Aim To establish the pyroptosis model of rat chondrocytes induced by tumor necrosis factor α(TNF-α)in order to study the effect of lysine acetyl-transferase 7(KAT7)on pyroptosis of chondrocytes.Methods Chondrocytes of rat knee joint were isolated by type Ⅱ collagenase digestion,and were identified by toluidine blue staining and Col Ⅱ immunofluorescence.CCK-8 was used to evaluate cell viability.Western blot was used to detect the expression of pyroptosis-related proteins NLRP3,GSDMD,caspase-8 and KAT7 in cells intervened with TNF-α,adenovirus overexpression of KAT7(KAT7-oe)and KAT7 inhibitor WM-3835.The microstructure of the cells was observed by scanning e-lectron microscopy.Pyroptosis was detected by TUNEL staining,and the expression of pyroptosis-related pro-tein and KAT7 was detected by immunofluorescence.Results Compared with the empty virus group,KAT7-oe inhibited cell viability,promoted the expression of pyroptosis-related proteins,and TNF-α enhanced this effect.At the same time,the expression of KAT7 and pyroptosis-related proteins in the TNF-α stimulation group increased,and WM-3835 reduced the related proteins expression.Electron microscopy showed that KAT7-oe caused cell swelling,deformation,membrane perforation and rupture,while WM-3835 could restore cell morphology.TUNEL staining and immunofluores-cence results also confirmed that KAT7-oe induced chondrocyte pyroptosis,and WM-3835 could down-reg-ulate the fluorescence of pyroptosis-related proteins.Conclusions The expression of KAT7 increases in rat chondrocyte pyroptosis model,and the intervention of KAT7 expression affects signal molecules related to py-roptosis pathway,suggesting that KAT7 may be related to chondrocyte pyroptosis.

Objective To investigate the effects of Amanita caojizong on cardiomyocyte apoptosis and the expression of apoptosis-related factors Bcl-2 and Bax,thereby providing experimental evidence for the prevention and treatment of Amanita caojizong poisoning.Methods Mouse cardiomyocytes(HL-1 cells)cultured in vitro were divided into an experimental group(treated with Amanita caojizong extract)and a control group(treated with PBS).After treatment with Amanita caojizong extract,apoptosis of HL-1 cells was observed using TUNEL staining,and the protein expression levels of Bax,Bcl-2,Caspase-3,and Cleaved Caspase-3 in HL-1 cardiomyocytes were detected by Western blot.Results Compared with the control group,the TUNEL staining showed significantly increased apoptotic fluorescence intensity in the Amanita caojizong extract-treated group.The protein expressions of Bax,Caspase-3,and Cleaved Caspase-3 in HL-1 cells in the Amanita caojizong-treated group were upregulated,while the expression of Bcl-2 was downregulated.Conclusion Amanita caojizong can promote apoptosis of mouse cardiomyocytes,and its mechanism may be associated with the Bcl-2/Bax pathway.

Aim To establish the pyroptosis model of rat chondrocytes induced by tumor necrosis factor α(TNF-α)in order to study the effect of lysine acetyl-transferase 7(KAT7)on pyroptosis of chondrocytes.Methods Chondrocytes of rat knee joint were isolated by type Ⅱ collagenase digestion,and were identified by toluidine blue staining and Col Ⅱ immunofluorescence.CCK-8 was used to evaluate cell viability.Western blot was used to detect the expression of pyroptosis-related proteins NLRP3,GSDMD,caspase-8 and KAT7 in cells intervened with TNF-α,adenovirus overexpression of KAT7(KAT7-oe)and KAT7 inhibitor WM-3835.The microstructure of the cells was observed by scanning e-lectron microscopy.Pyroptosis was detected by TUNEL staining,and the expression of pyroptosis-related pro-tein and KAT7 was detected by immunofluorescence.Results Compared with the empty virus group,KAT7-oe inhibited cell viability,promoted the expression of pyroptosis-related proteins,and TNF-α enhanced this effect.At the same time,the expression of KAT7 and pyroptosis-related proteins in the TNF-α stimulation group increased,and WM-3835 reduced the related proteins expression.Electron microscopy showed that KAT7-oe caused cell swelling,deformation,membrane perforation and rupture,while WM-3835 could restore cell morphology.TUNEL staining and immunofluores-cence results also confirmed that KAT7-oe induced chondrocyte pyroptosis,and WM-3835 could down-reg-ulate the fluorescence of pyroptosis-related proteins.Conclusions The expression of KAT7 increases in rat chondrocyte pyroptosis model,and the intervention of KAT7 expression affects signal molecules related to py-roptosis pathway,suggesting that KAT7 may be related to chondrocyte pyroptosis.

Objective To investigate the effects of Amanita caojizong on cardiomyocyte apoptosis and the expression of apoptosis-related factors Bcl-2 and Bax,thereby providing experimental evidence for the prevention and treatment of Amanita caojizong poisoning.Methods Mouse cardiomyocytes(HL-1 cells)cultured in vitro were divided into an experimental group(treated with Amanita caojizong extract)and a control group(treated with PBS).After treatment with Amanita caojizong extract,apoptosis of HL-1 cells was observed using TUNEL staining,and the protein expression levels of Bax,Bcl-2,Caspase-3,and Cleaved Caspase-3 in HL-1 cardiomyocytes were detected by Western blot.Results Compared with the control group,the TUNEL staining showed significantly increased apoptotic fluorescence intensity in the Amanita caojizong extract-treated group.The protein expressions of Bax,Caspase-3,and Cleaved Caspase-3 in HL-1 cells in the Amanita caojizong-treated group were upregulated,while the expression of Bcl-2 was downregulated.Conclusion Amanita caojizong can promote apoptosis of mouse cardiomyocytes,and its mechanism may be associated with the Bcl-2/Bax pathway.

Objective To explore the anatomical landmarks and segmentation method for the intraoperative identification of the cervical segment of the internal carotid artery by studying cadaveric dissections with an endoscopic transoral medial pterygomandibular fold approach and to investigate its clinical significance.Methods The head specimens of five fresh frozen cadavers were dissected in the anatomical laboratory of the Surgical Treatment Technology Innovation Unit of Nasal Skull Base Tumor in Eye&ENT Hospital of Fudan University.The parapharyngeal space was dissected layer by layer through the endoscopic transoral medial pterygomandibular fold approach,and the location marks of parapharyngeal internal carotid artery(ppICA)and adjacent structures of ppICA were anatomically studied.The anatomical landmarks associated with ppICA were observed and characterized,and the ppICA was segmented anatomically according to its adjacent structures.Then,the length of each ppICA segment was measured.Results Muscle structures were essential anatomical landmarks for an endoscopic transoral pterygoid medial approach that identifies mandibular folds.The first layer of muscles included the superior pharyngeal constrictor,tensor veli palatini,and medial pterygoid muscles.The second layer includes the stylopharyngeus,styloglossus,longus capitis,and levator veli palatini muscles.The stylopharyngeal and levator veli palatini muscles were close to the ppICA and were reliable landmarks for locating the ppICA.Furthermore,the ppICA was divided into three segments according to their positional relationship with the ppICA.The first segment of ppICA(P1 ICA)was located between the greater horn plane of the hyoid bone and the intersection plane between the upper margin of stylopharyngeal muscle and ppICA.The second segment of ppICA(P2 ICA)was between the plane where the upper edge of the stylopharyngeal muscle intersected with the ppICA and the plane where the projection of inferior edge of the levator veli palatini muscle intersected with the ppICA.The third segment of ppICA(P3 ICA)was between the intersection of the lower margin projection of the levator veli palatini muscle and ppICA and the external orifice of the carotid canal.The P2 ICA was within an anatomical region bounded by the levator veli palatini muscle,longus capitis muscle,and stylopharyngeus muscle.This region was termed"ICA window"in this paper measured under the cadaver head specimen,the lengths of P1 ICA,P2 ICA,and P3 ICA were(36.5±7.3)mm,(15.5±1.6)mm,(7.4±1.7)mm respectively.Conclusion The muscular structure refers to the relatively constant anatomical reference landmarks within the endoscopic transoral medial pterygomandibular fold.The stylopharyngeus and levator veli palatini muscles are reliable landmarks for precisely locating and segmenting the ppICA,thus having essential clinical implications.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a complex disease that is often accompanied by mental health disorders. However, the potential mechanisms underlying the heterogeneous clinical presentation of CP/CPPS remain uncertain. This study analyzed widely targeted metabolomic data of expressed prostatic secretions (EPS) and plasma to reveal the underlying pathological mechanisms of CP/CPPS. A total of 24 CP/CPPS patients from The Second Nanning People's Hospital (Nanning, China), and 35 asymptomatic control individuals from First Affiliated Hospital of Guangxi Medical University (Nanning, China) were enrolled. The indicators related to CP/CPPS and psychiatric symptoms were recorded. Differential analysis, coexpression network analysis, and correlation analysis were performed to identify metabolites that were specifically altered in patients and associated with various phenotypes of CP/CPPS. The crucial links between EPS and plasma were further investigated. The metabolomic data of EPS from CP/CPPS patients were significantly different from those from control individuals. Pathway analysis revealed dysregulation of amino acid metabolism, lipid metabolism, and the citrate cycle in EPS. The tryptophan metabolic pathway was found to be the most significantly altered pathway associated with distinct CP/CPPS phenotypes. Moreover, the dysregulation of tryptophan and tyrosine metabolism and elevation of oxidative stress-related metabolites in plasma were found to effectively elucidate the development of depression in CP/CPPS. Overall, metabolomic alterations in the EPS and plasma of patients were primarily associated with oxidative damage, energy metabolism abnormalities, neurological impairment, and immune dysregulation. These alterations may be associated with chronic pain, voiding symptoms, reduced fertility, and depression in CP/CPPS. This study provides a local-global perspective for understanding the pathological mechanisms of CP/CPPS and offers potential diagnostic and therapeutic targets.
Humans ; Male ; Prostatitis/blood* ; Adult ; Pelvic Pain/blood* ; Metabolomics ; Prostate/metabolism* ; Middle Aged ; Chronic Pain/blood* ; Metabolome ; Case-Control Studies ; Tryptophan/blood* ; Depression/blood* ; Oxidative Stress/physiology* ; Chronic Disease ; Lipid Metabolism/physiology*

Postoperative infection of internal fixation of closed fractures the lower limbs in adults represents a devastating complication, characterized by diagnostic challenges, prolonged treatment duration and high disability rates. Current management of these infections faces multiple challenges, such as difficulties in early accurate diagnosis, and various controversies about the treatment plan, leading to poor overall diagnosis and treatment results. To address these issues, based on evidence-based medicine and principles with emphasis on scientific rigor, clinical applicability and innovation, the Trauma Branch of the Chinese Medical Association, Orthopedic Branch of the Chinese Medical Doctor Association, Orthopedics Branch of the Chinese Medical Association, and Trauma Orthopedics and Polytrauma Group of the Resuscitation and Emergency Committee of the Chinese Medical Doctor Association have collaboratively organized a panel of relevant experts to develop the Guideline for diagnosis and treatment of infection after internal fixation of closed lower limb fractures in adults ( version 2025). The guideline proposed 10 recommendations, aiming to provide a foundation for standardized diagnosis and treatment of postoperative infection in adults with closed lower limb fractures.

Postoperative infection of internal fixation of closed fractures the lower limbs in adults represents a devastating complication, characterized by diagnostic challenges, prolonged treatment duration and high disability rates. Current management of these infections faces multiple challenges, such as difficulties in early accurate diagnosis, and various controversies about the treatment plan, leading to poor overall diagnosis and treatment results. To address these issues, based on evidence-based medicine and principles with emphasis on scientific rigor, clinical applicability and innovation, the Trauma Branch of the Chinese Medical Association, Orthopedic Branch of the Chinese Medical Doctor Association, Orthopedics Branch of the Chinese Medical Association, and Trauma Orthopedics and Polytrauma Group of the Resuscitation and Emergency Committee of the Chinese Medical Doctor Association have collaboratively organized a panel of relevant experts to develop the Guideline for diagnosis and treatment of infection after internal fixation of closed lower limb fractures in adults ( version 2025). The guideline proposed 10 recommendations, aiming to provide a foundation for standardized diagnosis and treatment of postoperative infection in adults with closed lower limb fractures.

Objective To compare the radiation dose of in vitro pre-fenestration and in situ fenestration thoracic endovascular aortic repair(TEVAR)in treatment of aortic disease.Methods Data of 51 patients with aortic diseases who received in vitro pre-fenestration(group A)and 21 cases who underwent in situ fenestration(group B)TEVAR were retrospectively analyzed.The fluoroscopy duration,total reference air kerma(AK),total dose area product(DAP)and TEVAR time were compared between groups.Results TEVAR was successfully completed in all 72 patients.Fluoroscopy duration([21.42±8.04]min vs.[34.57±9.07]min)and total DAP(44315.0[31157.0,56307.5]μGy·m2 vs.72153.0[45460.0,82354.0]μGy·m2)in group A were both significantly lower than those in group B(both P＜0.05),while total AK(2423[1638,3533]mGy vs.3600[1898,3921]mGy)and TEVAR time([83.41±22.89]min vs.[81.00±22.13]min)in group A were not significant different from those in group B(both P＞0.05).Conclusion Compared with in situ fenestration TEVAR,both the fluoroscopy time and total DAP of in vitro pre-fenestration TEVAR significantly reduced for treating aortic diseases.

Lipopolysaccharides (LPS) are major outer membrane components of Gram-negative bacteria. Unlike most Gram-negative bacteria, Acinetobacter baumannii can still survive and acquire polymyxin resistance after complete loss of LPS. Previous studies of LPS-deficient Acinetobacter baumannii mostly focused on LPS-deficient strains induced by polymyxin, whose background was complex and unstable. To investigate LPS loss-mediated polymyxin resistant-Acinetobacter baumannii, this study constructed a stable and clear background LPS-deficient strain by knocking out lpxC gene in Acinetobacter baumannii ATCC 19606 with CIRSPR/Cas9, and then studied the phenotypic changes of the lpxC-deficient strain including morphology, growth rate, antibiotic susceptibility, virulence, membrane permeability, and membrane potential. Animal experiments were approved by the Animal Care and Welfare Committee Institute of Medicinal Biotechnology, CAMS and PUMC (approval number: IMB-20240119D₉). The results indicated that the lpxC gene of Acinetobacter baumannii ATCC 19606 was successfully knocked out. After losing the lpxC, the strain underwent the morphological change from rod-shaped to spherical. Furthermore, it leads to reduced growth rate, enhanced membrane permeability, decreased membrane potential, lower virulence, and increased antibiotic susceptibility to β-lactams, quinolones, aminoglycosides, macrolides, glycopeptides. The lpxC deletion results in significant changes in membrane homeostasis and adaptability of Acinetobacter baumannii. Understanding the phenotypic changes of colistin-resistant Acinetobacter baumannii mediated by LPS loss is useful for exploring the resistance mechanism of Acinetobacter baumannii and developing new therapeutic strategies.