Objective To evaluate the surgical efficacy of unilateral pneumonectomy for the treatment of tuberculous destroyed lung, analyze the causes of severe postoperative complications, and explore clinical management strategies. Methods A retrospective analysis was conducted on the clinical data of patients with tuberculous destroyed lung who underwent unilateral pneumonectomy at the Public Health Clinical Center of Chengdu from 2017 to 2023. Postoperative severe complications were statistically analyzed. Patients were divided into a non-severe complication group and a severe-complication group, and the causes, management, and outcomes of complications were analyzed. Results A total of 134 patients were included, comprising 69 males and 65 females, with a mean age of 17-73 (40.43±12.69) years. There were 93 patients undergoing left pneumonectomy and 41 patients undergoing right pneumonectomy. Preoperative sputum smear was positive in 35 patients, all of which converted to negative postoperatively. There were 58 patients with hemoptysis preoperatively, and none experienced hemoptysis postoperatively. Postoperative incisional infection occurred in 8 (5.97%) patients, and postoperative pulmonary infection in 26 (19.40%) patients. Severe postoperative complications occurred in 17 (12.69%) patients, including empyema in 9 (6.72%) patients, bronchopleural fistula with empyema in 1 (0.75%) patient, severe pneumonia in 3 (2.24%) patients, postpneumonectomy syndrome in 1 (0.75%) patient, chylothorax in 1 (0.75%) patient, ketoacidosis in 1 (0.75%) patient, and heart failure with severe pneumonia in 1 (0.75%) patient. Perioperative mortality occurred in 2 (1.49%) patients, both of whom underwent right pneumonectomy. Multivariate logistic regression analysis revealed that a history of ipsilateral thoracic surgery, concomitant Aspergillus infection, and greater blood loss were independent risk factors for severe complications following unilateral pneumonectomy for tuberculous destroyed lung (P<0.05). Conclusion Unilateral pneumonectomy for patients with tuberculous destroyed lung can significantly improve the clinical cure rate, sputum conversion rate, and hemoptysis cessation rate. However, there is a certain risk of severe perioperative complications and mortality, requiring thorough perioperative management and appropriate management of postoperative complications.

Background: Diabetes-induced testicular damage (DITD) is a common complication of diabetes. We investigated underlying mechanism of retinoblastoma-binding protein 6 (Rbbp6)-mediated brain and muscle ARNT-like 1 (Bmal1) ubiquitination in modulating ferroptosis in DITD. Methods: Spermatogenic cell apoptosis and viability were measured by flow cytometry and cell counting kit 8 (CCK-8), respectively. The impact of Rbbp6 and Bmal1 on ferroptosis was assessed by determining expression of ferroptosis markers glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11), and levels of malondialdehyde (MDA), glutathione (GSH), iron, and lipid peroxidation. Co-immunoprecipitation was performed to determine the interaction between Rbbp6 and Bmal1, as well as the ubiquitination level of Bmal1. The expression levels of Rbbp6, Bmal1, Yes-associated protein 1 (YAP1), ferroptosis markers, and testicular steroidogenic enzymes were tested by Western blot. Results: Bmal1 protein expression was significantly downregulated, while Rbbp6 was upregulated in DITD mouse model and high glucose (HG)-induced GC-1 spg cells. Overexpression of Bmal1 improved testicular injury in diabetic mice, reduced 4-hydroxynonenal (4-HNE), MDA, iron levels, and increased expression levels of GPX4, SLC7A11, GSH, as well as testicular steroidogenic enzymes. Rbbp6 decreased Bmal1 level through promoting its ubiquitination. Meanwhile, Rbbp6 knockdown inhibited the ferroptosis of HG-induced GC-1 spg cells, which were abolished by silencing Bmal1. In addition, knockdown of YAP1 or treatment with ferroptosis inducer erastin blocked the above effects caused by Bmal1 overexpression. Conclusion Rbbp6-mediated Bmal1 ubiquitination suppressed YAP1 pathway, promoting ferroptosis in DITD. This study highlighted Rbbp6/Bmal1/YAP1 axis as a potential therapeutic target for mitigating DITD.

Background: Diabetes-induced testicular damage (DITD) is a common complication of diabetes. We investigated underlying mechanism of retinoblastoma-binding protein 6 (Rbbp6)-mediated brain and muscle ARNT-like 1 (Bmal1) ubiquitination in modulating ferroptosis in DITD. Methods: Spermatogenic cell apoptosis and viability were measured by flow cytometry and cell counting kit 8 (CCK-8), respectively. The impact of Rbbp6 and Bmal1 on ferroptosis was assessed by determining expression of ferroptosis markers glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11), and levels of malondialdehyde (MDA), glutathione (GSH), iron, and lipid peroxidation. Co-immunoprecipitation was performed to determine the interaction between Rbbp6 and Bmal1, as well as the ubiquitination level of Bmal1. The expression levels of Rbbp6, Bmal1, Yes-associated protein 1 (YAP1), ferroptosis markers, and testicular steroidogenic enzymes were tested by Western blot. Results: Bmal1 protein expression was significantly downregulated, while Rbbp6 was upregulated in DITD mouse model and high glucose (HG)-induced GC-1 spg cells. Overexpression of Bmal1 improved testicular injury in diabetic mice, reduced 4-hydroxynonenal (4-HNE), MDA, iron levels, and increased expression levels of GPX4, SLC7A11, GSH, as well as testicular steroidogenic enzymes. Rbbp6 decreased Bmal1 level through promoting its ubiquitination. Meanwhile, Rbbp6 knockdown inhibited the ferroptosis of HG-induced GC-1 spg cells, which were abolished by silencing Bmal1. In addition, knockdown of YAP1 or treatment with ferroptosis inducer erastin blocked the above effects caused by Bmal1 overexpression. Conclusion Rbbp6-mediated Bmal1 ubiquitination suppressed YAP1 pathway, promoting ferroptosis in DITD. This study highlighted Rbbp6/Bmal1/YAP1 axis as a potential therapeutic target for mitigating DITD.

Background: Diabetes-induced testicular damage (DITD) is a common complication of diabetes. We investigated underlying mechanism of retinoblastoma-binding protein 6 (Rbbp6)-mediated brain and muscle ARNT-like 1 (Bmal1) ubiquitination in modulating ferroptosis in DITD. Methods: Spermatogenic cell apoptosis and viability were measured by flow cytometry and cell counting kit 8 (CCK-8), respectively. The impact of Rbbp6 and Bmal1 on ferroptosis was assessed by determining expression of ferroptosis markers glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11), and levels of malondialdehyde (MDA), glutathione (GSH), iron, and lipid peroxidation. Co-immunoprecipitation was performed to determine the interaction between Rbbp6 and Bmal1, as well as the ubiquitination level of Bmal1. The expression levels of Rbbp6, Bmal1, Yes-associated protein 1 (YAP1), ferroptosis markers, and testicular steroidogenic enzymes were tested by Western blot. Results: Bmal1 protein expression was significantly downregulated, while Rbbp6 was upregulated in DITD mouse model and high glucose (HG)-induced GC-1 spg cells. Overexpression of Bmal1 improved testicular injury in diabetic mice, reduced 4-hydroxynonenal (4-HNE), MDA, iron levels, and increased expression levels of GPX4, SLC7A11, GSH, as well as testicular steroidogenic enzymes. Rbbp6 decreased Bmal1 level through promoting its ubiquitination. Meanwhile, Rbbp6 knockdown inhibited the ferroptosis of HG-induced GC-1 spg cells, which were abolished by silencing Bmal1. In addition, knockdown of YAP1 or treatment with ferroptosis inducer erastin blocked the above effects caused by Bmal1 overexpression. Conclusion Rbbp6-mediated Bmal1 ubiquitination suppressed YAP1 pathway, promoting ferroptosis in DITD. This study highlighted Rbbp6/Bmal1/YAP1 axis as a potential therapeutic target for mitigating DITD.

Background: Diabetes-induced testicular damage (DITD) is a common complication of diabetes. We investigated underlying mechanism of retinoblastoma-binding protein 6 (Rbbp6)-mediated brain and muscle ARNT-like 1 (Bmal1) ubiquitination in modulating ferroptosis in DITD. Methods: Spermatogenic cell apoptosis and viability were measured by flow cytometry and cell counting kit 8 (CCK-8), respectively. The impact of Rbbp6 and Bmal1 on ferroptosis was assessed by determining expression of ferroptosis markers glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11), and levels of malondialdehyde (MDA), glutathione (GSH), iron, and lipid peroxidation. Co-immunoprecipitation was performed to determine the interaction between Rbbp6 and Bmal1, as well as the ubiquitination level of Bmal1. The expression levels of Rbbp6, Bmal1, Yes-associated protein 1 (YAP1), ferroptosis markers, and testicular steroidogenic enzymes were tested by Western blot. Results: Bmal1 protein expression was significantly downregulated, while Rbbp6 was upregulated in DITD mouse model and high glucose (HG)-induced GC-1 spg cells. Overexpression of Bmal1 improved testicular injury in diabetic mice, reduced 4-hydroxynonenal (4-HNE), MDA, iron levels, and increased expression levels of GPX4, SLC7A11, GSH, as well as testicular steroidogenic enzymes. Rbbp6 decreased Bmal1 level through promoting its ubiquitination. Meanwhile, Rbbp6 knockdown inhibited the ferroptosis of HG-induced GC-1 spg cells, which were abolished by silencing Bmal1. In addition, knockdown of YAP1 or treatment with ferroptosis inducer erastin blocked the above effects caused by Bmal1 overexpression. Conclusion Rbbp6-mediated Bmal1 ubiquitination suppressed YAP1 pathway, promoting ferroptosis in DITD. This study highlighted Rbbp6/Bmal1/YAP1 axis as a potential therapeutic target for mitigating DITD.

Pancreatic cancer is highly aggressive and often diagnosed at an advanced stage,leaving most patients ineligible for radical resection.This study retrospectively analyzed four patients with locally advanced or advanced pancreatic cancer to evaluate the clinical efficacy and safety of high-intensity focused ultrasound(HIFU)ablation combined with chemotherapy as a neoadjuvant and conversion therapy.All cases were reviewed and individualized treatment plans were formulated through a multidisciplinary team evaluation.All patients received HIFU plus gemcitabine and nab-paclitaxel chemotherapy,with assessments of tumor volume,vascular involvement,surgical conversion,symptom relief,and adverse events.Three patients achieved marked tumor shrinkage and reduction of vascular invasion,enabling successful R0 resection without recurrence during follow-up.The remaining patient achieved disease stability,significant pain relief,and maintained good quality of life under repeated HIFU therapy.All treatments were well tolerated,and no severe adverse reactions occurred.The combination of HIFU and chemotherapy demonstrated synergistic local and systemic effects,effectively achieving tumor downstaging,improving resectability,and alleviating symptoms.As a safe,noninvasive,and repeatable therapeutic approach,this strategy offers a promising option for patients with advanced pancreatic cancer.Further large-scale prospective studies are warranted to validate its long-term efficacy and elucidate underlying mechanisms.

Background and Aims:Acute pancreatitis(AP)is an acute inflammatory disease of the pancreas caused by abnormal activation of pancreatic enzymes.Although gallstones,hyperlipidemia,and alcohol use are the most common causes,a subset of patients develop AP secondary to rare etiologies that are often misdiagnosed or diagnosed late,leading to recurrence or inappropriate management.This study aims to summarize the clinical characteristics,diagnostic strategies,and treatment outcomes of four cases of AP caused by uncommon etiologies,supported by a literature review.Methods:Clinical data of 4 patients admitted to the Department of Hepatobiliary and Pancreatic Surgery,the Third Xiangya Hospital of Central South University,between November 2021 and September 2024,were retrospectively analyzed.Their etiological characteristics,diagnostic approaches,and treatment strategies were reviewed in combination with relevant literature.Results:The underlying causes of AP were intraductal papillary mucinous neoplasm,pancreatic neuroendocrine tumor,pancreatic ductal adenocarcinoma,and duodenojejunal intussusception.All cases initially presented as idiopathic AP.Three patients underwent definitive surgical treatment and recovered well,while one patient with pancreatic cancer received only palliative care due to delayed diagnosis and died three months later.Conclusion:AP secondary to rare etiologies often mimics common forms in clinical presentation but poses diagnostic challenges.For patients with recurrent or idiopathic AP,clinicians should emphasize etiological tracing and utilize advanced imaging and endoscopic modalities for early identification.Timely etiological intervention,particularly surgical management when appropriate,is essential for preventing recurrence and improving prognosis.

Background and Aims:Infected necrotizing pancreatitis(INP),particularly with diffuse distribution,is a life-threatening condition.The optimal initial intervention-minimally invasive step-up therapy vs.direct open necrosectomy-remains controversial.Moreover,the impact of necrosis morphology("wet"or"dry")and the presence of severe acute pancreatitis(SAP)on treatment selection has not been fully clarified.This study aimed to compare the efficacy and safety of these two approaches in diffuse INP and to evaluate the guiding value of CT-based necrosis type and SAP status in clinical decision-making.Methods:A retrospective analysis was conducted on 458 patients with diffuse INP admitted to the Third Xiangya Hospital of Central South University from January 2012 to March 2023.Patients were divided into a minimally invasive step-up group(n=256)and a direct open surgery group(n=202).SAP was defined according to the determinant-based classification,and necrosis was categorized as"wet"or"dry"based on CT features.The primary endpoint was a composite of death or major complications,while secondary endpoints included mortality,length of hospital stay,and incision-related complications,were compared between the two groups,with subgroup analyses performed accordingly.Results:Overall,the open surgery group had higher rates of the primary endpoint(62.4%vs.48.1%,P=0.003)and mortality(27.2%vs.16.8%,P=0.008)compared with the step-up group.Among SAP patients,the step-up approach resulted in a significantly lower primary endpoint rate(66.7%vs.97.7%,P=0.003).In non-SAP patients,the primary endpoint rates were similar,but open surgery was associated with a shorter hospital stay[(36.5±10.4)d vs.(45.6±18.6)d,P<0.001]and higher incidences of wound infection and incisional hernia(both P<0.001).Multivariate analysis identified infection onset time,effusion characteristics,gas bubbles,and necrosis location as independent predictors of prolonged hospitalization in the step-up group(all P<0.05).Patients with"wet"necrosis benefited more from the step-up approach,whereas those with"dry"necrosis experienced shorter hospitalization following open surgery.Conclusion:For diffusely distributed INP,treatment strategies should be individualized based on SAP status and necrosis liquefaction/imaging characteristics.The step-up minimally invasive approach is preferred for SAP patients and those with"wet"necrosis on CT,while direct open necrosectomy may be advantageous for"dry"necrosis(particularly with limited liquefaction)by shortening hospital stay and reducing certain major outcomes,though at the cost of increased incision infection and incision herina.CT imaging features and SAP classification can serve as valuable tools for risk stratification and guiding individualized timing and modality of intervention.

Background and purpose:Internal mammary sentinel lymph node biopsy(IMSLNB)is a minimally invasive diagnostic technique for regional lymph nodes in breast cancer,which can provide accurate lymph staging and guide adjuvant treatment decision,but its clinical application has been controversial.The purpose of this study was to investigate the prognosis of IMSLNB in early breast cancer.Methods:In this study,a retrospective cohort of 7 949 patients with breast cancer from January 1,2016 to December 31,2021 was analyzed.After applying propensity score matching,the patients were divided into IMSLNB group and no-IMSLNB group,and the regional recurrence-free survival(RRFS),local recurrence-free survival(LRFS),distant metastasis-free survival(DMFS),disease-free survival(DFS)and overall survival(OS)of the two groups were compared.This study was approved by the Clinical Research Ethics Committee of the Affiliated Tumor Hospital of Shandong First Medical University(approval number:SDTHEC20130324).Results:A total of 990 patients were included in the final analysis(330 in the IMSLNB group and 660 in the no-IMSLNB group).IMSLN metastasis was found in 54 patients in the IMSLNB group,including 47 patients with axillary lymph node(ALN)metastasis and 7 patients with IMSLN metastasis only.The IMSLN transfer rate was 16.4%.The median follow-up of 41 months showed that the IMSLNB group demonstrated better 3-year DFS[98.4%vs 94.2%,hazard ratio(HR)=0.509;95%CI:0.312-0.828,P=0.007]and 5-year DFS(92.5%vs 87.3%,HR=0.214,95%CI:0.206-0.222,P=0.011)compared with no-IMSLNB group.However,no significant differences were observed in 3-year OS(99.1%vs 99.4%,HR=0.618,95%CI:0.231-1.655,P=0.338)or 5-year OS(98.5%vs 99.1%,HR=0.52,95%CI:0.51-0.53,P=0.392)between the two groups.The 3-year RRFS in the IMSLNB group was better compared with the no-IMSLNB group(99.09%vs 97.73%,HR=0.066;95%CI:0.061-0.071,P=0.048),while no significant differences were observed in 3-year LRFS(99.70%vs 98.19%,HR=0.209;95%CI:0.201-0.217,P=0.130)or DMFS(95.76%vs 96.06%,HR=0.865,95%CI:0.858-0.872,P=0.820)between the two groups.The exploratory subgroup analysis of DFS revealed that patients in the following subgroups could significantly benefit from IM-SLNB(P＜0.05):diagnosis age(≤50 years),premenopausal status,BMI(≤24),lymphovascular invasion(LVI,present),tumor location(lateral),molecular subtype[hormone receptor positive(HR+)/human epidermal growth factor receptor 2 negative(HER2-)],histological type(invasive ductal carcinoma),and axillary lymph node status(positive).Conclusion:IMSLNB can provide more accurate regional lymph node staging for early breast cancer,help optimize adjuvant radiotherapy strategies,and improve patients'DFS and RRFS.It can be promoted as a minimally invasive staging technique for regional lymph nodes.

Objective:To investigate the role and molecular mechanism of dual-specificity phosphatase 26(DUSP26)in the proliferation,migration and invasion of lung adenocarcinoma(LUAD)A549 cells.Methods:The expression profile of DUSP26 was retrieved from the GEPIA2 tumor database,and its differential expression in LUAD tissues and normal human lung tissues were analyzed.Twelve pairs of LUAD tissue and paracancerous tissue surgically resected at Pingxiang People's Hospital between October 2022 and October 2023 were collected.The difference in DUSP26 expression between LUAD tissues and paracancerous tissues was analyzed using immunohistochemical(IHC)staining and Western blotting(WB).Additionally,the expression of DUSP26 in four LUAD cells(A549,SK-LU-1,Calu-3,H1299)and two normal bronchial epithelial cells(BEAS-2B,HBEC)was detected using WB method.A549 cells stably overexpressing DUSP26(DUSP26-OE)or corresponding negative control(DUSP26-OENC)were constructed via lentiviral transfection.The effects of DUSP26 overexpression on cell proliferation,migration and invasion were detected using colony formation,scratch assay,and Transwell chamber assay,respectively.The expression levels of TGF-β1/SMAD2/3 pathway-and epithelial-mesenchymal transition(EMT)-related proteins were detected using WB method,and the expression levels of Ki-67 and cyclin D1 in cells were detected by immunofluorescence staining.Rescue experiments were conducted by adding 5 ng/mL recombinant TGF-β1.A nude mouse xenograft model was established using A549 cells to observe the effect of DUSP26 overexpression on the in vivo growth of transplanted tumors.The expression levels of TGF-β1/SMAD2/3 pathway-and EMT-related proteins in transplanted tumor tissues were assessed using WB method,and the expression levels of Ki-67 and cyclin D1 in transplanted tumor tissues were detected using immunofluorescence staining.Results:DUSP26 expression was downregulated in both LUAD tissues and cells(P<0.05,P<0.01,P<0.001 or P<0.000 1).Compared with the DUSP26-OENC group,the DUSP26-OE group showed significantly reduced proliferation,migration and invasion of A549 cells(P<0.01 or P<0.001).Furthermore,the protein levels of TGF-β1,p-SMAD2/3,vimentin,N-cadherin,snail,Ki-67,and cyclin D1 were significantly reduced(P<0.01,P<0.001 or P<0.000 1),while E-cadherin level was increased in the DUSP26-OE group(P<0.000 1).The addition of 5 ng/mL TGF-β1 recombinant protein partially reversed the effects of DUSP26 overexpression in vitro experiments.The nude mice A549 cell xenograft model was successfully constructed.The growth rate of transplanted tumors was significantly slower in the DUSP26-OE group,with reduced volume and mass(all P<0.001).The protein levels of TGF-β1,p-SMAD2/3,vimentin,N-cadherin,snail,Ki-67,and cyclin D1 in the transplanted tumor tissues were all reduced(P<0.01 or P<0.001),while E-cadherin level was increased(P<0.000 1).Conclusion:DUSP26 is downregulated in both LUAD tissues and cells.Upregulation of DUSP26 suppresses the proliferation,migration and invasion of A549 cells by inhibiting the TGF-β1/SMAD2/3 signaling pathway.