3.Comparison on Characteristics of Tumor Recurrence of Hepatocellular Carcinoma after Liver Transplantation and Hepatectomy
Bo LV ; Tian-Fu WEN ;
Chinese Journal of Bases and Clinics in General Surgery 2003;0(03):-
Objective To explore the different characteristics of tumor recurrence after liver transplantation (LT)and hepatectomy(HC)in patients with hepatocellular carcinoma(HCC).Methods The literatures about tumor recurrence of HCC after LT and HC were reviewed and their characteristics were compared.Results There are distinctions of recurrence rates,time,common sites between the recurred tumors after LT and HC,and their correlation factors and mechanisms of recurrence are also different.Conclusion Preventive measures should be strengthened and treatments should be more targeted according to the different characteristics of tumor recurrence after LT and HC to improve postoperative life quality and increase the survival rate.
4.Inertial Measurement Unit and Fall Risk Assessment in the Elderly (review)
Chinese Journal of Rehabilitation Theory and Practice 2015;21(7):780-784
Falling in the elderly is a major health problem and may cause severe consequences. Fall risk assessment is important for preventing and intervening fall incidence. Inertial Measurement Unit (IMU) has been introduced to evaluate motion/balance function and fall risk among the older people. Some researches indicated that it might have advantages over the usual tools, and can be used in the hospitals, communities, nursing homes, etc. IMU is a good way to measure gait variability, which may be strongly related with the risk of falls.
6.First visit for hoarseness: a rare case of a fish bone in paraglottic space.
Li-bo DAI ; Ling LING ; Yong FU
Chinese Journal of Otorhinolaryngology Head and Neck Surgery 2009;44(4):334-334
Foreign Bodies
;
complications
;
diagnosis
;
Glottis
;
Hoarseness
;
diagnosis
;
etiology
;
Humans
;
Male
;
Middle Aged
7.Hypoxia/reoxygenation and lipopolysaccharide induced nuclear factor-κB and hypoxia-inducible factor-1α signaling pathways in intestinal epithelial cell injury and the interventional effect of emodin
Chinese Critical Care Medicine 2014;26(6):409-414
Objective To observe pathological process of intestinal epithelial cells subjected to ischemia,ischemia/reperfusion injury and inflammation simulated hypoxia/reoxygenation (H/R) and lipopolysaccharide (LPS) challenged human fetal normal colonic cell (FHC) line in vivo,and to observe the changes when the assaulted intestinal epithelial cells were treated with emodin,in order to explore the possible intervention targets of emodin.Methods Normoxia group:the FHC cells were cultured in 95% air and 5% CO2 at 37 ℃.Hypoxia (H) group:the cells were cultured with a mixed anaerobic gas of 1% O2,5% CO2 and 94% N2 at 37 ℃ for 1,2,3,4 hours.H + LPS group:the cells were cultured in hypoxic condition as H group with simultaneous challenge of LPS (1 mg/L).H/R group:the cells were cultured in hypoxia for 3 hours followed by reoxygenation for 1,2,3 and 4 hours,respectively.H/R + LPS group:the cells were cultured in H/R as H/R group and LPS (1 mg/L) simultaneously.Emodin intervention group:the cells were cultured in H3 h/R2 h + LPS and emodin (20,40,60,80 μmol/L) simultaneously.The variation trends of phosphorylation nuclear factor-κB profilin-o (pIκB-α),phosphorylation NF-κBp65 (pNF-κBp65) and their downstream target gene cyclooxygenase-2 (COX-2),and hypoxia-inducible factor-1α (HIF-1 α) were determined by Western Blot.The morphological changes in intestinal epithelium in different groups were observed using light microscope.The effect of emodin on the proliferation of intestinal epithelial cell was measured by methyl thiazolyl tetrazolium (MTT) assay.Results ① H group:the expressions of pIκB-α,pNF-κBp65 and COX-2 were upregulated,peaking at H1 h (0.350 ± 0.018,1.083 ± 0.054,0.903 ± 0.045),and then they gradually lowered (F value was 3.011,7.247,5.754,P value was 0.013,0.000,0.005,respectively).The expression of HIF-1 α peaked at H3 h (1.511 ± 0.076),but there was no significant difference among different groups (F=1.881,P=0.062).H + LPS group:the expressions of pIκB-α,pNF-κBp65,COX-2,HIF-1α were increased with elongation of duration of hypoxia,and a maximal induction was observed at H3 h (0.504 ± 0.025,1.255 ± 0.063,0.812 ± 0.041,1.209 ± 0.075,F value was 2.683,8.774,9.765,2.432,and P value was 0.011,0.000,0.000,0.026,respectively).H/R group:with the prolonged duration of reoxygenation,the expressions of NF-κB signaling pathway proteins (pIκB-α,pNF-κBp65,COX-2) were decreased and dropped to nadir at H3 h/R4 h (0.712 ± 0.034,1.202 ± 0.048,0.691 ± 0.042,F value was 1.923,6.765,2.719,and P value was 0.063,0.000,0.016,respectively).Compared with H group,HIF-1α was decreased with a prolonged duration of reoxygenation in H/R group,but there was no significant difference in value among different time points (F=1.280,P=0.081).H/R + LPS group:pIκB-o,pNF-κBp65,COX-2,HIF-1α showed no sign of degradation with the prolonged duration of reoxygenation,and their expression increased to maximum analogously at R2-3 h (3.302 ± 0.061,2.315 ± 0.055,2.017 ± 0.043,2.413 ± 0.098,Fvalue was 4.614,1.652,5.970,2.076,and Pvalue was 0.001,0.067,0.000,0.037,respectively).Emodin group:emodin when co-treated with H/R + LPS inhibited the expression of HIF-1o and NF-κB pathways with a dose-effect relationship (P<0.05 or P<0.01).Emodin at the dose of 80 μmol/L showed most marked inhibition (2.599 ± 0.130,1.772 ± 0.089,2.590 ± 0.129,2.518 ± 0.125).However,after treatment of emodin did not show such effect.② After treatment with H/R + LPS,there were morphological changes in cells:vacuoles,deformation and fusion.The speed of cell growth became much slower compared with H group.③ Emodin (20-80 μmol/L) had no significant effect on cell proliferation.Although emodin produced biological effect in this concentration range,it had no cellular toxicity.Conclusions Both hypoxia and inflammation can activate the hypoxia pathway of HIF-1α and the pro-inflammatory pathway of NF-κB,but different stimuli cause varying degrees of activation in these two pathways.In H/R group,both pathways were weakened during reoxygenation.However,in H/R + LPS group,the proteins remained to show a relatively high expression during the process of reoxygenation.This may be related to the pathophysiological mechanism of intestinal ischemia/reperfusion injury:hypoxia/reperfusion injury and LPS act together to destroy the intestinal epithelial cells and induce gut-derived sepsis.Emodin may inhibit inflammation by blocking HIF-1α/NF-κB-COX-2 signaling pathways.
8.Clinical Observation of Low Molecular Weight Heparin Calcium in the Prevention of Venous Thromboem-bolism of ICU Patients
Zhenhui FU ; Bo REN ; Qundu ZHAO
China Pharmacy 2016;27(20):2838-2840,2841
OBJECTIVE:To observe the safety and therapeutic efficacy of low molecular weight heparin calcium in the preven-tion of venous thromboembolism (VTE) of ICU patients. METHODS:572 VTE patients were randomly divided into trial group and control group,with 286 cases in each group. Trial group was given Low molecular weight heparin calcium injection 0.3-0.6 ml, im,qd;control group was given Rivaroxaban tablet 10 mg,po,qd. The incidence of VTE,platelet count,coagulation function, quality score of life and the occurrence of ADR were compared between 2 groups. RESULTS:The incidence of VTE in trial group (0.3%)was significantly lower than control group(2.1%),with statistical significance(P<0.05). There was no statistical signifi-cance in platelet count,prothrombin time,APPT, fibrinogen and other indexes between 2 groups before and after treatment(P>0.05). The physical health,body function and role,general health,emotional role function,mental health and other aspects of trial group were improved significantly,compared to control group,with statistical significance(P>0.05). No obvious ADR was found in 2 groups. CONCLUSIONS:Low molecular weight heparin calcium can effectively prevent VTE and improve the quality of life, while doesn’t influence platelet count and coagulation function with good safety.
9.The statistical analysis of association between serum level of chlamydia pneumonia immunoglobulin A antibody and the attack of ischemic stroke
Bo ZHOU ; Jingpu SHI ; Lingyu FU
Chinese Journal of Practical Internal Medicine 2001;0(04):-
0.05),the odds ratio(OR)being 0.873,[95% confidential interval(CI):0.428~1.782].(3)The relationship between ischemic stroke and the risk factors was illuminated by the Logistic Regression analysis.The results showed that there was no significant difference of the positive rate of IgA antibody between the case group and control group.Conclusion There may be not relationship between CP IgA antibody and ischemic stroke.There is no relationship between IgA CP antibody and the other risk factors of ischemic stroke.
10.EFFECTS OF ANGIOTENSIN Ⅱ ON PAI-1 GENE EXPRESSION IN HUMAN GLOMERULAR MESANGIAL CELLS AND ITS MECHANISM
Bo FU ; Xiangmei CHEN ; Weng LI
Medical Journal of Chinese People's Liberation Army 1982;0(01):-
To explore the effects of angiotensin Ⅱ on plasminogen activator inhibitor 1 (PAI 1) gene expression in human glomerular mesangial cells.Glomerular mesangial cells (GMCs) were cultured from a healthy adult human kidney (unsuitable for renal transplantation) and then treated with angiotensin Ⅱ at concentration of 10 -9 ,10 -8 , 10 -7 and 10 -6 mol/L, respectively. The mRNA expressions of angiotensinⅡAT1 and AT2 receptor, and PAI I were examined with RT PCR and Northern blot analysis, respectively. Plasminogen activator activity in the supernatants of the GMCs was measured with fibrin plate method. After the GMCs were stimulated by angiotensin Ⅱ, the mRNA level of the AT1 receptor was markedly enhanced, but the AT2 receptor mRNA level was still undetectable as that in normal condition. When GMCs were treated with angiotensin Ⅱ for 48 hours, PAI 1 mRNA expression was increased in a dose dependent manner. The plasminogen activator activity was significantly reduced in the supernatants of the angiotensinⅡ treated GMCs. the results suggested that angiotensinⅡ promote PAI 1 gene expression of the GMCs possibly through its AT1 receptor.