ObjectiveTo explore the effectiveness of the first-stage debridement and Ilizarov metatarsal bone lengthening in treatment of diabetic foot ulcer complicated with chronic osteomyelitis of metatarsal head.MethodsBetween January 2015 and October 2018, 8 cases (9 feet, 11 sites) of diabetic foot ulcer complicated with chronic osteomyelitis of metatarsal head were treated by first-stage debridement and Ilizarov metatarsal bone lengthening. There were 3 males (4 feet, 5 sites) and 5 females (5 feet, 6 sites), with an average age of 57.5 years (range, 44-65 years). According to diabetic foot Wagner grade, 6 cases (7 feet) were grade 3 and 2 cases (2 feet) were grade 4. The chronic osteomyelitis located at left foot in 4 cases, right foot in 3 cases, and bilateral feet in 1 case. The duration of chronic osteomyelitis was 1-5 years (mean, 3.1 years). The chronic osteomyelitis site was the 1st metatarsal head in 3 feet, the 3rd metatarsal head in 1 foot, the 4th metatarsal head in 1 foot, and the 5th metatarsal head in 6 feet. Two patients had chronic osteomyelitis at 2 sites on 1 foot. The length of lengthened metatarsal bone, lengthening time, and the time of wearing external fixation frame were recorded, and the external fixation frame index was calculated. The healing conditions of foot ulcer and lengthening bone segment were observed, the healing time was recorded, and the healing index of lengthening bone was calculated. The ankle function was evaluated according to the American Orthopedic Foot and Ankle Society (AOFAS) score criteria.ResultsAll patients were followed up 9-26 months with an average of 15.0 months. Except pin tract infection during the bone lengthening period, there was no complications such as skin necrosis and vascular or nerve injury occurred during treatment. The length of lengthened metatarsal bone was 12-35 mm with an average of 20.5 mm; the metatarsal bone lengthening time were 21-84 days with an average of 57.8 days. The average time of wearing external fixation frame was 14.6 weeks (range, 10.4-21.1 weeks) and the external fixation frame index was 54.3 days/cm (range, 42.9-59.2 days/cm). The ulcer wound healed with an average healing time of 30.5 days (range, 19-70 days) and no ulcer recurrence was observed during follow-up. Bone healing was obtained in all bone lengthening segments, and the average healing index was 42.5 days/cm (range, 37-51 days/cm). The average AOFAS score was 91.7 (range, 87-95); 5 feet were excellent and 4 feet were good. The excellent and good rate was 100%.ConclusionThe metatarsal bone lengthening under Ilizarov law of tension-stress after debridement can promote diabetic foot ulcers healing and reconstructing the length of metatarsal to retain the function of metatarsal load and avoid amputation. This is an effective method for the treatment of diabetic foot ulcer complicated with chronic osteomyelitis of metatarsal head.
Objective To explore the effectiveness of Ilizarov external fixation without bone graft in the treatment of atrophic femoral shaft nonunion. Methods The clinical data of 12 patients with atrophic femoral shaft nonunion admitted between October 2010 and January 2017 were retrospectively analyzed. There were 8 males and 4 females, aged from 24 to 61 years, with an average age of 41.7 years. The nonunion sites located in the middle and upper femur in 7 cases and in the distal femur or supracondylar in 5 cases. The disease duration ranged from 1 to 9 years, with an average of 3.7 years. Previous operations ranged from 1 to 9 times, with an average of 2.8 times. The original fixator was removed, the fracture end of nonunion was debrided, and Ilizarov external fixator was installed. In patients with the length of bone defect less than 4 cm, direct compression fixation was performed during operation; in patients with limb shortening more than 2.5 cm, proximal femoral osteotomy and bone lengthening components were required to prepare limb lengthening after operation; all patients did not receive bone graft. The wearing time of external fixator, clinical bone healing time of nonunion fracture end, and complications were recorded. The effectiveness was evaluated by Paley’s nonunion evaluation criteria. Results All patients were followed up 24-50 months, with an average of 30 months. Bony union was achieved in all 12 cases with a healing time of 6.0-23.5 months (mean, 11.5 months). The wearing time of external fixator ranged from 7 to 25 months, with an average of 13.5 months. At last follow-up, according to Paley’s nonunion evaluation criteria, the results were excellent in 6 cases, good in 4 cases, and fair in 2 cases, with an excellent and good rate of 83.3%. Sagittal angulation deformity of femur more than 7° occurred in 4 cases, with no significant effect on knee extension function, and no special treatment such as osteotomy was performed. Two patients had shorter limbs (>2.5 cm) after operation and were replaced by high shoes; 4 patients with trans-knee fixation lost knee joint mobility of 10-30° after operation; 10 cases of needle tract infection occurred, of which 4 cases with infection and loosening of fixed needle were replaced and re-fixed after needle extraction, the remaining 6 cases of infection without loosening of fixed needle were controlled by local dressing change, needle nursing, and oral cephalosporin anti-inflammatory drugs. No complications such as deep infection and vascular nerve injury occurred. Conclusion Ilizarov external fixation has a high healing rate for atrophic femoral shaft nonunion, which is relatively minimally invasive and can avoid bone grafting. Its preliminary effectiveness is exact, and it is also effective for patients who have experienced multiple failed operations. It is necessary to pay attention to the nursing and rehabilitation training after external fixation.
ObjectiveTo investigate the expression profile, prognostic value, gene co-expression network, and immunomodulatory role of BRF1 in a pan-cancer context, and to explore its biological functions and molecular regulatory mechanisms in esophageal squamous cell carcinoma (ESCC). MethodsThe pan-cancer dataset from The Cancer Genome Atlas (TCGA) was utilized to analyze the differential expression of BRF1 in tumor versus normal tissues, its association with patient survival, pathway enrichment for co-expressed genes, and immune features (including immune checkpoints, cytokines, and immune cell infiltration). The expression profile of BRF1 in ESCC was validated using the Gene Expression Omnibus (GEO) database. In vitro, BRF1 was knocked down in ESCC cells using siRNA. Cell proliferation and migration were assessed by MTT and Transwell assays, respectively. The expression levels of proliferation- and migration-related proteins were detected by Western blotting. The correlation between BRF1 and ferroptosis was analyzed using TCGA data. ResultsBRF1 was significantly upregulated in over 20 types of cancer, and its high expression was associated with poor prognosis in patients with adrenocortical carcinoma and prostate adenocarcinoma. BRF1 was found to positively regulate the T-cell-mediated cell death pathway in esophageal adenocarcinoma and was associated with the circadian rhythm regulation pathway in pancreatic adenocarcinoma. The correlation of BRF1 with immune checkpoints, cytokine networks, and immune cell infiltration was found to be cancer type-specific. In vitro experiments demonstrated that knocking down BRF1 significantly inhibited the proliferation of ESCC cells, accompanied by the downregulation of the proliferation marker PCNA. Cell migration was also significantly impaired, with decreased expression of Vimentin and MMPs and increased expression of E-cadherin. Furthermore, the expression of BRF1 was positively correlated with that of ferroptosis-antagonizing genes, such as GPX4, HSPA5, and SLC7A11. ConclusionBRF1 plays complex roles in pan-cancer, participating in the regulation of tumorigenesis, progression, and immune infiltration. BRF1 promotes the proliferation and migration of ESCC cells, a mechanism potentially associated with the regulation of ferroptosis resistance. These findings suggest that BRF1 could be a potential therapeutic target for ESCC.