BACKGROUND:In the initial stage of growth plate injury inflammation,platelet-derived growth factor BB promotes the repair of growth plate injury by promoting mesenchymal progenitor cell infiltration,chondrogenesis,osteogenic response,and regulating bone remodeling. OBJECTIVE:To elucidate the action mechanism of platelet-derived growth factor BB after growth plate injury. METHODS:PubMed,VIP,WanFang,and CNKI databases were used as the literature sources.The search terms were"growth plate injury,bone bridge,platelet-derived growth factor BB,repair"in English and Chinese.Finally,66 articles were screened for this review. RESULTS AND CONCLUSION:Growth plate injury experienced early inflammation,vascular reconstruction,fibroossification,structural remodeling and other pathological processes,accompanied by the crosstalk of chondrocytes,vascular endothelial cells,stem cells,osteoblasts,osteoclasts and other cells.Platelet-derived growth factor BB,as an important factor in the early inflammatory response of injury,regulates the injury repair process by mediating a variety of cellular inflammatory responses.Targeting the inflammatory stimulation mediated by platelet-derived growth factor BB may delay the bone bridge formation process by improving the functional activities of osteoclasts,osteoblasts,and chondrocytes,so as to achieve the injury repair of growth plate.Platelet-derived growth factor BB plays an important role in angiogenesis and bone repair tissue formation at the injured site of growth plate and intrachondral bone lengthening function of uninjured growth plate.Inhibition of the coupling effect between angiogenesis initiated by platelet-derived growth factor BB and intrachondral bone formation may achieve the repair of growth plate injury.

This study was a single-center cross-sectional investigation aimed at identifying risk factors for cognitive dysfunction in patients undergoing maintenance hemodialysis (MHD), with the goal of providing a basis for improving patient prognosis. Patients receiving MHD in the Blood Purification Center of Hainan Provincial People's Hospital from June 1 to June 30, 2023, were enrolled. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), and potential risk factors for cognitive impairment were analyzed by using Logistic regression. A total of 278 patients were included, 69 patients (24.8%) of whom had cognitive impairment. Multivariate Logistic regression analysis indicated that the history of cerebrovascular disease ( OR=3.109, 95% CI 1.310-7.378, P=0.010), old age ( OR=1.077, 95% CI 1.040-1.115, P<0.001), low dialysis frequency ( OR=0.270, 95% CI 0.120-0.606, P=0.001), low academic qualification (using college/university as the control group: primary school group OR=26.960, 95% CI 7.519-96.673, P<0.001; Junior high school/technical secondary school group OR=4.264, 95% CI 1.330-13.650, P=0.015; High school group OR=9.554, 95% CI 2.861-31.904, P<0.001), high β2-microglobulin ( OR=1.609, 95% CI 1.044-2.480, P=0.031) and high C-reactive protein/albumin ( OR=2.672, 95% CI 1.226-5.826, P=0.013) were independent risk factors for cognitive impairment in MHD patients.

Autogenous arteriovenous fistula (AVF), compared to other vascular access routes, offers the advantages of stable blood flow, fewer complications, and a longer service life, making it the primary type of vascular access and the first choice for hemodialysis patients. The failure rate of AVF maturation is as high as 20% to 60%, primarily due to intimal hyperplasia following AVF surgery. Currently, the origin, function, and differentiation status of neointimal cells are not well understood, and most knowledge about neointimal cells was inferred from arterial neointima in non-AVF systems. Understanding the source of neointimal cells in AVF is crucial for experimental design and effectively providing strategies to reduce intimal hyperplasia. This article reviews the situation of venous intimal hyperplasia in patients with stage 5 chronic kidney disease, the relationship between changes in venous vessel wall and neointimal cells after AVF surgery, and the effects of outer membrane fibroblasts, local smooth muscle cells, and circulating bone marrow progenitor cells on AVF intimal hyperplasia. It is hoped that this will provide a reference for the treatment of intimal hyperplasia and experimental research.

Objective:To analyze effect of miR-532-3p on macrophage polarization in rats with chronic kidney disease(CKD)through targeted inhibition of Notch1 signal pathway.Methods:A total of 75 SD rats were divided into control group,CKD group,ago-NC group,ago-miR-532-3p group and FLI-06 group,except for control group,CKD models were constructed and corresponding plas-mids and inhibitors were injected,control group and CKD group were replaced with same amount of normal saline.Serum creatinine(Scr),blood urea nitrogen(BUN),TNF-α,IL-1β and IL-10 were measured by ELISA,HE staining and Masson staining were used to observe renal tissue pathology and renal fibrosis in rats,flow cytometry was used to detect CD11c+and CD206+of macrophages,miR-532-3p expression in rat kidney tissue was detected by qRT-PCR,Notch1 protein was detected by Western blot;target binding of miR-532-3p to Notch1 was determined by double luciferase reporter gene.Results:Structure of glomerulus,renal tubules and epithelial cells was complete,cell boundaries were clear,and cells were arranged neatly in control group;glomerular epithelial cell necrosis,mesangial matrix,glomerulosclerosis,inflammatory cell infiltration and renal fibrosis were increased in CKD group;compared with CKD group,damage degree of glomerulus and tubules,inflammatory infiltration cells and renal fibrosis degree in ago-miR-532-3p group and FLI-06 group were reduced;compared with control group,serum Scr,BUN,TNF-α,IL-1β,proportion of CD11c+,CD11c+/CD206+and Notch1 protein expression in macrophages of renal tissue were increased,serum IL-10 level,CD206+and miR-532-3p in renal tissue were decreased(P<0.05);compared with CKD group,serum Scr,BUN,TNF-α,IL-1β,proportion of CD11c+,CD11c+/CD206+and Notch1 protein expression in macrophages of renal tissue in ago-miR-532-3p group and FLI-06 group were decreased,serum IL-10 level,CD206+and miR-532-3p in renal tissue were increased(P<0.05);miR-532-3p targeted Notch1,and overexpression of miR-532-3p inhibited Notch1 protein expression.Conclusion:Promoting expression of miR-532-3p protects kidney tissue of CKD rats by inhibiting Notch1 pathway,which may be due to regulating polarization of macrophages.

Objective:To analyze effect of miR-532-3p on macrophage polarization in rats with chronic kidney disease(CKD)through targeted inhibition of Notch1 signal pathway.Methods:A total of 75 SD rats were divided into control group,CKD group,ago-NC group,ago-miR-532-3p group and FLI-06 group,except for control group,CKD models were constructed and corresponding plas-mids and inhibitors were injected,control group and CKD group were replaced with same amount of normal saline.Serum creatinine(Scr),blood urea nitrogen(BUN),TNF-α,IL-1β and IL-10 were measured by ELISA,HE staining and Masson staining were used to observe renal tissue pathology and renal fibrosis in rats,flow cytometry was used to detect CD11c+and CD206+of macrophages,miR-532-3p expression in rat kidney tissue was detected by qRT-PCR,Notch1 protein was detected by Western blot;target binding of miR-532-3p to Notch1 was determined by double luciferase reporter gene.Results:Structure of glomerulus,renal tubules and epithelial cells was complete,cell boundaries were clear,and cells were arranged neatly in control group;glomerular epithelial cell necrosis,mesangial matrix,glomerulosclerosis,inflammatory cell infiltration and renal fibrosis were increased in CKD group;compared with CKD group,damage degree of glomerulus and tubules,inflammatory infiltration cells and renal fibrosis degree in ago-miR-532-3p group and FLI-06 group were reduced;compared with control group,serum Scr,BUN,TNF-α,IL-1β,proportion of CD11c+,CD11c+/CD206+and Notch1 protein expression in macrophages of renal tissue were increased,serum IL-10 level,CD206+and miR-532-3p in renal tissue were decreased(P<0.05);compared with CKD group,serum Scr,BUN,TNF-α,IL-1β,proportion of CD11c+,CD11c+/CD206+and Notch1 protein expression in macrophages of renal tissue in ago-miR-532-3p group and FLI-06 group were decreased,serum IL-10 level,CD206+and miR-532-3p in renal tissue were increased(P<0.05);miR-532-3p targeted Notch1,and overexpression of miR-532-3p inhibited Notch1 protein expression.Conclusion:Promoting expression of miR-532-3p protects kidney tissue of CKD rats by inhibiting Notch1 pathway,which may be due to regulating polarization of macrophages.

This study was a single-center cross-sectional investigation aimed at identifying risk factors for cognitive dysfunction in patients undergoing maintenance hemodialysis (MHD), with the goal of providing a basis for improving patient prognosis. Patients receiving MHD in the Blood Purification Center of Hainan Provincial People's Hospital from June 1 to June 30, 2023, were enrolled. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), and potential risk factors for cognitive impairment were analyzed by using Logistic regression. A total of 278 patients were included, 69 patients (24.8%) of whom had cognitive impairment. Multivariate Logistic regression analysis indicated that the history of cerebrovascular disease ( OR=3.109, 95% CI 1.310-7.378, P=0.010), old age ( OR=1.077, 95% CI 1.040-1.115, P<0.001), low dialysis frequency ( OR=0.270, 95% CI 0.120-0.606, P=0.001), low academic qualification (using college/university as the control group: primary school group OR=26.960, 95% CI 7.519-96.673, P<0.001; Junior high school/technical secondary school group OR=4.264, 95% CI 1.330-13.650, P=0.015; High school group OR=9.554, 95% CI 2.861-31.904, P<0.001), high β2-microglobulin ( OR=1.609, 95% CI 1.044-2.480, P=0.031) and high C-reactive protein/albumin ( OR=2.672, 95% CI 1.226-5.826, P=0.013) were independent risk factors for cognitive impairment in MHD patients.

Autogenous arteriovenous fistula (AVF), compared to other vascular access routes, offers the advantages of stable blood flow, fewer complications, and a longer service life, making it the primary type of vascular access and the first choice for hemodialysis patients. The failure rate of AVF maturation is as high as 20% to 60%, primarily due to intimal hyperplasia following AVF surgery. Currently, the origin, function, and differentiation status of neointimal cells are not well understood, and most knowledge about neointimal cells was inferred from arterial neointima in non-AVF systems. Understanding the source of neointimal cells in AVF is crucial for experimental design and effectively providing strategies to reduce intimal hyperplasia. This article reviews the situation of venous intimal hyperplasia in patients with stage 5 chronic kidney disease, the relationship between changes in venous vessel wall and neointimal cells after AVF surgery, and the effects of outer membrane fibroblasts, local smooth muscle cells, and circulating bone marrow progenitor cells on AVF intimal hyperplasia. It is hoped that this will provide a reference for the treatment of intimal hyperplasia and experimental research.

OBJECTIVE To prepare a self-microemulsifying drug delivery system(SMEDDS) for the oral administration of nebivolol hydrochloride(NBH) and to conduct in vitro evaluation. METHODS The solubility of NBH was determined using various oil phases, surfactants, and co-surfactants. The composition of the blank self-microemulsifying formulation was determined using pseudo-ternary phase diagrams. A centralcomposite design-response surface method was employed to screen and optimize the formulation variables, and an excess amount of NBH raw material was incorporated to determine the drug loading capacity. RESULTS The optimized composition of the NBH-SMEDDS formulation consisted of medium-chain glycerides, capryl caproyl macrogol glycerides, and 2-(2-ethoxyethoxy) ethyl acetate at a ratio of 20∶48∶32, with a drug loading capacity of 20.05 mg. The particle size, self-emulsification time, and particle size distribution range of the formulation were in agreement with the predicted values. Dissolution testing demonstrated that the overall dissolution trend of NBH-SMEDDS in the medium was higher than that of NBH powder and NBH ordinary tablet. The stability of NBH-SMEDDS was found to be satisfactory under accelerated conditions for 1, 2, and 3 months. CONCLUSION The SMEDDS shows potential for enhancing the in vitro dissolution of NBH and demonstrates good stability.

OBJECTIVE To solve the problem of insolubility of itraconazole, improve its dissolution in vitro, and provide a reference for further industrial scale-up of the itraconazole multiparticle system. METHODS Itraconazole multiparticle system pellets were dissolved in an organic solvent and prepared in a fluidized bed by bottom spraying. Itraconazole and hydroxypropyl methylcellulose were sprayed onto the surface of the sucrose pellet core to form a uniform solid dispersion. The preparation parameters of the fluidized bed bottom spray coating were investigated by single factor method. The mass ratio of drug to carrier and core weight gain of the itraconazole multiparticle system were optimized by central composite design and response surface methodology with accumulative dissolution rate, application efficiency and adhesion rate as response values. Samples were prepared to verify the optimized prescription, the microscopic hierarchical structure of the itraconazole multiparticle system was observed by scanning electron microscope, and the solid dispersion in the itraconazole multiparticle system pellets was characterized by differential scanning calorimetry(DSC) and X-ray diffraction(XRD). The dissolution curves of itraconazole pellets and the physical mixture in 0.1 mol·L−1 HCl dissolution medium were compared to verify the solubilization effect. RESULTS Single factor method was used to determine the bottom spray coating parameters of the fluidized bed. The pumping speed was set as 3.0−5.0 mL·min−1, the atomization pressure was set as 1.5 bar, the inlet air volume was set as 110 m3·h−1, and the material temperature was set as 35 ℃. According to the central composite design and response surface methodology, the mass ratio of drug to carrier of the optimized prescription was 1∶1.5 and the core weight of the pill was 75%, and the response values reached the expected value. The result of scanning electron microscopy showed that the diameter of the itraconazole multiparticle system pellet was about 910 µm, the diameter of the sucrose pellet core was about 570 µm, the thickness of the drug loading layer was about 110 µm, and the thickness of encapsulation layer was about 11 µm. The results of DSC and XRD showed that itraconazole formed a uniform solid dispersion in the itraconazole multiparticle system pellets, which was amorphous. In the dissolution medium of 0.1 mol·L−1 HCl, the accumulative dissolution rate of the multiparticle system after 90 min was about 10 times that of the physical mixture, which showed that the solubilization effect was remarkable. CONCLUSION The dissolution of itraconazole in vitro can be significantly improved by processing itraconazole into pellets with multiparticle system and forming solid dispersion.

Objective:To investigate the clinical application value of commonly used preoperative indicators of sarcopenia in predicting postoperative pneumonia in patients aged 70 years and above with esophageal cancer.Methods:A retrospective analysis was conducted on the clinical data of 398 elderly patients(≥70 years old)with esophageal squamous cell carcinoma who underwent thoracic laparoscopic radical resection of esophageal cancer in our hospital from January 2020 to December 2021.The study aimed to investigate the correlation between clinical pathological indicators and commonly used measurement indicators of sarcopenia and postoperative pneumonia.Statistical analysis was performed to analyze the data.Results:The study found that the proportion of postoperative pneumonia in esophageal squamous cell carcinoma patients aged 70 years and above was 27.9%(111 out of 398). The pneumonia group had significantly lower preoperative BMI and peak expiratory flow(PEF)measurements compared to the non-pneumonia group, with statistically significant differences( t=2.799, 2.674, both P<0.05). Logistic multivariate analysis revealed that low PEF, low psoas major muscle index(PMI), and low psoas muscle density(PMD)were the primary risk factors for postoperative pneumonia in esophageal cancer patients aged 70 years and above(Wald χ2 values were 7.577, 6.091, 6.845, all P<0.05). The risk of postoperative pneumonia in esophageal cancer patients aged 70 years and above with low PEF, low PMI, and low PMD was found to be 1.969 times higher(95% CI: 1.215-3.185, P=0.006), 1.912 times higher(95% CI: 1.143-3.205, P=0.014), and 1.832 times higher(95% CI: 1.164-2.882, P=0.009)respectively, compared to patients with high PEF, high PMI, and high PMD. Conclusions:Low PEF, low PMI, and low PMD are significant risk factors for postoperative pneumonia in esophageal cancer patients aged 70 years and older.Preoperative PEF, PMI, and PMD, which are commonly utilized measurement indicators for sarcopenia, can be utilized as early screening indicators for postoperative pneumonia.