ObjectiveMitochondria are not only the central organelles responsible for cellular energy metabolism but also play essential roles in regulating cell cycle progression and cytoskeletal dynamics. In recent years, accumulating evidence has demonstrated that mitochondrial homeostasis is closely associated with mitotic progression and cytokinesis. Schizosaccharomyces pombe serves as a classical and well-established model organism. Because its cell cycle regulatory mechanisms are highly conserved throughout evolution, its genetic background is clearly defined, and experimental manipulation is efficient and convenient, it has been extensively applied in studies of cell growth, division, and reproductive mechanisms. The SPBC1604.04 gene encodes a previously uncharacterized mitochondrial carrier protein in Schizosaccharomyces pombe. This gene is located on chromosome II and spans 1 018 base pairs in length. It encodes a protein consisting of 238 amino acids with a predicted molecular mass of approximately 31.03 ku. Bioinformatic analysis predicts that this protein is responsible for the transport of thiamine pyrophosphate (TPP) into mitochondria. However, the effects of SPBC1604.04 gene deletion on mitotic cell dynamics under different temperature conditions have not been fully elucidated. MethodsThe SPBC1604.04 deletion strain of Schizosaccharomyces pombe was used as the experimental model. Fluorescent protein markers were constructed in the deletion background to label mitochondria, microtubules, actin, myosin, the nuclear envelope, and chromosomes. Live-cell imaging was performed using a TCS-SP8 laser scanning confocal microscope under normal temperature conditions (25℃) and heat stress conditions (37℃). Time-lapse microscopy was applied to dynamically monitor mitochondrial morphology and distribution, spindle assembly and elongation, chromosome segregation, as well as the formation and constriction of the actomyosin ring during cytokinesis. ImageJ software was used for quantitative measurements, including microtubule length during mitosis, spindle length at different mitotic stages, mitochondrial fluorescence intensity as an indicator of mitochondrial content, actomyosin ring length, nuclear envelope area, and chromosome segregation timing. Statistical analyses were conducted to compare phenotypic differences between the wild-type and SPBC1604.04 deletion strains at both temperature conditions. Through these analyses, we systematically investigated the impact of SPBC1604.04 deletion on mitotic cell dynamics in fission yeast under both normal physiological conditions and temperature stress. ResultsAt 25℃, compared with wild-type cells, the SPBC1604.04Δ strain exhibited a pronounced tendency toward mitochondrial fragmentation, accompanied by abnormal mitochondrial content and a significant reduction in mitochondrial fluorescence intensity. These observations suggest impaired mitochondrial homeostasis under normal growth conditions. In addition, the constriction time of actomyosin ring during cytokinesis was markedly prolonged, indicating that deletion of SPBC1604.04 affects the dynamics of the contractile machinery. However, no obvious defects were observed in spindle assembly, spindle elongation, or chromosome segregation. Under heat stress at 37℃, mitochondrial morphology in the SPBC1604.04Δ strain showed a tendency to recover toward a continuous tubular network structure. Mitochondrial content was restored, fluorescence intensity increased, and the constriction time of the actomyosin ring returned to levels comparable to those of wild-type cells. These results indicate that the mitotic defects observed at normal temperature are partially or fully alleviated under heat stress conditions. ConclusionThis study demonstrates that deletion of the SPBC1604.04 gene leads to abnormal mitochondrial content in Schizosaccharomyces pombe. The mitochondrial carrier protein SPBC1604.04 participates in regulating actomyosin ring constriction during mitosis but does not appear to be directly involved in the regulation of spindle dynamics or chromosome segregation. Our findings provide key experimental evidence for understanding the functional link between the SPBC1604.04 gene, mitochondrial homeostasis, and mitotic regulation.

ObjectiveMitochondria are not only the central organelles responsible for cellular energy metabolism but also play essential roles in regulating cell cycle progression and cytoskeletal dynamics. In recent years, accumulating evidence has demonstrated that mitochondrial homeostasis is closely associated with mitotic progression and cytokinesis. Schizosaccharomyces pombe serves as a classical and well-established model organism. Because its cell cycle regulatory mechanisms are highly conserved throughout evolution, its genetic background is clearly defined, and experimental manipulation is efficient and convenient, it has been extensively applied in studies of cell growth, division, and reproductive mechanisms. The SPBC1604.04 gene encodes a previously uncharacterized mitochondrial carrier protein in Schizosaccharomyces pombe. This gene is located on chromosome II and spans 1 018 base pairs in length. It encodes a protein consisting of 238 amino acids with a predicted molecular mass of approximately 31.03 ku. Bioinformatic analysis predicts that this protein is responsible for the transport of thiamine pyrophosphate (TPP) into mitochondria. However, the effects of SPBC1604.04 gene deletion on mitotic cell dynamics under different temperature conditions have not been fully elucidated. MethodsThe SPBC1604.04 deletion strain of Schizosaccharomyces pombe was used as the experimental model. Fluorescent protein markers were constructed in the deletion background to label mitochondria, microtubules, actin, myosin, the nuclear envelope, and chromosomes. Live-cell imaging was performed using a TCS-SP8 laser scanning confocal microscope under normal temperature conditions (25℃) and heat stress conditions (37℃). Time-lapse microscopy was applied to dynamically monitor mitochondrial morphology and distribution, spindle assembly and elongation, chromosome segregation, as well as the formation and constriction of the actomyosin ring during cytokinesis. ImageJ software was used for quantitative measurements, including microtubule length during mitosis, spindle length at different mitotic stages, mitochondrial fluorescence intensity as an indicator of mitochondrial content, actomyosin ring length, nuclear envelope area, and chromosome segregation timing. Statistical analyses were conducted to compare phenotypic differences between the wild-type and SPBC1604.04 deletion strains at both temperature conditions. Through these analyses, we systematically investigated the impact of SPBC1604.04 deletion on mitotic cell dynamics in fission yeast under both normal physiological conditions and temperature stress. ResultsAt 25℃, compared with wild-type cells, the SPBC1604.04Δ strain exhibited a pronounced tendency toward mitochondrial fragmentation, accompanied by abnormal mitochondrial content and a significant reduction in mitochondrial fluorescence intensity. These observations suggest impaired mitochondrial homeostasis under normal growth conditions. In addition, the constriction time of actomyosin ring during cytokinesis was markedly prolonged, indicating that deletion of SPBC1604.04 affects the dynamics of the contractile machinery. However, no obvious defects were observed in spindle assembly, spindle elongation, or chromosome segregation. Under heat stress at 37℃, mitochondrial morphology in the SPBC1604.04Δ strain showed a tendency to recover toward a continuous tubular network structure. Mitochondrial content was restored, fluorescence intensity increased, and the constriction time of the actomyosin ring returned to levels comparable to those of wild-type cells. These results indicate that the mitotic defects observed at normal temperature are partially or fully alleviated under heat stress conditions. ConclusionThis study demonstrates that deletion of the SPBC1604.04 gene leads to abnormal mitochondrial content in Schizosaccharomyces pombe. The mitochondrial carrier protein SPBC1604.04 participates in regulating actomyosin ring constriction during mitosis but does not appear to be directly involved in the regulation of spindle dynamics or chromosome segregation. Our findings provide key experimental evidence for understanding the functional link between the SPBC1604.04 gene, mitochondrial homeostasis, and mitotic regulation.

ObjectiveTo investigate the mechanism of Xiezhuo Jiedu prescription in the treatment of ulcerative colitis （UC） by inhibiting ferroptosis and alleviating intestinal mucosal injury based on the nuclear factor E₂ related factor 2/solute carrier family 7 member/glutathione peroxidase 4 （Nrf2/SLC7A11/GPX4） signaling pathway. MethodsA total of 60 male SD rats were divided into a normal group， a model group， high- and low-dose Xiezhuo Jiedu prescription groups （26.64 and 13.32 g·kg^-1， respectively）， a ferroptosis inhibitor group （Ferrostatin-1， 0.005 g·kg^-1）， and a mesalazine group （0.27 g·kg^-1）， with 10 rats in each group. A UC rat model was established by intrarectal administration of trinitrobenzene sulfonic acid （TNBS）-ethanol. The normal group and the model group were intragastrically administered normal saline. The other groups were given intragastric administration according to the corresponding dosage for 7 d. The general condition， disease activity index （DAI） score， colon length， and mucosal injury index （CDMI） score were observed in each group. The pathological changes of colon tissue in each group were observed by hematoxylin-eosin （HE） staining. The intestinal mucosa and mitochondrial morphology in each group were observed by transmission electron microscopy. The expression levels of Occludin， Claudin-1， mucin 2 （MUC2）， and E-cadherin in intestinal tissue were detected by immunofluorescence （IF）. Enzyme-linked immunosorbent assay （ELISA） was used to detect the expression levels of serum tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-10 （IL-10） in each group， and a lactic acid assay kit or ELISA was employed to detect the expression levels of reactive oxygen species （ROS）， ferrous ions （Fe²⁺）， glutathione （GSH）， malondialdehyde （MDA）， 4-hydroxynonenal （4-HNE）， diamine oxidase （DAO）， and D-lactate （D-LA）. Real-time quantitative polymerase chain reaction （Real-time PCR） was applied to detect the mRNA expression levels of Nrf2， SLC7A11， GPX4， Occludin， Claudin-1， MUC2， and E-cadherin in each group， and Western blot was adopted to detect the protein expression levels of Nrf2， p-Nrf2， SLC7A11， and GPX4 in each group. ResultsCompared with the normal group， rats in the model group exhibited listlessness， sluggish response， and mucopurulent and bloody stools. The model group also showed significantly increased DAI score， colon length， CDMI score， and expression levels of TNF-α， IL-6， ROS， Fe²⁺， MDA， 4-HNE， DAO， and D-LA （P<0.01）. In addition， it presented significantly decreased IF values of Occludin， Claudin-1， MUC2， and E-cadherin and mRNA and protein expression levels of IL-10， GSH， Nrf2， p-Nrf2， SLC7A11， and GPX4 （P<0.01）. There were different degrees of improvement in each administration group after treatment， and the improvement was the most significant in the high-dose Xiezhuo Jiedu prescription group （P<0.01）. ConclusionXiezhuo Jiedu prescription may alleviate intestinal mucosal injury by inhibiting ferroptosis of intestinal epithelial cells via regulating the Nrf2/SLC7A11/GPX4 signaling pathway， thereby exhibiting efficacy in the treatment of UC.

Objective To investigate the protective effect of benzoylaconine(BAC)on H9c2 cardio-myocytes after oxygen glucose deprivation/reoxyenation(OGD/R)injury.Methods After an in vitro model of OGD/R injury was established in H9c2 cells,the cells were treated with BAC at different concentrations(0,25,50,75,100 μmol/L)to determine its optimal dose.Then,H9c2 cells were randomly divided into control group,OGD/R group,OGD/R+BAC group(75 μmol),OGD/R+LY294002 group(PI3K/Akt inhibitor),and OGD/R+LY294002+BAC group.Corre-sponding reagent kits were used to determine cell viability and LDH level,as well as the expres-sion levels of TNF-α,IL-6,IL-1β,MDA and GSH-Px in the cells.Western blotting was applied to detect the expression of the PI3K/Akt pathway proteins,as well as autophagic proteins such as LC3,Beclin1,and P62.Results Compared to the control group,the cell viability was significantly decreased,and LDH level was obviously increased in the OGD/R group(P＜0.01).Treatment of 75 μmol/L BAC significantly increased the cell viability(0.87±0.06 vs 40.49±0.06,P＜0.01)and decreased the LDH level(86.75±7.79 U/L vs 234.42±6.20 U/L,P＜0.01)when compared to the levels of the OGD/R group.OGD/R injury induced notable increases in TNF-α,IL-6,IL-1β,and MDA expression levels,while decrease of GSH-Px expression level(P＜0.01),and down-regulation of p-PI3K,p-Akt and P62 and up-regulation of LC3 Ⅱ/LC3 Ⅰ and Beclin-1(P＜0.01)when compared with the control group.Treatment of 75 μmol/L BAC increased the levels of p-PI3K,p-Akt,and P62 proteins(0.90±0.07 vs 0.58±0.04,1.02±0.02 vs 0.49±0.01,1.48±0.05 vs 0.87±0.04)and decreased those of LC3 Ⅱ/LC3 Ⅰ and Beclin-1(0.52±0.01 vs 1.24±0.04,0.12±0.01 vs 0.32±0.02)when compared with the OGD/R group(P＜0.01).Conclusions BAC attenu-ates the inflammatory response and oxidative stress of myocardial cells after OGD/R injury,regu-lates autophagy homeostasis,and reduces myocardial cell damage.Its regulatory effect on myocar-dial autophagy homeostasis may be related to the activation of the PI3K/Akt pathway.

Objective The sample hospital is currently in the exploration stage of creating patient satisfaction service un-der the one-hospital and multi-district management mode.In order to improve the overall feeling of patients in the process of hos-pital treatment,the application effect of the existing all-round full-cycle patient service intelligent management platform in the hos-pital is quantitatively evaluated,so as to better improve the service mode.Methods A survey was conducted to collect satisfac-tion data from two groups:the experimental group,which utilized the comprehensive and full-cycle patient service intelligent man-agement platform for diagnosis and treatment services,and the control group,which followed the conventional patient admission and discharge process.The work efficiency number was obtained and calculated through the background of the system,including the average time to handle hospitalization procedures,the average waiting time for examination,the average time to handle dis-charge procedures,the time spent on each follow-up visit and the response rate of follow-up patients.The data were analyzed sta-tistically.Results The work efficiency of the experimental group was significantly better than that of the control group,and the satisfaction of hospitalized patients and staff was higher than that of the control group.Conclusion The application of the com-prehensive and full-cycle patient service intelligent management platform can improve the satisfaction of patients and staff,opti-mize the efficiency of treatment,and better serve the management mode of one hospital and multiple districts.

Objective The sample hospital is currently in the exploration stage of creating patient satisfaction service un-der the one-hospital and multi-district management mode.In order to improve the overall feeling of patients in the process of hos-pital treatment,the application effect of the existing all-round full-cycle patient service intelligent management platform in the hos-pital is quantitatively evaluated,so as to better improve the service mode.Methods A survey was conducted to collect satisfac-tion data from two groups:the experimental group,which utilized the comprehensive and full-cycle patient service intelligent man-agement platform for diagnosis and treatment services,and the control group,which followed the conventional patient admission and discharge process.The work efficiency number was obtained and calculated through the background of the system,including the average time to handle hospitalization procedures,the average waiting time for examination,the average time to handle dis-charge procedures,the time spent on each follow-up visit and the response rate of follow-up patients.The data were analyzed sta-tistically.Results The work efficiency of the experimental group was significantly better than that of the control group,and the satisfaction of hospitalized patients and staff was higher than that of the control group.Conclusion The application of the com-prehensive and full-cycle patient service intelligent management platform can improve the satisfaction of patients and staff,opti-mize the efficiency of treatment,and better serve the management mode of one hospital and multiple districts.

Objective To explore the mechanism of Huanglian Ganjiang Decoction in regulating the mitochondrial apoptotic pathway through the NF-κB/CXCL1/CXCR2 pathway in ulcerative colitis(UC).Methods Sixty C57BL/6J mice were divided into normal group,model group,Huanglian Ganzhang Decoction groups(low,medium and high doses)and mesalazine group.Except for the normal group,UC models were established in the other groups.The general conditions of the mice of all groups were recorded.HE staining was used to observe the pathological changes of the colon and rectum;electron microscopy was used to observe the mitochondrial condition;ELISA was used to determine the contents of IL-6,IL-10,D-lactic acid and DAO;Real-time PCR was used to detect the mRNA expression of NF-κB p65,CXCL1,CXCR2,Bcl-2 and Bax;Western blot was used to determine the protein expression levels of NF-κB p65,CXCL1,CXCR2,p-JAK2,p-STAT3,Bcl-2 and Bax.Results Compared with the normal group,the model group of mice showed a decline in condition,shortened length of the colon and rectum,and mitochondrial structural damage,furthermore,the levels of IL-6,DAO and D-lactic acid were increased,IL-10 level was decreased,the mRNA expression of NF-κB p65,CXCL1,CXCR2 and Bax were enhanced,Bcl-2 mRNA expression was weakened,the protein expression of NF-κB p65,CXCL1,CXCR2,p-JAK2,p-STAT3 and Bax were enhanced,Bcl-2 protein expression was weakened.Compared with the model group,the indexes mentioned above were reversed in the drug groups,especially in the high-dose group.Conclusion Huanglian Ganjiang Decoction may exert its therapeutic effect on UC in mice by regulating the NF-κB/CXCL1/CXCR2 pathway and mitochondrial apoptotic pathway.

Objective:To evaluate the outcomes of minimally invasive therapy for aortic arch pathology after ascending aortic replacement.Methods:A retrospective analysis was conducted at the Department of Cardiovascular Surgery, West China Hospital of Sichuan University from 2016 to 2024. After multidisciplinary discussion, these included patients were evaluated to be at high risk for traditional open surgery. Various minimally invasive repair techniques were employed, including Ⅳb hybrid technique, physician-modified endograft and novel unibody endograft. The study outcomes were technical success, in-hospital and follow-up mortality, stroke, endoleak, and the patency of the supra-aortic vessels.Results:A total of 40 patients(32 males and 8 females) with a median age of 60 years old were included in this study. The technique success rate was 100%, with no deaths or strokes reported. The patency of the supra-aortic vessels was 100%. 10 patients underwent Type Ⅳb hybrid surgery without any endoleaks occurring. Among the 22 patients who received physician-modified endograft, endoleaks were observed in 2 cases. One of these type Ⅰc endoleaks persisted and underwent reintervention. One patient underwent femoral artery replacement due to vascular injury. For the 8 patients who received novel unibody endograft, one case required reintervention due to persistent type Ⅰc endoleaks.Conclusion:With the development of different endovascular techniques and novel branched endograft, patients with aortic arch pathology who are at high risk for redo open surgery can achieve favorable outcomes with various minimal invasive techniques. However, long-term and large-sample follow-up studies are needed for further evaluation.

Background: Adrenal venous sampling (AVS) is essential for diagnosing unilateral aldosterone oversecretion in primary aldosteronism (PA). Traditionally, AVS relies on radioimmunoassay (RIA) to measure plasma aldosterone concentration (PAC), although RIA has limited specificity and considerable variability. This study evaluated the role of liquid chromatography-tandem mass spectrometry (LC-MS/MS) in AVS and its impact on clinical outcomes. Methods: Among 230 patients with PA (May 2020 to April 2023) who underwent AVS, successful sampling was achieved in 182 patients (79.1%) under unstimulated conditions and 206 patients (89.6%) under stimulated conditions. PAC levels from peripheral and adrenal veins measured by LC-MS/MS were compared with RIA results. Patient outcomes were categorized according to the Primary Aldosteronism Surgical Outcomes criteria. Results: LC-MS/MS showed significant correlations with PAC levels measured by RIA in AVS (r=0.40 [unstimulated] and r=0.56 [stimulated]; both P<0.001). However, lateralization concordance between RIA and LC-MS/MS was moderate, at only 57.7% (unstimulated) and 64.6% (stimulated). LC-MS/MS identified more unilateral disease than RIA under both unstimulated (61.5% vs. 37.4%, P<0.001) and stimulated conditions (36.4% vs. 9.7%, P<0.001). Patients achieving complete clinical success after adrenalectomy were more accurately identified by LC-MS/MS than RIA under stimulated (55.6% vs. 22.2%, P=0.035), but not in unstimulated conditions. Conclusion LC-MS/MS outperformed RIA in identifying unilateral disease, resulting in higher rates of complete clinical success in adrenalectomy patients when surgical decisions were based on LC-MS/MS lateralization results.

Objective To observe the effect of hypoxia(HX)on autophagy and pyroptosis-related protein expression of interleukin(IL)-1β-induced chondrocytes,and explore its mechanism of cartilage protection.Methods The expression of Bcl2/adenovirus E1B interacting protein 3-like(BNIP3L/NIX)in normal and osteoarthritis chondrocytes was analyzed by bioinformatics method.The primary chondrocytes from the knee joints of C57BL/6J neonatal mice were extracted and assigned to control group,IL-1β group,HX group,or IL-1β+HX group.The cells were treated with 10 ng/mL IL-1β for 24 h to simulate osteoarthritis-like chondrocyte injury,and HX treatment was by incubation with 1%O2 for 24 h.The expression levels of collagen typeⅡ α1(COL2α1),matrix metalloproteinase 13(MMP13),a disintegrin and metalloproteinase with thrombospondin 5(ADAMTS5),nucleotide-binding oligomerization domain-like receptor 3(NLRP3),gasdermin D N-terminal domain(GSDMD-N),apoptosis-associated speck-like protein containing a CARD(ASC),IL-18,hypoxia induced factor 1α(HIF1α),NIX,Beclin1,microtubule-associated protein-light chain 3(LC3),and p62 proteins were detected by Western blotting in each group.Results Bioinformatics analysis showed that the expression of NIX was lower in osteoarthritis chondrocytes than in normal chondrocytes.Western blotting showed that compared to the control group,the IL-1β group showed significant decreases in COL2α1 and NIX protein expression(both P＜0.05)and significant increases in MMP13,ADAMTS5,NLRP3,GSDMD-N,ASC,IL-18 and HIF1α protein expression(all P＜0.01).Compared to the IL-1β group,the IL-1β+HX group showed significant increases in COL2α1,HIF1α,NIX,Beclin1,and LC3 Ⅱ/LC3Ⅰ(all P＜0.01)and significant decreases in MMP13,ADAMTS5,NLRP3,GSDMD-N,ASC,IL-18 and p62(all P＜0.01).Compared to the control group,the HX group exhibited significant increases in HIF1α,NIX,Beclin1,and LC3Ⅱ/LC3Ⅰ(all P＜0.01)and decreases in p62,NLRP3,GSDMD-N and IL-18(all P＜0.05).Conclusion Hypoxia may eliminate NLRP3 inflammasome and inhibit chondrocyte pyroptosis through HIF1α/NIX-mediated mitochondrial autophagy,thereby reducing IL-1β-induced chondrocyte injury.