Background:Clear cell renal cell carcinoma (ccRCC) is the most common kidney cancer subtype. While localized disease is treated surgically, therapeutic options for advanced cases remain limited. This highlights an urgent need for reliable prognostic markers and novel therapeutic targets. Therefore, this study aimed to clarify the clinical significance and functional role of MAGI3 in ccRCC. Methods:We analyzed MAGI3 expression in ccRCC and normal tissues using public datasets and clinical samples. Its correlation with clinicopathological features and patient survival was evaluated. The biological role of MAGI3 and its underlying mechanism were investigated through in vitro and in vivo functional assays. Results:MAGI3 expression was significantly downregulated in tumor tissues compared with adjacent normal kidney specimens. Lower MAGI3 levels correlated positively with advanced tumor stage, higher Fuhrman nuclear grade, lymph node metastasis, increased infiltration of immunosuppressive cell populations, and poorer overall patient prognosis. Functional experiments further demonstrated that MAGI3 overexpression effectively suppressed ccRCC cell proliferation, migration, and invasion in vitro and in vivo by inhibiting STAT3 signaling phosphorylation and downstream transcriptional activity. Conclusions:Our study identifies MAGI3 as a novel tumor suppressor in ccRCC that constrains cancer progression via the STAT3 pathway. These results firmly establish MAGI3 as a potential prognostic biomarker for ccRCC.

Background:Prostate adenocarcinoma (PRAD) is a common malignancy with marked clinical heterogeneity, complicating prognosis and disease monitoring. Traditional tools like the Gleason score lack molecular and microenvironmental insights, underscoring the need for biomarker-driven predictive models. Methods:Single-cell RNA-seq data from GEO and bulk RNA-seq data from TCGA were analyzed. scRNA-seq processing used the Seurat package, with cluster-specific genes identified via FindAllMarkers. Differentially expressed genes (DEGs) from bulk data were obtained using limma, and key gene modules were identified through WGCNA. Using univariate Cox regression and LASSO analysis, a prognostic model was developed based on cluster-specific genes, key module genes, and differentially expressed genes. Clinical validation included comparison of tumor and adjacent normal tissues, revealing significantly elevated GDPD3 expression, further confirmed by immunohistochemistry. In vitro knockdown experiments were conducted in DU145 cells to assess GDPD3's role in promoting proliferation, migration, and epithelial-mesenchymal transition (EMT). Results:In this study, through integrated single-cell sequencing and Bulk-RNA-seq analyses, we established a 21-gene prognostic model. QPCR confirmed significant upregulation of three candidates, including GDPD3, which was also elevatedin malignant tissues. Knockdown of GDPD3 inhibited tumor cell proliferation, invasion, and migration. Mechanistically, GDPD3 regulated the levels of lysophosphatidic acid (LPA), which in turn induced EMT in tumor cells. Inhibition or knockdown of the LPA receptor LPAR1 suppressed EMT. LPA promoted EMT through activation of the AKT signaling pathway, and inhibition of this pathway reversed LPA-induced EMT. Conclusion:This study underscores key molecular mechanisms underlying prostate cancer progression, with GDPD3 emerging as a potential therapeutic target.

Chronic kidney disease (CKD) is a major global health issue. Kidney fibrosis is a key mechanism leading to end-stage renal disease. Senescence of renal tubular epithelial cells (RTECs) and the senescence-associated secretory phenotype (SASP) factors they release are crucial in kidney fibrosis progression. While isorhamnetin, the active component of Astragalus membranaceus , has demonstrated promise in combating senescence/aging and fibrosis, its precise mechanism of action remains poorly understood. This study aims to elucidate the mechanisms through which isorhamnetin mitigates RTEC senescence and kidney fibrosis, specifically by modulating the interleukin-6 (IL-6) signaling pathway. The findings indicate that isorhamnetin significantly attenuates kidney fibrosis in aging mice, inhibiting IL-6 secretion from senescent RTECs and reducing its accumulation in kidney tissues. In vitro analyses further revealed that isorhamnetin disrupted IL-6 signaling by competitively binding to the IL-6 receptor, thereby slowing RTEC senescence. Additional investigations demonstrated that isorhamnetin's inhibition of IL-6 secretion from senescent RTECs impacted macrophage M2 polarization and the transformation of fibroblasts into myofibroblasts, thus decelerating the progression of kidney fibrosis. This study highlights the critical role of isorhamnetin in alleviating RTEC senescence and kidney fibrosis through the suppression of the IL-6 signaling pathway, underscoring its potential for clinical application in CKD treatment.

BACKGROUND:Renal fibrosis is a critical pathological characteristic of chronic kidney disease, and current antifibrotic therapies has limited efficacy. Sodium butyrate (NaB) has been shown to be highly effective in mitigating bleomycin-induced pulmonary fibrosis; however, its specific impact on renal fibrosis and the underlying mechanisms remain unclear. This study aims to elucidate the role and mechanism of NaB in renal fibrosis by using a mouse model of renal fibrosis induced through Unilateral Ureteral Obstruction (UUO) and folic acid (FA) administration. RESULTS:NaB significantly decreased the distribution of collagen fibers in renal tissues and mitigated fibrosis in a dose-dependent manner. Further analysis indicated that NaB inhibited M2 macrophage polarization in the renal tissues of UUO model mice by blocking the phosphorylation of STAT6, hence reducing renal fibrosis. Additionally, in vitro experiments demonstrated that NaB inhibited fibroblast activation induced by M2 macrophages. Mechanistic studies revealed that NaB attenuates fibroblast activation and M2 macrophage polarization by upregulating LKB1 and inhibiting the activation of the STAT6 signaling pathway. CONCLUSION:NaB may exert its effects by inhibiting the activation of the IL-4/STAT6 signaling pathway through the upregulation of LKB1, which suppress the polarization of M2 macrophages and consequently reduce renal fibrosis. These findings establish a theoretical foundation for NaB as a novel drug candidate for renal fibrosis and indicate its potential applicability in clinical treatments for this condition.

Prostate cancer (PCa) is one of the most common malignant tumors that exhibit both chemoresistance and recurrence. SUV39H2 is highly expressed in many types of human tumors, but its role in the development and progression of PCa has never been clarified. The aim of this study is to elucidate the role of SUV39H2 in the development and progression of PCa, its association with the AKT/FOXO signaling pathway, and its potential implications for PCa diagnosis and treatment. SUV39H2 expression was analyzed in The Cancer Genome Atlas (TCGA) and genotype tissue expression pan-cancer data. The TCGA database was evaluated for SUV39H2 enrichment and its correlation to immune cell infiltration. SUV39H2 levels in PCa tissues and control tissues were determined in 30 patients using qPCR and IHC. Clinical relevance was assessed via The Cancer Genome Atlas (TCGA). In vitro assessments including colony formation assays, Western Blot analysis, CCK-8 assays, and flow cytometry were utilized to establish SUV39H2’s contribution to PCa cell growth. The influence of SUV39H2 on PC3 and DU145 cell proliferation was assessed through a cell line-derived xenograft model. Sphere formation assays and qPCR were employed to delineate SUV39H2’s role in PCa stemness and chemosensitivity. In vitro macrophage polarization assays provided insights into SUV39H2’s association with M2 macrophages, while enrichment analysis shed light on its role in FOXO signaling. PCa tissues expressed higher levels of SUV39H2 than normal tissues. By knocking down SUV39H2, PCa cells were made more chemosensitive to docetaxel and cell proliferation and stemness were inhibited. Additionally, SUV39H2 knockdown significantly inhibited in vivo PCa cell growth and inhibited the polarization of macrophages. Furthermore, SUV39H2 was found to regulate AKT/FOXO signaling by increasing Akt and FOXO3a phosphorylation. Our findings highlight SUV39H2’s role in PCa cell apoptosis and chemosensitivity mainly by regulating the AKT/FOXO signaling pathway and suggest that SUV39H2 could be a potential target for PCa diagnosis and treatment.

Abstract Background The prognostic management of Prostate adenocarcinoma (PRAD) presents a considerable challenge to healthcare professionals. However, it fails to accurately capture the fundamental cellular and molecular functions within tumor cells. Methods The data for PRAD scRNA-seq were retrieved from the Gene Expression Omnibus (GEO) database. The limma program was utilized to identify differentially expressed genes (DEGs) in PRAD patients that exert an influence on overall survival (OS). For the identification of key modules associated with PRAD, Weighted Gene Correlation Network Analysis (WGCNA) was employed. The intersection of core cell marker genes, PRAD key module genes, and DEGs was utilized to build a predictive model using univariate Cox and Least Absolute Shrinkage and Selection Operator (LASSO) analyses. Furthermore, we conducted experimental validation by collecting patient samples. Results Analysis of 162,897 scRNA-seq datasets and identified 7 central cell types. From the scRNA-seq dataset, 1805 marker genes were identified, while the bulk RNA-seq dataset yielded 1086 DEGs. Additionally, 2545 genes were linked to a key module identified through WGCNA. A predictive model was derived from the expression levels of 21 signature genes following intersection, univariate Cox, and LASSO analyses. And we confirmed the accuracy of our analysis through the patient samples we collected. Conclusion This study developed a unique prognosis-predictive model to predict the survival condition of individuals with PRAD through the integration of scRNA-seq and bulk RNA-seq data. The risk score emerges as a potential independent predictive indicator, demonstrating a strong relationship with the immunological microenvironment.

OBJECTIVES:Circular RNAs (circRNAs) are involved in carcinogenesis, though their expression profile in renal cell carcinoma (RCC) is uncharacterized. The tumor suppressor gene miR-145-5p is expressed in RCC tissues, but its relationship with circRNAs is unknown. Thus, we aimed to identify differentially expressed circRNAs in RCC tissues and to explore the interaction between these circRNAs and miR-145 in the development of RCC.METHODS:We performed high-throughput sequencing and bioinformatics analyses to examine the expression pattern of circRNAs in RCC. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were used to functionally annotate differentially expressed circRNAs. Quantitative real-time polymerase chain reaction (qRT-PCR) was used for sequence verification. Small interfering RNAs were employed to investigate the function and mechanism of circRNAs in RCC. The relationship between miR-145-5p and circRNAs was confirmed using luciferase, RNA immunoprecipitation (RIP), and biotin-coupled probe RNA pull-down assays.RESULTS:Fifty-three circRNAs were significantly and differentially expressed in RCC compared to normal control tissue. Bioinformatic analyses indicated that two significantly upregulated circRNAs, circ-AFF2 and circ-ASAP1, had sequences corresponding to miR-145 response elements. Consistently, the luciferase reporter, RIP, and biotin-coupled probe RNA pull-down assays showed that circ-AFF2 and circ-ASAP1 may repress miR-145 by acting as sponges. circ-AFF2 and circ-ASAP1 were highly expressed in RCC patient-derived tumor samples; their overexpression correlated with poor prognosis and low miR-145 levels. Knockdown of circ-AFF2 or circ-ASAP1 in RCC cell lines inhibited proliferation, underscoring their oncogenic function. A circRNA-miRNA network was constructed for RCC using the differentially expressed circRNAs and projected miRNAs. Candidate genes were verified by RT-qPCR and western blot, indicating that circ-AFF2 and circ-ASAP1 may be connected to RCC proliferation and metastasis.CONCLUSION:circ-AFF2 and circ-ASAP1 were upregulated in RCC and likely promote tumor progression by sponging miR-145. Therefore, both circRNAs should be investigated further as potential diagnostic and therapeutic targets for RCC.

Purpose:We examined whether anlotinib can attenuate folic acid-induced and unilateral ureteral obstruction-induced renal fibrosis and explored the underlying antifibrotic mechanism.Materials and Methods:We have evaluated the effects of anlotinib on folic acid-induced and unilateral ureteral obstruction-induced renal fibrosis in mice through in vivo experiments of unilateral ureteral obstruction or folic acid-induced interstitial fibrosis and in vitro models of transforming growth factor-β1 induced HK-2 human renal proximal tubule cells. Serum renal function parameters and inflammatory cytokine levels were measured, and histological changes of renal injury and fibrosis were analyzed by HE staining and immunohistochemistry. Immunohistochemistry and Western blotting were used to determine the mechanism of action of anlotinib in ameliorating renal fibrosis.Results:Anlotinib improved proteinuria and reduced renal impairment in folic acid-induced mouse models of renal fibrosis. Anlotinib reduced tubular injury, deposition of tubular extracellular matrix, and expression of alpha-smooth muscle actin, transforming growth factor-β1, and cytosolic inflammatory factors compared with controls.Conclusions:Anlotinib ameliorated renal function, improved extracellular matrix deposition, reduced protein levels of epithelial-mesenchymal transition markers, and decreased cellular inflammatory factors. Anlotinib reduced renal injury and fibrosis by inhibiting the transforming growth factor-β1 signaling pathway through AKT and ERK channels.

Dear Editor, Chronic kidney disease (CKD) with characteristics of progressive deterioration of renal function is regarded as one major public health problem around the world. The patients are often diagnosed at advanced stages with most kidney functions lost, since they have few signs or symptoms at early stage. Renal fibrosis is the pathologic hallmark and prognostic indicator for CKD. The effective methods except biopsy for early detection of renal fibrosis are required to improve the diagnosis of CKD. Our data revealed that RelB can not only discriminate CKD patients from normal subjects but also can distinguish CKD patients at different stages. We prove that RelB is capable to work as a promising serum biomarker to diagnose and monitor the renal fibrosis in CKD patients. Renal inflammation is actively participating in the evolution of renal fibrosis and CKD.1 In kidney tubular cells, hyperactivation of noncanonical NF-κB signaling induced by TWEAK, TNF-like weak inducer of apoptosis, contributes to inflammatory responses.2 Through analyzing a whole transcriptome RNA sequencing of mouse renal fibrosis model with unilateral ureteral obstruction (UUO), we found that RelB, the key transactivator of noncanonical NF-κB signaling pathway, was profoundly elevated in fibrotic renal tissues (Figure S1).3 Therefore, we established UUO model to validate the upregulation of RelB in the progressive renal fibrosis. The results showed a consistent and significant increase in RelB along with α-SMA and Col1α1 at mRNA and protein levels in fibrotic kidneys after UUO (Figure 1A and B), and the level of RelB mRNA was positively correlated with α-SMA, Col1α1, and Tgfβ1 (Figure S2A–C), while the RelB protein was correlated with fibrosis (Figure S2D and E). Then, we measured the concentration of serum RelB in mice with ureteric ligation and found it increased significantly from the 8th day after UUO as well (Figure 1C). The immunohistochemical analysis further showed that RelB, specifically expressed in the renal tubular epithelial cells, gradually increased with the fibrosis progression (Figure 1D-F ), and was positively correlated with the severity of fibrosis reflected by the Masson's staining (r = 0.5861, p = 0.0106) (Figure 1G ). Correspondingly, the concentration of serum RelB protein was positively correlated with the severity of fibrosis (r = 0.5726, p = 0.0130) (Figure 1H) and the renal RelB staining (r = 0.8260, p < 0.0001) (Figure S2F). These data clearly manifested that RelB is gradually induced in fibrotic kidney after UUO in mice and the expression of RelB can be an indicator of renal fibrosis. A cohort of the biopsy-proven CKD patients was subsequently studied. Kidney biopsy specimens were collected from 34 CKD patients for immunohistochemical staining (Figure 2A). Among these samples, the protein expressions of RelB were disclosed with positive correlations with the intensity of kidney fibrosis (r = 0.6994, p < 0.0001) (Figure 2B). We collected serum from 15 patients among these 34 patients and measured the content of RelB in sera. The serum RelB level was positively correlated with the intensity of renal fibrosis as well (r = 0.8388, p = 0.003) (Figure 2C). We next analyzed more blood samples including 32 CKD patients and 60 healthy people, and found that the concentration of RelB and HE4 (a literature reported serum biomarker for renal fibrosis in CKD4-7) in sera from CKD patients expressed higher levels than from healthy controls (Figure 2D, Table 1). More importantly, we found the serum RelB or HE4 level was also significantly correlated with the renal function. They were positively correlated with serum creatinine (SCr) and blood urea nitrogen (BUN), and negatively correlated with estimated glomerular filtration rate (eGFR) (Figure 2E and F, Figure S3), indicating that it can reflect the injury of renal function. In addition, the serum RelB level was positively correlated with the serum HE4 level (Figure 2G). Being evaluated within the receiver operating curve (ROC) analysis afterwards, serum RelB and HE4 showed predictive significance for CKD detection. The area under the curve (AUC) value of RelB and HE4 was 0.873 and 0.849, respectively, while the AUC of RelB-HE4 combination was 0.920 (Figure 2H). In addition, the Hosmer–Lemeshow test was used to check the calibration of predictive model (Figure S4A). Summarily, it suggests that RelB is likely to be a better predictor of renal fibrosis and CKD compared with HE4, while its predictive accuracy can be improved when combined with HE4 (Table S1). When dividing the 32 CKD patients into two groups: CKD I & II and CKD III & IV, we showed that not only the level of serum RelB was significantly upregulated in the early-stage patients, but it also increased remarkedly along with the progression of stages (Figure 3A). Nevertheless, no significant differences were identified in the levels of serum HE4 between stage I and II and stage III and IV of CKD patients (Figure 3A). The serum levels of RelB and HE4 were observed with significant correlations (Figure 3D) and were additionally associated with SCr, BUN, or eGFR (Figure 3B and C, Figure S3). Then, the ROC analysis indicated the ability of RelB, but not HE4, to discriminate the CKD I & II patients with the CKD III & IV ones (Figure 3E). The Hosmer–Lemeshow test further indicated RelB or RelB-HE4 combination was better calibrated in distinguishing CKD I & II and CKD III & IV patients (Figure S4B). These results indicated that the serum RelB can well discriminate CKD patients at different stages. Recently, accumulated evidence has revealed the importance of noncanonical NF-κB signaling in regulating both innate and adaptive immune responses, as well as the pathogenesis of inflammatory diseases.8-10 The present study revealed that its pivotal transcription factor RelB has the potential as the biomarker for renal fibrosis identification at CKD early stages. Since it can distinguish CKD patients from healthy controls and discriminate CKD patients at different stages, it might be useful to supplement the existing biochemical indexes of kidney disease. Due to the sampling limitation in this study, it is ideal to expand the patient samples for comparative study on CKD patients with different kidney disease types and for better evaluation of the diagnostic value of RelB in CKD. The authors declare no conflict of interest. Xiaoren Zhang, Ningxia Xie, and Li Wang designed the research. Donglin Sun and Ningxia Xie performed the experiments and interpreted the data. Donglin Sun, Ningxia Xie, Xi Wang, Wenquan Wu, Xiuyong Li, and Jingyao Wang collected and prepared human samples. Xiaoren Zhang, Li Wang, Donglin Sun, Ningxia Xie, Yiming Hu, Xiangqiu Chen, Guojun Qian, Cuifeng Li, Haohao Zhang, Yuhang Jiang, Dandan Liu, Weifeng Chen, Qiumei Zhao, and Deji Ye wrote and/or reviewed the manuscript. Li Wang, Min Zeng, and Junwei Zhang applied ethic approval and signed informed consent. All authors approved the final manuscript. This work was supported by the National Key R&D Program of China (2018YFA0107500), the National Natural Science Foundation of China (91949102, 91742113), and the Guangzhou Key Medical Discipline Construction Project Fund. Supplemental Figure 1. Altered expression of genes in NF-κB and TGF-β signaling pathways between UUO groups and sham group. The heatmap shows the renal tissue transcriptome-wide changes in gene expression among three different groups (sham-operated group, 2 days post-UUO group and 8 days post-UUO group). Normalized read counts values are recorded. 34 genes related to NF-κB and TGF-β signaling pathways were analyzed from a set of RNA-seq data available at the NCBI GEO repository. GEO accession: GSE79443. Supplemental Figure 2. The correlation between RelB and kidney fibrosis at mRNA levels and protein levels. (A, B, C) Scatter plot with linear regression shows a correlation between mRNA expression of RelB and kidney fibrosis in obstructive nephropathy after UUO. (D) Quantification of the RelB Western blot results. (E) Correlation between RelB protein levels measured by Western blot and kidney fibrosis. r = 0.8854; p = 0.0001; n = 12. (F) Correlation between renal RelB staining and serum RelB, r = 0.8260; p < 0.0001; n = 18. Data were exhibited as means ± S.D. *p < 0.05 and **p < 0.001. Supplemental Figure 3. The correlation between the serum RelB and BUN. (A) Scatter plot with linear regression shows the serum RelB and HE4 levels are positively correlated with BUN in healthy controls and CKD patients. (B) Scatter plot with linear regression shows the serum RelB levels are positively correlated with BUN in CKD patients. However, correlation analysis revealed no significant associations between the serum HE4 and BUN. The Spearman correlation coefficient (r) and p value are shown. Supplemental Figure 4. Calibration of the model. (A) The calibration curve and Hosmer-Lemeshow test for the predictive ability of RelB (χ2 = 13.16, p = 0.106), HE4 (χ2 = 14.12, p = 0.079) and the RelB + HE4 combination (χ2 = 9.11, p = 0.333) in healthy group and CKD patients demonstrated good agreement with observation. (B) Similarly, the predictive ability of the RelB (χ2 = 10.61, p = 0.225), HE4 (χ2 = 10.31, p = 0.244) and the RelB + HE4 combination (χ2 = 10.35, p = 0.241) between early-stage CKD patients (I & II) and advanced-stage CKD patients (III & IV) showed good agreement with observation by the calibration curve and Hosmer-Lemeshow test. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

目的 了解深圳某综合医院(2016～2020)年淋病奈瑟菌(淋球菌)的检出情况,了解本地区淋球菌的流行状况和为制订淋病的防控措施提供依据.方法 统计分析南方医科大学深圳医院(2016～2020)年淋球菌送检情况和阳性患者的临床信息,检测阳性结果定义为革兰阴性双球菌涂片、淋球菌培养或淋球菌核酸定性检测任一结果为阳性.结果 共收到6362份送检标本,其中涂片705份、分离培养868份、核酸定性检测4789份.共检出921例淋球菌阳性(14.5％),其中涂片291份(41.3％)、分离培养132份(15.2％)、核酸检测498份(10.4％).(2016～2020)年送检标本的淋球菌检出率分别为15.1％、18.2％、18.0％、10.0％、14.3％.921例淋球菌感染患者中男女比例为23∶1;(21～30)岁年龄段占比最高(43.4％),其次为(31～～40)岁(33.9％).结论 (2016～2020)年本地区淋球菌的检出率较高,多种检测方法联合可提高淋球菌的检出率.淋球菌感染者以男性为主,(21～40)岁中青年为主要感染人群,应对该人群加强宣传教育.

目的 提高对成人附睾横纹肌肉瘤的认识.方法 报道南方医科大学深圳医院收治的1例附睾横纹肌肉瘤合并附睾炎患者的临床资料并复习总结国内外文献.结果 本例患者表现为附睾肿块合并附睾炎,予抗炎治疗效果欠佳,行根治性睾丸切除术,术后病理为胚胎型横纹肌肉瘤侵犯骨髓.另总结国内外附睾横纹肌肉瘤29例,多表现为无痛性阴囊肿大,肿瘤最大径3～13 cm.19例发生远处转移,8例出现腹膜后淋巴结转移.所有病例均行根治性手术,病理主要为胚胎型(18例).24例术后采取辅助化疗,常用V AC方案(长春新碱、阿霉素、环磷酰胺).平均随访17.9个月,期间12例未见复发或转移,8例肿瘤无进展(带瘤生存).9例经治疗后死亡,死亡病例中位生存期仅9个月.结论 附睾横纹肌肉瘤罕见且进展快,易于早期转移,术前诊断困难,若合并附睾炎、鞘膜积液等易于混淆原发病的诊断.诊断主要依赖病理检查,早期诊断及尽早行根治性睾丸切除术辅以术后化疗是治疗的关键.

1 临床资料 患者,女,41岁.于2015年7月因"肉眼血尿伴左侧腰痛3天"收治入院.肾脏增强CT提示左肾中下极见不规则肿块影,密度不均匀,增强扫描后见肿物不规则强化,肿物无明显包膜,考虑恶性肿瘤可能性大(图1a、b);肾动脉+肾静脉ce-MRA增强提示左肾静脉受侵犯(图2);MRU示:未见尿路积水,左肾肿物累及肾门(图3).

Abstract Purpose: The aim of the present study was to assess whether SARS-CoV-2 can be detected in the expressed prostatic secretion (EPS) of patients with corona virus disease 2019 (COVID-19). Methods: 18 cases of COVID-19, and 5 suspected cases, were selected from three medical centers to detect the RNA expression of SARS-CoV-2 in their EPS with RT-PCR. Results: Results were negative in all EPS samples for SARS-CoV-2 of suspected and confirmed patients. Conclusions: No SARS-CoV-2 was expressed in EPS of patients with COVID-19.

目的:探索长期服用黄体生成素释放激素类似物(LHRH-a)对肾结石形成的风险,以及与骨质疏松、代谢综合征副反应之间的相关性.方法:采用前瞻性研究,共纳入40例前列腺癌患者,自纳入日均开始接受LHRH-a持续治疗方案;随访1年后,采集相关临床进行统计学指标分析.结果:在治疗1年后,患者PSA和睾酮水平明显下降(P<0.0001),股骨颈、全髋关节、腰椎部分骨密度T得分及Z得分均明显下降(P<0.001).患者血清指标中碱性磷酸酶、甘油三酯、钙、磷、骨钙素、beta-crosslaps、维生素D均升高(P<0.001);iPTH、雌二醇、PSA和睾酮指标均下降(P<0.001).患者空腹尿及24 h尿中钙/肌酐指标均高于治疗前(P<0.05、<0.001).24 h尿分析中钙排泄指数、钙排泄分数、肾小管再吸收磷酸盐、柠檬酸盐水平均高于治疗前(P<0.05).随访结束时检出随访期间形成肾结石患者共12例(30％).形成结石组患者腰椎骨密度T评分低于未形成结石组,beta-crosslaps水平高于未形成结石组,空腹尿钙/肌酐水平高于未形成结石组,差异均有统计学意义(P<0.05).进一步,对腰椎骨密度评分、beta-crosslaps水平和空腹尿钙/肌酐水平3个因素进行多因素非条件Logistic回归分析,结果提示只有beta-crosslaps水平与结石出现呈现相关性(P=0.012).结论:LHRH类似物在治疗前列腺癌的同时对机体骨代谢存在显著影响,将造成肾结石形成;而监测血清beta-crosslaps水平变化将有助于对肾结石的早期发现和干预.

目的:评价同期双侧输尿管软镜碎石术(SB-FURL)治疗双侧≤1.5 cm肾结石的有效性及安全性.方法:回顾性分析71例双侧≤1.5 cm肾结石的患者的临床资料,均采用SB-FURL治疗,结石最大径(11.8±2.3) mm.评估手术时间、结石清除率(SFR)、术后并发症发生率和重复治疗率.结果:71例患者平均手术时间为(55.3±25.7) min,住院天数为(2.4±2.1)d.一次SB-FURL术后SFR为73.2％(52/71),5例(7％)接受了≥2次的治疗.71例共行逆行软性输尿管镜下钬激光碎石术77次,平均1.08次/人.术后3个月总SFR为88.7％(63/71),总并发症发生率为12.6％(9/71),其中输尿管假道形成1例,输尿管穿孔并肾周血肿1例,术后发热6例(8.4％).结论:SB-FURL治疗双侧≤1.5cm肾结石是安全有效的,值得临床推广和应用.

目的 分析戈舍瑞林联合比卡鲁胺治疗前列腺癌的效果及不良反应.方法 40例前列腺癌患者,根据计算机随机分组法将其分为对照组及试验组,各20例.对照组采用比卡鲁胺治疗,试验组采用戈舍瑞林联合比卡鲁胺治疗.比较两组治疗效果及不良反应发生情况.结果 试验组总有效率为95％,对照组总有效率为65％,试验组总有效率高于对照组,差异具有统计学意义(P<0.05).试验组不良反应发生率为30％,对照组不良反应发生率为35％,试验组不良反应发生率低于对照组,但差异无统计学意义(P>0.05).结论 戈舍瑞林联合比卡鲁胺治疗前列腺癌效果显著,且不增加不良反应,值得临床推广应用.

Objective To retrospectively analyze the different clinical stages of patients with prostate cancer,and to investigate it's correlation with body mass index (BMI).Methods 363 patients with prostate cancer were enrolled from January 2008 to December 2016.There were 141 cases of stage Ⅱ,Ⅲ in 20 cases,202 cases of stage Ⅳ.According to the stratification of BMI (emaciation group,normal group,overweight group,obesity group),clinical data of different groups of prostate cancer patients were compared to analyze there correlation with BMI.Results Patient's age,pre-PSA concentration,Gleason scores and PSA density were significantly correlated with clinical stage (P ＜ 0.05).Prostate volume and weight had no significant correlation with staging.There was a significant correlation between different strata of BMI and clinical stage (P ＜ 0.05).Conclusion The different strata of BMI are closely related to the clinical stage.The higher BMI,the higher risk of the prostate cancer.

目的:探讨膀胱癌术前药物保留灌注膀胱降低手术切口膀胱癌种植转移率的有效性及其可能机制.方法:构建大鼠膀胱癌模型,分别获取药物处理后及生理盐水处理后的定量膀胱肿瘤组织.取部分两组处理后组织进行流式细胞仪检测,观察两组处理后肿瘤组织细胞凋亡率.健康SD大鼠60只随机分为实验组及对照组,实验组大鼠腹壁切口种植药物处理后的肿瘤组织,对照组种植生理盐水处理后的肿瘤组织,种植后观察两组在不同时间段成瘤情况及是否可以减少膀胱癌组织在手术切口处的种植转移率.结果:种植后不同时间段切口出现可触摸肿物的实验组及对照组的大鼠例数,2周后分别为1只(3.3％)和4只(13.3％),3周后分别为4只(13.3％)和10只(33.3％),4周后分别为5只(16.6％)和16只(53.3％),观察至第6周,未再见新增转移大鼠.种植后实验组及对照组的大鼠切口肿物直径平均大小,2周后分别为0.3 cm和0.45 cm,3周后分别为0.65 t.m和1.25 cm,4周后分别为1.05 cm和1.87 cm,6周后分别为1.56 cm和2.45c.m.实验组及对照组处理后肿物组织细胞凋亡率分别为:(36.67±1.63)％,(9.23±1.03)％.结论:在大鼠膀胱癌切口种植转移模型中,膀胱药物保留灌注后的肿瘤组织有较低的种植转移率.抗肿瘤药物的膀胱灌注对肿瘤的细胞及组织有杀灭作用,减少了具有转移能力的肿瘤细胞及组织的数量.

Objective To investigate clinicopathological features of primary testicular carcinoid tumor and diagnosis and treatment.Methods Light microscopy and immunofluorescence staining were used to detect 3 cases of primary testicular carci-noid tumor.Results 3 cases of primary carcinoid tumors had clear dividing line ,tender swelling of the testis,and luidity of sec-tion.Its cells were small,columnar or polygon,and its cytoplasm medium with uniform size ,stippling chromatin and eosinophilic granular cytoplasm.The nucleus was located in center ,round and single,chromatin of punctiform,without mitosis.Tumor cells were arranged as cords and nested compilation .There were some large and irregular adenoid structures .Fiber spacing was seen a-mong tumor cells and without lymphocytic infiltration .The cellular level was obscure with indistinctive atypia and vascular circle . Immunofluorescence staining showed that NSE ,Syn and CgA were positively expressed ,Vimentin was negatively expressed .Con-clusion Primary testicular carcinoid tumor is extremely rare in the clinic ,without the unity of its character ,and it has to be dif-ferentiated from other orchioncuses and metastatic carcinoid tumor .