Gleason score 7 prostate cancer comprises two biologically distinct subgroups—Gleason 3 + 4 and Gleason 4 + 3—with differing prognoses and therapeutic implications. However, reliable non-invasive methods to distinguish these subtypes prior to treatment remain limited. This exploratory study evaluated whether systemic inflammatory markers and prostate volume (PV) provide preliminary signals differentiating Gleason 3 + 4 from 4 + 3 disease. We analyzed 26 patients with biopsy-confirmed Gleason score 7 prostate cancer (3 + 4, n = 15; 4 + 3, n = 11). Pre-biopsy complete blood counts were used to calculate inflammation-based indices, including neutrophil-to-lymphocyte-to-platelet ratio (NLPR), systemic immune-inflammation index (SII), and others. Prostate volume (PV) was measured by a transrectal ultrasonography. Group comparisons used non-parametric tests, and receiver operating characteristic (ROC) analyses were performed. NLPR and PV showed modest separation between groups (NLPR AUC = 0.715; PV AUC = 0.709). Most other inflammatory markers-including NLR, PLR, MLR, AISI and SIRI-showed limited discriminatory performance. A multivariable combining NLPR and PV yielded an AUC of 0.776, which improved to 0.82 after adding SII. Given the very small cohort size (n = 26), these findings should be regarded strictly as preliminary and hypothesis-generating. This exploratory analysis suggests that NLPR and PV may reflect biological difference between Gleason 3 + 4 and 4 + 3 tumors. These observations require validation in larger, prospective, multi-institutional cohorts before any clinical interpretation or application can be considered.

Objective Prostate-specific antigen (PSA) testing is widely used for prostate cancer (PCa) screening; however, its limited specificity remains a major challenge, as elevated PSA levels also occur in benign prostatic hyperplasia (BPH). Systemic inflammatory markers, including neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and systemic immune-inflammation index (SII), have been proposed as adjunctive diagnostic tools. Method This retrospective study included 100 patients (50 PCa and 50 BPH) who underwent transrectal ultrasound-guided prostate biopsy between October 2018 and October 2021. Clinical data, including PSA, prostate volume (PV), and complete blood counts, were collected. Inflammatory indices were calculated and evaluated using receiver operating characteristic (ROC) analysis. Results NLR, MLR, RLR, and SII were significantly elevated in PCa patients (p < 0.05). However, their individual diagnostic performance was modest (AUC range: 0.624–0.656). The combined inflammatory model showed limited improvement (AUC = 0.662). In contrast, PV demonstrated superior diagnostic accuracy (AUC = 0.774) with high specificity. When combined with inflammatory markers, PV further improved predictive performance, achieving a positive predictive value of 70.3% and a negative predictive value of 73.9%. Conclusion Systemic inflammatory markers alone have limited diagnostic value in distinguishing PCa from BPH. However, their combination with prostate volume may enhance diagnostic accuracy and provide a simple, non-invasive approach for risk stratification in clinical practice.

Introduction:Evidence on the impact of different stent sizes on stone-free rate (SFR) and ureteral stent-related symptom questionnaire (USSQ) scores in endoscopic lithotripsy remains limited. This study aimed to evaluate the effects of 2 commonly used double-J stents of different diameters on these outcomes. Material and methods:We retrospectively reviewed 108 patients with upper urinary tract stones who underwent lithotripsy between January 2022 and December 2023. Patients were stratified into 4.7F and 6F groups based on stent diameter. Primary outcomes were SFR at 24 h and 30 days. USSQ scores and complications were compared between groups. Results:SFR was similar between groups at 24 h (52.5% vs 55.1%; p = 0.791) and 30 days (74.6% vs 77.6%; p = 0.719). USSQ scores were comparable (Urinary Symptoms: 29 vs 29, p = 0.473; Body Pain: 12 vs 12.5, p = 0.347; General Health: 13 vs 13, p = 0.706; Work Performance: 8 vs 8, p = 0.072; Sexual Matters: 4 vs 3, p = 0.242; Additional Problems: 12 vs 12, p = 0.485). More patients in the 4.7F group reported hematuria (83.1% vs 69.4%; p = 0.094) and changes in daily work activities. Many experienced body pain (76.9%) and absence of sexual activity (88.9%). No complications exceeded grade II. Conclusions:Both 4.7F and 6F stents showed similar efficacy and safety. Stent size did not significantly impact USSQ scores or SFR.

The incidence of prostate cancer (PCa) is increasing annually, making it the leading cause of tumor-related mortality in males. The available treatment options for metastatic PCa are limited. Vasculogenic mimicry (VM), an emerging phenomenon involving aggressive tumor cells, has a significant impact on patient survival. Misregulation of Wnt5a expression is commonly observed during cancer progression. However, there is a lack of comprehensive studies investigating the effects of Wnt5a on tumor VM formation. In this study, we demonstrate that alterations in wnt5a expression, either through gain or loss, have a significant influence on the formation of VM in tumor cells mediated by cell stemness and EMT progression. Further research has demonstrated that Wnt5a regulates the formation of VM through the PI3K/JNK signaling pathway. These experimental findings offer a novel avenue for the clinical management of prostate cancer.

Prostate cancer (PCa) is the most prevalent cancer in men and the leading cause of cancer-related mortality. Recent studies have highlighted the pivotal role of glycolysis in tumor progression. This study aimed to investigate the involvement of the EDNRB gene and its ligand endothelin 3 (EDN3) in glycolysis in PCa and to elucidate its underlying molecular mechanism. Quantitative reverse transcription PCR (RT-qPCR) and methylation-specific PCR (MSP) were used to probe EDNRB expression and methylation in PCa tissues. Cell proliferation and glycolysis in PCa cells were evaluated using Cell Counting Kit-8 (CCK-8), EDU staining, Seahorse assay, and biochemical kits to analyze the effects of EDN3/EDNRB. The underlying molecular mechanism was further explored through Western blotting. The in vivo effect of EDNRB on tumor growth was examined using a xenograft tumor model. Our findings revealed that EDNRB was hypermethylated and downregulated in PCa tissues and cell lines. Overexpression of EDNRB or EDN3 led to reduced cell proliferation and downregulation of glycolytic markers. EDNRB also decreased the extracellular acidification rate (ECAR) baseline and increased the oxygen consumption rate (OCR) baseline, indicating a shift away from glycolysis. Additionally, the anticancer effects of EDNRB or EDN3 was reversed upon inhibition of the cGMP/PKG pathway. In vivo, enhanced EDNRB expression significantly suppressed tumor growth. Therefore, EDNRB or EDN3 possess anticancer potential in PCa, primarily through the regulation of glycolysis via the cGMP/PKG pathway.

Prostate-specific antigen (PSA) is used to screen for prostate cancer for decades. However, PSA has poor specificity in prostate cancer screening within the 4.0- to 10.0-ng/mL range. This study aimed to develop a new prediction model for PCa in patients with a PSA level of 2.5–20 ng/mL. The clinical data of 80 patients with PSA 4–22 ng/mL from 2016 to 2022 were selected for retrospective analysis. Prostate volume was estimated by suprapubic ultrasonography. PSA and the inflammatory markers like neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-lymphocyte ratio (MLR) in peripheral blood were analyyzed to assess their value in PCa. The diagnostic performance of PSA, PSA density (PSAD), and inflammatory markers, respectively, was estimated by ROC curve. The areas under the ROC curve for f/t PSA, PV, PSAD, MLR, NLR, and PLR for predicting PCa in patients with a PSA level of 4.0–22.0 ng/mL were 0.7375, 0.7774, 0.8294, 0.5945, 0.5571, and 0.5437, respectively. The PSAD performed better than f/t PSA and PV in the diagnosis of PCa. The specificity of PSAD was higher than that of f/tPSA when tPSA was in the gray zone (between 4 and 10 ng/mL). The area under the curve (AUC) increased when PSAD was combined with MLR in patients with PSA 4–10 ng/mL and patients with PSA 10–22 ng/mL, and the positive predictive values were 81.81% and 90.91%, respectively (P = 0.0008 and P = 0.0002). PSAD has a moderate diagnostic value for PCa detection. The combination of PSAD and MLR could improve the diagnostic accuracy in PCa diagnosis.

ObjectiveMetabolic syndrome is an important risk factor for calcium oxalate stone, yet the underlying mechanism remain unclear. Gut microbiota is involved in human metabolic processes and is associated with both metabolic syndrome and calcium oxalate stone formation.MethodsIn this study, 100 subjects were divided into four groups: calcium oxalate stone with metabolic syndrome (Group A), metabolic syndrome only (Group B), calcium oxalate stone only (Group C), and healthy controls (Group D), with 25 cases in each group. Gut microbiota composition and function were analyzed using 16S rRNA gene sequencing. Microbiota diversity, species differences, and metabolic function changes were assessed by combining clinical parameters and metabolic pathway (KEGG) annotation.ResultsThe α diversity in Group A was significantly lower than in the other three groups (Shannon index, P < 0.05), and β diversity analysis revealed significant differences in bacterial community structure among all four groups (ANOSIM, P < 0.05). In Group A, short-chain fatty acid (SCFA)-producing probiotics (e.g., Faecalibacterium, Faecalibacillus, Prevotella) were reduced, while pro-inflammatory bacteria (e.g., Eggerthella and Anaerobacteriaceae) were enriched. RDA correlation analysis indicated that Faecalibacterium is negatively correlated with blood glucose levels, Faecalibacterium and Roseburia are positively correlated with urinary pH. KEGG analysis showed that the bisphenol degradation pathway was reduced (logFC = −1.45, P = 0.027) and the retinol metabolism pathway was enriched (logFC = 0.928, P = 0.006) in Group A compared to Group B.ConclusionPatients with calcium oxalate stone and metabolic syndrome exhibit a “double imbalance” in gut microbiota: on the one hand, the reduced diversity of the microbiota and the decrease of SCFAs-producing microbiota weakened the metabolic protective effect of the gut microbiota; on the other hand, the enrichment of pro-inflammatory and pathogenic bacteria exacerbated metabolic disorders and inflammatory reactions. The present study reveals that gut microbiota play a role in the mechanism of metabolic syndrome promoting calcium oxalate stone formation, and these findings provide a theoretical basis for the use of probiotics to prevent calcium oxalate stone.

Prolonged operation time has been associated with an increased incidence of postoperative complications in various surgical procedures. However, its role in pediatric percutaneous nephrolithotomy (PCNL) remains unclear. This study aimed to investigate the relationship between operation time and systemic inflammatory response syndrome (SIRS) incidence in pediatric patients undergoing PCNL. This retrospective study included 472 pediatric patients who underwent PCNL, the primary exposure of interest was operation time, while the primary outcome was the incidence of postoperative SIRS. Multivariate logistic regression, restricted cubic spline (RCS) analysis, and two-piecewise linear regression models were used to assess the relationship and potential threshold effects between operation time and postoperative SIRS. Subgroup analyses were used to investigate the association across different subgroups. The median age of the patients was 7 years (interquartile range: 3–12), and 56.36

Objective To investigate the correlation of Wnt5a expression and vasculogenic mimicry(VM)in prostate cancer tissues,and analyze their relationships with cancer stem cells(CSCs)characteristics and epithelial-mesenchymal transition(EMT).Methods Immunohistochemistry was conducted to detect the expression of Wnt5a in 50 prostate cancer tissues and 50 benign prostatic hyperplasia tissues.The expression levels of CD133,vimentin,and E-cadherin were detected in the prostate cancer tissues,and CD34/PAS double staining was used to detect VM structures.We analyzed the difference in Wnt5a level between prostate cancer and benign prostatic hyperplasia tissues,the clinical significance of Wnt5a and VM,the relationship of Wnt5a expression and VM,and the relationships of Wnt5a expression and VM with CD133,Vimentin,E-cadherin.Results The expression of Wnt5a was significantly higher in prostate cancer tissues than in benign prostatic hyperplasia(P<0.05).A positive correlation was observed between Wnt5a expression and VM(P<0.05).The expression levels of Wnt5a and VM were positively correlated with those of CD133 and vimentin(P<0.05).Wnt5a expression and VM were positively correlated with Gleason score,vas deferens invasion and lymphatic metastasis(P<0.05)of prostate cancer,and VM was also positively correlated with T stage of prostate cancer(P<0.05).Conclusion The expression level of Wnt5a in prostate cancer tissues is elevated and positively related with VM formation.Wnt5a expression and VM are correlated with cancer stem cells characteristics and the expression of epithelial-mesenchymal transition marker proteins.

Prostate cancer (PCa) represents a substantial global health concern and a prominent contributor to male cancer-related mortality. The aim of this study is to explore the role of B-type endothelin receptor (EDNRB) in PCa and evaluate its therapeutic potential. The investigation employed predictive methodologies encompassing data acquisition from the GEO and TCGA databases, gene screening, enrichment analysis, in vitro experiments involving PCR, Western blotting, wound healing, and Transwell assays, as well as animal experiments. Analysis revealed a significant downregulation of EDNRB expression in PCa cells. Overexpression of EDNRB demonstrated inhibitory effects on tumor cell growth, migration, and invasion, likely mediated through activation of the cGMP-Protein Kinase G pathway. In vivo experiments further confirmed the tumor-suppressive properties of EDNRB overexpression. These findings underscore the prospect of EDNRB as a therapeutic target for PCa, offering novel avenues for PCa treatment strategies.

BACKGROUND:Docetaxel (DTX) resistance attenuates anti-tumor effects of DTX on prostate cancer (mCRPC) and drug resistance was related to Treg expansion in tumors. ZNF667-AS1 played a suppressing role in various tumors and tumor-derived exosomes carry lncRNAs to participate in tumor progression. Here, the effects of ZNF667-AS1 on malignant characteristics and DTX resistance in PC and the effect and its underlying molecular mechanism of tumor-derived exosomes carrying ZNF667-AS1 on Treg expansion were investigated. METHODS:The identification of exosomes were determined using TEM, NTA and western blot. The abundance of genes and proteins were evaluated using IHC, RT-qPCR, western blot and FISH. Malignant phenotypes of PC cells were evaluated by means of Edu, scratch test, transwell, CCK-8 and flow cytometry. The percentage of CD4+CD25+Foxp3+ Tregs was detected using flow cytometry. The location of ZNF667-AS1 was detected using nuclear-cytoplasmic fractionation. The co-location of ZNF667-AS1 and U2AF1 protein was detected using IF-FISH assay. The interactions among ZNF667-AS1, TGFBR1 and U2AF1 were verified using RNA pull-down, RIP and dual luciferase activity. RESULTS:ZNF667-AS1 expression in PC samples was lowered, which was negatively relative to poor prognosis and DTX resistance. ZNF667-AS1 overexpression inhibited malignant phenotypes of PC cells, tumor growth and DTX resistance. Besides, DTX resistant cell-derived exosomes expressed lower ZNF667-AS1 expression. Exosomes carrying exogenously high ZNF667-AS1 expression derived PC cells or serum of mice suppressed Treg expansion. On the mechanism, ZNF667-AS1 interacted with U2AF1 to destabilize TGFBR1 mRNA and reduce TGFBR1 expression in CD4+T cells. CONCLUSION:ZNF667-AS1 suppressed cell growth of PC cells, tumor growth of mice and DTX resistance to PC cells and exogenously high ZNF667-AS1 expression in tumor-derived exosomes destabilized TGFBR1 mRNA and reduce TGFBR1 expression through interacting with U2AF1, thus resulting in attenuated Treg expansion, which was related to DTX resistance.

本文基于Hill动力学与Michaelis-Menten方程,建立理论模型研究胰岛素通过环磷腺苷效应元件结合蛋白(CREB)调节肝糖异生的物理机制.理论模型考虑胰岛素通过CREB调节过氧化物酶体增活化受体γ辅助活化因子(PGC)联级信号,进而调控肝脏糖异生,影响糖代谢信号通路特性.研究发现,在异常胰岛素(Ginsulin)作用下CREB表达提升,进一步刺激了磷酸烯醇式丙酮酸羧激酶1(Pck1)表达.通过Pck1的调控,柠檬酸盐酯(citrate)、α-酮戊二酸(α-keto glutarate)、苹果酸酯(Malate)、草酰乙酸盐(Oxaloacetate)出现了不同的代谢水平.高表达的CREB会上调Pck1的表达水平,通过CREB、Pck1的调节作用,磷酸烯醇式丙酮酸羧化酶(phosphoenolpyruvate)转化为白藜芦醇(Pyruvate)的水平提升,进而促使citrate、α-keto glutarate、Malate、Oxaloacetate大幅度升高,最终影响细胞葡萄糖代谢.在糖异生基因的调控作用下,较高浓度的葡萄糖(Glocose),使得phosphoenolpyruvate浓度提升,并且在Pck1的调控作用下,phosphoenolpyruvate转化为Pyruvate的量增多,也会使得citrate、α-keto glutarate、Malate、Oxaloacetate大幅度提升.理论结果进一步深刻揭示了胰岛素、CREB蛋白,以及糖异生基因对细胞糖代谢新的调控机理,可为设计阻断糖尿病转变通路的治疗方案提供理论依据.

目的 研究输尿管软镜碎石术教学中采用操作技能直接观察(DOPS)评估效果.方法 选择2021—2023年本院泌尿外科带教的学生56名,按照带教形式与评估方式的不同,分为试验组和对照组,分析带教效果.结果 试验组学生末期SOAP量表评分明显高于中期SOAP量表评分,P<0.05,但初期、中期SOAP量表评分组间对比,差异无显著性,P>0.05;试验组学生综合能力、学生对带教老师满意度、学生批判性思维评分高于对照组,P<0.05.结论 DOPS评估作为高效的一种教学和评估形式,可明显提升教学的效果.

Prostate cancer (PCa) is one of the leading causes of cancer-related death in males worldwide and exploring more reliable biomarkers for PCa is essential for the diagnosis and therapeutics for the disease. Although the functions of miR-141-3p and AlkB homolog 5 (ALKBH5) were identified in some cancers, whether they were involved in the development of PCa remains unclear. In this study, reverse transcription-quantitative polymerase chain reaction unveiled that the expression of ALKBH5 was reduced in PCa tissues and was negatively correlated with miR-141-3p. ALKBH5 attenuated the malignant development of PCa through suppressing the growth, migration, invasion, and sphere formation abilities of PCa cells. In addition, the luciferase activity assay identified that ALKBH5 was corroborated as a downstream target of miR-141-3p. Moreover, miR-141-3p expression was boosted in PCa tissues and cells and inhibition of miR-141-3p suppressed the tumor growth of PCa in vivo. Moreover, ALKBH5 was confirmed to suppress protein arginine methyltransferase 6 (PRMT6) expression through N6-methyladenosine (m6A) modification. We further identified that miR-141-3p-modulated PRMT6 level through mediating ALKBH5. Furthermore, PRMT6 level was positively correlated with miR-141-3p level and negatively associated with ALKBH5 level. Finally, rescue assays also uncovered that miR-141-3p aggravated PCa development by regulating PRMT6. In conclusion, miR-141-3p accelerated the malignant progression of PCa through ALKBH5-mediated m6A modification of PRMT6, which might offer a novel insight into the role of miR-141-3p and ALKBH5 in the treatments of PCa patients.

Objective To explore the inhibition effect and mechanism of miR-146a-5p on proliferation and invasion of prostate cancer (PCa) cell line PC-3 by targeting SMAD4. Methods RT-qPCR was used to detect the expression of miR-146a-5p in PCa tissues and cell lines. The relevance of miR-146a-5p expression with Gleason score was also analyzed. MTT, BrdU experiment, cell colony formation experiment, scratch experiment, Transwell assay and nude mouse xenograft model experiment were conducted to detect the effect of miR-146a-5p on cell proliferation, tumorigenicity, migration and invasion. The expression of SMAD4 in PCa tissues was detected by RT-qPCR, and the targeting relationship of SMAD4 and miR-146a-5p was confirmed by double luciferase reporter gene assay and rescue experiment. Western blot was used to detect the expression of SMAD2/SMAD3 complex in nucleus affected by miR-146a-5p and SMAD4. Finally, double luciferase reporter gene assay and ChIP experiment were performed to examine the targeting regulation of TIM3 by miR-146a-5p/SMAD4/SMAD2/SMAD3 signaling axis. Results miR-146a-5p was low expressed in PCa tissues and cell lines; its expression was negatively correlated to Gleason score and had the lowest expression in PC-3 cells. miR-146a-5p inhibited the proliferation and invasion of PC-3 cells by targeting SMAD4. SMAD2/SMAD3/TIM3 axis seemed to be the downstream mechanism of miR-146a-5p/SMAD4 signaling pathway. Conclusions miR-146a-5p can inhibit the proliferation and invasion of PC-3 cells by targeting SMAD4, and the downstream mechanism might be related to the SMAD2/SMAD3/TIM3 signaling pathway.

目的:分析上尿路结石梗阻所致脓毒血症患者的菌群分布及抗生素敏感谱特点.方法:回顾性分析2004年1月至2021年9月在新疆维吾尔自治区人民医院住院治疗的上尿路结石梗阻所致脓毒血症患者的病历资料,收集其性别、年龄、合并症、病原菌培养及药敏试验结果,并进行统计学分析,探讨其病原菌分布及抗生素敏感谱的特点.结果:本研究共纳入215例患者,男性76例,女性139例,其中病原菌培养阳性结果为151例(70.2％),阴性结果为64例(29.8％).在阳性结果患者中,共分离出菌株154株,其中革兰阴性菌125株(81.2％),革兰阳性菌25株(16.2％),真菌4株(2.6％).最常见的病原菌为大肠埃希菌,共98株(63.6％),其在革兰阴性菌中占比高达78.4％.在性别方面,女性感染大肠埃希菌的比例(74.0％)与男性(51.0％)有明显的统计学差异(P<0.05).革兰阳性菌中最常见的病原菌为屎肠球菌,共6株(3.9％).本研究中,革兰阴性菌对亚胺培南的敏感率最高,达99.2％.大肠埃希菌对碳青霉烯类抗生素(亚胺培南和美洛培南)的敏感率为100.0％.除亚胺培南和美洛培南外,大肠埃希菌对阿米卡星、呋喃妥因、哌拉西林/他唑巴坦、头孢哌酮/舒巴坦的敏感率也较高.革兰阳性菌对万古霉素、利奈唑烷、替拉考宁的敏感率最高,均为100.0％.在治疗大肠埃希菌感染时,女性对头孢他啶的敏感率(70.8％)明显高于男性(47.8％),差异具有统计学意义(P<0.05).结论:引起上尿路结石梗阻所致脓毒血症的主要病原菌为革兰阴性菌中的大肠埃希菌,女性更易感染大肠埃希菌,且女性大肠埃希菌感染者对头孢他啶的敏感性更高.临床可选用碳青霉烯类抗菌药物、头孢他啶等治疗上尿路结石梗阻所致脓毒血症.

Background: Prostate cancer (PC) is a malignant tumor with higher death rate. Chromodomain-helicase-DNA-binding-protein 1-like (CHD1L) has been shown to be a key facilitator in cancers' progression. High expression of methionine aminopeptidase 2 (METAP2) has been demonstrated in PC. However, the effects of CHD1L/METAP2 axis on PC progression are still undefined. Methods: The expressions of genes were confirmed by Real-Time quantitative Polymerase Chain Reaction (RT-qPCR), western bot or Immunohistochemistry (IHC) assay. Cell proliferation was tested by Cell counting kit-8 (CCK-8) and colony formation. Cell invasion and migration were examined using Transwell assay. The angiogenesis ability was assessed using tube formation. Tumor growth was evaluated in vivo assay. Results: CHD1L expression was up-regulated in the prostate adenocarcinoma (PRAD) tissues as compared to that in normal tissues using UALCAN and TIMER2.0 online websites. Further studies demonstrated that CHD1L exhibited higher mRNA and protein expression in PC tissues and cell lines. In addition, knockdown of CHD1L suppressed cell proliferation, migration and angiogenesis in PC. Positive correlation between CHD1L and METAP2 was shown in analysis based on TIMER2.0 and GEPIA online websites. Moreover, it was shown that CHD1L upregulated METAP2 expression in PC. METAP2 overexpression was shown to rescue the decreased cell proliferation, migration and angiogenesis mediated by CHD1L knockdown. Suppression of CHD1L was shown to inhibit tumor growth in vivo. Conclusions: Knockdown of CHD1L reduced PC cell proliferation, migration and angiogenesis through reducing METAP2. Our findings illustrated that the CHD1L/METAP2 axis may be useful bio-targets for PC treatment.

目的 探讨基于膳食炎症指数(DII)分析肾结石发病的影响因素.方法 选取2020年8月至2021年7月的新疆维吾尔自治区人民医院泌尿中心确诊的192例肾结石患者为结石组,选取同期于新疆维吾尔自治区人民医院体检健康的192名参与者为非结石组.比较两组的性别、年龄、体重指数、DII评分等因素,分析肾结石发病的影响因素.结果 所有参与者DII评分为0.91(-4.36,4.85),结石组的促炎饮食参与者(DII>0.91分)多于非结石组,差异有统计学意义(P<0.05).单因素分析结果显示,两组的不同能量摄入、不同体重指数、是否吸烟、是否饮酒、不同饮水量和不同DII评分比较,差异有统计学意义(P<0.05).多因素logistic回归分析结果显示,能量摄入(β=0.622,OR=1.980,95％CI=1.631～5.019)、体重指数>28 kg/m2(β=0.854,OR=2.349,95％CI=1.328～4.155)及DII评分>0.91分(β=0.544,OR=1.740,95％CI=1.126～2.687)是肾结石发病的危险因素.饮水量>2000 ml/d(β=-0.885,OR=0.413,95％CI=0.199～0.856)是肾结石发病的保护因素.结论 建议人群调整饮食结构偏向于低DII状态即抑炎饮食,同时建议人群通过控制体重指数、增加饮水量达>2000 ml/d以上,可能对结石预防起到重要作用.

目的 分析短期(2个月内)留置输尿管支架形成结石垢的危险因素.方法 回顾性分析2019年6月 -2021年6月因上尿路结石于新疆维吾尔自治区人民医院接受手术治疗并放置输尿管支架管的358例患者资料,分为结石垢组(123例)和非结石垢组(235例),收集患者基线资料及结石、输尿管支架管和尿液相关数据,通过单因素和多因素分析确定与结石垢形成相关的危险因素.结果 结石垢组患者的年龄、糖尿病和前列腺增生患病比例明显高于非结石垢组;与非结石垢组相比结石垢组患者中感染性结石患者比例、结石含感染性成分者、置管前尿路感染者、拔管前尿蛋白和尿结晶的阳性率均明显较高.单因素及多因素分析表明年龄＞60岁(OR:2.659,95％C I:1.360～5.199,P=0.004)、结石含感染性成分(OR:2.638,95％C I:1.392～4.998,P=0.003)及拔管前尿结晶(OR:8.125,95％C I:4.793～13.773,P＜0.001)为结石垢形成的独立危险因素.结论 年龄＞60岁、结石含感染性成分及拔管前尿结晶阳性为短期(2个月内)留置输尿管支架形成结石垢的独立危险因素.

目的:评价双源CT在儿童尿路结石成分检测中的应用价值。方法:回顾性选取2018年3月—2021年1月新疆维吾尔自治区人民医院泌尿中心收治的433例因泌尿系结石就诊的儿童，并行双源CT检查，数据经后处理工作站处理，将结石成分分析结果与红外光谱分析结果进行对比，比较双源CT分析结石的准确率及双源CT各测量指标对结石类型的预测价值。计量资料以均数±标准差( Mean± SD)表示，各结石类型的测量指标[平均CT值、双能差、双能比及双能量指数(DEI)]的比较采用单因素Anova方差分析。绘制受试者操作特征(ROC)曲线，计算各指标的曲线下面积(AUC)，对各指标进行诊断效能评价。 结果:双源CT检测到282枚草酸钙结石、238枚磷酸钙结石、39枚尿酸结石和7枚胱氨酸结石。与红外光谱分析结果比较，双源CT对草酸钙结石和羟基磷灰石的准确率分别为84.2%和81.8%，尿酸结石和胱氨酸结石均被准确检到。此外，双能差、双能比、DEI对草酸钙结石和磷酸钙结石均具有可靠的预测价值，尤其是双能比和DEI，均AUC>0.75。结论:利用先进的后处理分析方法，双源CT可以可靠地分析儿童尿路结石成分，为选择个性化治疗方案提供参考。