Objective To explore the feasibility and reference value of allogeneic lung transplantation and postoperative monitoring in miniature pigs for lung transplantation research. Methods Two miniature pigs (R1 and R2) underwent left lung allogeneic transplantation. Complement-dependent cytotoxicity tests and blood cross-matching were performed before surgery. The main operative times and partial pressure of arterial oxygen (PaO₂) after opening the pulmonary artery were recorded during surgery. Postoperatively, routine blood tests, biochemical blood indicators and inflammatory factors were detected, and pathological examinations of multiple organs were conducted. Results The complement-dependent cytotoxicity test showed that the survival rate of lymphocytes between donors and recipients was 42.5%-47.3%, and no agglutination reaction occurred in the cross-matching. The first warm ischemia times of D1 and D2 were 17 min and 10 min, respectively, and the cold ischemia times were 246 min and 216 min, respectively. Ultimately, R1 and R2 survived for 1.5 h and 104 h, respectively. Postoperatively, in R1, albumin (ALB) and globulin (GLB) decreased, and alanine aminotransferase increased; in R2, ALB, GLB and aspartate aminotransferase all increased. Urea nitrogen and serum creatinine increased in both recipients. Pathological results showed that in R1, the transplanted lung had partial consolidation with inflammatory cell infiltration, and multiple organs were congested and damaged. In R2, the transplanted lung had severe necrosis with fibrosis, and multiple organs had mild to moderate damage. The expression levels of interleukin-1β and interleukin-6 increased in the transplanted lungs. Conclusions The allogeneic lung transplantation model in miniature pigs may systematically evaluate immunological compatibility, intraoperative function and postoperative organ damage. The data obtained may provide technical references for subsequent lung transplantation research.

Radiotherapy is a cornerstone in the treatment of malignant tumors. It induces DNA damage through high-energy radiation, preferentially eliminating rapidly proliferating tumor cells. However, its clinical efficacy is often limited by tumor radioresistance and collateral damage to normal tissues. Consequently, elucidating the cellular response mechanisms to radiation stress and identifying key targets that can both sensitize tumor cells and protect normal tissues have become critical strategies for improving radiotherapy outcomes. Radiation stress triggers structural remodeling of the nucleolus, leading to the dissociation of certain ribosomal proteins from the ribosome and enabling them to acquire extra-ribosomal functions. Among these, RPL11 can be released and specifically binds to MDM2, thus inhibiting its E3 ubiquitin ligase activity, stabilizing p53, and mediating cell cycle arrest and apoptosis. The RPL11-MDM2-p53 pathway, acting as a signaling hub that links nucleolar dysfunction to cell fate determination, plays a pivotal role in maintaining genomic stability and regulating cellular responses to radiation. This review first introduces the basic characteristics of RPL11 and elucidates the molecular basis of radiation-induced ribosomal stress. It then outlines the core regulatory mechanisms of the cell cycle. On this basis, it focuses on the mechanisms by which radiation-induced RPL11 regulates the cell cycle and analyzes the specific effects of RPL11 on cell cycle. Furthermore, it discusses the role of the RPL11-MDM2-p53 pathway in cell cycle regulation. Finally, it explores the role of this pathway in maintaining genomic stability and determining cell fate, and highlights its potential value as a target for radiosensitization, aiming to provide new perspectives for enhancing tumor radiosensitivity and reducing damage to normal tissues.

Radiotherapy is a cornerstone in the treatment of malignant tumors. It induces DNA damage through high-energy radiation, preferentially eliminating rapidly proliferating tumor cells. However, its clinical efficacy is often limited by tumor radioresistance and collateral damage to normal tissues. Consequently, elucidating the cellular response mechanisms to radiation stress and identifying key targets that can both sensitize tumor cells and protect normal tissues have become critical strategies for improving radiotherapy outcomes. Radiation stress triggers structural remodeling of the nucleolus, leading to the dissociation of certain ribosomal proteins from the ribosome and enabling them to acquire extra-ribosomal functions. Among these, RPL11 can be released and specifically binds to MDM2, thus inhibiting its E3 ubiquitin ligase activity, stabilizing p53, and mediating cell cycle arrest and apoptosis. The RPL11-MDM2-p53 pathway, acting as a signaling hub that links nucleolar dysfunction to cell fate determination, plays a pivotal role in maintaining genomic stability and regulating cellular responses to radiation. This review first introduces the basic characteristics of RPL11 and elucidates the molecular basis of radiation-induced ribosomal stress. It then outlines the core regulatory mechanisms of the cell cycle. On this basis, it focuses on the mechanisms by which radiation-induced RPL11 regulates the cell cycle and analyzes the specific effects of RPL11 on cell cycle. Furthermore, it discusses the role of the RPL11-MDM2-p53 pathway in cell cycle regulation. Finally, it explores the role of this pathway in maintaining genomic stability and determining cell fate, and highlights its potential value as a target for radiosensitization, aiming to provide new perspectives for enhancing tumor radiosensitivity and reducing damage to normal tissues.

Radiotherapy is a cornerstone in the treatment of malignant tumors. It induces DNA damage through high-energy radiation, preferentially eliminating rapidly proliferating tumor cells. However, its clinical efficacy is often limited by tumor radioresistance and collateral damage to normal tissues. Consequently, elucidating the cellular response mechanisms to radiation stress and identifying key targets that can both sensitize tumor cells and protect normal tissues have become critical strategies for improving radiotherapy outcomes. Radiation stress triggers structural remodeling of the nucleolus, leading to the dissociation of certain ribosomal proteins from the ribosome and enabling them to acquire extra-ribosomal functions. Among these, RPL11 can be released and specifically binds to MDM2, thus inhibiting its E3 ubiquitin ligase activity, stabilizing p53, and mediating cell cycle arrest and apoptosis. The RPL11-MDM2-p53 pathway, acting as a signaling hub that links nucleolar dysfunction to cell fate determination, plays a pivotal role in maintaining genomic stability and regulating cellular responses to radiation. This review first introduces the basic characteristics of RPL11 and elucidates the molecular basis of radiation-induced ribosomal stress. It then outlines the core regulatory mechanisms of the cell cycle. On this basis, it focuses on the mechanisms by which radiation-induced RPL11 regulates the cell cycle and analyzes the specific effects of RPL11 on cell cycle. Furthermore, it discusses the role of the RPL11-MDM2-p53 pathway in cell cycle regulation. Finally, it explores the role of this pathway in maintaining genomic stability and determining cell fate, and highlights its potential value as a target for radiosensitization, aiming to provide new perspectives for enhancing tumor radiosensitivity and reducing damage to normal tissues.

ObjectiveTo investigate the repair effects of Zhengan Xifengtang on intestinal mucosal barrier in spontaneously hypertensive rats （SHRs） through the pathways of farnesoid X receptor （FXR）-myosin light chain kinase （MLCK）/phosphorylated myosin light chain （p-MLC） and its potential mechanism. MethodsForty 10-week-old male SHRs were randomly divided into model group， amlodipine besylate group （0.5 mg·kg^-1·d^-1）， and high， middle and low dose groups of Zhengan Xifengtang （34.5， 17.25， 8.625 g·kg^-1·d^-1）； eight age-matched male Wistar-Kyoto （WKY） rats of the same origin served as the normal control group. Drug intervention was carried out for 8 weeks， and the blood pressure of the rats was measured regularly. After the intervention， the rats were euthanized to collect tissue samples. Hematoxylin and eosin （HE） staining and Alcian blue-periodic acid-Schiff （AB-PAS） staining were used to evaluate the pathological morphology and the number of goblet cells in colonic mucosa. Enzyme-linked immunosorbent assay （ELISA） was employed to measure plasma lipopolysaccharide （LPS） and diamine oxidase （DAO） levels in each group of rats. Immunofluorescence （IF） assay was used to detect the relative fluorescence intensity of FXR and p-MLC in colonic tissue. Western blot was used to detect the zonula occludens-1 （ZO-1）， Occludin， Claudin-1， junctional adhesion molecule-1 （JAM-1）， mucin-2 （MUC2）， FXR， MLCK， and p-MLC protein expression in colon tissue. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect mRNA expression levels of ZO-1， Occludin， Claudin-1， JAM-1， MUC2， FXR， MLCK， and MLC in colon tissue. ResultsCompared with the normal group， the blood pressure in the model group increased significantly （P<0.01）， the colonic mucosal structure was seriously damaged， and the number of goblet cells decreased significantly. The contents of LPS and DAO increased significantly （P<0.01）， the relative fluorescence intensity of FXR in colon decreased， while that of p-MLC increased （P<0.01）. The protein and mRNA expressions of ZO-1， Claudin-1， JAM-1， Occludin， MUC2 and FXR decreased significantly （P<0.01）， whereas the protein expression of MLCK and p-MLC increased significantly （P<0.01）. Additionally， the mRNA expression of MLCK and MLC increased significantly （P<0.01）. Compared with the model group， the Zhengan Xifengtang groups at various dosages and the amlodipine besylate group showed significantly reduced blood pressure （P<0.01）. The damage of colonic mucosa structure was alleviated， the infiltration of inflammatory cells decreased， and the number of goblet cells increased. LPS and DAO levels were decreased （P<0.05， P<0.01）. In the colon， the relative fluorescence intensity of FXR increased， while that of p-MLC decreased （P<0.05， P<0.01）. The protein and mRNA expression levels of ZO-1， Claudin-1， JAM-1， Occludin， and FXR increased significantly （P<0.05， P<0.01）， while the protein expression of MLCK and p-MLC decreased significantly （P<0.05， P<0.01）. Furthermore， the mRNA expression of MLCK and MLC decreased significantly （P<0.05， P<0.01）， and the protein expression of MUC2 increased significantly （P<0.05， P<0.01）. The expression of MUC2 mRNA in each dose group of Zhengan Xifengtang increased significantly （P<0.05， P<0.01）. ConclusionZhengan Xifengtang may regulate the FXR-MLCK/p-MLC signaling pathway and enhance the expression of tight junction protein， thereby reducing intestinal mucosal permeability， promoting mucosal barrier repair， decreasing LPS release into the blood， and ultimately lowering blood pressure.

ObjectiveTo investigate the repair effects of Zhengan Xifengtang on intestinal mucosal barrier in spontaneously hypertensive rats （SHRs） through the pathways of farnesoid X receptor （FXR）-myosin light chain kinase （MLCK）/phosphorylated myosin light chain （p-MLC） and its potential mechanism. MethodsForty 10-week-old male SHRs were randomly divided into model group， amlodipine besylate group （0.5 mg·kg^-1·d^-1）， and high， middle and low dose groups of Zhengan Xifengtang （34.5， 17.25， 8.625 g·kg^-1·d^-1）； eight age-matched male Wistar-Kyoto （WKY） rats of the same origin served as the normal control group. Drug intervention was carried out for 8 weeks， and the blood pressure of the rats was measured regularly. After the intervention， the rats were euthanized to collect tissue samples. Hematoxylin and eosin （HE） staining and Alcian blue-periodic acid-Schiff （AB-PAS） staining were used to evaluate the pathological morphology and the number of goblet cells in colonic mucosa. Enzyme-linked immunosorbent assay （ELISA） was employed to measure plasma lipopolysaccharide （LPS） and diamine oxidase （DAO） levels in each group of rats. Immunofluorescence （IF） assay was used to detect the relative fluorescence intensity of FXR and p-MLC in colonic tissue. Western blot was used to detect the zonula occludens-1 （ZO-1）， Occludin， Claudin-1， junctional adhesion molecule-1 （JAM-1）， mucin-2 （MUC2）， FXR， MLCK， and p-MLC protein expression in colon tissue. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect mRNA expression levels of ZO-1， Occludin， Claudin-1， JAM-1， MUC2， FXR， MLCK， and MLC in colon tissue. ResultsCompared with the normal group， the blood pressure in the model group increased significantly （P<0.01）， the colonic mucosal structure was seriously damaged， and the number of goblet cells decreased significantly. The contents of LPS and DAO increased significantly （P<0.01）， the relative fluorescence intensity of FXR in colon decreased， while that of p-MLC increased （P<0.01）. The protein and mRNA expressions of ZO-1， Claudin-1， JAM-1， Occludin， MUC2 and FXR decreased significantly （P<0.01）， whereas the protein expression of MLCK and p-MLC increased significantly （P<0.01）. Additionally， the mRNA expression of MLCK and MLC increased significantly （P<0.01）. Compared with the model group， the Zhengan Xifengtang groups at various dosages and the amlodipine besylate group showed significantly reduced blood pressure （P<0.01）. The damage of colonic mucosa structure was alleviated， the infiltration of inflammatory cells decreased， and the number of goblet cells increased. LPS and DAO levels were decreased （P<0.05， P<0.01）. In the colon， the relative fluorescence intensity of FXR increased， while that of p-MLC decreased （P<0.05， P<0.01）. The protein and mRNA expression levels of ZO-1， Claudin-1， JAM-1， Occludin， and FXR increased significantly （P<0.05， P<0.01）， while the protein expression of MLCK and p-MLC decreased significantly （P<0.05， P<0.01）. Furthermore， the mRNA expression of MLCK and MLC decreased significantly （P<0.05， P<0.01）， and the protein expression of MUC2 increased significantly （P<0.05， P<0.01）. The expression of MUC2 mRNA in each dose group of Zhengan Xifengtang increased significantly （P<0.05， P<0.01）. ConclusionZhengan Xifengtang may regulate the FXR-MLCK/p-MLC signaling pathway and enhance the expression of tight junction protein， thereby reducing intestinal mucosal permeability， promoting mucosal barrier repair， decreasing LPS release into the blood， and ultimately lowering blood pressure.

Objective: To analyze the trends in incidence and mortality of prostate cancer in Ningbo City, Zhejiang Province, so as to provide insights into the prevention and control of prostate cancer. Methods: Data of the incidence and mortality of prostate cancer in Ningbo City from 2011 to 2023 were collected through Ningbo Chronic Disease Collaborative Management System. The incidence and mortality of prostate cancer were calculated and standardized by the data from the sixth national population census in 2010 and the Segi's world standard population in 1960. The trends in incidence and mortality of prostate cancer were evaluated using average annual percent change (AAPC). Results: A total of 15 411 cases of prostate cancer were reported in Ningbo City from 2011 to 2023, and the crude incidence, Chinese-standardized incidence and world-standardized incidence were 39.62/105, 22.18/105 and 16.49/105, respectively, showing upward trends (AAPC=14.782%, 10.390% and 10.608%, all P<0.05). The Chinese-standardized incidence of prostate cancer was higher in urban areas than in rural areas, and both showed upward trends (25.14/105 vs. 19.44/105; AAPC=9.057% and 14.272%, both P<0.05). The crude incidence of prostate cancer in the groups aged 50-<60 years, 60-<70 years, 70-<80 years and ≥80 years showed upward trends (AAPC=11.657%, 14.031%, 10.734% and 5.300%, all P<0.05). A total of 3 739 deaths were reported, and the crude mortality, Chinese-standardized mortality and world-standardized mortality were 9.66/105, 5.23/105 and 3.71/105, respectively, showing upward trends (AAPC=8.458%, 3.620% and 3.602%, all P<0.05). The Chinese-standardized mortality of prostate cancer was higher in urban areas than in rural areas, and both showed upward trends (5.35/105 vs. 5.13/105; AAPC=3.183% and 3.962%, both P<0.05). The crude mortality of prostate cancer the groups ageds ≥80 years showed an upward trend (AAPC=7.482%, P<0.05). Conclusions From 2011 to 2023, the incidence and mortality of prostate cancer in Ningbo City showed upward trends. Special attention should be paid to urban residents, and prostate cancer screening should be strengthened among males aged 50 years and older.

Objective:To investigate the impact of correcting rotational subluxation through circumferential fusion and transforaminal lumbar interbody fusion (TLIF) on postoperative coronal plane imbalance in degenerative scoliosis.Methods:A retrospective analysis was conducted on the data of 108 patients with type A degenerative scoliosis in the Nanjing classification who underwent primary multi-segment posterior column osteotomy (PCO) with deformity correction and internal fixation at Nanjing Gulou Hospital from June 2017 to June 2021. Patients were divided into two groups based on the presence of preoperative rotational subluxation: the rotational subluxation group and the non-rotational subluxation group. The rotational subluxation group consisted of 60 patients, with 8 males and 52 females, aged 63.7±5.5 years (range, 56-75 years). The non-rotational subluxation group included 48 patients, with 5 males and 43 females, aged 64.4±5.2 years (range, 53-72 years). Within the rotational subluxation group, depending on whether TLIF was performed on the rotational subluxation segment, they were further categorized into the TLIF group and the PCO group. The TLIF group comprised 28 patients, while the PCO group had 32 patients. Full-spine anteroposterior and lateral X-rays were taken preoperatively, postoperatively, and at the last follow-up to measure coronal balance types and radiographic parameters. The differences in the lumbar Cobb angle, coronal balance distance (CBD), and the Cobb angle of the lumbosacral curve (Cobb-Fra angle) were compared between the rotational subluxation group and the non-rotational subluxation group, as well as between the TLIF group and the PCO group.Results:The average surgery duration ranged from 200 to 310 min, with a mean of 235±47 min. The intraoperative blood loss ranged from 700 to 2,400 ml, with an average of 950±355 ml. The number of fused segments in the rotational subluxation group was 7.6±2.1, ranging from 5 to 11 segments, while in the non-rotational subluxation group, it was 7.4±2.0, ranging from 5 to 10 segments. Postoperatively, 13%(8/60) of patients in the rotational subluxation group developed type C coronal imbalance, significantly higher than the 2%(1/48) in the non-rotational subluxation group. The immediate postoperative and final follow-up lumbar Cobb angles, CBD, and Cobb-Fra angles in the rotational subluxation group were 20.60°±10.73° and 20.33°±10.92°, 22.53±16.45 mm and 18.53±17.31 mm, 13.14°±4.40° and 11.23°±4.92°, respectively, which were higher than those in the non-rotational subluxation group (13.92°±7.02° and 12.92°±6.64°, 18.62±17.44 mm and 8.83±8.95 mm, 11.91°±3.03° and 9.52°±3.30°), with statistical significance ( P<0.05).. Among patients in the rotational subluxation group, the probability of new-onset coronal imbalance postoperatively was 4%(1/28) in the TLIF group, which was lower than the 22%(7/32) in the PCO group, with a statistically significant difference (χ 2=4.330, P=0.037). The immediate postoperative and final follow-up lumbar Cobb angles, CBD, and Cobb-Fra angles in the PCO group were 25.63°±11.00° and 25.13°±11.04°, 27.37±18.95 mm and 25.25±18.67 mm, 15.50°±3.62° and 14.08°±4.77°, respectively, which were significantly higher than those in the TLIF group (14.86°±6.96° and 14.86°±5.37°, 17.08±10.94 mm and 10.86±7.86 mm, 10.14°±3.37° and 8.46°±2.66°), with statistical significance ( P<0.05). Conclusion:For patients with Type A degenerative scoliosis combined with rotational subluxation according to the Nanjing classification, performing a 360-degree circumferential release and interbody fusion at the segment with rotatory subluxation can reduce the risk of developing new postoperative coronal imbalances.

Aim To explore the key components and mechanisms of Lizhong decoction in treating rats with cold-damp diarrhea based on network pharmacology,molecular docking technology and animal experiments.Methods By literature review and database collec-tion,the components of Lizhong decoction,therapeutic targets,and the mapping with diarrhea disease targets were conducted to construct an intersection target pro-tein-protein interaction network for screening core tar-gets,and GO and KEGG pathway enrichment analysis was performed to build an"active component-target-pathway"network,followed by molecular docking vali-dation.Forty-eight rats were randomly divided into the normal control group(K),model group(DG),Lizhong decoction group(LZDG),and Pulsatilla decoction group(BTDG).Subsequently,a rat cold-damp diar-rhea model was established using Senna combined with low-temperature high-humidity environment,and the rats were intervened with Lizhong decoction and Pul-satilla decoction.HE staining was used to detect path-ological changes in intestinal tissue,ELISA was em-ployed to measure the levels of peripheral blood IL-6,IL-10,IL-1 β,and TNF-α,and western blot was used to determine the expression of colon tight junction pro-teins.Results Network pharmacology initially identi-fied 125 compounds in Lizhong decoction,5 186 drug target components,438 disease targets,and 60"drug-disease"shared targets.GO and KEGG enrichment a-nalysis showed that signaling pathways such as IL-17 and TNF were highly enriched.Molecular docking in-dicated that the core components of the drug had good binding activity with corresponding key targets.Liz-hong decoction could effectively improve the clinical symptoms of rats with cold-damp diarrhea,and com-pared with the DG group,the diarrhea rate,diarrhea in-dex,and other related indicators also gradually de-creased to normal levels.Compared with the DG group,the LZDG group showed reduced inflammation levels and a recovery in energy metabolism levels.Conclusion It can regulate targets such as MMP9 and IL-17 signaling pathways through multi-components like Calycosin and formononetin to exert its therapeutic effect on cold-damp diarrhea.

Lens injury is an important etiological factor in the reduction of visual function following ocular trauma.Currently, there are no clear standards for the classification of lens injury, and comprehensive diagnostic tools are lacking.This deficiency leads to numerous controversies and challenges in critical areas, such as diagnosis and preoperative evalution, timing of surgery, surgical strategy, and assessment of postoperative prognosis.Tomographic imaging technology, such as computed tomography, magnetic resonance imaging, optical coherence tomography, has introduced a new dimension to the evaluation of lens injury, which is crucial for assessing the transparency, texture, location, morphology, and integrity of the lens, as well as the zonules and nearby intraocular structures.However, the use of tomographic imaging technology is somewhat limited due to the limitations of relying on a single method.With the ongoing advancement of imaging technologies and the rapid development of big data and artificial intelligence, tomographic imaging will become an increasingly essential tool in the future management of lens injury.Our expert group reviewed the epidemiological characteristics and classification of lens injury and the major challenges currently faced in the diagnosis and treatment of lens injury, and provided expert recommendations mainly focusing on the application, shortcomings and limitations of current tomographic imaging technology in the diagnosis and treatment of lens injury, and future development directions.