Objective To assess the value of MSCT in the evaluation of the anatomy and variation of hepatic veins for living donor liver transplantation (LDLT) donors and the significance of vessel variation in surgical operation. Methods A total of 238 subjects who wanted to be the donors of LDLT underwent MSCT plain and enhanced examination, and the hepatic veins were evaluated. Results Among all 238 subjects, according to Nakamura's classification of hepatic veins, 164 were type Ⅰ, 60 were type Ⅱ, 14 were type Ⅲ. The left hepatic vein (LHV) shared a common trunk with the middle one in 167 subjects. Branches of Ⅷ going along the cross section and diameter larger than 5 mm were detected in 105 subjects. The Ⅳ segment veins drained into MHV in 68, into LHV in 7 subjects. Right inferior hepatic vein with diameter larger than 3 mm was found in 108 subjects, while the distance between RHV and IRHV were larger than 4 cm in 55 subjects. Conclusion MSCT can offer details and exact information about the donors pre-operation, and is an important non-invasive method for the evaluation of hepatic veins of potential LDLT donors.

Objective: To investigate the alteration of bcl- 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague -Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of mo derate severity. Bcl-2, Bcl-x and Bax protein expression was detected by immun ohistochemistry. Results: (1) The immunoreactivity of Bcl-2 and Bcl-x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post-injury, and this was the main cause of down-regulation of the ratio of Bcl-2+Bcl-x to Bax. (2) During 1-3 d after injury, the Bax protein express i on increased significantly, while the Bcl-2 and Bcl-x protein expression decre ased relatively slow. The decreased ratio of Bcl-2+Bcl-x to Bax was mainly due to the Bax up-regulation. Conclusion: The bcl-2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

Objective To investigate the regulation of protein kinase C(PKC) to the expression of β-1,4-galactusyhransferase- Ⅰ ( β-1,4-GalT- Ⅰ ) and the influence on cytoskeleton and adherence ability of human umbilical vein endothelial cells(HUVECs) when stimulated by lipopolysaccharide (LPS). Methods Cultured HUVECs were pretreated by various PKC inhibitors or phorbol 12-myristate 13-acctate( PMA), an excitomotor of PKC respectively for 30 min, then stimulated by LPS for 4 h. β-1,4-GalT-Ⅰ expression were detected by RT-PCR and Western blot, expression of β-1,4-galactosylated carbohydrate chains and cytoskeleton were assayed by immumofluorescence, and adherence ability of HUVECs was observed by endothelialmonocyte cell adherence test. Results Up-regulated expression of β-1,4-GalT- Ⅰ and β-1,4-galactosylated carbohydrate chains in HUVECs stimulated by LPS were suppressed by PKC inhibitors and increased by PMA. F-actin and β-1,4-GalT- Ⅰ were partly co-localized in HUVECs. PKC inhibitor inhibited the effect of LPS on the distribution of F-actin and β-1,4-GalT- Ⅰ. Adherence ability of HUVECs enhanced by LPS was significantly suppressed by PKC inhibitor. Conclusion PKC signal transduction pathway may participate in regulating β-1,4-GalT-Ⅰ expression in endothelial cells stimulated by LPS. Furthermore, polytypes of PKC may participate in this regulating process; PKC might regulate cytoskeleton reorganization and adherence ability of EC through β-1,4-GalT-Ⅰ during inflammation.

Objective: To investigate the alterations of bcl-2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis follow ing traumatic brain injury (TBI). Methods: Male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury(FPBI) of moderate severity. bax and bcl-xL mRNA and protein expression was detected by RT-PCR an d immunohistochemistry. In addition to morphological evidence of apoptosis, TUNE L histochemistry was used to identify DNA fragmentation in situ under both l ight and electron microscope, whereas characteristic internucleosomal DN A fragm entation of apoptosis was demonstrated by DNA gel electrophoresis. Resul ts: bcl-xL mRNA and protein decreased in the ipsilateral hemisphere t o the impact site as early as 6 h post-injury［(67.42±7.54)% and (85.85±5.72)% r espectively］. The decrease in bcl-xL mRNA and protein preceded apoptosis was observed 12 h post-injury. And this was the main cause of up-regulation of the ratio of bax to bcl-xL in the acute period(minutes-hours) followin g FPBI. bax mRNA and protein were observed to rise slowly, doubled 3 d post- injury, returned to sham level slowly. The delayed cell death (days-weeks) migh t associated with the up-regulation of pro-apoptotic gene bax. Conclusio n: The expression of bcl-xL and bax coincide with apoptosis following TBI. The reg ulation of bax and bcl-xL by TBI occur before transcription. The balance of bax/bcl-xL ratio determines the neurocytes to survive or die following FPBI.

BACKGROUND/AIMS: Infliximab has proven to be effective in the treatment of perianal fistulas in Crohn's disease (CD) but the efficacy of adalimumab is still unclear. The aim of this study is to assess the clinical efficacy of adalimumab and compare the results with those for infliximab. METHODS: Forty-seven CD patients treated for perianal fistulas with infliximab from September 2005 to December 2010 (n=31), or with adalimumab from November 2010 to May 2012 (n=16), were enrolled in this retrospective study. The following patient characteristics were analyzed; intestinal lesion site, fistula classification, seton placement, index of inflammatory bowel disease, C-reactive protein level, follow-up period, and the cumulative rate of nonrecurrence or aggravation of fistula. RESULTS: There were no significant differences in the intestinal lesion site, fistula classification, inflammatory bowel disease index, C-reactive protein level, and the frequency of injection between the infliximab group and the adalimumab group. The cumulative rate of nonrecurrence or aggravation of fistula was 62.5% in the adalimumab group and 83.9% in the infliximab group at 24 months after treatment (P=0.09). The risk factors for recurrence or aggravation may be related to seton placement (P=0.02), gender (P=0.06), and fistula classification (P=0.07). CONCLUSIONS: There was no significant difference in the clinical efficacy of adalimumab and infliximab in the treatment of perianal fistulas in CD. However, fistula classification may be an important risk factor for recurrence or aggravation. The preliminary findings in this study show that further research is warranted.
Adalimumab* ; C-Reactive Protein ; Classification ; Crohn Disease* ; Fistula ; Follow-Up Studies ; Humans ; Inflammatory Bowel Diseases ; Infliximab* ; Rectal Fistula* ; Recurrence* ; Retrospective Studies ; Risk Factors ; Treatment Outcome*

Objective To analysis and determine the possibility of the Citellus undulatus infected with Yersinia pestis surviving the winter in an experimental study, and to provide scientific experimental basis for the study on the mechanism of Yersinia pestis preservation. Method In 2006,09 to 2007,04 and 2007,09 to 2008,04 in Xinjiang Wusu-Gurtu natural foci of plague, under natural conditions, the over the winter process of Citellus undulatus carrying the plague bacteria was simulated, and 178 Citellus undulatus were infected with Yersinia pestis (1×107 Bacteria/mouse) using artificial injection method. One hundred seventy-eight Citellus undulatus infected with Yersinia pestis were kept into a construction of the black (1-5 ℃) basement (2 meters under the ground) in the plague focus. In doing so, these Citellus undulatuses almost simultaneously stepped into hibernation. After waking up from hibernation in following year in April, the survived mice carrying the plague bacteria were observed. Results Sixty-eight mice survived among the 178 infected with Yersinia pestis after 6 months of hibernation (through October to the following year in April), and the remaining 110 were all dead without pulling through the hibernation period. The survival rate was 38.2% (68/178). The organ culture of Yersinia pestis of the 110 dead mice(Citellus undnlatus) were tested, 67 were negative(-), 43 positive(+), with a positive rate of 39.1%(43/110). Among the rats with positive plague bacteria, the congestive pulmonary edema and the pathological changes of the hemorrhagic inflammation of the heart, liver, spleen, kidney and injection site could be seen clearly; the plague-free mice were not found to have any pathological changes. The survived 68 mice over the winter were autopsied and observed after being fed up for 20 days. No any pathological changes were found among these mice, and culturing of Yersinia pestis of the heart, liver, spleen, lungs and the tissue of injection site of these mice were all negative (-). Conclusions Citellus undulatus can carry Yersinia pestis during hibernation, but some fail to carry the bacteria through the entire process of hibernation persistently. Yersinia pestis was negative in the survived mice at the end of hibernation. The results showed that Citellus undulatus can not carry Yersinia pestis over the winter.

Objective To improve the knowledge and diagnostic ability of imagiology on neonatal respiratory distress syndrome (NRDS) computed radiograph(CR).Methods The doubtful patients were done to photographs bedside using the high resolution imaging plate, 50 cases of newborn with NRDS were selected whose clinical diagnosed clearly and had been treated and had the complete CR image documents.The CR change and clinical characteristics were observed dynamically.Results Nine of 50 cases were combined with aspirated pneumonia,8 cases with infective pneumonia,3 cases with intra-alveolar hemorrage,and 2 cases with pneumothorax.Accoding to X-ray manifestations,all cases were divided into four stages:Ⅰ stage(n=5), Ⅱ stage(n=20),Ⅲ stage(n=22),Ⅳstage(n=3).Typical CR signs included:the pulmonary lucency decreasd,wide-ranging net and grain shadowes of high density, and in companing with a lot of air brunchus sing.Conclusions Computed radiography is the most important imaging method in diagnosis of NRDS bedside ,and shall be improved the ability of diagnosis and differential of NRDS combined with the clinic.

Objective:To study the effects of LPS and TNF-? on the expression of SSeCKS and morphology as well as cytoskeleton of endothelial cell, so as to explore the role of SSeCKS in cell morphology changes.Methods:The cultured Bovine pulmonary artery endothelial cells(BPAEC) was induced by LPS, TNF-? and the expression of SSeCKS was detected by in situ hybridization,Western blot and immunohistology. Immunofluorescent staining method with confocal laser-scanning fluorescence microscope was used to observe the effects of LPS and TNF-? on the morphology of endothelial cells and the organisation of SSeCKS as well as cytoskeleton.Results:Firstly, we found that TNF-? could induce the expression of SSeCKS in a concentration and time dependent manner , meanwhile LPS had no effects on SSeCKS expression. Secondly, it was observed that LPS and TNF-? induced reorganization of F-actin and SSeCKS in endothelial cell. Thirdly,PKC inhibitor Ro-31-8220 reversed the effect of LPS,TNF-? on F-actin and SSeCKS in endothelial cells.Conclusion:The results demonstrate that TNF-? could induce endothelial cell to express SSeCKS; PKC plays a role in the reorganization of SSeCKS and F-actin in endothelial cells induced by LPS and TNF-?; the results suggest that the mechanism for reorganization of cytoskeleton induced by LPS, TNF-? be partially related to the SSeCKS of ECs.

BACKGROUNDCellular cardiomyoplasty by transplantation of various cell types has been investigated as potential treatments for the improvement of cardiac function after myocardial injury. A major barrier for the clinical application of cell transplantation is obtaining sufficiently large quantities of suitable cells. Allogeneic cellular cardiomyoplasty may provide an alternative source of abundant, transplantable, myogenic cells by in vitro manipulation of cardiac fibroblasts using chemicals including 5-azacytidine. This study evaluated cardiomyogenic differentiation of cardiac fibroblasts, their survival in myocardial scar tissue, and the effect of the implanted cells on heart function.

METHODSPrimary cardiac fibroblasts from neonatal rats were treated with 5-azacytidine (10 µmol/L) or control. Treatment of 5-azacytidine caused myogenic differentiation of cultured cardiac fibroblasts, as defined by elongation and fusion into multinucleated myotubes with sarcomeric structures as identified by electron microscopy, and positive immunostaining for cardiac specific proteins, troponin I and β-myosin heavy chain (β-MHC) and the gap junction protein connexin 43. The myogenic cells (1.0 × 10⁶) were transplanted into the infarcted myocardium 2 weeks after coronary artery occlusion.

RESULTSBy 1 month after transplantation, the converted fibroblasts gave rise to a cluster of cardiac-like muscle cells that in the hearts occupied a large part of the scar with positive immunostaining for the myogenic proteins troponin I and β-MHC. Engrafted cells also expressed the gap junction protein connexin 43 in a disorganized manner. There was no positive staining in the control hearts treated with injections of culture medium. Heart function was evaluated at 6 weeks after myocardial injury with echocardiographic and hemodynamic measurements. Improvement in cardiac function was seen in the hearts transplanted with the 5-azacytidine-treated cardiac fibroblasts which was absent in the hearts treated with control.

CONCLUSIONThe 5-azacytidine has a unique capacity to induce myogenesis in cardiac fibroblasts in vitro and transplantation of cardiac-like muscle cells into ventricular scar tissue improves myocardial function.

Animals ; Azacitidine ; therapeutic use ; Cells, Cultured ; Fibroblasts ; drug effects ; transplantation ; ultrastructure ; Immunohistochemistry ; Microscopy, Electron, Transmission ; Myocardial Infarction ; drug therapy ; therapy ; Rats

The activity of nano carbon fullerene lipidosome (NCFL) against influenza virus HINI in vitro was studied by observing the cytotoxicities and its activity rendered by different intensities of lighting with various periods of time. Rimantadine hydrochloride was used as the positive control drug. By using microcultural technique, the morphological changes of cells were observed and by using the gentian violet staining, antiviral activity of the NCFL against influenza virus was assayed. The results showed that: (1) The maximal concentration of the NCFL was 7μg/mL and the 50% toxic concentration (TC50) was 13.54μg/mL respectively; (2) NCFL had a significant activity of directly killing the influenza virus, while the activities in antiadsorption and antireplication were not obvious; (3) There was a dose-activity relationship between the dosages of NCFL and the direct killing effect against the influenza virus, and the periods of lighting-time could influence the activity partly. It was concluded that NCFL had a significant activity of directly killing the influenza virus.