Background Mitochondrial biogenesis is pivotal in coal workers' pneumoconiosis fibrosis, yet the role of the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)-nuclear respiratory factor 1 (NRF1)-mitochondrial transcription factor A (TFAM) pathway inmitochondrial biogenesis remains elusive, warranting further investigation. Objective To elucidate the role of the PGC-1α-NRF1-TFAM pathway in mitochondrial biogenesis in a rat coal workers' pneumoconiosis model through in vivo and in vitro experiments. Methods (1)n vivo: twelve SPF male SD rats (200-220 g) were randomized into a control group and a coal dust group (n=6 per group). After acclimatization, the coal dust group received 1 mL 50 mg·mL⁻¹ coal dust suspension via intratracheal instillation; the controls received saline. Lung tissues were harvested after two months for histopathology [HE, Masson, and transmission electron microscopy (TEM) ], protein and mRNA analysis, and mitochondrial DNA (mtDNA) quantification by quantitative real-time polymerase chain reaction (qPCR). (2) In vitro: rat lung type II epithelial cells (RLE-6TN) cells were exposed to coal dust (50, 100, 200, and 400 mg·L⁻¹, 24 h). CCK-8 assay determined optimal doses. Ultrastructural changes were analyzed by TEM. Cells were transfected with OE-PGC-1α (PGC-1α overexpression) or shRNA-PGC-1α plasmids (PGC-1α knockdown), and the transfection efficiency was determined by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). The expression levels of alpah-smooth muscle actin (α-SMA), citrate synthase (CS), PGC-1α, NRF1, TFAM, and fibronectin (Fn) proteins and their corresponding mRNA were detected using Western blot and RT-qPCR, respectively. The relative content of mtDNA was determined by qPCR. Results In vivo: the control group lung samples exhibited soft, pink parenchyma, while the coal dust-exposed lungs showed blackened surfaces with soft texture. The histopathological evaluation revealed intact alveolar walls in the controls versus structural destruction, micro-nodules, and fibrotic areas in the coal dust group. After Masson staining, coal dust deposits were found surrounded by blue collagen fibers in the exposed lungs, but absent in the controls. The coal dust group displayed significant upregulation of fibrotic marker α-SMA and downregulation of mitochondrial biogenesis markers (CS, PGC-1α, NRF1, TFAM) and mtDNA compared to the controls (P<0.05). In vitro: coal dust exposure reduced cell density and induced morphological alterations. TEM revealed evenly distributed normal mitochondria in controls versus mitochondrial swelling, disrupted cristae, and reduced numbers in exposed cells. The mitochondrial biogenesis markers were elevated in the coal dust + OE-PGC-1α group compared to the coal dust + OE-NC group (P<0.05); in contrast, they were decreased in the coal dust + shRNA-PGC-1α group compared to the coal dust + shRNA-NC group (P<0.05). Compared to the control group, the expression levels of the fibrosis marker α-SMA mRNA and protein were increased in the coal dust group (P<0.05). Overexpression of PGC-1α reduced α-SMA expression, while downregulation of PGC-1α increased its expression (P<0.05). Conclusion Coal dust exposure induces mitochondrial dysfunction and pulmonary fibrosis in vivo and in vitro via the PGC-1α-NRF1-TFAM pathway dysregulation. Targeting this pathway may mitigate coal dust-induced fibrosis by restoring mitochondrial biogenesis.

China is one of the countries with the highest incidence of esophageal cancer, which is still increasing year by year in recent years. Surgical treatment is the first choice for early and middle esophageal cancer. Surgeons have been exploring how to remove the tumor as completely as possible and reduce the trauma as far as possible. In recent years, with the rapid development of minimally invasive surgery and endoscopic technology, minimally invasive esophagectomy(MIE)has led the trend of radical surgery for esophageal cancer. At present, the mainstream minimally invasive surgery is thoracoscopic thoracoscopic(VATS)resection of esophageal cancer, which requires thoracotomy and anesthesia, resulting in large surgical trauma and more complications of postoperative circulatory respiratory system. Mediastinose-assisted esophagectomy(MAE), which eliminates a thoracotomy, is also an important part of MIE. Overseas MAE application started early, but the domestic development is relatively slow. This article summarizes the experience of different MAE surgical methods in China, and provides the basis for its promotion in China.

Objective To evaluate endovascular treatment of Budd-Chiari syndrome(BCS)with occlusion of hepatic veins.Methods Retrospective analysis on the clinical materials of 32 BCS cases with occlusion of hepatic veins was made.Four cases received inferior vena cava(IVC)angioplasty or stent implant and splenorenal shunt;Transfemoral vein or transjugular hepatic vein angioplasty was performed in 10 cases,and percutaneous transhepatic recanalization combined with transjugular and/or transfemoral vein angioplasty of hepatic veins was performed in 16 cases,respectively.Two cases failed therapy attempt.Results A failure to find the main hepatic vein in percutaneous transhepatic venography lead to the abandent of therapy in 2 cases.Hepatic vein angioplasty and IVC angioplasty was successful in the other 30 cases.The pressure of hepatic vein decreased from(43±8)cm H_2O to(16±4)cm H_2O(t=21.23,P<0.01).The symptoms were obviously relieved,ascites disappeared,abdominal distension palliated,chest and abdominal wall varicose veins collapsed one week after endovascular treatment.During perioperative procedure,2 cases with liver puncture bleeding were cured by laparotomy.The follow-up duration was 5 months to 65 months and mean(26.0±2.0)months.There was no stent migration and hepatic vein restenosis and occlusion.Chest and abdominal wall varicose veins disappeared and esophagus phlebeurysma were ameliorated as shown by esophageal barium series.There were no pulmonary embolism and death.Conclusions The procedure of endovascular treatment of BCS with occlusion of hepatic veins is simple,mini-traumatic and effective.

AIM: To investigate the effect of Shexiang Baoxin Pill(SXBXP) on endothelial in stable angina pectoris patients and its underlying mechanisms. METHODS: Sixty-eight stable angina pectoris patients were randomly divided into two groups,the conventional group(34cases),SXBXP treatment group(34cases).The conventional group was treated with standard treatment,and SXBXP group was treated with standard treatment and SXBXP.FMD,NO,ET,TXB_2,6-Keto-PGF-1a were determined before and after three months treatment. RESULTS: FMD,NO,6-Keto-PGF-1a of SXBXP group were (9.35%?0.78%)、(77.25?6.36)?mmol/L、(93.87?(10.28))?/(ng/L) after treatment,ET、TXB_2 were(81.15?5.43) pg/mL、(43.02?4.19)?/(ng/L).There were significant improvement as compared with in SXBXP group before treatment and in conventional group after treatment(P