Risk factors for amputation in diabetic foot ulcers: A retrospective analysis.

Diabetic foot ulcers (DFUs) are chronic, difficult-to-heal wounds with a very high incidence of amputation. For patients with DFUs, prevention of amputation is crucial. However, the risk factors associated with DFU amputation and the extent to which different risk factors increase the risk of amputation are still uncertain. This study intends to provide a clinical basis for early intervention in DFU by retrospectively analysing the risk factors for DFU amputation. A retrospective analysis of 200 patients with DFUs admitted between October 2019 and October 2023 was conducted. Sixty-eight of the 200 underwent amputations. The overall amputation rate was 34%. Multiple logistic regression model showed that neutrophil/lymphocyte ratio (OR = 1.943; 95% CI:1.826-2.139), white blood cell (OR = 1.143; 95% CI:1.034-1.267), C-reactive protein (OR = 1.307; 95% CI:1.113-2.194) and Wagner grading (OR = 2.783; 95% CI: 1.751-4.302) were independent risk factors for amputation, while haemoglobin (OR = 0.742; 95% CI:0.638-0.965) and high density lipoprotein were independent protective factors for amputation (OR = 0.168; 95% CI:0.037-0.716), and further Receiver Operating Characteristic Curve curves showed that they showed high accuracy and were good predictors of amputation of DFUs.

TP53-mediated miR-2861 promotes osteogenic differentiation of BMSCs by targeting Smad7.

Bone defect seriously affects the quality of life. Meanwhile, osteogenic differentiation in BMSCs could regulate the progression of bone defect. Transcription factors are known to regulate the osteogenic differentiation in BMSCs. The study aimed to investigate the detailed mechanism by which TP53 regulates the osteogenic differentiation. To study bone defect in vitro, BMSCs were isolated from spinal cord injury rats. CCK-8 assay was applied to test the cell viability. The mineralized nodules in BMSCs was tested by alizarin red staining. Meanwhile, TUNEL staining and flow cytometry were performed to test the cell apoptosis. mRNA expression was tested by qRT-PCR. Starbase and dual-luciferase reporter assay were used to predict the downstream mRNA of miR-2861. Moreover, western blot was applied to detect the protein expressions (TP53 and Smad7). BMSCs were successfully isolated from rats. The expressions of miR-2861 were significantly upregulated in osteogenic medium, compared with growth medium. MiR-2861 inhibitor significantly decreased the levels of OCN, ALP, BSP, and Runx2 in BMSCs. In addition, miR-2861 inhibitor notably inhibited the mineralized nodules, viability, and induced the apoptosis of BMSCs. Smad7 was identified to be the downstream target of miR-2861, and knockdown of Smad7 notably reversed miR-2861 inhibitor-induced inhibition of osteogenic differentiation and promotion of apoptosis in BMSCs. Moreover, miR-2861 was transcriptionally regulated by TP53 in BMSCs. TP53-meidiated miR-2861 promotes osteogenic differentiation of BMSCs by targeting Smad7. Thereby, our research might provide new methods for bone defect treatment.