The evaluation of the immunosuppression state in liver transplanted recipients is vital for a correct posttransplantation management and a major step towards the personalized treatment of the immunosuppression.To date,immunological monitoring after liver transplantation relies mainly on clinical judgment and pathological examination of the graft,without a proper assessment of the actual state.Previous studies have ever identified many markers for acute rejection(AR) and immune tolerance after liver transplantation.Many markers for AR are pro-inflammatory or immunoregulatory cytokines and other proteins related to inflammation.However,many markers have been proved to be also able to predict other diseases and only a few of the markers for AR have been validated.Standard liver tests cannot be used as markers for graft rejection due to the low sensitivity and specificity.This review summarized the potential markers for AR and immune tolerance after liver transplantation based on published literatures in recent years and to provide evidence for clinical application.

Objective:To study the protective effect and effect of SphK1 overexpression on the injury of nerve cells induced by acrylamide.Methods:ACR with 99% purity was prepared into 1.25 mmol/L and 2.5 mmol/L solutions. SH-SY5Y cells were divided into control group (NC group) , experimental group and SphK1 activator group. The experimental group was given ACR solution with final concentration of 1.25 mmol/L and 2.5 mmol/L respectively for 24 h. In the SphK1 activator group, on the basis of the exposure concentration of the experimental group, the SphK1 specific activator (12-) phorbol tetradecanoate (-13-) acetate (PMA) solution[prepared by dimethyl sulfoxide (DMSO) , the final concentration was 100 nmol/l], and other treatments were the same as the experimental group. Control group (NC group) added PMA solution into normal cells. Western blot was used to detect the expression of SphK1 protein; CCK-8 was used to detect the proliferation of SH-SY5Y cells; hoechst33342 method was used to observe the morphological changes of nerve cells; flow cytometry was used to analyze the apoptosis of cells.Results:Compared with NC group, the expression of SphK1 protein in the experimental group and the SphK1 activator group was significantly lower ( P<0.05) . Compared with the experimental group, the expression of SphK1 protein in each concentration of SphK1 activator group was increased, and the difference was statistically significant ( P<0.05) . In addition to 1.25 mmol/L SphK1 activator group, compared with NC group, the relative growth survival rate of experimental group and 2.5 mmol/L SphK1 activator group were lower, the difference was statistically significant ( P<0.05) . Compared with the experimental group, the relative survival rate of cells in the SphK1 activator group was higher, and the difference was statistically significant ( P<0.05) . With the increase of exposure concentration, the cells in the experimental group showed the morphological characteristics of early apoptosis at ACR 1.25 mmol/L and late apoptosis at ACR 2.5 mmol/L. Compared with NC group, the apoptosis rate of experimental group and SphK1 activator group at ACR 2.5 mmol/L was significantly different ( P<0.05) ; compared with experimental group, the apoptosis rate of SphK1 activator group at ACR 2.5 mmol/L was lower, the difference was statistically significant ( P<0.05) . Conclusion:The SphK1 excessive expression plays the protective function to the nerve cell damage caused by acrylamide.

Objective:To study the protective effect and effect of SphK1 overexpression on the injury of nerve cells induced by acrylamide.Methods:ACR with 99% purity was prepared into 1.25 mmol/L and 2.5 mmol/L solutions. SH-SY5Y cells were divided into control group (NC group) , experimental group and SphK1 activator group. The experimental group was given ACR solution with final concentration of 1.25 mmol/L and 2.5 mmol/L respectively for 24 h. In the SphK1 activator group, on the basis of the exposure concentration of the experimental group, the SphK1 specific activator (12-) phorbol tetradecanoate (-13-) acetate (PMA) solution[prepared by dimethyl sulfoxide (DMSO) , the final concentration was 100 nmol/l], and other treatments were the same as the experimental group. Control group (NC group) added PMA solution into normal cells. Western blot was used to detect the expression of SphK1 protein; CCK-8 was used to detect the proliferation of SH-SY5Y cells; hoechst33342 method was used to observe the morphological changes of nerve cells; flow cytometry was used to analyze the apoptosis of cells.Results:Compared with NC group, the expression of SphK1 protein in the experimental group and the SphK1 activator group was significantly lower ( P<0.05) . Compared with the experimental group, the expression of SphK1 protein in each concentration of SphK1 activator group was increased, and the difference was statistically significant ( P<0.05) . In addition to 1.25 mmol/L SphK1 activator group, compared with NC group, the relative growth survival rate of experimental group and 2.5 mmol/L SphK1 activator group were lower, the difference was statistically significant ( P<0.05) . Compared with the experimental group, the relative survival rate of cells in the SphK1 activator group was higher, and the difference was statistically significant ( P<0.05) . With the increase of exposure concentration, the cells in the experimental group showed the morphological characteristics of early apoptosis at ACR 1.25 mmol/L and late apoptosis at ACR 2.5 mmol/L. Compared with NC group, the apoptosis rate of experimental group and SphK1 activator group at ACR 2.5 mmol/L was significantly different ( P<0.05) ; compared with experimental group, the apoptosis rate of SphK1 activator group at ACR 2.5 mmol/L was lower, the difference was statistically significant ( P<0.05) . Conclusion:The SphK1 excessive expression plays the protective function to the nerve cell damage caused by acrylamide.

BACKGROUNDAngiogenesis is a prerequisite for tumor growth and plays an important role in rapidly growing tumors, such as malignant gliomas. A variety of factors controlling the angiogenic balance have been described, and among these, the endogenous inhibitor of angiogenesis, tumstatin, has drawn considerable attention. The current study investigated whether expression of tumstatin by glioma cells could alter this balance and prevent tumor formation.

METHODSWe engineered stable transfectants from human glioma cell line U251 to constitutively secrete a human tumstatin protein with c-myc and polyhistidine tags. Production and secretion of the tumstatin-c-myc-His fusion protein by tumstatin-transfected cells were confirmed by Western blotting analysis. In the present study, we identify the anti-angiogenic capacity of tumstatin using several in vitro and in vivo assays. Student's t-test and one-way analysis of variance (ANOVA) test were used to determine the statistical significance in this study.

RESULTSThe tumstatin transfectants and control transfectants (stably transfected with a control plasmid) had similar in vitro growth rates compared to their parental cell lines. However, the conditioned medium from the tumstatin transfected tumor cells significantly inhibits proliferation and causes apoptosis of endothelial cells. It also inhibits tube formation of endothelial cells on Matrigel. Examination of armpit tumors arising from cells overexpressing tumstatin repress the growth of tumor, accompanying the decreased density of CD31 positive vessels in tumors ((5.62 ± 1.32)/HP), compared to the control-transfectants group ((23.84 + 1.71)/HP) and wild type U251 glioma cells group ((29.33 + 4.45)/HP).

CONCLUSIONAnti-angiogenic gene therapy using human tumstatin gene may be an effective strategy for the treatment of glioma.

Animals ; Autoantigens ; genetics ; Brain Neoplasms ; blood supply ; therapy ; Cell Line, Tumor ; Cell Proliferation ; Collagen Type IV ; genetics ; Genetic Therapy ; Glioma ; blood supply ; pathology ; therapy ; Humans ; Mice ; Mice, Inbred BALB C ; Neovascularization, Pathologic ; prevention & control ; Platelet Endothelial Cell Adhesion Molecule-1 ; analysis ; Transfection

OBJECTIVETo evaluate the clinical outcome of posterior total vertebral resection in treating thoracic vertebrae tumor in order to provide a safe and effective method in rebuilding spine stability.

METHODSFrom 2002.1 to 2007.12, 18 patients with thoracic spine tumor underwent posterior total vertebral resection and internal fixation. Among the patients, 10 patients were male and 8 patients were female, ranging in age from 45 to 78 years, with an average of 56 years. The course of the diseases ranged from 2 to 13 months. After the operation, the tumor reccurence was monitored by X-ray, and the tumor markers were detected.

RESULTSAll the patients were followed up for a period ranging from 12 to 60 months, averaged 29 months. All the patients showed a postoperative neurologic improvement, as well as showed radiographic evidence of solid fusion in the follow-up examinations during 3 to 9 months, with an average of (8 +/- 1.4) months.

CONCLUSIONPosterior total vertebral resection for the treatment of thoracic spine tumor is safe and effective.

Aged ; Female ; Fracture Fixation, Internal ; methods ; Humans ; Male ; Middle Aged ; Spinal Neoplasms ; pathology ; surgery ; Thoracic Vertebrae ; pathology ; surgery ; Treatment Outcome

Objective To evaluate the technical feasibility and safety of endoscopic retrograde catheterization of gallbladder (ERCG) and endoscopic transpapillary gallbladder stenting (ETGS) for gallbladder diseases.Methods Patients who underwent ERCG and ETGS in Eastern Hepatobiliary Hospital from January 2010 to June 2016 were enrolled to this retrospective study.The superselection time of cystic duct,the catheterization time of gallbladder,postoperative symptoms and complications were analyzed.Results A total of 10 patients were enrolled to this study,including 2 cases of acute calculous cholecystitis,4 cases of percutaneous transhepatic gallbladder drainage (PTGBD) and 4 cases of cholecystocholedocholithiasis.The success rates of ERCG and ETGS were 100％.Symptoms were relieved in all patients and PTGBD catheter was removed after ETGS.The mean times of ERCG and ETGS were 10.2 ± 6.9 min and 17.0 ± 8.0 min respectively.The mean times of ERCG were 18.5±4.9 min,13.0±3.6 min and 3.3± 1.3 min,respectively (F=18.86,P =0.002).The mean times of ETGS were 25.5±4.9 min,21.0± 4.7 min and 8.8 ± 1.0 min,respectively (F =18.04,P =0.002).Complications included 1 case of cholangitis and 1 case of hyperamylasemia.Cholangitis was relieved after anti-inflammatory treatment.No acute pancreatitis,bleeding,perforation or procedure-related death occurred.Conclusion ERCG and ETGS are safe and feasible,which can play important roles in the treatment of specific gallbladder diseases or gallbladder with bile duct diseases.

Objective To determine whether the susceptibility to ischemia-reperfusion injury in aged heart is higher than that in adult heart and,if so,to clarify the mechanisms underlying this change.Methods Wister rats(5-or 20-month-old)were randomly divided into 4 groups(6 animals in each group).The rats were subjected to 30 minutes of myocardial ischemia via ligating the left anterior descending coronary artery,followed by 3 hours of reperfusion(Young-MI/R group and Old-MI/R group);A silk suture around the left anterior descending coronary artery was not ligated in young and old rats(Young-sham group and Old-sham group).Myocardial apoptosis was detected by terminal deoxynueleotidyl transferase biotin-d UTP nick end labeling(TUNEL)staining and caspase-3 activity was detected by using a caspase-3 colorimetrie assay.Nitrotyrosine content,a footprint of in vivo ONOO~-formation,and total NO content were determined by ELISA and chemiluminescence method respectively.Results A significantly exacerbated cardiac reperfusion injury was found in Old-MI/R group as evidenced by increased TUNEL positive myocytes[(19.0?2.1)% vs.(14.6?1.7)%],and increased myocardial caspase-3 activity[(436?35)?mool/mg vs.(340?32)?mol/mg] compared with Young-MI/R group(P＜0.05).Aged hearts had a markedly increased basal NOx level compared with young adult hearts.Marked higher myocardial nitrotyrosine content was found in OId-MI/R group[(7.25?0.18)nmol/g]than that in Young-MI/R group[(4.68?0.15)nmol/g] (P＜0.05).Conclusions In aged hearts,high levels of NO might form highly toxie derivant, ONOO~-,and its subsequent nitrified protein.This may attribute to the increased susceptibility of the aged heart to isehemic-reperfusion injury.

Objective To evaluate the diagnostic value of MRI in brachial plexus injury.Methods Total 98 patients with brachial plexus injury were examined by MRI before operation.Fifty-four of 98 patients MR imaging were obtained by 0.5 Tesla scanner and other 44 patients were obtained by 1.5 Tesla scanner.The scanning sequences include: SE T_1WI,T_2WI,FFE T_2WI and T_2WI SPIR. Exploration of the supraclavicular plexus was carried out and the MR imaging were compared with the operative finding in 63 patients.Thirty-five patients who had not surgery were followed-up.Results MR imaging found pre-ganglionic injuries in 45 patients and post-ganglionic injuries in 56 patients.Pre-and post-ganglionic injuries simultaneously in 16 patients among them.MR imaging can not find injury sings in 13 patients.The positive rate was 86.73%.MR imaging finding of pre-ganglionic injuries include:(1) Spinal cord edema and hemorrhage,2 patients (4.44% ).(2)Displacement of spinal cord,17 patients (37.78%).(3)Traumatic meningoceles,37 patients (82.22%).(4)Absence of roots in spinal canal, 25 patients(55.56% ).(5)Scarring in the spinal cnanl,24 patients (53.33%).(6)Denervation of erector spine,13 patients (28.89%).MR imaging finding of post-ganglionic injuries include:(1)Trunk thickening with hypointensities in T_2WI,23 patients (41.07%).(2)Nerve trunk complete loss of continuity with disappeared of nerve structure,16 patients (28.57%).(3)Continuity of nerve trunk was well with disappearance of nerve structure,14 patients(25.00%).(4)Traumatic neurofibroma,3 patients (5.36%).Conclusion MR imaging can reveal Pre-and post-ganglionic injuries of brachial plexus simultaneously.MR imaging is able to determine the location (pre-or post-ganglionic)and extent of brachial plexus injury,provided important information for treatment method selection.

Objective To improve recognition and imaging diagnosis of aneurysmal bone cyst secondary to a giant cell tumor.Methods To collect the dates of 12 patients with aneurysmal bone cyst secondary to a giant cell tumor were proved by operation and pathology from January 2003 to October 2006. Analyzed and summarized their imaging manifestations and correlation with pathohistology.Results Six lesions were located in epiphysis and metaphysic regions of long bone.Six lesions were located in pelvis.All cases showed a cystic lesion with expanded and osteolytic,eccentric 10 cases and centric 2 cases.Four cases display trabeculate,the margin is well define with a rim of bone sclerosis in 2 cases.Magnetic resonance imaging(MRI)scans were available in 10 patients.All case showed cystic,dilated lesions with solid areas. Eight cases manifested single or multitude solid nodules in big cystic wall.Two cases appeared solid masses with multitude cysts.The sign of multitude fluid-fluid level,best seen on T_2-weighted images,was present in all patients.Seven cases emerged soft-tissue masses.MR found indicative of large amounts of hemosiderin in one cases.Eight cases were examined by spiral CT with plain scanning and enhancement scanning. Reconstructed image were CTA and 3D-MPR(three dimensions multiplanar reconstruction)imaging.All cases showed cystic,dilated lesions with solid areas.The sign of multitude fluid-fluid level was present in 6 patients.The solid areas and cystic-wall of lesions showed contrast enhancement in 8 patients.3D-MPR imaging showed supply blood vessel of tumors in 3 cases.Arteriovenous malformation did not found in all patients.The surgeons'operative findings and the gross specimens were studied in all patients.All lesions were composed of solid areas and cystic areas.The diagnosis of pathology were ABC with GCT(grade Ⅱ)in 10 cases and ABC with GCT(grade Ⅲ).Conclusion Aneurysmai bone cyst secondary to a giant cell tumor is not rare.Adequately recognizing the pathologic basis of ABC,and selecting imaging techniques correctly (X-ray and MRI,or X-ray and CT)is especially important to diagnose a giant-cell tumor with secondary aneurysmai bone cyst.When an eccentric,expanded,lytic tumor with a cystic-solid lesion in epiphysis of long bone or pelvis shows multiple fluid levels,a giant-cell tumor with secondary aneurysmai bone cyst components should be sufficiently considered.

A new and a known anthraquinone glycosides were isolated from the ethanol extract of the roots of Rheum officinale Baill. The extract was purified by various chromatographies, such as silica gel, Sephadex LH-20, RP-C18 column chromatography and HPLC. Two compounds were identified by the spectroscopic techniques of NMR, MS, and chemical method. In addition, they were tested for their cytotoxic effects against HepG2 cell. Unfortunately, they showed no or weak activity.
Anthraquinones ; chemistry ; isolation & purification ; pharmacology ; Glycosides ; chemistry ; isolation & purification ; pharmacology ; Hep G2 Cells ; Humans ; Molecular Structure ; Plant Roots ; chemistry ; Plants, Medicinal ; chemistry ; Rheum ; chemistry