Jin-Lai Lei

Lateral compression type1 (LC-1) pelvic fractures represent a wide spectrum of heterogeneous injuries. These include both stable and unstable patterns; however, determining whether a LC-1 fracture is stable or unstable is a challenge, and the method used to evaluate fracture stability is complicated. We prospectively collected and analyzed data from 22 patients with LC-1 pelvic fractures, who underwent ultrasonography and a pelvic compression and separation test, in order to evaluate the role of ultrasonography in determining fracture stability and assist decision-making for treatment strategy. Twenty-two patients (15 men and 7 women) were included in the study. Following an ultrasound examination, 10 patients were classified into the stable group and 12 into the unstable group. In total, 13 patients received conservative treatment and 9 underwent surgery. At follow-up, there were no differences in fracture healing times or fracture-related complications between the two groups. The Majeed score was comparable between the two groups and most patients recovered well. There was a moderate degree of consistency in Kappa values (Kappa = 0.571, P = 0.01) between the classification of stability and the final treatment received. In addition, the sensitivity of ultrasonography was 66.67% and the specificity was 76.92%. In conclusion, ultrasonography is a useful tool for diagnosing the stability of LC-1 pelvic fractures and assists the determination of treatment strategy. Left-right mobility ≥ 0.3 cm may be used as the criterion for determining instability. ChiCTR-DDD-16008722.

Inflammation plays a crucial role in kidney damage after crush syndrome (CS). Several researchers report that high mobility group box-1 protein (HMGB1) may be the vital trigger in kidney damage, and tumor necrosis factor-α (TNF-α) and c-Jun N-terminal kinase (JNK) are involve in this pathophysiological process, but their biological roles are unclear. This study aimed to explore the relationship between HMGB1, JNK, and TNF-α in kidney damage. The crush injury model was established using weight compression. The reliability of the crush injury model was determined by hematoxylin-eosin (HE) staining. Western blot was used to detect the expression of HMGB1, JNK, and TNF-α, and TUNEL was used to mark apoptotic cells in the renal cortex. The results showed that the highest expression of HMGB1 in muscle was 12 h after CS. JNK and TNF-α increased and peaked at 1 day after CS in kidneys. Western blot analysis revealed that anti-HMGB1 antibody could downregulate the expression of JNK and TNF-α. Anti-TNF-α could downregulate activation of JNK, and SP600125 could downregulate expression of TNF-α in the kidneys. In addition, anti-HMGB1 antibody, anti-TNF-α antibody, and SP600125 could reduce cellular apoptosis in the renal cortex. It is possible that JNK and TNF-α commonly contribute to kidney damage by assembling a positive feedback cycle after CS, leading to increased apoptosis in the renal cortex. HMGB1 from the muscle may be the trigger.