1.High glucose downregulates the expression of podocalyxin protein in glomerular podocytes of mice
Journal of Peking University(Health Sciences) 2004;0(02):-
Objective:To examine the expression of podocalyxin protein in glomerular podocytes by long-term high glucose exposure in vitro and in vivo.Methods:Immunohistochemical staining and computer image analysis were applied to detect the expression of podocalyxin protein in glomeruli from db/db mice and Wt mice.The effects of high glucose on the expression of podocalyxin protein were analized by Western blotting.The activation of MAPKS signaling pathway(ERK,p38 and JNK)by high glucose was also examined.Results:The expressions of podocalyxin protein in db/db mice were obviously less than that in Wt mice[(0.18?0.07)vs(0.25?0.05),P
3.Research of the effect of persisters in Candida albicans biofilm on antifungal therapy using a Caenorhabditis elegans infection model
Chinese Journal of Microbiology and Immunology 2011;31(7):588-591
Objective To illuminate the effect of persisters on antifungal therapy by infecting Caenorhabditis elegans as a live-animal model with Candida albicans isolates of different persister levels, treating them with amphotericin B and comparing the survival rate. Methods Glp-4 (bn2ts); sek-1 (km4) worms were synchronized and grown to sterile to L4-stage, put on different Candida albicans strains lawns separately for 2 h. Dispensed 15-20 worms per well of the 96-well plate, and added serial dilutions of amphotericin B for each strain group. Wells filled without any amphotericin B were used as negative controls intra-group. Incubated the plate at 25C for 5 days, counted the survival rate of each well. Results Compared with negative controls, survival rate of drug wells in each group increased. In the same drug concentration, the increase for high-persister group was significantly lower than that for low-persister group (P<0.01). Conclusion Caenorhabditis elegans provides a model for the study of persisters and antifungal pharmacodynamics.The drug tolerance of persisters may be a critical component responsible for antifungal drug failure and relapsing infections.
4.Effects of low-dose T-2 toxin on cultured cartilage cells and molecular mechanism
Chinese Journal of Endemiology 2015;34(7):485-489
Objective Through observing the effect of low-dose T-2 toxin on chondrocyte,to study the molecular mechanism of cartilage damage.Methods The primary chondrocytes were isolated from articular cartilage of d 1-2 Wistar neonate rats through enzymatic digestion.Different doses (0.005,0.010,0.100 μg/L) of T-2 toxin were added after 24 h in vitro culture.The survival rate of chondrocytes was detected with Trypan blue staining.Echylosis (matrix metalloproteinase,MMP1) was analyzed by immunohistochemistry.The damage of articular chondrocyte was observed by transmission electron microscope.Results ①Cell morphology of in vitro cultured chondrocyte:the newly isolated chondrocytes were spherical.After 24 hours,the adherent cells gradually began to stretch the triangle or polygon;the nucleus was large and round;the cell was clear and transparent,containing secretory granules.②Cell proliferation:T-2 toxin had a significant inhibitory effect on chondrocyte proliferation,the higher the concentration of T-2 toxin,the significant the inhibitory effects [0.000 μg/L (control) group:3.45 × 108/L,0.005 μg/L T-2 toxin group:3.45 × 108/L,0.010 μg/L T-2 toxin group:2.06 × 108/L,x2 =9.554,P < 0.05].③Immunohistochemical observation:dysplasia,nucleus condensation and membrane rupture were observed in T-2 toxin treated group,brown staining was observed in all groups at varying degrees.The deepest staining was in 0.005 μg/L T-2 toxin group,with the strongest secretion of MMP1;with increasing doses of the toxin,the damage to cartilage cells was severe,MMP1 secretion was less,staining was weak,and the weakest staining was in the 0.100 μg/L T-toxin group.④Under transmission electron microscopy:in control group,cytoplasm was rich in rough endoplasmic reticulum,nuclear membrane and cell membrane were clear;in 0.005 μg/L T-2 toxin group,the cell nucleus showed pyknosis,organelles were decreased in cytoplasm;in 0.100 μg/L T-2 toxin group,the microvilli was dropped out of cartilage surface,nuclear changes were obvious,and mitochondria was myeloid degeneration;rough endoplasmic reticulum was degranulation and expansion into cystiform,chondrocytes were apoptosis occasionally,the cell nucleus showed pyknosis,and the formation of high-density plaque.Conclusion Low dose of T-2 toxin could damage the primary cultured articular chondrocyte in vitro.The results have showed that there are damaged cytostasis,chondrocyte degeneration,necrosis and apoptosis.
5.Clinical research progress of Boston type l keratoprosthesis
International Eye Science 2015;(1):1-5
?Boston Type l keratoprosthesis is currently widely used. ln this article, the indication, number of cases, best-corrected visual acuity ( BCVA ) , retention, and complications in all the international published case reports will be sum up; then the main post-operative complications and their respective treatments one by one, which include retrospective membrane, glaucoma, infection will be introduced.
6.Advances in the study of aldehyde oxidases.
Acta Pharmaceutica Sinica 2014;49(5):582-589
Aldehyde oxidase (AOX), a highly conserved molybdoflavoenzyme in mammal cytoplasm, has broad substrate specificity and ability to catalyze the oxidation of aldehydes and nitrogen, oxygen-containing heterocyclic rings. AOX was found to widely distribute with the individual differences in vivo and plays an important role in phase I metabolism of drugs and xenobiotics. The biological characteristics of AOX and its contributions in drug metabolism are introduced briefly in this review.
Aldehyde Oxidase
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antagonists & inhibitors
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chemistry
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metabolism
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Animals
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Drug Discovery
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Humans
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Liver
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enzymology
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Oxidation-Reduction
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Pharmaceutical Preparations
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metabolism
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Raloxifene Hydrochloride
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pharmacology
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Substrate Specificity
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Xenobiotics
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chemistry
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metabolism
9.Current status of tissue engineering in urology
Journal of Shanghai Jiaotong University(Medical Science) 2006;0(09):-
Tissue engineering provides urologists a new way to fix or reconstruct the impaired organs.Reconstitution of corporal bodies of penis with engineered tissue substitutes has been applied in animal models.In hypospadias reconstruction,the use of engineered tissue substitutes has been applied clinically.The clinical application of bladder tissue substitutes has been ongoing phase II clinical trial.Great progress has been made in renal replacement therapy with clinical application of human progenitor cells in hemofiltration units,and the engineered intracorporeal renal replacement unit will come true by additional studies.The current status of tissue engineering in clinical practice of urology is reviewed in this paper.
10. Therapeutic effect of low-dose aspirin on chronic allograft nephropathy in renal recipient rats
Academic Journal of Second Military Medical University 2010;31(6):650-652
Objective: To observe the effect of low-dose aspirin on allogeneic chronic allograft nephropathy in renal recipient rats and the possible mechanisms. Methods: Chronic allograft nephropathy model of rats were established and the recipient rats were randomly divided into 2 groups with 10 in each group. Cyclosporine A (5 mg/kg) was administered as a basic treatment one day before surgery to prevent and treat acute rejection. Aspirin therapy group was given oral aspirin (5 mg/kg) daily, and control group were given oral saline 2 ml/d. Animals were sacrificed 8 weeks after operation and the serum creatinine, urea nitrogen levels were determined. Renal histomorphology and immunohistochemistry approaches were used to examine TGF-β1 expression. Results: The severity of pathological lesion, increase of serum creatinine and blood urea nitrogen levels, and expression of fibrosis associated factor TGF-β1 in aspirin therapy group were significantly slighter than those of the saline control group (P<0.05). Conclusion: Low-dose aspirin in addition to routine anti-rejection treatment can be used for treatment of chronic allograft nephropathy in rats, which might be associated with the decreased expression of anticoagulation factor TGF-β1.