BACKGROUND:As one of the most serious pathological types of lumbar disc herniation, the nucleus pulposus of prolapsed style lumbar intervertebral disc herniation is like a cord or mass. And the nucleus pulposus compresses nerve roots and dural sac, which brings severe low back pain and/or cauda equina injury symptoms.OBJECTIVE:To compare the clinical efficacy of simple discectomy under the Quadrant system and minimally invasive transforaminal lumbar interbody Concorde fusion (MIS-TLIF) in the treatment of prolapsed and sequestrated lumbar disc herniation.METHODS:From January 2012 to January 2015, 58 patients with prolapsed and sequestrated lumbar disc herniation were enrolled in this study, including 36 patients in simple Quadrant group and 22 patients in MIS-TLIF group.RESULTS AND CONCLUSION:Significant difference was recorded in the visual analogue scale scores and Oswestry disability index at 1 week, 3 months and 18 months postoperation compared with preoperation in the two groups (P < 0.05). Compared with the simple Quadrant group, the visual analogue scale scores of low back pain and Oswestry disability index were significantly decreased in the MIS-TLIF group at postoperative 18 months (P < 0.05), but there was no significant difference in the visual analogue scale score of leg pain between two groups (P > 0.05). There were two patients with recurrent lumbar disc herniation in the simple Quadrant group. In summary, simple discectomy under the Quadrant system could achieve the similar satisfied effect as the MIS-TLIF, but the MIS-TLIF provides less low back pain.

BACKGROUND: Dexmedetomidine has been shown to fight against ischemia/reperfusion injury induced by tourniquets. OBJECTIVE: To study the effects of dexmedetomidine on the oxidative stress and inflammatory damage caused by tourniquet-induced ischemia/reperfusion injury. METHODS: Seventy-six patients scheduled for lower limb operation were randomized into two groups: patients in dexmedetomidine group were given the intravenous injection of 1 μg/kg dexmedetomidine for 10 minutes, followed by 0.5 μg/kg?h until the end of operation; while the controls were subjected to 0.9% saline injection at an equivalent velocity and volume. The levels of serum propanediol, lactic dehydrogenase, superoxyde dismutase, tumor necrosis factor-α, interleukin-6 and -8 were detected before tourniquet inflation, 10, 60 and 120 minutes after tourniquet release. RESULTS AND CONCLUSION: In both two groups, the serum levels of propanediol, lactic dehydrogenase, tumor necrosis factor-α, interleukin-6 and -8 after tourniquet release were significantly higher and the serum superoxide dismutase level was significantly lower than those before tourniquet inflation (P < 0.05). Compared with the control group, dexmedetomidine significantly reduced the serum levels of propanediol, lactic dehydrogenase, tumor necrosis factor-α, interleukin-6 and -8, and increased the serum superoxyde dismutase level after tourniquet release (P < 0.05). These results suggest that dexmedetomidine can attenuate the oxidative stress and inflammatory damage resulting from tourniquet-induced ischemia/reperfusion injury probably by up-regulating the serum superoxyde dismutase level, and down-regulating the serum levels of propanediol, lactic dehydrogenase, tumor necrosis factor-α, interleukin-6 and -8.

ObjectiveTo study the dynamic express of CD57 on T cell of PBMC and clinical significance in acute HIV infection.MethodsSeventeen patients with acute HIV infection were enrolled study randomly diagnosed from 2006.11 to 2009.12 and 15 healthy donors as control group.The PBMCs from 1th,3th and 6th during acute infection were collected.The proportion of CD3+CD57+T lymphocytes,CD3+ CD8+CD57 +T lymphocytes and CD3 + CD4 + CD57 + T lymphocytes were evaluated by flow cytometric analysis with three or double color staining.The relationship between the proportion of CD57+ T phenotypes and virus load and CD4+T cells count was analyzed.ResultsThe proportion of CD57+T lymphocytes in PMBC in 1th,3th and 6th during acute HIV acute was 15.24％ ±1.49％,13.51％ ±2.45％ and 14.65％ ±1.83％,respectively,and was higher than normal control group and the difference was significantly(P＜0.0001 ).The proportion of CD8+ CD57+T lymphocytes was 7.79％ ±2.10％ and 9.88％ ±2.36％ in 1th and 3th month during acute infection,respectively.The proportion of CD8+ CD57+T lymphocytes in 1th and 3th month during acute infection were positive relationship with virus load in corresponding time,and R2 was 0.3700 and 0.3768,and P value was 0.0096 and 0.0088,respectively.The proportion of CD8+CD57+T lymphocytes in the 1th and 3th month during acute infection was negative relationship with CD4+T lymphocytes count.The R2 was 0.3768 and 0.4235,and P value was 0.0215 and 0.0017,respectively.In 6 rapid progressors and 11 no rapid progressors on the 1th month after HIV infection,CD8+ CD57+T lymphocytes percentage was 11.20％±2.21％ and 6.16％ ±1.09％,respectively,and CD4+CD57+T lymphocytes percentage 2.79％ ±0.31％and 1.40％ ±0.30％,respectively.Both CD8+CD57+T and CD4+CD57+T in rapid progressors were higher than no rapid progressors,and P value was 0.0338 and 0.0106,respectively.ConclusionCD57+ T lymphocytes percentage in peripheral blood increase in acute HIV infection patients,in which the increasing CD8+CD57+T lymphocyte may mirror the dynamic of HIV replication and CD4+T cell count.The CD57 high express on T lymphocyte on the early HIV acute infection predicts rapid progression.

ObjectiveTo investigate the impact of icariin （ICA） on autophagy in glucocorticoid-induced bone microvascular endothelial cells （BMECs） mediated by the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR） signaling pathway. MethodBMECs were isolated and cultured from femoral heads obtained during total hip arthroplasty and identified using immunofluorescence staining. The experimental cells were divided into four groups： A control group， a glucocorticoid group （100 mg·L^-1 hydrocortisone）， an ICA group （100 mg·L^-1 hydrocortisone+6.7×10^-3 mg·L^-1 ICA）， and a Rapamycin group （100 mg·L^-1 hydrocortisone+6.7×10^-3 mg·L^-1 ICA+1 mg·L^-1 rapamycin）. Autophagy in BMECs was induced using 100 mg·L^-1 hydrocortisone. LC3 fluorescence staining was used to observe the peak of autophagy at different time points. Western blot analysis was employed to analyze the expression of autophagy-related proteins and PI3K/Akt/mTOR pathway proteins in each group. Electron microscopy was used to observe autophagosomes and autolysosomes in the cells. ResultHydrocortisone at 100 mg·L^-1 induced autophagy in BMECs， reaching a peak at around 5 hours， which then declined with further intervention. Compared to the control group， the glucocorticoid group showed cell membrane damage， disordered organelle arrangement， and a large number of autophagosomes and autolysosomes. Compared to the glucocorticoid group， the ICA group had more intact cell membranes， sparser organelle arrangement， and fewer autophagosomes and autolysosomes. Compared to the ICA group， the Rapamycin group showed cell membrane damage， disordered organelle arrangement， and more autophagosomes and autolysosomes. Compared to the control group， the glucocorticoid group had significantly increased expression of light chain 3B （LC3B）， Atg4B， and p62 （P<0.01）. Compared to the glucocorticoid group， the ICA group showed significantly decreased expression of LC3B， Atg4B， p62， and Beclin-1 （P<0.01）. Compared to the ICA group， the Rapamycin group had significantly increased expression of Atg4B and p62 （P<0.01）. Compared to the control group， the glucocorticoid group had significantly decreased expression of p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR （P<0.01）. Compared to the glucocorticoid group， the ICA group showed significantly increased expression of p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR （P<0.01）. Compared to the ICA group， the Rapamycin group had significantly decreased expression of p-PI3K/PI3K， p-Akt/Akt， and p-mTOR/mTOR （P<0.01）. Ubiquitination levels were significantly decreased in the glucocorticoid group compared to the control group （P<0.01）. Compared to the glucocorticoid group， ubiquitination levels were significantly increased in the ICA group （P<0.01）， and significantly decreased in the Rapamycin group compared to the ICA group （P<0.01）. ConclusionThe glucocorticoid-induced autophagy in BMECs is time-dependent. ICA inhibits glucocorticoid-induced autophagy in BMECs， and this effect may be related to the regulation of the PI3K/Akt/mTOR pathway.

Objective: To establish a quantitative assay of serum Golgi protein 73 (GP73) using xMAP technology and evaluate its performance. Methods: Monoclonal antibodies against GP73 were prepared and purified, and antibody pair screening was performed by double-antibody sandwich enzyme-linked immunosorbent assay. The screened antibodies were used to construct a Luminex liquid chip detection system, and the analysis performance of the detection system was evaluated. The serum levels of GP73 were detected in 90 clinical samples from healthy controls and patients with chronic hepatitis B infection (CHB) and hepatocellular carcinoma (HCC). Results: Five anti-GP73 monoclonal antibodies were prepared and purified, and 5 antibody pairs were successfully screened. The Luminex liquid chip detection system of GP73 was successfully constructed using 8F10D1 and 10B9F11 antibody pairs. The analytical performance evaluation showed that the sensitivity of this system was 0.25 ng/ml and the dynamic range was 0.25-100 ng/ml. No cross reactivity was observed. The intra- and inter-assay variation for GP73 was <8% and <11%, respectively. The recovery was 83%-92%. The linear regression equation was y=1.141x+ 6.436 (r²=0.998 4, P<0.001). The GP73 concentrations in the serum samples of healthy control, CHB group, and HCC group were 42.8 (38.68, 55.90) ng/ml, 61.49 (43.59, 81) ng/ml, and 122.78 (49.36 liter, 264.55) ng/ml, respectively. The levels of GP73 in HCC group were significantly higher than those in CHB group and healthy controls (P<0.05). Moreover, the levels of GP73 in CHB group were significantly higher than those in healthy controls (P<0.05). Conclusions A liquid chip detection system of GP73 was successfully constructed. It provides a powerful tool for the clinical application of GP73 in the future.

DNA/metabolism* ; Gene Editing ; HEK293 Cells ; Humans

CRISPR-Associated Protein 9 ; Gene Editing ; CRISPR-Cas Systems/genetics*