Objective To explore the change pattern of quantitative parameters in contrast-enhanced computed tomography (CECT) scans during the cortical and nephrographic phases in patients with clear cell renal cell carcinoma (ccRCC), evaluate the diagnostic efficiency of these quantitative parameters in predicting the pathological grade of ccRCC preoperatively, and provide imaging reference for clinically evaluating preoperative disease severity and formulating individualized therapeutic regimens. Methods A retrospective analysis was performed on the clinical data of 84 patients with ccRCC treated in our hospital between September 2022 and September 2024. According to the World Health Organization/International Society of Urological Pathology (WHO/ISUP) pathological grading system, patients were divided into a high-grade group (n = 32) and a low-grade group (n = 52). CECT features and quantitative parameters were compared between the two groups. The relationships between CECT quantitative parameters and pathological grading in ccRCC patients were analyzed using Spearman correlation. The diagnostic value of these parameters for preoperative pathological grading was evaluated using receiver operating characteristic curves. Results The maximum tumor diameter and the proportion of tumors with blurred margins were higher in the high-grade group than in the low-grade group (P<0.05). The CT values, net enhancement values, and enhancement rates during both the cortical and nephrographic phases were lower in the high-grade group than in the low-grade group (P<0.05). Spearman correlation analysis showed that the CT values, net enhancement values, and enhancement rates during both the cortical and nephrographic phases were negatively correlated with preoperative pathological grades in ccRCC patients (P<0.05). Receiver operating characteristic curve analysis revealed that the area under the curve for preoperative pathological grading using the combination of cortical phase CT value, cortical phase net enhancement value, cortical phase enhancement rate, nephrographic phase CT value, nephrographic phase net enhancement value, and nephrographic phase enhancement rate was 0.912, which was higher than the areas for any individual parameter used alone (0.770, 0.748, 0.763, 0.751, 0.739, and 0.718, respectively; P<0.05). The sensitivity, specificity, and 95% confidence interval for the parameters used in combination were 96.88%, 69.23%, and 0.853-0.970, respectively. Conclusion CECT quantitative parameters were negatively correlated with pathological grades in patients with single ccRCC and demonstrated high diagnostic efficiency for pathological grading, providing a reference for clinical treatment planning.

ObjectiveTo explore the molecular mechanisms by which serum containing Gegen Qinlian Tang （GQT） inhibits glycolysis and enhances chemotherapy sensitivity in 5-fluorouracil （5-FU）-resistant colorectal cancer （CRC） cells based on the cyclin-dependent kinase 16 （CDK16）/MYC proto-oncogene （MYC） pathway. MethodsHCT-116/5-FU cells were treated with different concentrations （5%， 10%， 20%， 30%） of GQT-containing serum. Cell viability and 5-FU sensitivity were assessed using the cell counting kit-8 （CCK-8） assay， and the experimental concentrations of 5-FU and GQT for subsequent experiments were determined. Cell proliferation and apoptosis under individual 5-FU， GQT， and combined 5-FU + GQT treatments were evaluated using 5-ethynyl-2′-deoxyuridine （EDU） staining and annexin V-FITC/PI double staining， respectively. Glucose consumption， adenosine triphosphate （ATP） production， and lactate levels were measured by colorimetric assays. Expression levels of glycolysis-related proteins， CDK16， MYC， and phosphorylated MYC were detected by Western blot. Co-immunoprecipitation （CoIP） was used to examine the protein interaction between CDK16 and MYC， and cycloheximide （CHX） treatment was applied to assess the effect of CDK16 overexpression on MYC protein stability. ResultsCCK-8 assays showed that 2.5 mg·L^-1 5-FU significantly inhibited HCT-116 cell viability in a dose-dependent manner. In HCT-116/5-FU cells， significant inhibition was observed only at 5 mg·L^-1 5-FU （P<0.05）， which was used for model establishment. Compared with 5-FU alone， addition of 5% GQT-containing serum significantly suppressed HCT-116/5-FU cell viability （P<0.05）， with stronger inhibition at higher serum concentrations. Thus， 5% GQT-containing serum was used in subsequent experiments. Compared with the control group， 5-FU， GQT， and 5-FU + GQT treatments all significantly reduced cell proliferation （P<0.05） and increased apoptosis （P<0.01）. The 5-FU + GQT combination showed superior inhibition of proliferation compared with 5-FU or GQT alone （P<0.01）， accompanied by more pronounced reductions in glucose consumption， ATP production， and lactate generation （P<0.01）. Additionally， compared with control， 5-FU， and GQT groups， the 5-FU + GQT group exhibited stronger suppression of MYC and its phosphorylated forms （P<0.01） and greater inhibition of glycolytic enzymes， including hexokinase 2 （HK2）， 3-phosphoinositide-dependent protein kinase 1 （PDK1）， lactate dehydrogenase A （LDHA）， and pyruvate kinase M2 （PKM2） （P<0.01）. CDK16， MYC， and MYC phosphorylation expression levels were significantly downregulated in the 5-FU + GQT group compared with the 5-FU group （all P<0.01）. MYC protein stability decreased in a time-dependent manner in the 5-FU + GQT group （P<0.05）， which was rescued by CDK16 overexpression （P<0.05）. ConclusionGQT significantly enhances the sensitivity of HCT-116/5-FU cells to 5-FU， potentially by inhibiting CDK16 and thereby reducing MYC-mediated glycolysis.

ObjectiveTo explore the molecular mechanisms by which serum containing Gegen Qinlian Tang （GQT） inhibits glycolysis and enhances chemotherapy sensitivity in 5-fluorouracil （5-FU）-resistant colorectal cancer （CRC） cells based on the cyclin-dependent kinase 16 （CDK16）/MYC proto-oncogene （MYC） pathway. MethodsHCT-116/5-FU cells were treated with different concentrations （5%， 10%， 20%， 30%） of GQT-containing serum. Cell viability and 5-FU sensitivity were assessed using the cell counting kit-8 （CCK-8） assay， and the experimental concentrations of 5-FU and GQT for subsequent experiments were determined. Cell proliferation and apoptosis under individual 5-FU， GQT， and combined 5-FU + GQT treatments were evaluated using 5-ethynyl-2′-deoxyuridine （EDU） staining and annexin V-FITC/PI double staining， respectively. Glucose consumption， adenosine triphosphate （ATP） production， and lactate levels were measured by colorimetric assays. Expression levels of glycolysis-related proteins， CDK16， MYC， and phosphorylated MYC were detected by Western blot. Co-immunoprecipitation （CoIP） was used to examine the protein interaction between CDK16 and MYC， and cycloheximide （CHX） treatment was applied to assess the effect of CDK16 overexpression on MYC protein stability. ResultsCCK-8 assays showed that 2.5 mg·L^-1 5-FU significantly inhibited HCT-116 cell viability in a dose-dependent manner. In HCT-116/5-FU cells， significant inhibition was observed only at 5 mg·L^-1 5-FU （P<0.05）， which was used for model establishment. Compared with 5-FU alone， addition of 5% GQT-containing serum significantly suppressed HCT-116/5-FU cell viability （P<0.05）， with stronger inhibition at higher serum concentrations. Thus， 5% GQT-containing serum was used in subsequent experiments. Compared with the control group， 5-FU， GQT， and 5-FU + GQT treatments all significantly reduced cell proliferation （P<0.05） and increased apoptosis （P<0.01）. The 5-FU + GQT combination showed superior inhibition of proliferation compared with 5-FU or GQT alone （P<0.01）， accompanied by more pronounced reductions in glucose consumption， ATP production， and lactate generation （P<0.01）. Additionally， compared with control， 5-FU， and GQT groups， the 5-FU + GQT group exhibited stronger suppression of MYC and its phosphorylated forms （P<0.01） and greater inhibition of glycolytic enzymes， including hexokinase 2 （HK2）， 3-phosphoinositide-dependent protein kinase 1 （PDK1）， lactate dehydrogenase A （LDHA）， and pyruvate kinase M2 （PKM2） （P<0.01）. CDK16， MYC， and MYC phosphorylation expression levels were significantly downregulated in the 5-FU + GQT group compared with the 5-FU group （all P<0.01）. MYC protein stability decreased in a time-dependent manner in the 5-FU + GQT group （P<0.05）， which was rescued by CDK16 overexpression （P<0.05）. ConclusionGQT significantly enhances the sensitivity of HCT-116/5-FU cells to 5-FU， potentially by inhibiting CDK16 and thereby reducing MYC-mediated glycolysis.

Objective To explore the clinical efficacy of plasma exchange (PE) and double-filtration plasmapheresis (DFPP) pretreatment regimens for high-titer ABO-incompatible kidney transplantation (ABOi-KT). Methods A retrospective analysis was conducted on 31 cases of ABOi-KT with a follow-up period ≥1 year admitted to Zhongshan Hospital Affiliated to Fudan University from April 2016 to August 2025. The efficacy differences between the PE combined with rituximab (RTX) + oral triple immunosuppressive regimen and the DFPP combined with RTX + oral triple immunosuppressive regimen were compared and analyzed. The titers of blood group antibodies and serum creatinine levels before and after the operation were monitored. The survival curves and cumulative risk occurrence curves were plotted using the Kaplan-Meier method. The survival rates of recipients and transplanted kidneys and the occurrence of complications were analyzed. Results Both the PE regimen and the DFPP regimen may effectively reduce the preoperative blood group antibody titer of the recipients to ≤1∶16. The one-year survival rate of the recipients and the transplanted kidneys both reached 100% after the operation. The postoperative serum creatinine levels of recipients who received the DFPP regimen were lower and more stable. There was no statistically significant difference in the incidence of complications between the two regimens during the same follow-up period. Conclusions Both the PE and DFPP regimens are effective pretreatment regimens for ABOi-KT. The DFPP regimen has more advantages in reducing treatment operations, lowering drug dosage and maintaining the stability of postoperative renal function. For recipients with a high initial antibody titer (≥ 1∶32), individualized determination of the number and frequency of plasma processing for pretreatment may achieve ideal therapeutic effects.

Background Previous studies have found that exposure to benzo[a]pyrene (BaP) can lead to functional impairment of the human pancreas. Pancreatic and duodenal homeobox factor 1 (PDX-1) may play a role in regulating mitochondrial function. It is hypothesized that BaP exposure may interfere with PDX-1 expression in human pancreatic ductal epithelial cells (H6C7), thereby affecting mitochondrial transcription factor A (TFAM). This process could induce mitochondrial DNA (mtDNA) damage, disrupt pancreatic development and function, and elevate the risk of diabetes onset. Objective To investigate the mechanism of BaP-induced mtDNA damage through disruption of the PDX-1/TFAM pathway in a H6C7 cell model. Methods A H6C7 cell injury model was established using different concentrations of BaP. Cell viability was determined using cell counting kit-8 (CCK-8). After 24 h of BaP exposure (5,10, and 20 μmol·L⁻¹), cell morphological and mitochondrial membrane potential (MMP) changes were observed via confocalmicroscopy, and PDX-1/TFAM protein expression levels were assessed. Bioinformatics analysis combined with dual-luciferase reporter assays was used to confirm PDX-1 directly targeting the TFAM promoter. Following PDX-1 overexpression or silencing in BaP treated cells, flow cytometry was used to evaluate viability and apoptosis, while Western blot and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) measured PDX-1/TFAM expression and mitochondrial DNA copy number (mtDNA-cn). Results The cell injury model demonstrated that, compared with the control group, BaP exposure reduced cell viability, disrupted membrane integrity, induced nuclear fragmentation, and decreased MMP. Protein expression levels of PDX-1 and TFAM were significantly downregulated in the 10 and 20 μmol·L⁻¹ groups (P<0.05). Dual-luciferase reporter assays confirmed that PDX-1 overexpression upregulated TFAM levels. Flow cytometry revealed that PDX-1 overexpression significantly reduced apoptosis rate (P<0.001), whereas PDX-1 silencing increased apoptosis rate (P<0.001). Compared with the BaP-only group, BaP+PDX-1 overexpression elevated TFAM protein and mRNA expression as well as mtDNA-cn (P<0.01), while BaP+siRNA-PDX-1 suppressed these parameters (P<0.001). Conclusion BaP exposure promotes apoptosis in human pancreatic cells. PDX-1, a key gene in pancreatic development, regulates the expression of TFAM, a core regulator of mitochondrial function. This interaction triggers changes in MMP and mtDNA-cn, activates the PDX-1/TFAM/mtDNA axis, and ultimately leads to pancreatic cell injury.

Background Previous studies have found that exposure to benzo[a]pyrene (BaP) can lead to functional impairment of the human pancreas. Pancreatic and duodenal homeobox factor 1 (PDX-1) may play a role in regulating mitochondrial function. It is hypothesized that BaP exposure may interfere with PDX-1 expression in human pancreatic ductal epithelial cells (H6C7), thereby affecting mitochondrial transcription factor A (TFAM). This process could induce mitochondrial DNA (mtDNA) damage, disrupt pancreatic development and function, and elevate the risk of diabetes onset. Objective To investigate the mechanism of BaP-induced mtDNA damage through disruption of the PDX-1/TFAM pathway in a H6C7 cell model. Methods A H6C7 cell injury model was established using different concentrations of BaP. Cell viability was determined using cell counting kit-8 (CCK-8). After 24 h of BaP exposure (5,10, and 20 μmol·L⁻¹), cell morphological and mitochondrial membrane potential (MMP) changes were observed via confocalmicroscopy, and PDX-1/TFAM protein expression levels were assessed. Bioinformatics analysis combined with dual-luciferase reporter assays was used to confirm PDX-1 directly targeting the TFAM promoter. Following PDX-1 overexpression or silencing in BaP treated cells, flow cytometry was used to evaluate viability and apoptosis, while Western blot and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) measured PDX-1/TFAM expression and mitochondrial DNA copy number (mtDNA-cn). Results The cell injury model demonstrated that, compared with the control group, BaP exposure reduced cell viability, disrupted membrane integrity, induced nuclear fragmentation, and decreased MMP. Protein expression levels of PDX-1 and TFAM were significantly downregulated in the 10 and 20 μmol·L⁻¹ groups (P<0.05). Dual-luciferase reporter assays confirmed that PDX-1 overexpression upregulated TFAM levels. Flow cytometry revealed that PDX-1 overexpression significantly reduced apoptosis rate (P<0.001), whereas PDX-1 silencing increased apoptosis rate (P<0.001). Compared with the BaP-only group, BaP+PDX-1 overexpression elevated TFAM protein and mRNA expression as well as mtDNA-cn (P<0.01), while BaP+siRNA-PDX-1 suppressed these parameters (P<0.001). Conclusion BaP exposure promotes apoptosis in human pancreatic cells. PDX-1, a key gene in pancreatic development, regulates the expression of TFAM, a core regulator of mitochondrial function. This interaction triggers changes in MMP and mtDNA-cn, activates the PDX-1/TFAM/mtDNA axis, and ultimately leads to pancreatic cell injury.

The European Society of Cardiology (ESC) released the "2024 ESC guidelines for the management of elevated blood pressure and hypertension" on August 30, 2024. This guideline updates the 2018 "Guidelines for the management of arterial hypertension." One notable update is the introduction of the concept of "elevated blood pressure" (120-139/70-89 mm Hg). Additionally, a new systolic blood pressure target range of 120-129 mm Hg has been proposed for most patients receiving antihypertensive treatment. The guideline also includes numerous additions or revisions in areas such as non-pharmacological interventions and device-based treatments for hypertension. This article interprets the guideline's recommendations on definition and classification of elevated blood pressure and hypertension, and cardiovascular disease risk assessment, diagnosing hypertension and investigating underlying causes, preventing and treating elevated blood pressure and hypertension. We provide a comparison interpretation with the 2018 "Guidelines for the management of arterial hypertension" and the "2017 ACC/AHA guideline on the prevention, detection, evaluation, and management of high blood pressure in adults."

Diabetic macular edema(DME), a serious complication of diabetic retinopathy(DR), is a chronic condition caused by multiple factors. Throughout its progression, inflammatory factors and vascular endothelial growth factor(VEGF)play a critical role. Anti-VEGF drugs have shown significant effectiveness in the treatment of DME; however, some patients may experience persistent DME after injection or require frequent injections. Dexamethasone intravitreal implants(DEX implants)serve as a sustained-release implant characterized by a reasonable release profile and high bioavailability. They offer safe, effective, and prolonged anti-inflammatory effects, aiding in the repair of retinal barrier and reduction of exudation. To further enhance patients' visual quality, exploring the efficacy of DEX implants in combination with existing treatment regimens has great clinical significance. This review primarily discusses the research advancements in DEX implants, focusing on their pharmacological properties, indications for use, and their combination with existing drugs and treatment methods. It also evaluates the advantages and disadvantages of combination therapy or switching to DEX implants compared to current standard treatments, aiming to provide guidance for personalized treatment options for patients with DME.

To understand the background of Escherichia coli(E.coli)carried by artificially bred sika deer and the biological characteristics of the isolated strains,such as drug resistance and pathogenicity,in April 2024,we collected 184 fresh deer fecal samples from four deer farms in Luxiang Township,Shuangyang District,Changchun City,Jilin Province,for isolation and cultivation of E.coli.The isolates were tested for drug resistance and biochemical identification with a BD PhoenixTM-100 Automated Microbiology System.The virulence genes were detected with PCR,and the strains were molecularly typed with ERIC-PCR.A total of 165 E.coli strains were isolated from 184 samples of deer feces,with an isolation rate of 89.67%.Twenty strains had a drug resistance phenotype,and the drug resistance rate was 12.12%;these strains included 15 strains of multi-drug resistant bacteria and 11 strains of ESBL-producing bacteria.Virulence gene detection indicated that the sika deer isolates carried multiple diarrhea-associated virulence genes,such as EAST-1(12.12%),eae(1.21%),stx1(7.88%),stx2(7.27%),and STa(1.82%).ERIC-PCR demonstrated that the isolates showed high polymorphism.The ESBL-producing E.coli carried by sika deer are likely to spread drug resistance in the community and livestock population.Some isolates carried multiple diarrhea-associated virulence genes,thus posing a human transmission risk.Therefore,monitoring of drug resistance and virulence genes must be strengthened,and antibiotics must be used reasonably during the breeding process to avoid excessive use and misuse.

Objective To study the clinical features,management,and outcomes of benign lesions of the vocal folds in children.Methods A retrospective study was conducted on 686 children diagnosed with benign lesions of vocal folds from 2010 to 2021.The clinical features were analyzed.One hundred children with follow-up records were divided in-to conservative observation group(66 cases)and surgical treatment group(34 cases),and the outcomes was analyzed.Results A total of 455(66.3％)children with benign lesions of vocal folds were boys,and most children(249 cases,36.3％)were within the age group of 6～10 years old.Vocal fold polyps were the most common cases(451 cases,65.7％).The long-term effective rates of the conservative observation and the surgery groups were 63.6％and 79.4％,respectively.The recurrence rate of vocal fold polyps was 31.8％in children aged 3 to 10 years.All the children with vocal fold cyst failed to respond to conservative treatment.Conclusion Benign lesions in children are more common in boys and those aged 6～10 years old,and vocal fold polyps being the most common lesions.Conservative observation is preferred when children with vocal fold polyps are under six years old,and surgical treatment is considered when they are aged 10 and above.Surgery is recommended for children with vocal fold cysts.