Purpose. The objective of this study was to investigate the preliminary effectiveness of percutaneous endoscopic transforaminal lumbar interbody fusion (PE-TLIF) for the treatment of lumbar spinal stenosis (LSS). Methods. From September 2016 to June 2017, a series of seven patients consisting of six females and one male with an average age of 55.25 years (range 43–77 years) who were diagnosed with LSS were involved in this study. All patients were treated by PE-TLIF. During perioperative and follow-up period, demographic data, operation time, intraoperative blood loss, Visual Analogue Scale (VAS), Oswestry Disability Index (ODI), and modified MacNab criteria were evaluated and perioperative complications were documented. Results. All patients were followed up for more than 12 months, with an average follow-up time of 15 (range 12-21) months. The mean VAS of back pain was 7.43 (range 6-8) preoperatively and 0.86 (range 0-2) at the final follow-up. The mean VAS of leg pain was 6.14 (range 4-9) preoperatively and 0.71 (range 0-1) at the final follow-up. The mean ODI was 53.57% (range 38%-63%) preoperatively and 15.57% (range 5%-26%) at the final follow-up. In three-month follow-up, continuous bone trabeculae bridging between intervertebral bodies was seen in 3 cases, and the remaining 4 cases could identify continuous bone trabeculae bridging at 6-month follow-up, reaching the standard of spinal intervertebral fusion. At the final follow-up, 4 patients were rated as excellent (4/7) and 3 patients were rated as good (3/7) according to the modified MacNab criteria. Conclusions. Our study suggested that percutaneous endoscopic transforaminal lumbar interbody fusion could acquire satisfactory treatment effects for the patients with lumbar spinal stenosis, even for the patient who could not afford general anesthesia.
Microcystis, the dominant species among cyanobacterial blooms, normally forms colonies under natural conditions but exists as single cells or paired cells in axenic laboratory cultures after long-term cultivation. Here, a bloom-forming Microcystis aeruginosa strain CHAOHU 1326 was studied because it presents a colonial morphology and grows on the water surface during axenic laboratory culturing. We first examined the morphological features of strain CHAOHU 1326 and three other unicellular M. aeruginosa strains FACHB-925, FACHB-940, and FACHB-975 cultured under the same conditions by scanning and transmission electron microscopy. Then, we compared the extracellular polysaccharide (EPS)-producing ability of colonial strain CHAOHU 1326 to that of the three unicellular M. aeruginosa strains, and found that strain CHAOHU 1326 produced a higher amount of EPS than the other strains during growth. Moreover, based on genome sequencing, multiple gene clusters implicated in EPS biosynthesis and a cluster of 12 genes predicted to be involved in gas vesicle synthesis in strain CHAOHU 1326 were detected. These predicted genes were all functional and expressed in M. aeruginosa CHAOHU 1326 as determined by reverse transcription PCR. These findings provide a physiological and genetic basis to better understand colony formation and buoyancy control during M. aeruginosa blooming.
Lipid metabolism disorder and inflammation are essential promoters in pathogenesis of liver injury in type 2 diabetes. Puerarin (PUR) has been reported to exert beneficial effects on many diabetic cardiovascular diseases and chemical-induced liver injuries, but its effects on diabetic liver injury and its mechanism are still unclear. The current study was designed to explore the therapeutic effect and mechanism of PUR on liver injury in a type 2 diabetic rat model induced by a high-fat diet combined with low-dose streptozotocin. The diabetic rats were treated with or without PUR (100 mg/kg/day) by gavaging for 8 weeks, and biochemical and histological changes in liver were examined. Results showed that treatment with PUR significantly attenuated hepatic steatosis by regulating blood glucose and ameliorating lipid metabolism disorder. Liver fibrosis was relieved by PUR treatment. PUR inhibited oxidative stress and inflammation which was associated with inactivation of NF-κB signaling, thereby blocking the upregulation of proinflammatory cytokines (IL-1β, TNF-α) and chemokine (MCP-1). This protection of PUR on diabetic liver injury is possibly related with inhibition on TGF-β/Smad signaling. In conclusion, the present study provides evidence that PUR attenuated type 2 diabetic liver injury by inhibiting NF-κB-driven liver inflammation and the TGF-β/Smad signaling pathway.
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