Clinical Effect of Minimally Invasive Microendoscopic-Assisted Transforaminal Lumbar Interbody Fusion for Single-Level Lumbar Disc Herniation.

OBJECTIVE: This retrospective study aimed to compare the clinical and radiological outcomes of transforaminal lumbar interbody fusion (TLIF) through the Wiltse approach (W-TLIF) vs minimally invasive microendoscopy-assisted transforaminal lumbar interbody fusion (ME-TLIF) in single-segment lumbar disc herniation (LDH). METHODS: A retrospective study was conducted to study the differences in specific clinical outcomes between single-segment LDH patients receiving W-TLIF and ME-TLIF. Single-segment LDH patients admitted to the Fujian Medical University Union Hospital from March 2015 to June 2018 were included. All the participants were divided into the ME-TLIF group or the W-TLIF group according to their TLIF surgery types. Demographic characteristics, the visual analog score (VAS), Oswestry Disability Index (ODI), Japanese Orthopaedic Association (JOA) scale, blood loss volume, postoperative drainage, ambulated time, initial postoperative back pain, hospitalization duration, expenses, and improvement rates of patients in the two groups were collected for analysis. Radiographic fusion was ultimately assessed via the Bridwell interbody fusion grading system. All selected patients with TLIF were followed up for 1 year. RESULTS: Fifty-seven patients were selected, with 26 in the ME-TLIF group and 31 in the W-TLIF group, both of whom were followed up for 1 year. The mean age of the included patients was 53.75 ± 9.313 years, and the sex ratio was indiscrimination. There was no significant difference in demographic data or operating time between the two groups prior to surgery. The blood loss volume (ME-TLIF: 228.5 vs W-TLIF: 681.3), postoperative drainage (ME-TLIF:82.1 ± 23.5 vs W-TLIF: 345.8 ± 65.2), initial postoperative back pain (ME-TLIF: VAS_3 days: 1.96 ± 0.60 VAS_7 days: 1.73 ± 0.53, W-TLIF: VAS_3 days: 2.48 ± 0.51 VAS_7 days: 1.87 ± 0.43), and hospitalization duration (ME-TLIF: 9.04 vs. W-TLIF: 11.29) were all significantly lower in the ME-TILF group (p < 0.05). However, there were no statistical differences between the two groups in VAS, ODI, and JOA at 1 month, 3 months, 6 months, and 1 year postoperatively (p > 0.05). The fusion rates of the two groups showed no notable difference (p > 0.05), while the X-ray exposure time in the ME-TLIF group was significantly longer than in the W-TLIF group (p < 0.05). CONCLUSIONS: ME-TLIF surgery was an effective and satisfactory surgical technique to manage LDH. Although ME-TLIF increased the operation time and intraoperative fluoroscopic irradiation volume, it could effectively relieve low back pain from early postoperative onset and promote early postoperative recovery compared with W-TLIF.

Inhibitory effect of CCR3 signal on alkali-induced corneal neovascularization.

AIM: To investigate the effect of CC chemokine receptor 3 (CCR3) signal on corneal neovascularization (CRNV) induced by alkali burn and to explore its mechanism. METHODS: Specific pathogen-free male BALB/C mice (aged 6-8 weeks) were randomly divided into CCR3-antagonist treated group (experimental group) and control group. CRNV was induced by alkali burn in mice. The time kinetic CCR3 expression in injured corneas was examined by reverse transcription polymerase chain reaction (RT-PCR). CCR3-antagonist (SB-328437 at different concentration of 125µg/mL, 250µg/mL, and 500µg/mL) was locally administrated after alkali injury. The formation of CRNV was assessed by CD31 corneal whole mount staining at two weeks after injury. Monocyte chemotactic protein 1 (MCP-1), monocyte chemotactic protein 3 (MCP-3) expressions in the early phase after injury were quantified and compared by RT-PCR. Macrophage intracorneal accumulation in the early phase after injury was evaluated and compared by immunohistochemistry. RESULTS: Alkali injury induced the time kinetic intracorneal CCR3 expression. 500µg/mL of CCR3-antagonist treatment in the early phase but not the late phase resulted in significant impaired CRNV as compared to control group (P<0.05). CCR3-antagonist treatment in the early phase significantly reduced the intracorneal MCP-1 and MCP-3 enhancement compare to control group at day 2 and day 4 (P<0.05). Moreover, the number of intracorneal macrophage infiltration in the experimental group was reduced than those in control group at day 4 (P<0.05). CONCLUSION: CCR3 signal is involved in alkali-induced CRNV. CCR3-antagonist can inhibit alkali-induced CRNV by reducing the intracorneal MCP-1 and MCP-3 mRNA expression and the intracorneal macrophage infiltration.

Inhibited experimental corneal neovascularization by neutralizing anti-SDF-1α antibody.

AIM: To explore the effect of SDF-1α on the development of experimental corneal neovascularization (CRNV). METHODS: CRNV was induced by alkali injury in mice. The expression of SDF-1α and CXCR4 in burned corneas was examined by Flow Cytometry. Neutralizing anti-mouse SDF-1α antibody was locally administrated after alkali injury and the formation of CRNV 2 weeks after injury was assessed by Immunohistochemistry. The expression of VEGF and C-Kit in burned corneas was detected by RT-PCR. RESULTS: The number of CRNV peaks at 2 weeks after alkali injury. Compared to control group, SDF-1α neutralizing antibody treatment significantly decreased the number of CRNV. RT-PCR confirmed that SDF-1α neutralizing antibody treatment resulted in decreased intracorneal VEGF and C-Kit expression. CONCLUSION: SDF-1α neutralizing antibody treated mice exhibited impaired experimental CRNV through down regulated VEGF and C-Kit expression.

[Eukaryotic expression and biological activity of recombinant human IL-17B protein].

AIM: To construct pCEP4/hIL-17B recombinant expression vector and express it stably in eukaryotic cells and investigate the biological activity in vitro. METHODS: The CDS region of human IL-17B gene was cloned by RT-PCR. After identification by sequencing, the hIL-17B gene was inserted into expression vector of pCEP4 to construct the recombinant vector pCEP4/hIL-17B, then transfected into 293T cells. The transgenic 293T cell line stably expressing rhIL-17B protein was selected in the presence of Hygromycin B. After FCS-free cultivation and sub-cloning, The IL-17B/mFc gene and protein expression was confirmed by RT-PCR, ELISA and Western blot analysis. To investigate the ability of combination with IL-17B receptor on human leukemic monocytic cell line, THP-1, by Flow cytometrical analysis (FACS) and of stimulation to secret cytokines in vitro. RESULTS: The recombinant pCEP4/hIL-17B and its transgenic 293T cells stably expressing rhIL-17B protein were obtained successfully. FACS analysis showed its high affinity with its receptor and it can stimulated THP-1 cell line to excrete IL-1ß and TNF-α in vitro and consistently caused a dose-dependent influx of neutrophil into the peritoneal cavity by intraperitoneal injection in vivo. CONCLUSION: The obtainment of transgenic 293T cell line stably expressing rhIL-17B protein paved the way for further study on biological functions of hIL-17B.

[Prokaryotic expression and biological activity of recombinant human IL-17F/His protein].

AIM: To Prepare recombinant human IL-17F/His protein and investigate its biological activity in vitro. METHODS: The gene region of human IL-17F was cloned by RT-PCR. After identification by sequencing, the hIL-17F gene encoding function domain was cloned into expression plasmid PQE3.0 and transfected into E.coli M15. By the induction of Isopropyl-ß-D-Thiogalacto-Pyranoside(IPTG), recombinant IL-17F/His protein was effectively expressed in E.coli M15. The recombinant protein was identified by Western blot. RESULTS: After renaturation and purification by HiTrap(TM); affinity column, the recombinant protein can up-regulate macrophages to secret TNF-α, IL-6 and other relative cytokines. It also promoted proliferation of HeLa cells in vitro. CONCLUSION: hIL-17F/His recombinant protein is of high biological activity, which can be used to make further study of its special characteristic.