in yeast, which allows a convenient purification of the MpAFP protein that has the cryoprotective effect.
Animals ; Antifreeze Proteins ; biosynthesis ; Blotting, Western ; Cold Temperature ; Coleoptera ; Cryoprotective Agents ; chemistry ; Electrophoresis, Polyacrylamide Gel ; Freezing ; Insect Proteins ; biosynthesis ; Mice ; Pichia ; metabolism ; Sf9 Cells

Objective To test the changes of lymphocyte subsets and anti-GP Ⅱ b/Ⅲa,anti-GP Ⅰ b/Ⅸ specific antibodies in patients with idiopathic thrombocytopenic purpura(ITP),and discuss the related factors involved in pathogenesis of ITP.Methods The changes of lymphocyte subsets CD3+,CD4+,CD8+,CD4+CD8+,CD19+ in 72 patients with ITP (ITP group) and 50 healthy controls (control group) were measured by flow cytometry (FCM).Expression of anti-GP Ⅱ b/Ⅲ a,anti-GP Ⅰ b/Ⅸ specific antibodies were tested by monoclonal antibody immobilization of platelet antigens assay (modified MAIPA).Results Optical density of anti-GP Ⅱ b/Ⅲ a,anti-GP Ⅰ b/Ⅸ specific antibodies in ITP group was much higher than that in control group (P ＜0.05).In changes of lymphocyte subsets,the number of the CD3+,CD4+,CD4+/CD8+ in ITP group were obviously lower than those in control group (P ＜0.01),but CD8+ and CD19+ were much higher than those in control group(P ＜0.01).Conclusions Expression of lymphocyte subsets and platelet specific antibodies can reflect the pathogenesis of ITP well.The abnormal function and ratio of lymphocyte subsets,as well as the immunologic mechanism disorder of lymphocytes play important roles in the pathogenesis of ITP.

Objective To investigate the pathological significance of DEK-AP-2α interaction in HER2 overexpres-sion and breast tumorigenesis. Methods The protein level of DEK,AP-2α and HER-2 in breast tumor tissues was detected by Western blot. The interaction of DEK and AP-2α in MDA-MB-453 mammary cancer cells was detected by immuno-coprecipitation. Furthermore the impact of DEK and AP-2α on HER2 expression was investigated by siRNA in MDA-MB-453 mammary cancer cells followed by semi-quantitive RT-PCR and Western blot. Results A correlation between DEK, AP-2α and HER2 levels in breast cancer tissues were found. The interaction between DEK and AP-2α in MDA-MB-453 cells was verified by co-immunoprecipitation assay. Depletion of DEK and AP-2α in MDA-MB-453 cell by siRNA cooperatively repressed HER2 expression at both the mRNA and protein levels. Conclusion Oncogene DEK has synergestic effect with AP-2α transcriptional factor to promote HER2 overexpres-sion in breast cancer.

[Objective]To observe the growth status and osteogenic potential of gene transferred mesenchymal stem cells with Ad-BMP-2 planted on allogenetic acellular and decalcified bone matrix served as tissue engineering scaffold.[Method]Rabbit mesanchymal stem cells transferred with Ad-BMP-2 were seeded on allogenetic acellular and decalcified bone matrix,the growth status of gene transferred MSCs on the scaffold was observed by scanning electron microscopy and the ostengenic potential was observed by testing contents of ALP and BGP and secretion of Collagen I in the culture supermatant.[Result]The MSCs transfected with Ad-BMP-2 grew well on the tissue engineering scaffold,the osteogenic ability of the gene transfected MSCs showed great significant difference compared with that of the control group.[Conclusion]The MSCs transfected with Ad-BMP-2 can grow well on the acellular and decalcified bone matrix and the osteogenic potential can be great improved by gene transfection.

Objective To study the effect of hyperthermia-induced MMP-9 on expression of claudin-1 in in vitro BBB model.Methods BMEC and astrocytes were cultured.An in vitro BBB model was established with its permeability assayed by LY test.The BBB model was randomly divided into 37℃ group,39℃ group,37℃+MMP-9 group and 39℃+MMP-9 group.The permeability of BBB model was recorded at 30,60 and 90 min respectively.Expression of claudin-1 in BMEC was detected by Western blot with immunocytochemical staining.Results The permeability of BBB model was higher in 39℃ group than in 37℃ group (P＜0.05) and was significantly higher in 39℃ +MMP-9 group than in 37℃ group (P＜0.05).The number of claudin-1 positive BMEC was smaller in 39℃ +MMP-9 group than in 37℃ group at the same time points (P＜0.05) and in 39℃ +MMP-9 group than in 39℃ group at 90 min (75.0±12.8/HP vs 97.0±6.1/HP,P＜0.05).The expression level of claudin-1 was lower in 39℃ group than in 37℃ group (P＜0.05) and was significantly higher in 39℃ +MMP-9 group than in 37℃ group (P＜0.05),which further increased with the increasing time.Conclusion Hyperthermia can downregulate the expression of claudin-1 in in vitro BBB model and upregulate the permeability of in vitro BBB model.Adding MMP-9 can further aggrevate the damage of in vitro BBB model,indicating that hyperthermia can aggrevate the damage of in vitro BBB model through MMP-9.