Objective To explore the change of venous blood phase values detected by enhanced gradient echo T2 star weighted angiography(ESWAN)sequence in mild and severe traumatic brain injury (TBI) models of rabbits in diverse phases and investigate their association with neurological severity scale (NSS) scores. Methods Fifty-one New Zealand rabbits, which were randomly divided into control group (n=3) ,mild injured group (n=24) , and severe injured group (n=24) by random digital table method, underwent routine MRI and ESWAN sequence at the time points of baseline, 1 h, 6 h, 12 h, 24 h, 48 h, 72 h, 1 week, and 2 weeks after injury(3 rabbits per subgroup)respectively. Blood phase values in veins of interest were recorded. Observation of behavior characteristics and abnormalities, followed by NSS, was executed post injury, and the correlation between venous blood phase values and NSS scores was statistically analyzed. Two independent-samples t-test was applied to compare venous blood phase values of diverse measured veins in each group separately at every time ponits. One-way ANOVA was used to analyze venous blood phase values varying over time of measured vessels in each injured group. Least significant difference t-test was applied to compare blood phase values within the subgroups with each other at each time point. NSS scores of mild and severe injured groups were compared by two independent-samples t-test. Correlations between venous blood phase values and NSS scores in each vein and group was analyzed with Spearman correlation analysis. Results Blood phase values in veins of interest presented an inclination of descending, which was more obvious in severe injured groups than in the mild. Change of venous blood phase values over time featured continuing reduction in earlier phases which reached to the minimum in 24-48h, and then increased gradually, especially in VMV, VLV, DSS, and MDVB (P<0.05). ICV and DCV also showed similar trend. Values of NSS scores in the two group were (15.5 ± 3.1) and (33.2 ± 6.5) respectively (t=3.543,P=0.001). Blood phase values in most of the measured veins correlated with NSS scores (P<0.05) after 6h post injury, especially significant during 24-72h among all the measured veins(P<0.05). Higher accuracy and sensitivity were presented in the supratentorial or superficial veins compared with subtentorial or profound veins. Conclusions It is feasible to evaluate oxygen saturation of veins after TBI by measuring venous blood phase values on ESWAN images. The method is effective in the assessment of the degree of injury and clinical status, indicating a favorable application prospect.

Objective To investigate dynamic regulation of quantifying fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values in rotational brain injury models of rabbit using diffusion tensor imaging (DTI), and its correlation with β?amyloid precursor protein (β-APP). Methods Forty-two 6-month-old New Zealand rabbits were randomly divided into three groups, including control group (n=6), mild injured group (n=18) and severe injured group (n=18), and preformed on autonomous rapidly rotational brain injury device. The rotational angles of 45° for mild injured group and 90° for severe injured group were condemned, and MRI and pathology were conducted at 6 h, 12 h, 24 h, 48 h, 72 h and 1 week after injury (3 rabbits per subgroup). Routine sequences and DTI technique were performed on 3.0 T MRI. FA and ADC values in subcortical white matter, corpus callosum and brain stem were measured. Independent t?test was performed to evaluate the significance of the intergroup difference in FA and ADC values in mild and severe injured groups of verious brain regions by timing, one?way ANOVA was performed to evaluate its timing variation and its correlation with the number of the β-APP positive axons was analyzed by Pearson correlation analysis. Results FA and ADC values of the severe injured group were lower than that of the mild in most brain regions(P<0.05), and the difference in mild injured group was smaller than that in severe injured group. Both FA and ADC values in brain stem of the severe injured group were lower at 6 h after injury compared to mild injured group, which were sensitive to injury. Furthermore, FA and ADC values in each brain regions of mild and severe injured groups showed similar dynamic trends, namely gradually decreasing by time, and FA values were more sensitive to injury than ADC values. FA values in subcortical white matter and brain stem reduced in severe injured group at 6 h after injury compared with that before injury(P<0.05), and decreased in various brain area of both injured groups at 12 h after injury(P<0.05). Meanwhile, ADC values in all regions were declined in the severe injured group at 12 h after injury(P<0.05), and decreased in various regions in both injured groups at 24—48 h after injury(P<0.05)except for subcortical white matter in mild injured group. There were statistically negative correlations between FA and ADC values and the number of β-APP positive axons in 12—48 h after injury in most regions(P<0.05). Conclusions DTI can quantitatively detect and assess the pathological process in white matter and axons of TBI in earlier stage of the brain injury, and can be applied in evaluation and quantitative diagnose in these patients.

Abstract BACKGROUND: Sodium hyaluronate is an effective treatment for osteoarthritis, but the underlying mechanism remains unclear. There is evidence that abnormal expressions of matrix metaloproteinase (MMP)-1, -3 and -9 and tissue inhibitor of metaloproteinase (TIMP)-1 and -2 show great effects on osteoarthritis. OBJECTIVE: To assess the influence of intra-articular injection of sodium hyaluronate on expressions of MMPs-1, 3, 9 and tissue inhibitor of TIMPs-1, 2 in the rabbit cartilage after osteoarthritis. METHODS: Twenty-four mature New Zealand white rabbits were divided into normal control, model, and sodium hyaluronate groups. The model and sodium hyaluronate groups underwent unilateral anterior cruciate ligament transection, and rabbits in the sodium hyaluronate group received 0.3 mL of 1% sodium hyaluronate via intra-articular injection at 4 weeks after modeling, once a week for 5 weeks. At 11 weeks folowing surgery, the rabbits were kiled and the cartilage was harvested to extract total RNA. mRNA expressions of MMPs-1, 3, 9 and TIMPs-1, 2 in the cartilage were analyzed using real-time PCR for each group. RESULTS AND CONCLUSION:Compared with the model group, the range and extent of cartilage damage was reduced in the sodium hyaluronate group (P < 0.01), and Mankin scores were noticeably decreased (P < 0.05). In the cartilage, mRNA expressions of MMPs-1, 3, 9 were enhanced and mRNA expressions of TIMPs-1, 2 were down-regulated in the model group. However, the mRNA expression levels of MMPs-1, 3, 9 and TIMPs-1, 2 in the articular cartilage were not obviously changed in the sodium hyaluronate group. These results suggest that MMPs-1, 3, 9 and TIMPs-1, 2 are involved in the progression of osteoarthritis and the therapeutic mechanism of sodium hyaluronate is not realized through the down-regulation of their expressions during development of osteoarthritis. Sodium hyaluronate for treatment of osteoarthritis is a complex process and the underlying mechanisms require further investigation.

The effect of inhibition of proliferation of a novel human megakaryoblastic leukemia cell line (HIMeg) by two physiological factors, 1.25-dihydroxyvitamin D3 [1,25(OH)2 D3] and 13-cis-retinoic acid (RA), was investigated. At the range of 10-9 - 10-6 mol/L, 1,25(OH)2 D3 and RA showed significant inhibition of proliferation of the megakaryoblastic leukemia cells,which was demonstrated by count of survival cells,incorporation of [3H]-TdR and [3H]-UR, and cloning efficiency. From above, it can further explain the m.echanism of differentiation-inducers and the effect of 1,25(OH)2D3 on myelofibrosis. It is possible for 1,25(OH)2D3 and RA to be used for a new -treatment.

Objective To explore the strategy and outcomes of surgical treatment of thoracic ossification of ligamentum flavum(OLF),especially combined with ossification of posterior longitudinal ligament,thoracic kyphosis and epidural adhesion.Methods Fifty-three cases of thoracic OLF from January 2003 to December 2009 were reviewed retrospectively.All patients were treated by the methods of en bloc resection of semi-facet and lamina.All patients were followed up for more than half an year,including 32 males and 21 females,aged from 43 to 73 years(average 54.7 years).The lesions located in upper thoracic for 18 patients,and in thoracolumbar for 35 patients.For multi-level or jumping OLF patients,the responsible levels were determined by combination of images and clinical symptoms.For multi-level OLF with ossification of posterior longitudinal ligament(OPLL)or thoracic kyphosis(＞50°),multi-level pedicle screw fixation and correction of kyphosis were performed.For dural adhesion patients,part of cerebrospinal fluid was released with a caudal incision of dural sac resulting in collapse and epidural arachnoid separation.Ossific and adhesion dura mater were removed with integrity of arachnoid.The surgical outcomes were evaluated with preoperative and postoperative thoracic Japanese Orthopaedic Association(JOA)score,Nurick grade and neurologic functional recovery ratio.Results Fifty-three cases were followed up for 6 months to 6 years,with an average of 18 months.The average preoperative JOA score was 4.3±2.3,which significantly increased to 8.3±1.8 after operation.Postoperative neurologic functional recovery rates were 11% to 80%(average 65.8%),including excellent in 18 cases,good in 20,fair in 10,and poor in 5.The excellent or good rate was 71.7%.The mean preoperative Nurick grade was 3.7(2-5 grade)and decreased to 2.3 grade after operation.Conclusion En bloc resection of semi-facet and lamina is a safe and effective method for treatment of thoracic OLF.For the patients with OPLL or kyphosis,pedicle screws fixation and kyphosis correction was beneficial for recovery of neurologic function of thoracic OLF patients.

The expression of silence of death domains (SODD) and its clinical significance and relationship with phospho-NF-kappaB-p65 proteins in bone marrow cells of childhood acute lymphoblastic leukaemia (ALL) were explored, and the expression of SODD and phospho-NF-kappaB-p65 in Jurkat cells treated with chemotherapeutic drugs was detected in order to find a new chemotherapeutic target. The expression of SODD and phospho-NF-kappaB-p65 proteins in bone marrow cells was detected by immunohistochemistry in 25 children with ALL. The apoptosis rate was measured by Annexin-V-Fluorescence/PI double-labeling flow cytometry and the expression of SODD and phospho-NF-kappaB-p65 proteins determined by Western blotting in the Jurkat cells. It was found that the expression of SODD and active P65 in ALL was significantly higher than that in normal control group (P<0.05). The expression of the SODD and phospho-NF-kappaB-p65 proteins in the high-risk (HR) group was significantly higher than that in the standard-risk (SR) group (P<0.05). The Pearson rank correlation analysis revealed that there was a positive correlation between SODD and phospho-NF-kappaB-p65 expression (P<0.01, r=0.69). VCR could effectively induce the apoptosis of Jurkat cells, and down-regulate the expression of SODD and phospho-NF-kappaB-p65 proteins in a time-dependent manner, but DNR could not down-regulate the expression of SODD effectively. It was concluded that SODD may be closely related to the clinical classification and prognosis of ALL in children. The expression of SODD and phospho-NF-kappaB-p65 had a definite synergistic relationship with the onset and development of ALL. VCR could down-regulate the expression of SODD and inhibit the NF-kappaB activation, which could recover the sensibility of apoptosis in leukemic cells.

In order to investigate the inhibitory effects of all trans-retinoitc acid (ATRA) on differentiation and apoptosis of Walker-256 hepatocellular carcinoma cells and the therapeutic effects of ATRA combined with transarterial chemoembolization (TACE) on rat Walker-256 transplanted hepatocarcinoma, Walker-256 hepatocarcinoma cell lines were treated with ATRA at different concentrations. After culture for 48 h, the inhibitory rate of cell proliferation was determined by MTT assay; the changes of Fas and Bcl-2 mRNA expression were determined by RT-PCR, and the expression levels of Caspase3 and Caspase8 proteins were detected by Western blot. Twenty-seven Wistar rat models of hepatocarcinoma were set up successfully by implanting Walker-256 cell lines. The tumor volume at the 11th day after implantation (V(preoperation)) was measured by magnetic resonance imaging (MRI). The 27 rats were randomly and equally divided into three groups, and the therapy scheme was performed as follows: group A (ATRA 0.1 mg+mitomycin 0.05 mL+lipiodol 0.05 mL+gelfoam powder 0.025 mg); group B (mitomycin 0.05 mg+lipiodol 0.05 ml+gelfoam 0.025 mg; group C (0.9% NaCl 0.2 mL). After another 11 days, MRI was performed once again to measure the tumor volume (V(postoperation)). The expression of factor and Ki VIII -67 in the tumor tissues was detected by immunohistochemistry. The results showed that ATRA could suppress proliferation of Walker-256 cell lines. After treatment of Walker-256 cell lines with ATRA, the expression of Fas mRNA was significantly up-regulated and the Bcl-2 mRNA was significantly down-regulated by ATRA at the concentration of 10 mumol/L as compared with the control group (P<0.05). After treatment with 10 mumol/L ATRA for 48 h, the Caspase3 and Caspase8 were significantly activated as compared with the control group (P<0.05). Significant difference existed in growth rate among the three groups (P<0.01) and between either two groups (P<0.05). The expression rate of factor VIII and Ki-67 was gradually increased from group A, group B to group C. The study suggests that ATRA could inhibit the proliferation of Walker-256 cells and the effectiveness of the combined therapy (ATRA+TACE) for treating transplanted hepatoma of rats is superior to that of TACE alone.

BACKGROUND:Articular cartilage repair has been a difficulty in the clinical setting, which is mainly treated with autologous or al ogeneic osteochondral grafts, and cartilage periosteum or periosteum grafts. However, the limited source, secondary lesion and immunological rejection force some researchers to search for a novel treatment strategy, cartilage tissue engineering, that is of great significance for cartilage regeneration and repair. OBJECTIVE:To investigate the tissue-engineered scaffolds for the repair of articular cartilage defects. METHODS:The first author searched the PubMed and WanFang databases for the articles addressing tissue-engineered cartilage for articular cartilage defects published between 1991 and 2015 using the keywords“articular cartilage defect, scaffold, tissue engineered cartilage”in English and Chinese, respectively. The irrelative and repetitive literatures were excluded. RESULTS AND CONCLUSION:Final y 48 eligible literatures were enrol ed based on the inclusion and exclusion criteria. Cartilage tissue engineering possesses the advantages of control ability, little damage to tissue itself, and biological repair of injured cartilage. Tissue-engineered scaffold material is a critical factor in tissue engineering construction;therefore, it should hold biodegradability and histocompatibility. The commonly used scaffold materials include natural macromolecule materials (col agen, silk fibroin and chitosan), and synthetic polymer materials (polylactic acid and tricalcium phosphate). It is necessary to prepare composite scaffolds with high bioactivity integrate advantages of each material. The tissue engineering is bound to be a hotspot in the field of articular cartilage repair.

Objective To analyse the symptoms in discogenic low back pain and their neurological anatomic mechanism,and to explore the theoretical basis of symptomatic diagnosis of discogenic low back pain.Methods From January 2010 to December 2013, 289 patients were primarily diagnosed as discogenic discogenic low pain in our department, of which 164 patients showing only single abnormal segment on MRI were enrolled, including 99 male and 65 female patients, averaging 42 years old.All patients underwent discography.All the symptoms conform to the neurological anatomic mechanism of lumbar disc, i.e.extensive low back pain, posterior ilium pain, lateral thigh pain, groin pain, low abdomen pain, were recorded postoperatively.Then the occurrence rate of each symptom with positive discography was calculated.The positive rate (equal to sensitivity of the symptom to the diagnosis of discogenic low pain) of discography when each symptom occurred and the negative rate (equal to specificity of the diagnosis of the symptom to the discogenic low pain) of discography when each symptom did not occur were calculated respectively.Results The discographies of 129 (78.7％) in 164 patients were positive, of these patients 95 (73.6％) had the symptom of extensive low back pain, 99 (76.7％) had posterior ilium pain, 58 (45.0％) had lateral thigh pain, 29 (22.3％) had groin pain, and 24(18.6％) had low abdomen pain.The positive rate of discography in those with the symptom of extensive low back pain, posterior ilium pain, lateral thigh pain, groin pain and low abdomen pain was 89.6％, 90.8％, 90.6％, 90.6％ and 92.3％ respectively, i.e.the diagnostic sensitivity to the discogenic low back pain of the symptom of extensive low back pain, posterior ilium pain, lateral thigh pain, groin pain and low abdomen pain was 89.6％, 90.8％, 90.6％, 90.6％ and 92.3％ respectively.Conclusion The occurrence of the above-mentioned symptoms in the discogenic low back pain is conform to the neurological anatomic mechanism of efferent nerve of lumbar disc.These symptoms have great diagnostic significance for discogenic low back pain.

Objective To explore the signaling pathway of apoptosis induced by Paclitaxel (PTX) in leukemia cells and the chemosensitizing effect of adding short hairpin RNA(shRNA) on PTX,which targets the silencer of death domains(SODD).Methods After being treated with PTX,the expressions of SODD,B-cell lymphoma/leukemia-2 (Bcl-2),nuclear factor kappa B (NF-κB) and Caspase-3 proteins in Jurkat cells were determined by Western blot ;the shRNA-SODD vectors were constructed and transfected into Jurkat cells by electroporation,and then G418 was used to select the stable tranfected cell line expressing the shRNA-SODD recombinant plasmids.The incidence of cell apoptosis induced by PTX was determined by flow cytometry labeled with propidium iodide.Results During the process of inducing apoptosis of Jurkat cells,PTX could significantly down-regulate the expressions of SODD and Bcl-2 proteins,degrade Caspase-3 and activate NF-κB.The apoptotic sensibility of Jurkat cells transfected with shRNA-SODD to PTX was significantly increased compared with the control group,and the difference was statistically significant (F =10.35,P ＜ 0.05).Conclusions PTX can effectively induce apoptosis of Jurkat cells.Perhaps,SODD/Bcl-2 represents a specific apoptotic signaling pathway of PTX in leukemia cells and this apoptotic signaling pathway is Caspase-3-dependent,in which the function of NF-κB is to modulate the correlative apoptotic factors.Inhibiting the expression of SODD through transfecting shRNA-SODD vectors can significantly increase the apoptotic sensibility of leukemia cells to PTX.