Fibrosis, the pathological scarring of vital organs, is a severe and often irreversible condition that leads to progressive organ dysfunction. It is particularly pronounced in organs like the liver, kidneys, lungs, and heart. Despite its clinical significance, the full understanding of its etiology and complex pathogenesis remains incomplete, posing substantial challenges to diagnosing, treating, and preventing the progression of fibrosis. Among the various molecular players involved, platelet-derived growth factor-C (PDGF-C) has emerged as a crucial factor in fibrotic diseases, contributing to the pathological transformation of tissues in several key organs. PDGF-C is a member of the PDGFs family of growth factors and is synthesized and secreted by various cell types, including fibroblasts, smooth muscle cells, and endothelial cells. It acts through both autocrine and paracrine mechanisms, exerting its biological effects by binding to and activating the PDGF receptors (PDGFRs), specifically PDGFRα and PDGFRβ. This binding triggers multiple intracellular signaling pathways, such as JAK/STAT, PI3K/AKT and Ras-MAPK pathways. which are integral to the regulation of cell proliferation, survival, migration, and fibrosis. Notably, PDGF-C has been shown to promote the proliferation and migration of fibroblasts, key effector cells in the fibrotic process, thus accelerating the accumulation of extracellular matrix components and the formation of fibrotic tissue. Numerous studies have documented an upregulation of PDGF-C expression in various fibrotic diseases, suggesting its significant role in the initiation and progression of fibrosis. For instance, in liver fibrosis, PDGF-C stimulates hepatic stellate cell activation, contributing to the excessive deposition of collagen and other extracellular matrix proteins. Similarly, in pulmonary fibrosis, PDGF-C enhances the migration of fibroblasts into the damaged areas of lungs, thereby worsening the pathological process. Such findings highlight the pivotal role of PDGF-C in fibrotic diseases and underscore its potential as a therapeutic target for these conditions. Given its central role in the pathogenesis of fibrosis, PDGF-C has become an attractive target for therapeutic intervention. Several studies have focused on developing inhibitors that block the PDGF-C/PDGFR signaling pathway. These inhibitors aim to reduce fibroblast activation, prevent the excessive accumulation of extracellular matrix components, and halt the progression of fibrosis. Preclinical studies have demonstrated the efficacy of such inhibitors in animal models of liver, kidney, and lung fibrosis, with promising results in reducing fibrotic lesions and improving organ function. Furthermore, several clinical inhibitors, such as Olaratumab and Seralutinib, are ongoing to assess the safety and efficacy of these inhibitors in human patients, offering hope for novel therapeutic options in the treatment of fibrotic diseases. In conclusion, PDGF-C plays a critical role in the development and progression of fibrosis in vital organs. Its ability to regulate fibroblast activity and influence key signaling pathways makes it a promising target for therapeutic strategies aiming at combating fibrosis. Ongoing research into the regulation of PDGF-C expression and the development of PDGF-C/PDGFR inhibitors holds the potential to offer new insights and approaches for the diagnosis, treatment, and prevention of fibrotic diseases. Ultimately, these efforts may lead to the development of more effective and targeted therapies that can mitigate the impact of fibrosis and improve patient outcomes.

ObjectiveTo investigate the effect of Shugan Quyu Jiedu prescription （SGQYJDF） on inducing ferroptosis in hepatocellular carcinoma cells based on the tumor protein 53 （p53）/solute carrier family 7 member 11 （SLC7A11）/glutathione peroxidase 4 （GPX4） pathway. MethodMHCC97H cells were divided into the blank serum group （10% blank serum medium）， SGQYJDF-containing serum low concentration group （5% SGQYJDF-containing serum and 5% blank serum medium）， SGQYJDF-containing serum medium concentration group （7.5% SGQYJDF-containing serum and 2.5% blank serum medium）， SGQYJDF-containing serum high concentration group （10% SGQYJDF-containing serum medium） and sorafenib group （sorafenib concentration of 10 μmol·L^-1 in 10% blank serum medium）. After 24 hours of intervention， the cell survival rate was detected by cell counting kit-8 （CCK-8） assay. The cell proliferation ability was detected by 5-ethynyl-2′-deoxyuridine （EdU） staining. The intracellular ferrous ion （Fe²⁺） level was detected by ferrous ion fluorescent probe （FerroOrange） staining. The intracellular malondialdehyde （MDA） and glutathione （GSH） levels were detected by colorimetric assays. The ultrastructure of mitochondria was observed by transmission electron microscopy. The expression levels of ferroptosis-related proteins p53， SLC7A11 and GPX4 were detected by Western blot. ResultIn terms of cell viability， compared with the blank serum group， the SGQYJDF group showed a dose-dependent decrease in the survival rate of MHCC97H cells. Effect of the medium and high concentrations of SGQYJDF on the survival rate of MHCC97H cells were significantly decreased （P<0.01）. Additionally， the results of the EdU assay showed that both the medium and high concentrations of SGQYJDF were able to inhibit the proliferation ability of MHCC97H cells （P<0.05， P<0.01）. Regarding the biochemical indicators of ferroptosis， compared to the blank serum group， the medium and high concentrations of SGQYJDF were able to dose-dependently increase the intracellular Fe²⁺ level （P<0.01）. The low， medium， and high concentrations of SGQYJDF were able to dose-dependently decrease the level of GSH in MHCC97H cells （P<0.01） and increase the level of MDA in the cells （P<0.05， P<0.01）. In terms of pathway-related protein expression， compared to the blank serum group， the medium and high concentrations of SGQYJDF could significantly increase the expression of p53 （P<0.01）. The low， medium， and high concentrations of SGQYJDF could significantly decrease the expression of GPX4 （P<0.01）. The high concentration of SGQYJDF could decrease the expression of SLC7A11 （P<0.01）. In terms of the cell morphology of ferroptosis， compared with the blank serum group， transmission electron microscopy revealed that the low concentration of SGQYJDF caused mitochondrial deformation， while the medium and high concentrations of SGQYJDF resulted in reduced mitochondrial volume， increased double-layer membrane density， and decreased mitochondrial cristae. These features were similar to those of sorafenib-induced ferroptosis. Furthermore， compared with the sorafenib group， the high concentration of SGQYJDF showed no statistically significant differences in cell survival rate， proliferation ability， Fe²⁺ level， MDA level， and GSH level. ConclusionThe results suggest that SGQYJDF may induce ferroptosis and inhibit proliferation in hepatocellular carcinoma MHCC97H cells by upregulating the expression of p53， suppressing the expressions of GPX4 and SLC7A11， downregulating the level of GSH， and leading to the accumulation of intracellular Fe²⁺ and MDA.

AIM: To report three cases of viral keratitis caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2).METHODS: Slit lamp, intraocular pressure, corneal fluorescence staining, anterior segment photography, in vivo confocal microscopy(IVCM), and routine fundus screening were performed in the three confirmed patients. Treatment involved Ganciclovir, artificial tears and glucocorticoid eye drops.RESULTS: Three patients with SARS-CoV-2 keratitis(SCK)recovered well after standard treatment.CONCLUSION: SARS-CoV-2 keratitis typically presents as corneal subepithelial infiltration and can result in a decrease in corneal subepithelial nerve fiber density and an increase in dendritic cells(DC). Antiviral therapy in combination with glucocorticoid has proven to be effective.

Objective:To explore the characteristics, prevention and treatment strategies of lower urinary tract injury in transvaginal reconstructive pelvic surgery (vRPS).Methods:A retrospective analysis was conducted on 24 patients who suffered lower urinary tract injuries occuring in vRPS from January 2005 to June 2021, among which 4 cases were referred to our hospital from other hospitals.Results:(1) In our hospital, 1 952 patients underwent vRPS for anterior and (or) middle pelvic organ prolapse during that study period, with a 1.0% (20/1 952) incidence of lower urinary tract injuries occurring in 20 cases. (2) Ureteral injuries were observed in 14 cases who underwent transvaginal high uterosacral ligament suspension (1.4%, 14/966). The symptoms were relieved after the removal of sutures. (3) Bladder injuries occurred in 6 cases in our hospital, with 4 cases (0.7%, 4/576) in anterior transvaginal mesh surgery (aTVM), one (0.4%, 1/260) in colpocleisis, and one (0.7%, 1/150) in apical suspension for fornix prolapse. An additional 4 cases of bladder injury were referred to our hospital after aTVM. Among the 8 cases of bladder injury during aTVM, 2 cases were intraoperative incidents. Cystoscopy confirmed that the superficial branch or puncture rod of anterior vaginal mesh had penetrated into the bladder. Re-puncturing and placement of the mesh were successfully performed. No abnormalities were observed during a follow-up period of 4-5 years. Postoperative bladder injuries were identified in 6 cases, characterized by mesh erosion into the bladder and formation of calculi. These injuries were confirmed between 6 months to 2 years after vRPS. The exposed mesh and calculi in the bladder were removed through laparotomy or cystoscopy, followed up for 2-12 years. One case experienced slight re-erosion of mesh to the bladder.Conclusions:Lower urinary tract injuries are difficult to avoid in vRPS, particularly in transvaginal high uterosacral ligament suspension and aTVM. However, the incidence is low. Lower urinary tract injuries during vRPS could be easily detected and managed intraoperatively because of the use of cystoscopy. As long-term postoperative complications, erosion of transvaginal mesh to lower urinary tract postoperatively could be treated correctly, seldom with severe sequelae.

Objective To evaluate the effectiveness,safety and economy of the clinical application of levetiracetam(LEV)concentrated solution for injection generic drug and the original drug in the national centralized volume-based procurement.Methods The information of inpatients using original LEV concentrated solution for injection in the Xuanwu Hospital of Capital Medical University(original drug group)and inpatients using generic LEV concentrated solution for injection in the First Affiliated Hospital of Wannan Medical College(generic drug group)was retrospectively analyzed after the implementation of the procurement policy(from November 2021 to March 2022).To compare the effectiveness,safety and economy of the two in the prevention and treatment of epilepsy.Results In the original drug group and the generic drug group,18 and 17 patients were enrolled in the treatment of epilepsy respectively,the effective rates were 50.00％and 58.82％,the incidence of adverse reactions were both 0％,and the median daily cost was 255.00(255.00,510.00)yuan and 131.78(131.78,131.78)yuan.After propensity score matching,both the original drug group and the generic drug group had 76 patients each received preventive medication,the effective rates were 97.37％and 100％(P＞0.05),and the incidence of adverse reactions were both 0％.The median daily fee for the original the generic drug group was 170.00(170.00,170.00)yuan and 131.78(131.78,131.78)yuan,there were significant difference(P＜0.01).Conclusion The clinical effect of generic and original LEV concentrated solution for injection in preventing epilepsy is basically the same,the clinical safety are equivalent,the generic has better economy than the original.The effective rate of the treatment of epilepsy is similar,while the sample size needs to be further expanded to verify the results.

Objective To explore the value of droplet digital polymerase chain reaction(ddPCR)in the etiological diagnosis of severe acute pancreatitis(SAP)patients with suspected bloodstream infection(BSI).Methods SAP patients admitted to the department of critical care medicine in a hospital July to September 2022 were enrolled.When BSI was suspected,venous blood was collected for both ddPCR detection and blood culture(BC)with antimi-crobial susceptibility testing(AST)simultaneously.The time required for two detection methods was recorded,and the detection results of ddPCR and BC were compared.The etiological diagnostic efficacy of ddPCR was calculated,and the correlation between the value of pathogen load detected by ddPCR and the level of infection parameters was explored.Results A total of 22 patients were included in the analysis,and 52 venous blood specimens were collec-ted for detection.BC revealed 17 positive specimens(32.7％)and 29 pathogenic strains,while ddPCR showed 41 positive specimens(78.8％)and 73 pathogenic strains.Detection time required for ddPCR was significantly lower than that of BC([0.16±0.03]days vs[5.92±1.20]days,P＜0.001).Within the detection range of ddPCR and taking BC results as the gold standard,the sensitivity and specificity of ddPCR were 80.0％and 28.6％,respective-ly.With the combined assessment of BSI based on non-blood specimen microbial evidence within a week,the sensi-tivity and specificity of ddPCR detection increased to 91.9％and 76.9％,respectively.ddPCR detected resistance genes of blaKPC,blaNDM/IMP,VanA/VanM,and mecA from 19,9,6,and 5 specimens,respectively.Correlation analysis showed a positive correlation between pathogen load and levels of C-reactive protein as well as procalcitonin(r=0.347,0.414,P＜0.05).Conclusion As a supplementary detection method for BC in BSI diagnosis,ddPCR has the advantages of higher sensitivity and shorter detection time,and is worthy of further exploration in clinical application.

Objective To investigate the diagnostic value of contrast-enhanced ultrasound(CEUS)combined with serum Smad ubiquitin regulatory factor 1(SMURF1)detection for thyroid cancer.Methods A total of 144 suspected thyroid cancer patients admitted to Lishui branch of Zhongda Hospital Affiliated to Southeast University from February 2019 to February 2020 were selected as the study subjects.Based on the histopathological results,they were divided into the thyroid cancer group(76 cases)and the benign group(68 cases).All patients underwent contrast-enhanced ultrasound examination and serum SMURF1 level detection;the diagnostic value of contrast-enhanced ultrasound parameters,serum SMURF1 detection alone,and the combination of the two methods for thyroid cancer were analyzed.Results Contrast-enhanced ultrasound parameters peak intensity(PI),mean perfusion intensity(SImean)and maximum perfusion intensity(SImax)in the thyroid cancer group were lower than those in the benign group,and the level of SMURF1 mRNA was higher than that in the benign group(P<0.05).The sensitivity of contrast-enhanced ultrasound parameter SImax in the diagnosis of thyroid cancer was 82.89%,the specificity was 72.06%,the accuracy was 77.78%,and the Kappa value was 0.552.The sensitivity of serum SMURF1 in the diagnosis of thyroid cancer was 65.79%,the specificity was 94.12%,the accuracy was 79.17%,and the Kappa value was 0.589.The sensitivity,specificity,accuracy and Kappa value of SImax combined with serum SMURF1 in the diagnosis of thyroid cancer were 97.37%,85.29%,91.67%and 0.832,respectively,which were higher than those of SImax and SMURF1 alone(P<0.05),the AUC of the combination of the two methods was 0.927,which was significantly higher than that of the two methods alone(Zcombined vs.SImax=3.999,P<0.001;Zcombined vs.SMURF1=3.270,P=0.001).Conclusion Contrast-enhanced ultrasound combined with serum SMURF1 detection can improve the diagnostic efficiency of thyroid cancer,which may avoid the over-diagnosis on the premise of ensuring the effective diagnosis of thyroid cancer patients.

Objective To investigate whether curcumin is a potential drug for the treatment of gastrointestinal stromal tumors(GIST).Methods The differential genes of imatinib-resistant cells and non-resistant cells were analyzed by cell transcriptology.The antitumor activity of curcumin was verified by cell counting kit-8(CCK-8)method,and the concentration of Curcumin ranged from 5 to 80 μg·mL-1for GIST-T1 and GIST-T1/IMR cells.20 μg·mL-1 Curcumin as the experimental group,phosphate buffered solution as the control group.The contents of interleukin-6(IL-6),reactive oxygen species(ROS)and nitric oxide(NO)were measured by enzyme linked immunosorbent assay.The cell cycle changes were analyzed by flow cytometry.Results Using non-resistant cells as a contrast,the results showed that there were 1 300 up-regulated genes and 1 609 down-regulated genes in imatinib-resistant cells.The 50％inhibiting concentration values of Curcumin on GIST-T1 and GIST-T1/IMR cells were(15.33±1.36)and(10.49±2.12)μg·mL-1,respectively.In GIST-T1 cells,the IL-6 levels in experimental group and control group were(3.45±0.01)and(5.64±0.42)pg·mL-1;the ROS levels were(2 841.42±81.83)and(4 174.32±439.12)pg·mL-1;the iNOS levels were(7.02±0.08)and(8.08±0.03)μmol·L-1,respectively.In GIST-T1/IMR cells,the IL-6 levels in experimental group and control group were(2.47±0.30)and(6.30±0.01)pg·mL-1;the ROS levels were(4 706.40±146.71)and(8 254.34±342.35)pg·mL-1;the iNOS levels were(6.42±0.09)and(7.29±0.04)μmol·L-1,respectively.Among the 2 cells,the differences of above indicators were statistically significant between the experimental group and the control group(P＜0.05,P＜0.01).Curcumin blocked the cell cycle of GIST-T1 and GIST-T1/IMR in G1 phase,further shortens S phase and G2 phase.Conclusion Curcumin can inhibit the secretion of inflammation and regulate the proliferation of GIST.

Quercetin can mediate the activation of mitogen-activated protein kinase(MAPK)signaling pathways to prevent osteoporosis(OP).This paper comprehensively discusses the interrelationship between MAPK and osteoporosis-related cells based on the latest domestic and international research.Additionally,it elucidates the research progress of quercetin in mediating the MAPK signaling pathway for OP prevention.The aim is to provide an effective foundation for the clinical prevention and treatment of OP and the in-depth development of quercetin.

Thioredoxin-1(Trx-1)is a petite redox protein primarily encountered in mammalian cells.It responds to alterations in the redox environment by facilitating electron transfer and regulating associated proteins.This paper provides a concise overview of Trx-1,focusing on its altered expression patterns during cerebral ischemia.The emphasis is on its neuroprotective attributes following cerebral ischemia,encompassing anti-oxidation,anti-inflammation,anti-apoptosis,promotion of cell growth,angiogenesis,and its involvement in cerebral ischemia-related pathologies.