Purpose To investigate the clinical efficacy of percutaneous radiofrequency ablation and microwave ablation in the treatment of primary hepatic carcinoma.Materials and Methods Ninety-two patients with primary hepatocellular carcinoma (116 lesions) were randomly divided into 46 cases of radiofrequency ablation group and 46 cases of microwave ablation group, which were treated with radiofrequency ablation and microwave ablation, respectively, the ablation points and ablation time, complete ablation rate, local tumor progression rate, postoperative complications, hospitalization time, hospitalization expenses, recurrence rate and relapse-free survival rate 1 year, 2 years and 3 years after surgery were compared and analyzed.Results There was no significant difference between the two groups in average ablation points (P>0.05), and the ablation time of microwave ablation group was significantly shorter than that of radiofrequency ablation group (P<0.01). There was no significant difference in complete ablation rate and local tumor progression rate between the two groups (P>0.05). The difference of complete ablation rate and local tumor progression rate between the two groups of tumor <3 cm, tumor 3-5 cm and tumor near the vessel were not statistically significant (P>0.05). There were no significant differences in the incidence of fever, pain in liver area and average length of hospitalization between the two groups (P>0.05). The average hospitalization cost of microwave ablation group was significantly lower than that of radiofrequency ablation group (P<0.01). There was no statistically significant difference of the cumulative recurrence rate for 1 year, 2 years, 3 years after surgery between the two groups (P>0.05). There was no significant difference between the two groups in the overall relapse-free survival rate and relapse-free survival rate among tumors with different size of the two groups (P>0.05).Conclusion Using microwave ablation for the treatment of primary hepatocellular carcinoma shows a clinical efficacy and safety as good as radiofrequency ablation. Radiofrequency ablation may have better therapeutic effect for smaller tumors, but microwave ablation may have some advantages for medium or large tumors and tumors located near the vessels.

Fluorine is an important element widely present in nature, and moderate intake can prevent dental caries and promote bone development. However, long-term excessive intake can lead to fluorosis, damaging tissues or organs such as teeth, bones, heart muscle, and blood vessels. Bone marrow mesenchymal stem cells (BMSCs) play an important role in the repair process of bone injury due to their excellent multi-directional differentiation potential. Therefore, studying BMSCs is of great value in the treatment of fluorosis caused by fluoride poisoning. This article summarize the progress on the effect of fluoride on BMSCs, providing new ideas for the study of the pathogenesis and clinical treatment of fluorosis.

Objective:To explore the changes of mitophagy- and apoptosis-related protein expressions after spinal cord injury in rats and its related mechanism.Methods:Ninety-six healthy female SD rats were divided into sham surgery group ( n=48) and spinal cord injury group ( n=48) according to the random number table. Each group was divided into six time points of 1, 3, 7, 14, 21 and 28 days with 8 rats at each time point. In the sham surgery group, the T 8-9 spinous processes and vertebral plates were removed without damage to the spinal cord; in the spinal cord injury group, the spinal cord injury model was established using Allen′s method. At each post-injury time point in two groups, BBB score was used to evaluate the motor function of the rats; HE staining was used to observe the histopathological changes of the spinal cord; immunofluorescence was used to observe the co-localized positive cells of the voltage-dependent anion channel protein 1 (VDAC1) with microtubule-associated protein 1 light chain 3 (LC3) II, E3 ubiquitin ligase (Parkin), and polyubiquitin-binding protein (p62); Western blotting was used to observe expressions of the mitochondrial LC3 II/LC3 I, cytoplasmic Parkin, mitochondrial Parkin, cytoplasmic p62, mitochondrial p62, cytoplasmic apoptotic proteins (Bax), mitochondrial Bax, cytoplasmic cytochrome C (Cyt C), and mitochondrial Cyt C. Results:(1) Compared with the sham surgery group [(21.00±0.00)points at all time points], the BBB scores in the spinal cord injury group were (0.94±0.50)points, (1.69±0.70)points, (4.13±0.99)points, (11.81±1.03)points, (15.06±1.12)points and (18.38±0.83)points at 1, 3, 7, 14, 21 and 28 days after injury, respectively ( P<0.01). (2) Compared with the sham surgery group, the structure in the spinal cord injury group was significantly disrupted at 1 and 3 days after injury, when a large number of hemorrhagic foci, inflammatory cell infiltration, neuronal swelling, and cavity formation were observed. At 7 and 14 days after injury, the number of hemorrhagic foci was markedly reduced compared with the earlier period, when swollen neuronal cytosols, inflammatory cell infiltration and a large number of cavities were found. At 21 and 28 days after injury, a large number of cells were seen to be involved in the repair and the arrangement of cells was disorganized. (3) Compared with the sham surgery group, the number of co-localized positive cells of VDAC1 with LC3 II, Parkin and p62 separately in the spinal cord injury group, markedly increased at 1 and 3 days after surgery, and gradually decreased after that. (4) In the sham surgery group and at 1, 3, 7, 14, 21 and 28 days after injury in the spinal cord injury group, the mitochondrial LC3 II/LC3 I expression levels were 0.56±0.05, 1.00±0.05, 1.19±0.11, 0.86±0.05, 0.80±0.08, 0.66±0.13 and 0.51±0.11, respectively; the cytoplasmic Parkin expression levels were 0.80±0.13, 0.47±0.08, 0.29±0.06, 0.57±0.07, 0.70±0.05, 0.97±0.09 and 0.88±0.12, respectively; the mitochondrial Parkin expression levels were 0.67±0.09, 1.07±0.18, 1.27±0.15, 0.82±0.12, 0.59±0.09, 0.53±0.13 and 0.57±0.14, respectively; the cytoplasmic p62 expression levels were 1.25±0.08, 1.04±0.04, 0.94±0.05, 1.09±0.05, 1.19±0.06, 1.20±0.04 and 1.27±0.05, respectively; the mitochondrial p62 expression levels were 0.61±0.06, 0.88±0.07, 1.09±0.09, 0.98±0.07, 0.70±0.08, 0.68±0.08 and 0.60±0.09, respectively; the cytoplasmic Bax expression levels were 0.92±0.08, 0.67±0.07, 0.36±0.08, 0.48±0.08, 0.69±0.06, 0.88±0.11 and 0.94±0.08, respectively; the mitochondrial Bax expression levels were 0.57±0.04, 0.74±0.04, 0.91±0.05, 0.76±0.05, 0.63±0.08, 0.61±0.05 and 0.57±0.05, respectively; the cytoplasmic Cyt C expression levels were 0.28±0.05, 0.81±0.07, 1.12±0.08, 0.64±0.07, 0.67±0.13, 0.60±0.11 and 0.37±0.06, respectively; and the mitochondrial Cyt C expression levels were 1.02±0.07, 0.91±0.14, 0.37±0.07, 0.73±0.06, 0.91±0.11, 0.95±0.13 and 1.10±0.15, respectively. Compared with the sham surgery group, in the spinal cord injury group mitochondrial LC3II/LC3I had the highest expression level at 3 days after injury; cytoplasmic Parkin had the lowest expression level at 3 days after injury; mitochondrial Parkin had the highest expression level at 3 days after injury; cytoplasmic p62 had the lowest expression level at 3 days after injury; mitochondrial p62 had the highest expression level at 3 days after injury; cytoplasmic Bax had the lowest expression level at 3 days after injury; mitochondrial Bax had the highest expression level at 3 days after injury; cytoplasmic Cyt C had the highest expression level at 3 days after injury; and mitochondrial Cyt C had the lowest expression level at 3 days after injury. Conclusion:Mitochondrial autophagy and apoptosis are enhanced after spinal cord injury in rats, and the potential mechanism may be associated with the transfer of Parkin and P62 from the cytoplasm to the damaged mitochondria for enhanced mitophagy and the release of a large amount of Cyt C from the mitochondria caused by the transfer of Bax from the cytoplasm to the damaged mitochondria for enhanced apoptosis.

Fluorosis is an endemic disease caused by prolonged exposure to excessive fluoride and is considered a serious public health problem in many countries. In recent years, the damage of chronic fluorosis to the central nervous system has attracted extensive attention from scholars at home and abroad. The mechanisms of neurotoxicity caused by fluorosis include oxidative stress, inflammatory reaction, autophagy, neurotransmitters and related enzymes, changes in neural signaling pathways, abnormal neuronal energy metabolism of neurons, cell apoptosis, etc., causing permanent damage to human brain structure, impaired learning ability, memory dysfunction and behavioral problems. This article reviews the effects of fluorosis on the nervous system and related mechanisms, and provides a reliable basis for prevention and treatment of fluorosis.

Objective:To study the locational distribution characteristics of the heterotopic ossification (HO) following traumatic elbow stiffness and the risk factors for HO development at different locations.Methods:Consecutively included according to our inclusion criteria in the present study were the patients who had been admitted to Department of Orthopaedic Trauma, Beijing Jishuitan Hospital from January 2018 to December 2018 for elbow release due to traumatic elbow stiffness but developed postoperative HO. Their baseline data and CT data were collected and processed using Mimics 20.0. The HO distribution for each patient was characterized at the anteromedial, anterolateral, posteromedial, posterolateral, posterior, medial, lateral, and proximal radioulnar locations. The patient's original injury was categorized into 5 types: distal humerus fracture, olecranon fracture, radial head fracture, coronoid fracture, and elbow dislocation. After the univariate analysis with the HO occurrence at a specific location as the dependent variable and the original injury and baseline data as the independent variables, the factors with P value less than 0.1 were included in the logistic regression analysis to determine the risk factors for HO at each location.Results:A total of 91 patients were included in this study. Of them, 88 had posteromedial HO (96.7%, 88/91), 62 posterior HO (68.1%, 62/91), 60 posterolateral HO (65.9%, 60/91), 41 anteromedial HO (45.1%, 41/91), 26 anterolateral HO (28.6%, 26/91), 13 proximal radioulnar HO (14.3%, 13/91), 8 lateral HO (8.8%, 8/91), and 7 medial HO (7.7%, 7/91). Logistic regression analysis showed that presence of ulnar nerve symptoms ( OR=4.354, P=0.017) and presence of original elbow dislocation ( OR=2.927, P=0.042) were the independent risk factors for the anteromedial HO development and that presence of original olecranon fracture ( OR=0.277, P=0.023) was the protective factor for the anteromedial HO development. Presence of original radial head fracture was the independent risk factor for the anterolateral HO development ( OR=2.891, P=0.033) and the posterolateral HO development ( OR=3.123, P=0.043). Conclusions:HO development in patients with post-traumatic elbow stiffness is closely related to their original injury. Posteromedial HO may develop in almost all the patients. Patients with ulnar nerve symptoms and original elbow dislocation are more prone to anteromedial HO development, but patients with original olecranon fracture are less likely to develop anteromedial HO. Patients with original radial head fracture are more likely to develop anterolateral and posterolateral HO.

Osteoporotic vertebral compression fracture (OVCF) can lead to lower back pain and may be even accompanied by scoliosis, neurological dysfunction and other complications, which will affect the daily activities and life quality of patients. Vertebral augmentation is an effective treatment method for OVCF, but it cannot correct unbalance of bone metabolism or improve the osteoporotic status, causing complications like lower back pain, limited spinal activities and vertebral refracture. The post-operative systematic and standardized rehabilitation treatments can improve curative effect and therapeutic efficacy of anti-osteoporosis, reduce risk of vertebral refracture, increase patient compliance and improve quality of life. Since there still lack relevant clinical treatment guidelines for postoperative rehabilitation treatments following vertebral augmentation for OVCF, the current treatments are varied with uneven therapeutic effect. In order to standardize the postoperative rehabilitation treatment, the Spine Trauma Group of the Orthopedic Branch of Chinese Medical Doctor Association organized relevant experts to refer to relevant literature and develop the "Guideline for postoperative rehabilitation treatment following vertebral augmentation for osteoporotic vertebral compression fracture (2022 version)" based on the clinical guidelines published by the American Academy of Orthopedic Surgeons (AAOS) as well as on the principles of scientificity, practicality and advancement. The guideline provided evidence-based recommendations on 10 important issues related to postoperative rehabilitation treatments of OVCF.