Value-based medicine is a new medical model which develops on the basis of evidence-based medicine and perfectly combines the skills and experiences of doctors with patients and hospitals’ value. According to the definition and connotation of the value-based medicine,this paper introduced its preliminary application at different stages(theoretical teaching,internship and practice) of digestive disease courses by teaching theory courses and letting students involved in the management of different individuals of the same disease. Meanwhile,this paper discussed on its effects.

Objective:To evaluate the effect of portal vein restriction combined with hepatic artery ligation on Sprague Dawley(SD) rats liver regeneration and injury.Methods:Twenty-four healthy and clean SD male rats, 250-280 g, 7-8 weeks old, were randomly divided into portal vein ligation (PVL) group, mild restriction group and moderate restriction group with 8 rats in each group. In PVL group, the right, caudal and left branches of portal vein were ligated, and only the right branches of portal vein were preserved. The operation of mild and moderate restriction group was the same as PVL, however, the left branch of the portal vein was slightly and moderately restricted, and the left branch of the hepatic artery was ligated at the same time. At 72 hours after the operation, the left middle lobe was stained with hematoxylin-eosin and the total necrosis score was calculated. The right middle lobe was immunostained for Ki-67 and the number of positive cells was counted. The liver regeneration rate of the right middle lobe was calculated and the serum liver function indexes were measured.Results:The hepatic regeneration rate of right middle lobe in PVL group was (109.1±10.9)%, while that in moderate restriction group was (105.0±12.3)%, which was significantly higher than that in the mild restriction group (67.1±6.4)%, the differences were statistically significant ( P<0.05). The Ki-67 result was also higher in the PVL group than the mild restriction group. The total necrosis score was 4.50(3.25, 6.00) in moderate restriction group, 2.00(1.25, 3.00) in PVL group and 0(0, 0.75) in mild restriction group. The three groups showed a decreasing trend and the differences were statistically significant ( P<0.05). Alanine aminotransferase in mild restriction group was (48.4±11.4) U/L, was significantly lower than that in PVL group (67.2±12.2) U/L and moderate restriction group (74.3±14.2) U/L, the difference was statistically significant ( P<0.05). There were no significant differences in serum levels of aspartate aminotransferase, albumin and total bilirubin among the three groups ( P>0.05). Conclusion:Appropriate portal vein restriction combined with hepatic artery ligation can effectively induce the regeneration of liver tissue on the reserved lobe and control the damage of liver tissue on the occluded lobe.

OBJECTIVETo investigate the prophylactic and therapeutic effect of oxymatrine on experimental liver fibrosis and to reveal its mechanism.

METHODSBy establishing D-galactosamine-induced rat liver fibrosis model, we observed the effect of oxymatrine on serum and tissue biochemical indexes, content of liver hydroxyline, expression of TGF?1 mRNA and changes of tissue pathology.

RESULTSThere was a decline of liver hydroxyline and serum AST and ALT in oxymatrine group compared to those of the D-GalN group. The hydroxyline content in oxymatrine pretreatment group was (0.50 0.11)mug/mg compared with (0.99 0.14)mug/mg in D-GalN group (t=8.366, P<0.01). The content in oxymatrine treatment group was (0.44 0.04)mug/mg compared with 0.70 0.06 in D-GalN group (t=9.839, P<0.01). The SOD activity was (149.81 15.28) NU/mg in oxymatrine pretreatment group and (95.22 16.33) NU/mg in the model group (t=7.309, P<0.01); (157.68 19.54) NU/mg in the treatment group compared with (119.88 14.94) NU/mg in the model group (t=4.348, P<0.01). MDA in the pretreatment group was (2.06 0.17) nmol/mg, lower than (4.57 0.37) nmol/mg in the model group (t=17.529, P<0.01). In the treatment group, it was (1.76 0.24)nmol/mg, lower than (3.10 0.17) nmol/mg in the model group (t=12.697, P<0.01). TGF?1 mRNA reduced in the pretreatment and treatment groups as compared with that in the model group (0.21 0.01 vs 0.50 0.01, t=48.665, P<0.01; 0.18 0.02 vs 0.38 0.01, t=22.464, P<0.01). Electron microscopy showed that oxymatrine group had milder hepatocyte degeneration and less fibrosis accumulation than did the model group. Microscopy revealed wide septa expansion from the portal area to the central venous, piecemeal and confluent necrosis and pseudo-nodular formation in part of the lobular in the model group. While in oxymatrine group these lesions were much improved.

CONCLUSIONSOxymatrine shows prophylactic and therapeutic effect in D-galactosamine induced rat liver fibrosis. This is partly by protecting hepatocyte and suppressing fibrosis accumulation through anti-lipoperoxidation.

Alkaloids ; therapeutic use ; Animals ; Anti-Arrhythmia Agents ; therapeutic use ; Calcium Hydroxide ; metabolism ; Chemoprevention ; Disease Models, Animal ; Galactosamine ; Liver Cirrhosis ; chemically induced ; drug therapy ; metabolism ; pathology ; prevention & control ; Liver Function Tests ; Male ; Quinolizines ; RNA, Messenger ; metabolism ; Rats ; Rats, Wistar ; Superoxide Dismutase ; metabolism ; Transforming Growth Factor beta ; genetics ; metabolism

Objective To observe the changes of liver function,blood cell,and lung function of healthy young and middle-aged men before and after fast-advancing short-term high altitude exposure(FSHAE);and to explore the effects and possible mechanisms of FSHAE on the function of liver,blood cells,and lung tissues.Methods This study included 48 healthy young and middle-aged male volunteers,who collected physiological indicators,tested liver function indicators,blood cell indicators,and lung function-related indicators 1 day before entering the plateau(100m above sea level),and 15 days after FSHAE(3000m above sea level).Differences in the relevant parameters of each system were compared before and after FSHAE.Results Compared with those before entering the plateau,the physiological parameters of young and middle-aged men after 15 days of FSHAE heart rate increased significantly,respiratory rate increased,systolic blood pressure increased,mean arterial blood pressure increased,oxygen saturation decreased(P＜0.01),and diastolic blood pressure increased(P＜0.05),all of which were statistically significant;and the indicators of liver function:glutamic oxaloacetic aminotransferase,glutamic alanine aminotransferase increased(P＜0.01),glutamylamine aminotransferase,glutamate aminotransferase,glutaminase,and pulmonary function were increased(P＜0.01),glutamyl transpeptidase,alkaline phosphatase,and total bile acids were elevated,and total protein decreased(P＜0.05),and the differences were statistically significant.Hemocyte-related indexes:erythrocyte count,erythrocyte pressure volume,mean erythrocyte volume,mean hemoglobin volume,mean hemoglobin concentration,and hemoglobin were elevated,and platelet count decreased(P＜0.01),and the differences were statistically significant.although there was an elevation of leukocyte count(P＞0.05);Lung function-related indexes:decreased exertion lung volume(P＜0.05).There were decreased exertion expiratory volume in the first second,increased one-second rate(P＞0.05).Conclusion FSHAE can lead to oxidative stress in the organism,and acute hypoxic multisystemic injury will occur,with the simultaneous emergence of hypoxic adaptive regulation of various systems,self-compensatory repair of various organs of the organism,and there may be the possibility of interactions between various systems.

The integrity of lysosomes is of vital importance to survival of tumor cells. We demonstrated that LW-218, a synthetic flavonoid, induced rapid lysosomal enlargement accompanied with lysosomal membrane permeabilization in hematological malignancy. LW-218-induced lysosomal damage and lysosome-dependent cell death were mediated by cathepsin D, as the lysosomal damage and cell apoptosis could be suppressed by depletion of cathepsin D or lysosome alkalization agents, which can alter the activity of cathepsins. Lysophagy, was initiated for cell self-rescue after LW-218 treatment and correlated with calcium release and nuclei translocation of transcription factor EB. LW-218 treatment enhanced the expression of autophagy-related genes which could be inhibited by intracellular calcium chelator. Sustained exposure to LW-218 exhausted the lysosomal capacity so as to repress the normal autophagy. LW-218-induced enlargement and damage of lysosomes were triggered by abnormal cholesterol deposition on lysosome membrane which caused by interaction between LW-218 and NPC intracellular cholesterol transporter 1. Moreover, LW-218 inhibited the leukemia cell growth