Experimental study on determining the degree of bone healing by wall thickness ratio analysis.

To verify the reliability and accuracy of wall thickness ratio analysis to determine the degree of bone healing, fracture models were established with 6 beagles. X-ray, micro-CT, and CT scans were performed at 24 weeks. The healthy side and the affected side were used to simulate the three-dimensional geometric model after internal fixation, and the mesh was divided. The mean and median CT wall thickness values were obtained through the wall thickness analysis. X-ray, CT, micro-CT, and gross appearance were used to determine the degree of bone healing, which was compared with wall thickness analysis. There was a positive correlation between the average CT value and the median wall thickness. The correlation coefficient analysis of the median wall thickness ratio (R2) and healing index ratio (R3) showed a positive correlation. The results of the wall thickness ratio (R2) and the healing index ratio (R3) were used to determine bone healing, and the results were consistent with the results of the actual mechanical test and image analysis. The results of wall thickness ratio analysis were significantly correlated with the degree of bone healing. This method is simple, rapid, and practical to analyze and judge the degree of bone healing.

Wall thickness analysis method for judging the degree of lower extremity long bone healing.

To evaluate the possibility of judging the degree of bone healing by wall thickness analysis provide reference for quantitative analysis of bone healing. Patients with lower limb fracture from April 2014 to October 2019 were recruited and divided into bone healing (group A), poor bone healing (group B), and nonunion (group C). Models were built in Mimics 20.0 with DICOM 3.0 data obtained from patient's CT. Three-dimensional geometric models of unaffected limb and affected limb after simulated removal of internal fixation were established, corresponding to basic phase and simulated phase, respectively. Wall thickness analysis was performed to obtain median wall thickness after meshing. R2 (median wall thickness ratio), R4 (CT value ratio), and R5 (healing index ratio) were obtained by calculating the ratio of each value in simulated phase to that in basic phase. Receiver operating characteristic curve analysis was used to evaluate the ability of Wall Thickness Analysis to indicate fracture healing. 112 CT scans of 79 patients were included in the study. The frequency of categorization in groups A, B, and C was 49, 37 and 26, respectively. The median R2 in groups A, B, and C was 0.91, 0.80, and 0.67, respectively (group A > group B > group C, all P < 0.05). The best cutoff point for R2 in predicting bone healing was 0.84, and predicting bone nonunion was 0.74. The Wall Thickness Analysis can be used to quantitatively evaluate fracture healing state, with median wall thickness ratio as a more intuitive and reliable judgment index.

Pretreatment with a modified St. Thomas' solution in patients with severe upper limb injuries: Four case reports.

BACKGROUND: This study aims to describe the application of a modified St. Thomas' solution in patients with severe limb injuries. CASE SUMMARY: Four patients who sustained a high-energy trauma and underwent complete upper limb amputation were pretreated with a modified St. Thomas' solution before upper limb replantation. After the perfusion solution stopped flowing from the blood vessel, the amputated upper limb amputation was replanted. The patients were instructed to perform functional rehabilitation training after the operation. All 4 patients were followed up for 5 years. All the severed upper limbs survived. Routine re-examination after the operation showed that the function of the affected limb was restored. All the patients were satisfied with the sensory and functional recovery of the affected limb. CONCLUSION: The modified St. Thomas' solution can effectively improve the success rate of limb salvage surgery and the recovery of limb function in patients with a severe limb injury.

Correction to: Bilobalide protects against ischemia/reperfusion-induced oxidative stress and inflammatory responses via the MAPK/NF-κB pathways in rats.

An amendment to this paper has been published and can be accessed via the original article.

Bilobalide protects against ischemia/reperfusion-induced oxidative stress and inflammatory responses via the MAPK/NF-íœ B pathways in rats.

BACKGROUND: Clinically, skeletal muscle ischemia/reperfusion injury is a life-threatening syndrome that is often caused by skeletal muscle damage and is characterized by oxidative stress and inflammatory responses. Bilobalide has been found to have antioxidative and anti-inflammatory effects. However, it is unclear whether bilobalide can protect skeletal muscle from ischemia/reperfusion injury. METHODS: The effects of bilobalide on ischemia/reperfusion-injured skeletal muscle were investigated by performing hematoxylin and eosin staining and assessing the wet weight/dry weight ratio of muscle tissue. Then, we measured lipid peroxidation, antioxidant activity and inflammatory cytokine levels. Moreover, Western blotting was conducted to examine the protein levels of MAPK/NF-휅B pathway members. RESULTS: Bilobalide treatment could protected hind limb skeletal muscle from ischemia/reperfusion injury by alleviating oxidative stress and inflammatory responses via the MAPK/NF-휅B pathways. CONCLUSIONS: Bilobalide may be a promising drug for I/R-injured muscle tissue. However, the specific mechanisms for the protective effects still need further study.

miR-181c-5p mediates simulated microgravity-induced impaired osteoblast proliferation by promoting cell cycle arrested in the G2 phase.

Impaired osteoblast proliferation plays fundamental roles in microgravity-induced bone loss, and cell cycle imbalance may result in abnormal osteoblast proliferation. However, whether microgravity exerts an influence on the cell cycle in osteoblasts or what mechanisms may underlie such an effect remains to be fully elucidated. Herein, we confirmed that simulated microgravity inhibits osteoblast proliferation. Then, we investigated the effect of mechanical unloading on the osteoblast cell cycle and found that simulated microgravity arrested the osteoblast cell cycle in the G2 phase. In addition, our data showed that cell cycle arrest in osteoblasts from simulated microgravity was mainly because of decreased cyclin B1 expression. Furthermore, miR-181c-5p directly inhibited cyclin B1 protein translation by binding to a target site in the 3'UTR. Lastly, we demonstrated that inhibition of miR-181c-5p partially counteracted cell cycle arrest and decreased the osteoblast proliferation induced by simulated microgravity. In conclusion, our study demonstrates that simulated microgravity inhibits cell proliferation and induces cell cycle arrest in the G2 phase in primary mouse osteoblasts partially through the miR-181c-5p/cyclin B1 pathway. This work may provide a novel mechanism of microgravity-induced detrimental effects on osteoblasts and offer a new avenue to further investigate bone loss induced by mechanical unloading.

Simulated microgravity reduces intracellular-free calcium concentration by inhibiting calcium channels in primary mouse osteoblasts.

Calcium homeostasis in osteoblasts plays fundamental roles in the physiology and pathology of bone tissue. Various types of mechanical stimuli promote osteogenesis and increase bone formation elicit increases in intracellular-free calcium concentration in osteoblasts. However, whether microgravity, a condition of mechanical unloading, exerts an influence on intracellular-free calcium concentration in osteoblasts or what mechanisms may underlie such an effect are unclear. Herein, we show that simulated microgravity reduces intracellular-free calcium concentration in primary mouse osteoblasts. In addition, simulated microgravity substantially suppresses the activities of L-type voltage-sensitive calcium channels, which selectively allow calcium to cross the plasma membrane from the extracellular space. Moreover, the functional expression of ryanodine receptors and inositol 1,4,5-trisphosphate receptors, which mediate the release of calcium from intracellular storage, decreased under simulated microgravity conditions. These results suggest that simulated microgravity substantially reduces intracellular-free calcium concentration through inhibition of calcium channels in primary mouse osteoblasts. Our study may provide a novel mechanism for microgravity-induced detrimental effects in osteoblasts, offering a new avenue to further investigate bone loss induced by mechanical unloading.