ObjectiveTo explore the interaction and competitive binding of Homo sapiens long intergenic non-protein-coding RNA 1134 （LINC01134） to CCCTC-binding factor CTCF， affecting the transcription of cyclin-dependent kinase inhibitor （p21） and influencing the proliferation of A549 cells， in order to investigate the possible mechanism of Astragali Radix and Hedyotis diffusa （A-H） in inhibiting A549 proliferation by regulating this axis. MethodsRNA-binding protein immunoprecipitation （RIP） assays were conducted to examine the interaction between LINC01134 and CTCF， and chromatin immunoprecipitation （ChIP） assays were used to study the effect of LINC01134 overexpression on the interaction between CTCF and p21. Stable A549 cell lines （oe-NC and oe-LINC01134） were established using lentiviral transfection， and each group was treated with 10% A-H drug-containing serum. Real-time PCR and Western blot analyses were performed to detect the effects of A-H on the expression of LINC01134， CTCF， and p21 in A549 cells. Cell counting kit-8 （CCK-8） and colony formation assays were used to assess the effects of A-H on A549 cell proliferation via LINC01134. Flow cytometry was employed to evaluate the effects of A-H on the A549 cell cycle through LINC01134， and Western blot was used to detect changes in cell cycle proteins. ResultsCompared with the IgG group， the oe-CTCF group showed a significantly increased abundance of LINC01134 aggregates （P0.01）. Compared with the oe-Vector group， p21 abundance in CTCF complexes was significantly reduced in the oe-LINC01134 group （P0.01）. Compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed the expression of LINC01134 and p21 （P0.05）， but had no significant regulatory effect on CTCF. Compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed cell viability at 72 h （P0.05）， inhibited malignant proliferation （P0.05）， and reversed the proportions of cells in the G₀/G₁ and S phases （P0.01）. Furthermore， compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed the expression of Cyclin D₁， CDK4， Cyclin E， CDK2， phosphorylated retinoblastoma protein （p-Rb）， and E2F transcription factor 3 （E2F3） （P0.01）. ConclusionA-H regulates the LINC01134-CTCF-p21 axis to block the G₁/S phase transition of A549 cell cycle， accelerate cellular senescence， and inhibit malignant proliferation.

ObjectiveTo explore the interaction and competitive binding of Homo sapiens long intergenic non-protein-coding RNA 1134 （LINC01134） to CCCTC-binding factor CTCF， affecting the transcription of cyclin-dependent kinase inhibitor （p21） and influencing the proliferation of A549 cells， in order to investigate the possible mechanism of Astragali Radix and Hedyotis diffusa （A-H） in inhibiting A549 proliferation by regulating this axis. MethodsRNA-binding protein immunoprecipitation （RIP） assays were conducted to examine the interaction between LINC01134 and CTCF， and chromatin immunoprecipitation （ChIP） assays were used to study the effect of LINC01134 overexpression on the interaction between CTCF and p21. Stable A549 cell lines （oe-NC and oe-LINC01134） were established using lentiviral transfection， and each group was treated with 10% A-H drug-containing serum. Real-time PCR and Western blot analyses were performed to detect the effects of A-H on the expression of LINC01134， CTCF， and p21 in A549 cells. Cell counting kit-8 （CCK-8） and colony formation assays were used to assess the effects of A-H on A549 cell proliferation via LINC01134. Flow cytometry was employed to evaluate the effects of A-H on the A549 cell cycle through LINC01134， and Western blot was used to detect changes in cell cycle proteins. ResultsCompared with the IgG group， the oe-CTCF group showed a significantly increased abundance of LINC01134 aggregates （P0.01）. Compared with the oe-Vector group， p21 abundance in CTCF complexes was significantly reduced in the oe-LINC01134 group （P0.01）. Compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed the expression of LINC01134 and p21 （P0.05）， but had no significant regulatory effect on CTCF. Compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed cell viability at 72 h （P0.05）， inhibited malignant proliferation （P0.05）， and reversed the proportions of cells in the G₀/G₁ and S phases （P0.01）. Furthermore， compared with the 10% blank + oe-LINC01134 group， the 10% A-H + oe-LINC01134 group reversed the expression of Cyclin D₁， CDK4， Cyclin E， CDK2， phosphorylated retinoblastoma protein （p-Rb）， and E2F transcription factor 3 （E2F3） （P0.01）. ConclusionA-H regulates the LINC01134-CTCF-p21 axis to block the G₁/S phase transition of A549 cell cycle， accelerate cellular senescence， and inhibit malignant proliferation.

OBJECTIVE To investigate the effects and mechanism of the Yishen paidu formula on renal fibrosis in rats with chronic renal failure （CRF） through the reactive oxygen species （ROS）/thioredoxin-interacting protein （TXNIP）/NOD-like receptor thermal protein domain associated protein 3 （NLRP3） pathway. METHODS Rats were randomly divided into control group， model group， Yishen paidu formula low-dose （Yishen paidu formula-L） group， Yishen paidu formula high-dose （Yishen paidu formula- H） group， Yishen paidu formula-H+pcDNA-NC group， and Yishen paidu formula-H+ pcDNA-TXNIP group， with 10 rats in each group. Except for control group， all other rats were fed a diet containing 0.5% adenine to establish a CRF model； the rats were then administered corresponding drugs or normal saline intragastrically or via tail vein， once daily， for 8 consecutive weeks. After the last administration， the levels of serum creatinine （Scr）， blood urea nitrogen （BUN）， ROS， superoxide dismutase （SOD）， malondialdehyde （MDA）， tumor necrosis factor-α （TNF-α）， interleukin （IL）-6， and IL-1β were measured in each group. Pathological changes in renal tissue were observed， and the protein expression levels of Collagen Ⅲ， α-smooth muscle actin （α-SMA）， transforming growth factor-β1 （TGF-β1）， TXNIP and NLRP3 in renal tissue were detected. RESULTS Compared with model group， the renal histopathological damage and fibrosis of rats in Yishen paidu formula-L group and Yishen paidu formula-H group were significantly alleviated. The levels of Scr， BUN， ROS， MDA， TNF- α， IL-6 and IL-1β， and the protein expressions of Collagen Ⅲ， α-SMA， TGF-β1， TXNIP and NLRP3 were significantly decreased， while SOD levels were significantly increased （P＜0.05）. Moreover， the changes were more pronounced in the Yishen paidu formula-H group （P＜0.05）. Compared with Yishen paidu formula-H+pcDNA-NC group， above indexes of rats in Yishen paidu formula-H+pcDNA-TXNIP group were reversed significantly （P＜0.05）. CONCLUSIONS Yishen paidu formula can inhibit renal fibrosis in CRF rats by suppressing the ROS/TXNIP/NLRP3 pathway.

Chronic atrophic gastritis （CAG） is a digestive system disease characterized by the reduction and atrophy of the intrinsic glands of the gastric mucosa. This disease is closely related to risk factors such as Helicobacter pylori （Hp） infection，long-term unhealthy eating habits and lifestyle. As CAG is a key link in the development of gastric cancer，effectively preventing its deterioration is of great significance for the prevention of gastric cancer. At present，Western medicine mainly uses symptomatic treatments such as eradicating Hp，protecting gastric mucosa， and promoting gastrointestinal motility. However， long-term use is prone to drug resistance and cannot reverse limitations such as gland atrophy， making it urgent to explore new intervention strategies. In recent years，with the deepening of CAG mechanism research，the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway，as one of the classic signaling pathways，plays a significant role in the occurrence and development of CAG，while its systematic summary is still blank. Based on the regulatory advantages of "multi-target，multi-pathway，and low toxicity"，traditional Chinese medicine can improve the pathological process of CAG by intervening in key nodes of the PI3K/Akt pathway. In this paper，the research progress of traditional Chinese medicine regulating PI3K/Akt pathway to improve CAG was systematically reviewed for the first time. The expression of PI3K/Akt signaling pathway in CAG was discussed，including the regulation of inflammation and oxidative stress，cell proliferation and apoptosis，and autophagy. The traditional Chinese medicine flavonoids，alkaloids，terpenoids and other compounds that regulate this pathway were summarized. The traditional Chinese medicine compounds mainly include classic famous prescriptions such as Xiaochaihu Tang，Banxia Xiexin Tang，Morodan concentrated pills，Elian granules and other traditional Chinese patent medicines，as well as empirical prescriptions such as modified Leweiyin formula，and Qiling prescription. This study aims to give full play to the advantages of traditional Chinese medicine and lay a solid foundation for the wide application and further development of CAG treatment，and provide new ideas for clinical research and drug research on CAG.

Systemic autoimmune diseases represent a group of disorders characterized by loss of immune tolerance to self-antigens, leading to abnormal immune responses and subsequent tissue damage. Typical examples include systemic lupus erythematosus and systemic sclerosis. These conditions are marked by multi-system involvement, chronic progression, and recurrent flares. The pancreas, as a vital digestive and endocrine organ rich in glandular tissue and vascular supply, can also be affected by autoimmune processes. Pancreatic injury often indicates active and difficult-to-control disease, posing a serious threat to patient survival. Due to its relative rarity, diverse underlying mechanisms across different autoimmune diseases, and frequently nonspecific clinical presentations, pancreatic involvement is easily overlooked, resulting in delayed diagnosis and treatment.This article focuses on the clinical features and potential pathophysiological mechanisms of pancreatic injury associated with autoimmune diseases, such as systemic lupus erythematosus, systemic sclerosis, Sjögren's syndrome, and rheumatoid arthritis, aiming to enhance clinical awareness and facilitate early recognition and diagnosis of this condition.

Objective To analyze the characteristics of viral hepatitis mortality and life loss among residents in Pudong New Area from 2003 to 2023, and to provide a basis for related prevention and control work. Methods Viral hepatitis mortality data were obtained from the Pudong New Area mortality monitoring system. The crude mortality rate (CMR), standardized mortality rate (SMR), potential years of life lost (PYLL), average years of life lost (AYLL), and standardized potential years of life lost (SPYLL) were calculated to analyze viral hepatitis deaths. The average annual change (AAPC) and annual percentage change (APC) of the mortality rate were calculated by Joinpoint regression analysis to analyze the trend of mortality. Results The CMR and SMR of viral hepatitis among residents in Pudong New Area from 2003 to 2023 were 3.89/100000 and 1.98/100000, respectively. Both CMR and SMR of viral hepatitis showed a decreasing trend over time (CMR:APC=-5.476, t=-13.581, P<0.001; SMR:APC=- 7.624, t= -21.253, P<0.001). The CMR for males was 4.75/100000 and the SMR for males was 2.65/100000; the CMR for females was 3.04/100000 and the SMR for females was 1.32/100000, with a higher mortality rate for males than for females（Z_CME=12.094，P<0.001; Z_SMR=-14.718，P<0.001). Deaths were concentrated in the age groups of 45-64 years old and 65 years old and above, accounting for 91.62% of the total deaths. The PYLL of deaths due to viral hepatitis among residents in Pudong New Area from 2003 to 2023 was 26912 person-years, with a PYLLR of 0.45% and an AYLL of 8.88 years per person. Conclusion The mortality rate of viral hepatitis among the residents of Pudong New Area in 2003-2023 shows a decreasing trend over time. The mortality rate of males is higher than that of females, and the deaths of middle-aged and elderly people account for a large proportion of the total deaths. Chronic hepatitis B is the main cause of death.

Non-alcoholic fatty liver disease （NAFLD） is a chronic liver disease closely related to metabolism， which is mainly characterized by abnormal lipid deposition in hepatocytes. In recent years， with the increasing prevalence of obesity and metabolic syndrome， NAFLD has become one of the most common chronic diseases in the world. The pathogenesis of NAFLD is complex and varied， involving the cross-regulation of multiple signaling pathways such as glucose-lipid metabolism， oxidative stress， and inflammation. The TLR4 signaling pathway plays a key role in the development and progression of NAFLD， and abnormal activation of this pathway accelerates the deterioration of NAFLD by promoting the release of pro-inflammatory cytokines， inducing oxidative stress， and exacerbating insulin resistance. Studies have shown that traditional Chinese medicine （TCM） can regulate the TLR4 signaling pathway to alleviate the symptoms and pathological features of NAFLD. The present review summarizes the experimental research progress in the TCM regulation of the TLR4 signaling pathway in treating NAFLD in the past 5 years， covering a wide range of TCM active ingredients （such as polysaccharides， terpenoids， alkaloids， flavonoids） and compound prescriptions. The active ingredients and compound prescriptions of TCM can effectively ameliorate lipid metabolism disorders， reduce insulin resistance， regulate intestinal flora， and inhibit inflammation and oxidative stress by regulating the TLR4 signaling pathway via multiple targets and pathways， thus slowing down the progression of NAFLD. Through in-depth analysis of the pathological mechanisms of NAFLD and exploration of the potential of TLR4 signaling pathway as a therapeutic target， we can provide theoretical support for the application of TCM in the treatment of NAFLD， as well as new perspectives and directions for future clinical research and new drug development， thereby promoting the innovation and development of therapeutic strategies for NAFLD.

BACKGROUND: The contraction behaviors of cardiomyocytes (CMs), especially contraction synchrony, are crucial factors reflecting their maturity and response to drugs. A wider field of view helps to observe more pronounced synchrony differences, but the accompanied greater computational load, requiring more computing power or longer computational time. METHODS: We proposed a method that directly correlates variations in optical field brightness with cardiac tissue contraction status (CVB method), based on principles from physics and photometry, for rapid video analysis in wide field of view to obtain contraction parameters, such as period and contraction propagation direction and speed. RESULTS: Through video analysis of human induced pluripotent stem cell (hiPSC)-derived CMs labeled with green fluorescent protein (GFP) cultured on aligned and random nanofiber scaffolds, the CVB method was demonstrated to obtain contraction parameters and quantify the direction and speed of contraction within regions of interest (ROIs) in wide field of view. The CVB method required less computation time compared to one of the contour tracking methods, the LucasKanade (LK) optical flow method, and provided better stability and accuracy in the results. CONCLUSION This method has a smaller computational load, is less affected by motion blur and out-of-focus conditions, and provides a potential tool for accurate and rapid analysis of cardiac tissue contraction synchrony in wide field of view without the need for more powerful hardware.

After continuous development and improvement, lung transplantation has become the preferred means to treat a variety of benign end-stage lung diseases. However, the field of lung transplantation still faces many challenges, including shortage of donor resources, preservation and maintenance of donor lungs, and postoperative complications. Lung tissue samples removed after lung transplantation are excellent clinical resources for the study of benign end-stage lung disease and perioperative complications of lung transplantation. However, at present, the collection, storage and utilization of tissue samples after lung transplantation are limited to a single study, and unified technical specifications have not been formed. Based on the construction plan of the biobank for lung transplantation in the First Affiliated Hospital of Xi'an Jiaotong University, this study reviewed the practical experience in the collection, storage and utilization of lung transplant tissue samples in the aspects of ethical review, staffing, collection process, storage method, quality control and efficient utilization, in order to provide references for lung transplant related research.

ObjectiveTo investigate the effects of excessive activation of the Specific protein 1 （Sp1）-MicroRNA-582-3p （miR-582-3p）-cyclin-dependent kinase inhibitor （p27） axis on the cell cycle and proliferation of A549 lung adenocarcinoma cells at the cellular level， thereby investigating the possible mechanisms by which Astragali Radix and Hedyotis diffusa（A-H） regulate the axis to inhibit A549 cells proliferation. MethodsLentiviral plasmid transfection technology was used to obtain four stable A549 transgenic cell lines： shRNA-Sp1+LV-miR-582-3p mimic， shRNA-Sp1+LV-mNC， shRNA-NC+LV-miR-582-3p mimic， and shRNA-NC+LV-mNC. Real-time PCR was used to detect the effect of Sp1 on miR-582-3p expression in A549 lung adenocarcinoma cells. CCK-8 and colony formation assay were used to detect the effect of Sp1 on cell proliferation through miR-582-3p， while flow cytometry was used to detect the effect of Sp1 on cell cycle via miR-582-3p. Western blot was used to detect the effect of Sp1 on cyclin in A549 cells through miR-582-3p. CCK-8 was employed to detect the effects of different concentrations （5%， 10%， 20%， 40%， 80%） of A-H on A549 cell viability， and the optimal concentration was selected for subsequent mechanism exploration. Stable transgenic strains oe-Sp1 and control oe-Vector were constructed using the above-mentioned transfection techniques. Real-time PCR was then used to investigate the effect of A-H on miR-582-3p expression in A549 cells， while Western blot was employed to detect the effect of A-H on Sp1 and p27 expression in A549 lung adenocarcinoma cells. ResultsCompared with the shRNA-NC+LV-mNC group， the expression of miR-582-3p was significantly inhibited in the shRNA-Sp1+LV-mNC group （P<0.01）. Compared with the shRNA-Sp1+LV-mNC group， the shRNA-Sp1+LV-miR-582-3p mimic group significantly reversed miR-582-3p expression （P<0.01）， indicating that Sp1 has a significant regulatory effect on miR-582-3p. Compared with the shRNA-Sp1+LV-mNC group， the shRNA-Sp1+LV-miR-582-3p mimic group significantly reversed cell proliferation （P<0.01）， suggesting that miR-582-3p can partially reverse the proliferative effect of Sp1 on A549 lung adenocarcinoma. Compared with the shRNA-Sp1+LV-mNC group， the shRNA-Sp1+LV-miR-582-3p mimic group showed a significant decrease in G₀/G₁ proportions， while the G₂/M and S phase proportions increased significantly （P<0.01）， indicating that miR-582-3p can partially reverse the effect of Sp1 on the A549 cell cycle. Compared with the shRNA-Sp1+LV-mNC group， the shRNA-Sp1+LV-miR-582-3p mimic group significantly reversed the expression of various proteins with the decrease of p27 and the increase of Cyclin D₁， CDK4， Cyclin E， CDK2， p-Rb， and E2F3 （P<0.01）， indicating that miR-582-3p can partially reverse the effect of Sp1 on the cell cycle of A549 lung adenocarcinoma. Compared with the blank group， the serum containing A-H significantly inhibited A549 cell viability in a concentration-dependent manner. Therefore， 10% A-H was selected for intervention of subsequent mechanism experiments. Compared with A-H+oe-Vector， A-H+oe-Sp1 significantly reversed the downregulation of Sp1， miR-582-3p， and the upregulation of p27 （P<0.01）. This suggests that Sp1 can partially reverse the effects of A-H on miR-582-3p and p27 levels in A549 lung adenocarcinoma cells. ConclusionOveractivation of the Sp1-miR-582-3p-p27 axis significantly promotes the proliferation of A549 lung adenocarcinoma cells， and the potential mechanism of the inhibitory effect of A-H on the proliferation of A549 cells may be related to its inhibition on the overactivation of the Sp1-miR-582-3p-p27 axis.