Objective To investigate mitochondrial function mediated by phospholipase D1(PLD1)in the lungs of mice with bronchopulmonary dysplasia.Methods Wild-type(WT)and PLD1 knockout(PLD1-KO)newborn mice were assigned to four groups:normoxic+WT,normoxic+PLD1-KO,hyperoxic+WT,and hyperoxic+PLD1-KO,with nine mice in each group.Mice in the hyperoxia groups were exposed to hyperoxia(85％ O2)for 14 days.Mice in the normoxic groups were exposed to normoxic conditions(21％ O2)for 14 days.On the 14th day,the levels of oxidative stress,apoptosis,and fibrosis in lungs were evaluated using commercial kits for malondialdehyde(MDA)and superoxide dismutase(SOD),Western blot for BAX,BCL-2,and Cleaved Caspase-3,and immunohistochemistry for α-SMA and AIF.The following MLE-12 cell groups were prepared,normoxic+si-NC,hyperoxic+si-NC,normoxic+si-PLD1,and hyperoxic+si-PLD1.After transient transfection,the cells were exposed to normoxia or hyperoxia for 24 h.Mitochondrial reactive oxygen species(mtROS)and function were measured using MitoSOX Red and the hippocampus mitochondrial stress test.Results The levels of α-SMA and AIF staining,MDA,Cleaved Caspase 3,and BAX in lung tissue were significantly increased in the hyperoxic groups compared with the normoxic groups(P＜0.05),while SOD activity and BCL-2 levels were significantly decreased(P＜0.05).α-SMA and AIF staining,and the abundance of Cleaved Caspase-3 and BAX in lung tissue were lower in the hyperoxia+PLD1-KO group than in the hyperoxia+WT group(P＜0.05),while SOD activity and BCL-2 abundance were higher in the hyperoxia+PLD1-KO group than in the hyperoxia+WT group(P＜0.05).The level of AIF in MLE-12 cell mitochondria in the hyperoxic groups was significantly lower than that in the normoxic groups(P＜0.05);however,the level of AIF was increased significantly in the cytoplasm of the hyperoxic groups compared with the normoxic groups(P＜0.05).The level of AIF in MLE-12 cell mitochondria in the hyperoxic+si-PLD1 group was significantly increased compared with that in the hyperoxic+si-NC group(P＜0.05).The abundance of mtROS in hyperoxia MLE-12 cell groups was higher than that in the normoxia groups(P＜0.05),and the abundance of mtROS in the hyperoxia+si-PLD1 group was lower than that in the hyperoxia+si-NC group(P＜0.05).Compared with the normoxic+si-NC group,basic respiration,ATP production,maximum respiration,and spare respiratory capacity was significantly decreased in the hyperoxic+si-NC group(P＜0.05).Compared with the hyperoxic+si-NC group,the hyperoxic+si-PLD1 group had significantly increased basic respiration,ATP production,maximum respiration,and spare respiratory capacity(P＜0.05).Conclusions PLD1 is involved in hyperoxia-induced injury of mouse BPD and MLE-12 cells.Deletion of the PLD1 gene may alleviate hyperoxia-induced lung injury by inhibiting mitochondrial-dependent apoptosis.

Objective To investigate mitochondrial function mediated by phospholipase D1(PLD1)in the lungs of mice with bronchopulmonary dysplasia.Methods Wild-type(WT)and PLD1 knockout(PLD1-KO)newborn mice were assigned to four groups:normoxic+WT,normoxic+PLD1-KO,hyperoxic+WT,and hyperoxic+PLD1-KO,with nine mice in each group.Mice in the hyperoxia groups were exposed to hyperoxia(85％ O2)for 14 days.Mice in the normoxic groups were exposed to normoxic conditions(21％ O2)for 14 days.On the 14th day,the levels of oxidative stress,apoptosis,and fibrosis in lungs were evaluated using commercial kits for malondialdehyde(MDA)and superoxide dismutase(SOD),Western blot for BAX,BCL-2,and Cleaved Caspase-3,and immunohistochemistry for α-SMA and AIF.The following MLE-12 cell groups were prepared,normoxic+si-NC,hyperoxic+si-NC,normoxic+si-PLD1,and hyperoxic+si-PLD1.After transient transfection,the cells were exposed to normoxia or hyperoxia for 24 h.Mitochondrial reactive oxygen species(mtROS)and function were measured using MitoSOX Red and the hippocampus mitochondrial stress test.Results The levels of α-SMA and AIF staining,MDA,Cleaved Caspase 3,and BAX in lung tissue were significantly increased in the hyperoxic groups compared with the normoxic groups(P＜0.05),while SOD activity and BCL-2 levels were significantly decreased(P＜0.05).α-SMA and AIF staining,and the abundance of Cleaved Caspase-3 and BAX in lung tissue were lower in the hyperoxia+PLD1-KO group than in the hyperoxia+WT group(P＜0.05),while SOD activity and BCL-2 abundance were higher in the hyperoxia+PLD1-KO group than in the hyperoxia+WT group(P＜0.05).The level of AIF in MLE-12 cell mitochondria in the hyperoxic groups was significantly lower than that in the normoxic groups(P＜0.05);however,the level of AIF was increased significantly in the cytoplasm of the hyperoxic groups compared with the normoxic groups(P＜0.05).The level of AIF in MLE-12 cell mitochondria in the hyperoxic+si-PLD1 group was significantly increased compared with that in the hyperoxic+si-NC group(P＜0.05).The abundance of mtROS in hyperoxia MLE-12 cell groups was higher than that in the normoxia groups(P＜0.05),and the abundance of mtROS in the hyperoxia+si-PLD1 group was lower than that in the hyperoxia+si-NC group(P＜0.05).Compared with the normoxic+si-NC group,basic respiration,ATP production,maximum respiration,and spare respiratory capacity was significantly decreased in the hyperoxic+si-NC group(P＜0.05).Compared with the hyperoxic+si-NC group,the hyperoxic+si-PLD1 group had significantly increased basic respiration,ATP production,maximum respiration,and spare respiratory capacity(P＜0.05).Conclusions PLD1 is involved in hyperoxia-induced injury of mouse BPD and MLE-12 cells.Deletion of the PLD1 gene may alleviate hyperoxia-induced lung injury by inhibiting mitochondrial-dependent apoptosis.

The incidence of osteoporotic thoracolumbar vertebral fracture (OTLVF) in the elderly is gradually increasing. The kyphotic deformity caused by various factors has become an important characteristic of OTLVF and has received increasing attention. Its clinical manifestations include pain, delayed nerve damage, sagittal imbalance, etc. Currently, the definition and diagnosis of OTLVF with kyphotic deformity in the elderly are still unclear. Although there are many treatment options, they are controversial. Existing guidelines or consensuses pay little attention to this type of fracture with kyphotic deformity. To this end, the Lumbar Education Working Group of the Spine Branch of the Chinese Medicine Education Association and Editorial Committee of Chinese Journal of Trauma organized the experts in the relevant fields to jointly develop Clinical guidelines for the diagnosis and treatment of osteoporotic thoracolumbar vertebral fractures with kyphotic deformity in the elderly ( version 2024), based on evidence-based medical advancements and the principles of scientificity, practicality, and advanced nature, which provided 18 recommendations to standardize the clinical diagnosis and treatment.

Objective To study the characteristics of granulomatosis with polyangiitis (GPA) accompanied by pneumothorax.Methods We described a case of GPA accompanied by hydropneumothorax who was successfully treated.Relevant literature was also reviewed.Results A total of 25 cases were identified,consisting of 18 males and 7 females [the average age was (44±16)(16-70) years old].The time from disease onset to pneumothorax was 26±51 (0.83-216) weeks.Pneumothorax,hydropneumothorax,pyopneumothorax and hemopneumothorax occurred in 11,5,8 and 1 respectively.Nodules or excavated nodules on chest radiography or CT were seen in 22 cases.Erythrocyte sedimentation rate (ESR) and C reactive protein (CRP) were elevated in all cases.Sixteen cases received glucocorticoid and immunosuppressive agents treatment.Sixteen cases received drainage and 7 received open operation.Pseudomonas aeruginosa was the most commonmicrobiology findings.Granulomatosis with active vasculitis,bronchopleural fistula,pleural bleb with intensefibrosis,rupture of subpleural nodule were seen on lung biopsy or autopsy.Nine cases died of infections,respiratory failure,sepsis and respiratory arrest.Conclusion Pneumothorax in GPA can be caused by multiple factors such as rupture of subpleural nodule and with high mortality.Patients always died of infections and respiratory failure.Regular treatment of the underlying disease,apply sensitive antibiotics for infection and reasonable surgical intervention should be considered.

Objective:To explore the effect and mechanism of intracellular Zn2+ concentration ([Zn2+ ]i) in hypoxia‐induced regulation of metalloproteinases (MMPs) and extracellular matrix (ECM) expression in nucleus pulposus (NP) cells .Methods:NP cells from SD rats received plate culture at first and then three‐dimensional culture with sodium alginate gel .[Zn2+ ]i was assayed by FluoZin‐3 AM staining .Proteoglycan was assayed by Alcian blue staining .Glycosaminoglycan was detected by 1 ,9‐dimethylmethylene blue (DMMB) assay .And real‐time PCR were used to assay the mRNA expression of α1 type II collagen (COL2A1) ,matrix metalloproteinase 13 (MMP‐13) and a disintegrin and metalloproteinase with a thrombospondin motif 5 (ADAMTS‐5) .The expression of ZRT ,IRT‐like protein 8(ZIP8) was assayed by immunohistochemistry and Western blotting .Results:Interleukin (IL)‐1βand ZnCl2 could significantly increase the [Zn2+ ]i of NP cells ,however ,the effect could be inhibited by hypoxia .Hypoxia did significantly attenuate the decrease of proteoglycan ,glycosaminoglycan ,and COL2A1 mRNA ,which was induced by IL‐1βand ZnCl2 treatment ,in sodium alginate three‐dimensional culture . However ,ZnCl2 inhibited the protective effect of hypoxia .Both an intracellular Zn2+chelator and hypoxia could inhibit the increase of MMP‐13 mRNA expression .IL‐1βand ZnCl2 treatment promoted the increase of ZIP8 expression in NP cells ,however ,hypoxia inhibited ZIP8 expression .Conclusions:Hypoxia may regulate the Zn2+ influx in NP cells . Zn2+ mediates the regulation effect of hypoxia on ECM and MMP‐13 .Perhaps the changes of [Zn2+ ]i are involved in the process of intervertebral disc degeneration .