Objective To evalvate the efficacy of patient-controlled epidural analgesia (PCEA) combined with ganciclovir for treatment of postherpetic neuralgia in patients.Methods A total of 60 patients with PHN,aged 51-86 yr,of ASA physical status Ⅰ-Ⅲ,were randomly assigned into 2 groups (n =30 each) using a random number table:ganciclovir group (F group) and PCEA combined with ganciclovir group (FB group).In FB and F groups,ganciclovir 0.25 g was infused intravenously twice a day for 7 consecutive days.In addition,continuous PCEA was performed simultaneously in group FB and the PCEA solution contained ropivacaine 300 mg,prednisolone 20 mg and dezocine 10 mg in 250 ml of normal saline.At 1 day before treatment (T0) and 7 days,1 month,and 6 months after treatment (T1-3),pain was assessed with visual analogue scale (VAS),and the quality of life (QOL) score and pair relief rate were recorded.Results VAS and QOL scores were significantly lower at T1-3 than at T0 in the two groups.Compared with F group,VAS scores were significantly decreased,and QOL score and pain relief rate were increased at T1-3 in FB group.Conclusion PCEA combined with ganciclovir can effectively alleviate postherpetic neuralgia in the patients.

Objective To explore the molecular mechanism of Yixin Tongbi Mixture in the intervention of atherosclerosis(AS).Methods Thirty-six SD rats were divided into the normal control group,model con-trol group,low dose Yixin Tongbi Mixture group,medium dose Yixin Tongbi Mixture group,high dose Yixin Tongbi Mixture group and atorvastatin group,6 cases in each group.Except the normal control group,the oth-er groups adopted the high fat vitamin D3 mixed feed gavage for constructing the rat AS model.The low dose,medium dose and high doses Yixin Tongbi Mixture groups were gavaged by 10,20,40 g/kg Yixin Tongbi Mixture.The atorvastatin group was gavaged by 5 mg/kg atorvastatin;and the normal control group and mod-el control group were gavaged by placebo once a day for consecutive 14 d.The pathological changes of aortic tissues were observed by HE staining.The levels of serum TC,TG,HDL and LDL were detected by automatic biochemical analyzer.The expression levels of IL-6,TNF-α and ICAM-1 in aortic tissue were detected by ELISA.The expression levels of MMP-2 and MMP-9 in aortic tissue and Bax and Bcl-2 protein expression lev-els in cardiac tissue were detected by Western blot.Results Compared with the normal control group,the aor-tic wall of the model control group rats was significantly thickened,and the levels of serum TC,TG,HDL and LDL were increased.The expression levels of MMP-2,MMP-9,IL-6,TNF-α and ICAM-1 in the aortic tissues were also increased.The expression level of Bax in the myocardial tissues was increased,while the expression level of Bcl-2 was decreased,and the differences were statistically significant(P＜0.05).Compared with the model control group,the above indicators in the medium dose and high doses Yixin Tongbi Mixture groups and atorvastatin group were significantly improved(P＜0.05).Except Bax,IL-6 and ICAM-1 expression lev-els,the other indicators in the low dose Yixin Tongbi Mixture group had no statistically significant differences(P＞0.05).Conclusion Yixin Tongbi Mixture could inhibit the AS occurrence and development by inhibiting inflammation and cellular apoptosis,and its mechanism is related to the abnormal expression of IL-6/TNF-αand MMP-2/MMP-9.

【Objective】 To analyze the position of the feeding artery entering the renal cell carcinoma (RCC) with 3D Slicer software, so as to explore the distribution pattern of the tumor artery and to provide an anatomical basis for the accurate surgical resection. 【Methods】 The clinical data of RCC patients who underwent partial nephrectomy in the Department of Urology, The Second Affiliated Hospital of Xi'an Jiaotong University during Jan.2021 and Jun.2022 were collected.The preoperative renal artery CT angiography data were imported into 3D Slicer software in DICOM format to construct the relative positions of tumor-feeding artery from horizontal, sagittal and coronary planes.The number and distribution of tumor feeding arteries in each plane were analyzed. 【Results】 A total of 112 patients (59 male and 53 female) with single tumor were involved.RENAL score was 4-10.The tumor stages were T1a in 58 cases, T1b in 48 cases, and T2a in 6 cases.Among them, 38 cases (33.93%) had 1 tumor artery, 53 cases (47.32%) had 2 tumor arteries, and 21 cases (18.75%) had 3 tumor arteries.Of these 207 tumor arteries, 22 (10.63%) entered the tumor through the superficial part of the tumor bed, and 185 (89.37%) through the deep part. 【Conclusion】 In localized RCC, nearly 90% of the feeding arteries enter the tumor from deep part of the tumor bed, which provides an anatomical basis for accurate tumor resection and wound suture in partial nephrectomy.

Pathological vascular remodeling is a hallmark of various vascular diseases. Previous research has established the significance of andrographolide in maintaining gastric vascular homeostasis and its pivotal role in modulating endothelial barrier dysfunction, which leads to pathological vascular remodeling. Potassium dehydroandrographolide succinate (PDA), a derivative of andrographolide, has been clinically utilized in the treatment of inflammatory diseases precipitated by viral infections. This study investigates the potential of PDA in regulating pathological vascular remodeling. The effect of PDA on vascular remodeling was assessed through the complete ligation of the carotid artery in C57BL/6 mice. Experimental approaches, including rat aortic primary smooth muscle cell culture, flow cytometry, bromodeoxyuridine (BrdU) incorporation assay, Boyden chamber cell migration assay, spheroid sprouting assay, and Matrigel-based tube formation assay, were employed to evaluate the influence of PDA on the proliferation and motility of smooth muscle cells (SMCs). Molecular docking simulations and co-immunoprecipitation assays were conducted to examine protein interactions. The results revealed that PDA exacerbates vascular injury-induced pathological remodeling, as evidenced by enhanced neointima formation. PDA treatment significantly increased the proliferation and migration of SMCs. Further mechanistic studies disclosed that PDA upregulated myeloid differentiation factor 88 (MyD88) expression in SMCs and interacted with T-cadherin (CDH13). This interaction augmented proliferation, migration, and extracellular matrix deposition, culminating in pathological vascular remodeling. Our findings underscore the critical role of PDA in the regulation of pathological vascular remodeling, mediated through the MyD88/CDH13 signaling pathway.
Mice ; Rats ; Animals ; Myeloid Differentiation Factor 88/metabolism* ; Vascular Remodeling ; Cell Proliferation ; Vascular System Injuries/pathology* ; Carotid Artery Injuries/pathology* ; Molecular Docking Simulation ; Muscle, Smooth, Vascular ; Cell Movement ; Mice, Inbred C57BL ; Signal Transduction ; Succinates/pharmacology* ; Potassium/pharmacology* ; Cells, Cultured ; Diterpenes ; Cadherins