1.Long-term follow-up on disc renarrowing after anterior lumbar interbody fusion with autogenous tricortical iliac crest graft.
Yong-gang ZHANG ; Wen-zhi ZHANG ; Duo-sai LÜ ; Die-ji LU ; Yan WANG ; Zhi-ren LIANG
Chinese Journal of Surgery 2004;42(6):330-333
OBJECTIVETo have a retrospective review of the patients undergoing anterior lumbar interbody fusion (ALIF) with clinical and radiological assessment, and observe changing of graft after procedure and assess correlation between graft collapse and recurrence of radiculopathy.
METHODSSixty-seven consecutive patients undergoing ALIF only at L(4 - 5) with autologous iliac crest graft for intervertebral disc prolapse were followed-up for an average of 14 (2.5 - 32) years. The effect of the fusion was examined by the existence of radiolucent lines and bony continuity on plain radiographs and tomographs, or mobility on flexion-extension radiographs. The disc height was also measured. Lower limb radiculopathy was assessed based on the symptom and examination. Paired samples t-test was used for statistical analysis.
RESULTSSixty-four patients with successful fusion were analyzed (fusion rate: 96%). All measurements in this study were completed by the same author, and the measurement error of more than 2 mm was statistically significant. According to this, graft collapse occurred in 55 patients (86%) and 9 patients (14%) had no graft collapse. In these 55 cases, the original disc height was (12.1 +/- 2.9) mm, increased immediately after the surgery to (16.2 +/- 1.9) mm, however re-narrowed to (12.9 +/- 2.7) mm at the first observation of solid fusion (a mean of 9 months, ranging from 5 to 14 months), which was not significant different compared to the original. There was no significant change in disc height after solid fusion and the disc space at the final follow-up was (12.6 +/- 2.3) mm. There was no radiculopathy observed in 52 cases (95%) during the follow-up.
CONCLUSIONDisc space re-narrowing was observed in most cases after single level ALIF of L(4 - 5), however it was rarely less than the initial and unlikely to result in recurrence of radiculopathy.
Adult ; Equipment and Supplies ; Female ; Follow-Up Studies ; Humans ; Low Back Pain ; surgery ; Lumbar Vertebrae ; diagnostic imaging ; pathology ; surgery ; Lumbosacral Region ; diagnostic imaging ; Male ; Middle Aged ; Radiography ; Recurrence ; Spinal Fusion ; methods ; Spinal Osteophytosis ; surgery ; Time Factors ; Transplantation, Autologous ; methods ; Treatment Outcome
2.PKD3 promotes metastasis and growth of oral squamous cell carcinoma through positive feedback regulation with PD-L1 and activation of ERK-STAT1/3-EMT signalling.
Bomiao CUI ; Jiao CHEN ; Min LUO ; Yiying LIU ; Hongli CHEN ; Die LÜ ; Liwei WANG ; Yingzhu KANG ; Yun FENG ; Libin HUANG ; Ping ZHANG
International Journal of Oral Science 2021;13(1):8-8
Oral squamous cell carcinoma (OSCC) has a high incidence of metastasis. Tumour immunotherapy targeting PD-L1 or PD-1 has been revolutionary; however, only a few patients with OSCC respond to this treatment. Therefore, it is essential to gain insights into the molecular mechanisms underlying the growth and metastasis of OSCC. In this study, we analysed the expression levels of protein kinase D3 (PKD3) and PD-L1 and their correlation with the expression of mesenchymal and epithelial markers. We found that the expression of PKD3 and PD-L1 in OSCC cells and tissues was significantly increased, which correlated positively with that of mesenchymal markers but negatively with that of epithelial markers. Silencing PKD3 significantly inhibited the growth, metastasis and invasion of OSCC cells, while its overexpression promoted these processes. Our further analyses revealed that there was positive feedback regulation between PKD3 and PD-L1, which could drive EMT of OSCC cells via the ERK/STAT1/3 pathway, thereby promoting tumour growth and metastasis. Furthermore, silencing PKD3 significantly inhibited the expression of PD-L1, and lymph node metastasis of OSCC was investigated with a mouse footpad xenograft model. Thus, our findings provide a theoretical basis for targeting PKD3 as an alternative method to block EMT for regulating PD-L1 expression and inhibiting OSCC growth and metastasis.
Animals
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B7-H1 Antigen/metabolism*
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Carcinoma, Squamous Cell
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Cell Line, Tumor
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Feedback
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Head and Neck Neoplasms
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Humans
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Mice
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Mouth Neoplasms
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Protein Kinase C
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STAT1 Transcription Factor
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Squamous Cell Carcinoma of Head and Neck