Liver Imaging Reporting and Data System was released online in 2011 by America College of Radiology (ACR) for standardizing the performance,interpretation and reporting of CT and MR imaging examinations of the liver in patients at risk for hepatocellular carcinoma.This article overviewed the profile of this system,its updated version and recent progress on its clinical application.

AIM: To observe the effect of mouse Sim2 (mSim2) eukaryotic expression vector transfection on the cell cycle in PC12 cells in vitro and to explore the role of Sim2 in the pathogenesis of Down syndrome. METHODS: The full open reading frame of mSim2 was amplified by reverse transcription-polymerase chain reaction (RT-PCR) and cloned into the vector pcDNA3. Then the constructed pcDNA3-Sim2 vectors were transiently transfected into PC12 with Lipofectamine~ TM . The expression of mSim2 was detected by RT-PCR. The effect of mSim2 on the cell cycle was observed by flow cytometry. RESULTS: The eukaryotic expression vector mSim2 was successfully constructed. There was notable expression of mSim2 in the cells transfected with pcDNA3-Sim2. There were more cells in G_0/G_1 phase in the pcDNA3-Sim2 transfected cells than that in the control (P

To investigate the effects of ischemia-reperfusion on the levels of nitric oxide and nitric oxide synthase isoforms (nNOS and iNOS), rat organotypic hippocampus slice were cultured in vitro and subjected to ischemia by oxygen-glucose deprivation (OGD) for 30 min and then placed in the normal culture condition. The ischemia-reperfusion produced a time-dependent increase in nitrite levels in the culture medium. Reverse transcriptional-polymerase chain reaction showed augmented levels of mRNA for both nNOS and iNOS when compared with control at 12 h and remained increase at 36 h after OGD (P < 0.05). The protein levels of both nitric oxide synthase isoforms increased significantly as determined by Western Blot. OGD also caused neurotoxicity in this model as revealed by the elevated lactate dehydrogenase (LDH) efflux into the incubation solution. The results suggest that organotypic hippocampus slice is a useful model in studying ischemia-reperfusion brain injury. NO and NOS may play a critical role in the ischemia-reperfusion brain damage in vitro.
Animals, Newborn ; Cell Hypoxia ; Hippocampus/cytology ; Hippocampus/*metabolism ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase Type I/*metabolism ; Nitric Oxide Synthase Type II/*metabolism ; RNA, Messenger/metabolism ; Rats, Sprague-Dawley ; Reperfusion Injury/*metabolism ; Tissue Culture Techniques

The aim of this study was to express and purify human histydyl-tRNA synthetase related gene and to prepare its polyantibody. The open reading frame was amplified by PCR, and then recombined into prokaryotic expression vector pQE30 and transformed into E. coli M15 for expression. The expressed products were induced by IPTG after the reconstructed pQE30 was transferred into M15. After purified by Ni affinity chromatography, the product was identified to be a single band by SDS-PAGE. The rabbits were inoculated with purified products. High-titer polyantibody was successfully prepared. Highly-purified expression product and prepared polyantibody may provide a good basis for further study.
Antibodies/*genetics ; Antibodies/immunology ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Histidine-tRNA Ligase/biosynthesis ; Histidine-tRNA Ligase/*genetics ; Histidine-tRNA Ligase/immunology ; Open Reading Frames/genetics ; Prokaryotic Cells/metabolism

Aim To explore the possible protective effect of ginsenoside Rg1 on oligomeric Aβ1-42 induced apoptosis and its possible mechanism. Methods The damage was induced by oligomeric Aβ1-42 in primary cortical neurons. Cells were incubated in the absence or presence of Aβ, or co-incubated in sp600125 with Aβ, or pre-incubated in ginsenoside Rg1 then co-incu-bated in Aβ. The p-JNK, JNK, caspase-3 activity and TUNEL-positive cells were detected. Results In Aβ1-42 treated group, the ratio of p-JNK/JNK level was increased more than that in non-treated group for 15 min. However, in neurons preincubated with (2. 5, 5, 10 μmol·L-1 ) ginsenoside Rg1 and then co-incuba-ted with 5 μmol·L-1 oligomeric Aβ1-42 , the p-JNK/JNK ratio, caspase-3 activity and TUNEL positive neu-rons were significantly decreased compared with those of Aβ1-42 treated group. Conclusion Ginsenoside Rg1 can attenuate the oligomeric Aβ1-42-induced apop-tosis by JNK pathway.

Objective To investigate the possible effect of ginsenoside Rg1 and oligo Aβ1-42 on PKA/CREB pathway.Methods The damage was induced by oligomeric Aβ1-42 in primary cortical neuron.Neurons were incubated with or without glutamate,or incubated in Aβ,or pre-incubated in Rg1 and then co-incubated in Aβ.The proteins of p-CREB,t-CREB,PKA Ⅱ α and BDNF were detected by Western blot.Results After the treatment with Oligo Aβ1-42 for 2 h,the p-CREB/t-CREB level induced by glutamate was obviously lower (P＜ 0.001).However,in neurons pre incubatedwith 2.5,5.0,10.0 μmol/L of ginsenoside Rg1 and then co-incubated with 5μmol/L of oligo Aβ1-42,the p-CREB/t-CREB induced by glutamate was significantly increased as compared with that of Aβ1-42 group (P＜0.05).Upon Aβ1-42 exposure for 2 h,cortical neurons showed a statistically significant increase in PKA Ⅱ α as compared to the control group (P ＜ 0.001).Pre-treatmentwith varying doses of ginsenoside Rg1 (2.5,5,10μmol/L) showed a decrease in PKA Ⅱ α as compared to neurons treated with Aβ1-42 alone for 2 h (P＜0.001).Furthermore,BDNF level significantly increased in Rgl-pretreated cells as compared to cells treated with Aβ1-42 alone for 24h (P＜0.05).Conclusions Ginsenoside Rg1 attenuates the oligo Aβ142 inhibition of PKA/CREB pathway.

Objective To investigate the clinical outcome and treatment of portal vein thrombosis (PVT) following partial splenic embolization (PSE).Methods From April 2006 to April 2010,105patients with hypersplenism caused by cirrhotic portal hypertension were treated with PSE.Contrastenhanced abdominal computed tomography or magnetic resonance imaging was performed routinely in 60patients before PSE and 1 -3 months after PSE.PVT was detected in 10 patients on images after the procedures.After PVT was diagnosed,4 patients received anticoagulant therapy immediately,and the other 6 patients did not receive therapy.Clinical data of these 10 PVT patients were analyzed retrospectively.Results 3 of 4 patients who received anticoagulant therapy had complete or partial resolution of the thrombus,and one developed mild ascites without thrombosis progression.Of the 6 patients who did not receive anticoagulant therapy,follow-up studies (6- 48 months,mean 16.9 months) demonstrated partial clot calcification in one,thrombosis progression in 5.Among those 5 patients with thrombosis progression,two experienced hematemesis due to variceal rupture and underwent transjugular intrahepatic portosystemic shunt,2 developed cavernous transformation,extensive collateral circulation,ascites and variceal progression,and one had variceal progression with melena during the follow-up period.Conclusions PVT is a severe complication of PSE.Early diagnosis and prompt anticoagulant therapy is effective in preventing PVT.

Objective Using CT perfusion (CTP) technique,to investigate the graft perfusion changes in patients with hepatic artery stenosis (HAS) with or without ischemic-type biliary lesions (ITBL) after orthotopic liver transplantation (OLT).Methods Thirteen recipients with HAS received CTP scan of the liver,including 8 with ITBL and 5 without ITBL.For all patients,the diagnosis of HAS was made by CTA,and the diagnosis of ITBL by percutaneous transhepatic cholangiography.CT perfusion indices were obtained,including hepatic artery perfusion (HAP),portal vein perfusion (PVP),total liver perfusion (TLP) and hepatic perfusion index (HPI).Results Of the 13 patients with HAS,mean HAP in patients with and without ITBL was 59.8 and 35.1 ml·min-1 ·100 ml-1 (P =0.021,two-tailed paired Student t test) ; mean PVP was 125.4 and 166.2 ml·min-1·100 m1-1 (P =0.016) ; mean TLP was 185.2 and 201.3 ml· min-1 · 100 ml-1 (P =0.306) ; and mean HPI was 33.6 and 18.2 (P =0.005),respectively.Conclusion Using CTP technique,liver perfusion changes were reflected by measuring CTP indices noninvasively.Compared to those without ITBL in this study,HAP and HPI in patients with ITBL were higher and PVP was lower,which may be contributed to biliary inflammation.

Objective To evaluate the effects of limb ischemic preconditioning (LIP) on the intestinal injury during release of hepatic portal occlusion (RHPO) in rats.Methods Thirty-six male Sprague-Dawley rats,aged 6-7 weeks,weighing 200-250 g,were randomly divided into 3 groups using a random number table:sham operation group (group S,n =12),RHPO group (n =39) and LIP+ RHPO group (n =20).Hepatic ischemia/ reperfusion was produced by occluding portal vein and hepatic artery for 30 min followed by 6 h reperfusion according to Pringle's method.LIP was produced by tourniquet occlusion of the right femoral artery and vein for 10 min followed by 24 h reperfusion before hepatic ischemia.The animals were sacrificed at 6 h after hepatic portal occlusion was released and the mucous membrane of small intestine was obtained for microscopic examination and for determination of malondialdehyde (MDA) content,superoxide dismutase (SOD) activity,myeloperoxidase (MPO)activity,total antioxidant capacity (T-AOC) and intercellular adhesion molecule-1 (ICAM-1) mRNA and protein expression.The degree of damage to intestinal mucous membrane was scored according to Chiu.Results Compared with group S,Chiu's score and levels of MDA and MPO were significantly increased,SOD activity and TAOC were decreased,and ICAM-1 mRNA and protein expression was up-regulated in group RHPO (P ＜ 0.05 or 0.01).Compared with group RHPO,Chiu's score and levels of MDA and MPO were significantly decreased,SOD activity and T-AOC were increased,and ICAM-1 mRNA expression was down-regulated in group LIP + RHPO (P ＜ 0.05).Conclusion LIP can alleviate the intestinal injury during RHPO in rats by enhancing the antioxidant function and down-regulating the expression of ICAM-1.

Objective To investigate the imaging characteristics of different biliary strictures after liver transplantation and their relationship with causes. Methods Forty-six patients with jaundice and biliary stricture were enrolled in this study.The diagnosis was confirmed by percutaneous transhepatic cholangiography (PTC).All the patients had hepatic arteriography with DSA or CTA and underwent liver biopsy.Their imaging characteristics were analyzed and the related statistic analysis was conducted.Results Anastomosis biliary stricture (ABS) was demonstrated in 21 cases,and non-anastomosis biliary stricture (NBS) with hepatic artery thrombosis (HAT) occurred in 13 cases,and there were 12 cases of NBS without HAT.PTC examination confirmed there were 26 cases of biliary stricture at hepatic hilum,and the incidence of biliary stricture in NBS group was significantly higher than that in ABS group (92％ vs.14.35％,P＜0.05).There were 31 cases of intrahepatic bile duct stricture,and the incidence in NBS group was significantly higher than that in ABS group ( 100％ vs.28.6％,P＜0.05).There were 33 cases of dilatation of intrahepatic bile duct,and the incidence in NBS without HAT group was significantly lower than that in ABS group and NBS with HAT group (16.7％,100％ and 76.9％ respectively) (P＜0.05).There were 21 cases of extrahepatic biliary dilatation,and the incidence in ABS group was significantly higher than that in NBS group (85.7％ vs. 12％,P＜0.05). There were 18 cases of stricture and dilatation in intrahepatic bile duct,and the incidence in NBS with HAT group was significantly higher than that in ABS group and NBS without HAT group (76.9％,28.6％ and 16.7％ respectively,P＜0.05).The results of the liver biopsy were accorded with the diagnosis of biliary stricture,Conclusion The different biliary strictures carry different imaging characteristics,including location of biliary stricture,and location and type of secondary biliary dilatation.