Comparison between single anterior and single posterior approaches of debridement interbody fusion and fixation for the treatment of mono-segment lumbar spine tuberculosis.

PURPOSE: To compare the efficacy of single anterior and single posterior approach of debridement, interbody fusion, and fixation for the treatment of mono-segment lumbar spine tuberculosis (TB) patients. METHODS: Eighty-seven patients with mono-segment lumbar TB who underwent debridement, interbody fusion, and fixation through either single anterior (Group A) or single posterior approach (Group B) from January 2007 to January 2017 were enrolled in this study. The duration of the operation, blood loss, complication rate, visual analog scale (VAS), Oswestry disability index (ODI), Frankel scale, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), kyphosis angle, correction rate, correction loss, and time taken for bone graft fusion were compared between the groups. RESULTS: The average period of follow-up was 34.3 ± 9.5 months (24-56 months). No significant differences were observed between patients in Group A and patients in Group B in terms of gender, age, body mass index (BMI), duration of illness and preoperative evaluative indices (P > 0.05). The mean operation time and blood loss was significantly higher in Group A (P = 0.000), along with a slightly higher rate of complications compared with Group B (P = 0.848). The VAS, ODI and Frankel scale scores showed significant improvement in both groups (P = 0.000), along with the ESR, CRP and kyphosis indices (P = 0.000), which were similar in both groups at the final follow-up. CONCLUSION: Both single anterior and single posterior approaches of debridement, interbody fusion and fixation are effective for mono-segment lumbar TB patients, although the single posterior approach is of a shorter duration and results in less blood loss.

Effects of Phenanthrene Stress on Gonads and Vitellogenin of Loach (Misgurnus anguillicaudatus).

Phenanthrene (PHE) as a tricyclic polycyclic aromatic hydrocarbon is one of the common pollutants in water and sediments, which can cause reproductive toxicity to aquatic organisms. In this study, enzyme-linked immunosorbent assay (ELISA) was used to detect the vitellogenin (VTG) of loach, and then to explore the estrogenic toxicity effect of PHE on loach. The results were as follows: (1) with the increase of PHE concentrations and the extension of exposure time, the gonadosomatic index (GSI) of males decreased significantly, while it increased in female loaches. In addition, males had more obvious changes than females and were more sensitive to PHE. (2) The increase of VTG contents in serum of males were stronger than that in females. Those results reveal that PHE has estrogenic effect, which can affect the generation of VTG, thus causing damage to the gonad development of loach.

CTRP6 inhibits fibrogenesis in TGF-ß1-stimulated human dermal fibroblasts.

Skin fibrosis is characterized by excessive proliferation of fibroblasts and overproduction of extracellular matrix (ECM). C1q/tumor necrosis factor-related protein 6 (CTRP6), a member of CTRPs, has been involved in the development of cardiac fibrosis. However, the function and detailed regulatory mechanism of CTRP6 in skin fibrosis remain unclear. The aim of this study was to investigate the effect of CTRP6 on the activation of human dermal fibroblasts. Our results showed that CTRP6 was lowly expressed in scar tissues and transforming growth factor-ß1 (TGF-ß1)-treated dermal fibroblasts. CTRP6 overexpression significantly inhibited the proliferation of dermal fibroblasts, as well as suppressed the expression of ECM in TGF-ß1-treated dermal fibroblasts. Furthermore, CTRP6 overexpression markedly inhibited TGF-ß1-induced phosphorylation of Smad3 in dermal fibroblasts. In conclusion, the data reported here demonstrate that CTRP6 is able to inhibit the proliferation and ECM expression in human dermal fibroblasts through suppressing the TGF-ß1/Smad3 signaling pathway. These findings suggest that CTRP6 may be a potential therapeutic target for the prevention of skin fibrosis.

NF-YA promotes invasion and angiogenesis by upregulating EZH2-STAT3 signaling in human melanoma cells.

The process of angiogenesis is essential for tumor development and metastasis. Vascular endothelial growth factor (VEGF), which is overexpressed in most human cancers, has been demonstrated to be a major modulator of angiogenesis. Thus, inhibition of VEGF signaling has the potential for tumor anti-angiogenic therapy. Signal transducer and activator of transcription-3 (STAT3) is a key regulator for angiogenesis by directly binding to the VEGF promoter to upregulate its transcription. Several factors can enhance STAT3 activity to affect angiogenesis. Here, we found that overexpression of nuclear transcription factor-Y alpha (NF-YA) gene could promote cell invasion and angiogenesis accompanying the increase of STAT3 signaling in human melanoma cells. Moreover, the expression and secretion of VEGF was also found to be upregulated by the overexpression of NF-YA gene in melanoma cells. The STAT3 inhibitor was able to attenuate the upregulation of VEGF induced by NF-YA overexpression. Enhancer of zeste homolog 2 (EZH2), the catalytic subunit of the Polycomb repressive complex 2, enhances STAT3 activity by mediating its lysine methylation. We also showed that NF-YA upregulated the expression of EZH2 and NF-YA­induced angiogenesis could be inhibited by EZH2 knockdown. Taken together, these findings indicate that overexpression of NF-YA contributes to tumor angiogenesis through EZH2-STAT3 signaling in human melanoma cells, highlighting NF-YA as a potential therapeutic target in human melanoma.