The methods of diagnostic imaging for pulmonary embolism is diversified. However, the different characteristic features of diagnostic imaging and diagnostic accuracy impressive influenced the choice of selection by clinicians. Furthermore, the principle and indication of interventional therapy would have great impending force on the outcomings. This article presents a comprehension of diagnostic imagings and interventional therapy for pulmonary embolization.

ObjectiveTo observe the spinal cord pathological change and hindlimbs motor function of rats after decompression on chronic spinal cord injury.Methods 30 Wistar rats were divided randomly into conrol group ( n =5 ),compression group ( n =5 ) and decompression group ( n =20 ),then the decompression group was subdivided into 4 parts as 1 week,2 weeks,4 weeks,6 weeks after decompression.Decompression was made after 30 days of chronic spinal cord copression injury,rats'motor function was detected by inclined plate experiment,the histopathological change,Nissl body and neural cells apoptosis in different spinal cord sections were assessed by the stainings of HE,Nissl and TUNEL.ResultsCompared with control group,the behavior testing showed all rats in compression group presented with weakness of muscle power in their hindlimbs (P ＜ 0.01 ),but the hindlimbs motor functions recovered from the first week after decompression and the difference had statistical significance compared with the compression group(P＜ 0.01 ).Then the rats hindlimbs functions recovered gradually later on.The staining of HE,Nissl and TUNEL showed that the injured spinal cord section performed no improvement at the first 2 weeks after decompression,the neural apoptosis index(24.31 ± 4.73 )％ decreased until the forth week after decompression(P＜0.05).The spinal cord segments closed to the injured part recovered in early stage.At 1 week after decompression,lots of Nissl bodys were observed in spinal anterior horn,the neural apoptosis index in the 2 sections closed to the injured part were ( 15.21 ± 4.81 ) ％ and ( 16.21 ± 3.98 ) ％,which declined observably compared with compression group(P ＜ 0.05 ).ConclusionAfter decompression on chronic spinal cord injury,the recovery of rats'hindlimbs motor function in early stage is probably benefited by the functional compensation of the spinal cord segments closed to the injured section.

Based on the significance of the innovative experiment program for college students and the experience at home and abroad,this paper analyzes the current situation of the implementation of this plan by School of Medicine of Shanghai Jiaotong University.It summarizes the beneficial experience of training students' scientific research thinking in the implementation of the course plan,through literature reading,project design and so on.Practice has proved that,with rigorous and reasonable protection system and the scientific implementation of the process and the quality control system,the program can play a role in improving the students' ability of innovation and practice,stimulate their interest in scientific research,and excavate their research potential.

Hepatocellular carcinoma(HCC)has high incidence rate,recurrence rate after surgecal treat-ment,as well as fatality rate in China .HCC is not sensitive to radiotherapy or chemotherapy and no effective treat-ment is available for HCC patients at advanced stage .Sorafenib is the first effective molecularly targeted drug for the treatment of HCC,which represents a milestone in the treatment of HCC .However,it also shows drug resist-ance during clinical application .Therefore,it is important to investigate the mechanism of drug resistance and its molecular markers for HCC .In this review ,we summarize the current status of the studies in these fields .

OsRacD belonging to rice Rho family of the small GTP binding proteins,is a pivotal gene involved in rice photoperiod fertility conversion of photoperiod sensitive genic male sterile rice,which influences rice fertility via controlling the pollen tube growth.T20N site-directed mutation was introduced into its highly conserved G1 motif by PCR-mediated method to mimic its GDP-binding state based on the sequences alignment and conserved domains analysis.The prokaryotic expression vector of OsRacD and T20N-OsRacD were constructed,and the His6 tag fused proteins were expressed and purified from E.coli.After identified by Western blot,the GTP hydrolysis activities were detected.The results showed that the GTPase activities of T20N-OsRacD were significantly reduced comparing with that of OsRacD,suggested that OsRacD and T20N-OsRacD have different biochemical characteristics.

OBJECTIVETo investigate the injury stress responses caused by ischemia reperfusion and its effects on the salivary secretory function of rat submandibular glands.

METHODSAn in situ ischemia reperfusion experimental model of rat submandibular glands was developed. The rat submandibular glands were subjected to 90 min of ischemia without denervation followed by reperfusion for 1, 12, 24, and 72 h. Salivary secretion, histological changes, reactive oxygen species (ROS) levels, and cellular apoptosis of the involved submandibular glands were detected after reperfusion.

RESULTSThe secretory function of the glands decreased at 1 and 12 h, and the saliva secretion gradually had the same value as that of the control sample 72 h after reperfusion. Increasing inflammatory cells infiltration, cellular atrophy, and tissue edema were observed especially after reperfusion for 12 h. The level of ROS and the number of apoptotic cells exhibited the same tendency, and higher ROS levels and more apoptosis cells 1 and 12 h after reperfusion were observed.

CONCLUSIONOur study suggests that ischemia reperfusion can cause a series of injury stress responses in submandibular glands, which might have an important function in the early phase dysfunction of transplanted submandibular glands.

Objective:To investigate the expression and clinical significance of Nusap1 in hepatical carcinoma. Methods:The expression of Nusap1 protein in 61 specimens of hepatical carcinoma was examined by immunohistochemistry. Based on the levels of Nusap1 expression, the 61 specimens were divided into a high Nusap1 expression group and a low Nusap1 expression group. The correlation between Nusap1 expression with clinicopathologic features and prognosis of hepatical carcinoma was analyzed. Results:TherateofhighNusap1expressionwas54.1%inhepaticalcarcinoma.TherateofhighNusap1 expression was 21.3%in noncarcinoma, with signiifcant difference between the 2 groups (P<0.01).Nusap1 overexpression had signiifcant correlation with histological differentiation, tumor size, liver cirrhosis,lymphaticmetastasis,tumorthrombiandearlyrecurrence(P<0.05),butnotwithsex,age,AFP level,tumornumber,TNMclassificationandtumorencapsulation(P>0.05).Survivalanalysissuggested thatthe6monthand12monthnoncarcinomasurvivalratewassignificantlylowerinthehighNusap1 expression group [33.3%(11/33), 17.9%(5/33)] than that in the low Nusap1 expression group [89.3%(25/28), 53.6%(15/28);P<0.005]. Conclusion:Nusap1 is overexpressed in hepatical carcinoma and is a valuable prognostic factor for hepatical carcinoma.

Object To investigate the effect of PPARαactivation on PPARγ-induced fatty liver in the mouse. Methods Wild type mice ( C57BL/6) aged 4 to 5 weeks were used as animal models.All mice were divided into four groups.The mice in the first group were fed with chow diet.The mice in the second group were fed with a diet containing 0.125%Wy-14,643, an agonist of PPARa, for 8 days.The mice in the third group were injected with Ad/PPARγvia tail vein for 5 day.The mice in the fourth group were firstly fed with Wy-14,643 diet for 3 days and then injected with Ad/PPARγvia tail vein for another 5 day.Mouse livers were collected and photographed.The effect of PPARαactivation on PPARγ-induced fatty liver was observed by H&E and Oil red O staining.Results Compared with the controls, wild-type mice treated with Wy-14,643 for 8 days exhibited marked hypertrophy of hepatocytes with increased cytoplasmic eosinophil-ia and proliferation of peroxisomes.The liver size was significantly increased in the wild-type mice treated with Ad/PPARγfor 5 days, and over-expression of PPARγstrongly induced hepatic steatosis.Importantly, the wild-type mice pretreated with Wy-14,643 for 3 days and then given Ad/PPARγinjection exhibited dramatically the increase of liver size, which might be due to the dual function of PPARa and PPARγ.Compared with the Ad/PPARγgroup, the Wy-14,643 pretreat-ment group showed a reduced hepatic steatosis.Conclusions Activation of PPARαby Wy-14,643 effectively improves PPARγ-stimulated hepatic steatosis, which provides a novel target for prevention and therapy of fatty liver.

Objective To study the effects of endoplasmic reticulum stress on liver damage in young rats fed with high-fat diet.Methods We divided 48 male weaned young rats randomly into high-fat diet group and control group,which were separately fed with high-fat diet and normal diet.After feeding 8,12 and 1 6 weeks,the body weight and visceral fat of the rats were measured.The serum liver function was measured.The morphology of livers was observed by HE and transmission electron microscopy. The mRNA expressions of ATF6 and GRP78 in hepatocytes were measured with RT-PCR.Results ① The body weight and visceral fat weight of rats in high-fat diet group increased compared with those in control group (P <0.05).② Alanine aminotransferase and aspartate aminotransferase in high-fat diet group increased slightly over time (P >0.05);alanine aminotransferase at week 1 6 was increased significantly compared with that in controls (P < 0.05 ).③ Liver cells in high-fat diet group had steatosis at week 8 and the steatosis became more serious between week 12 and week 1 6.④ In high-fat diet group at week 8 there were a large number of lipid droplets in the cytoplasm,and the cell structure was close to that of normal cells;rough endoplasmic reticulum was nearly normal and the ribosome was visible.At week 12 and week 1 6,besides a large number of lipid droplets,we could also see that some substances with line-like structure deposited in rough endoplasmic reticulum pool.⑤ The expressions of ATF6 and GRP78 mRNA in hepatocytes in high-fat group at weeks 8, 12 and 1 6 were significantly increased compared with those in control group (P <0.05). Conclusion High-fat diet in infants can cause visceral fat accumulation,fatty degeneration of hepatocytes and liver injury.ATF6-mediated endoplasmic reticulum may be closely related to the liver injury which results from highfat diet.