A photo-switchable supramolecular glycochip was fabricated via host-guest complexation between surface-immobilized azobenzene and galactose-modified pillar[5]arene. This platform captures suspension tumor cells through multivalent carbohydrate-protein interactions for the construction of QCM cell sensors. UV irradiation triggers disassembly of the host-guest complex, enabling reagent-free cell release. The chip regeneration is then achieved by visible light irradiation to restore the trans-azobenzene configuration, followed by re-immersion in Gal-P[5] solution to reform the complex. The system allows real-time analysis of cell surface glycosylation under physiological conditions.

Multidrug resistance (MDR) has become a major challenge in tumor chemotherapy, primarily associated with the overexpression of P-glycoprotein (P-gp). Inhibiting P-gp expression and function through redox dyshomeostasis has shown great potential for reversing MDR. Here, a nanoscale system of copper-based metal-organic framework (HA-CuMOF@DOX) modified with hyaluronic acid (HA) was constructed to overcome MDR via two-way regulation of redox homeostasis under hypoxia. HA-CuMOF@DOX is a spherical glutathione (GSH) responsive nanoparticle with a drug loading capacity of 20.69 %, which could deplete GSH through Cu2+ and electrophilic ligands, and generate •OH via a Fenton-like reaction. In vitro experiments suggested that the nanoparticles had good targetability to cancer cells and biocompatibility to normal cells. HA-CuMOF@DOX was successfully internalized by drug-resistant human hepatoma carcinoma cell line (HepG2-ADR). It aggravated redox dyshomeostasis via dual regulation, inducing mitochondrial damage, reducing intracellular adenosine triphosphate (ATP) levels, and downregulating P-gp to overcome HepG2-ADR drug resistance. More importantly, in vivo experiments demonstrated an 80.69 % tumor growth inhibition in nude mice bearing HepG2-ADR cells. This work represents a significant advancement in the development of effective treatments for drug-resistant tumors.

Background: Kidney stone disease is a global disease; however, it has not been totally understood. Calcium oxalate (CaOx) stone is the dominant type of kidney stone, and the potential factors involved in its formation are yet to be explored. Clinically, we found that the CaOx stones in patients were mainly unilateral; therefore, systemic factors cannot explain them, although some local factors must be involved. Urinary microbiota is involved in stone formation. Therefore, this study aimed to explore the association between the urinary microbiota and CaOx stones and provide insight into the medical treatment and prevention of CaOx stones. Methods: Sixteen pelvic urine samples were collected from the stone and non-stone sides of patients with unilateral CaOx stones following strict criteria. The 16S rRNA gene sequencing was performed on each pair of pelvic urine samples at the species level. Many bioinformatic analyses were conducted to explore the potential factors affecting CaOx stone formation. Results: Although no statistically significant difference was found between the overall microbiota of the pelvis urine from the two sides. Many biologically distinct taxa were observed, including many bacteria found in previous studies, like Proteobacteria, Actinobacteria, Firmicute and Enterobacter cloacae and so on. What's more, despite these common bacteria, our current study added to these bacterial communities with additional identification of Deinococcus-Thermus, Coriobacteriia, Porphyromonas and Ralstonia. To predict the functions of these microbiota, Kyoto Encyclopedia for Genes and Genomes and MetaCyc analysis were conducted and immunometabolism might be an important pathway. Moreover, a random forest predictor was constructed to distinguish the stone side from the non-stone side, with an accuracy of 62.5%. Conclusion: Our research profiled the microbiome in the pelvis urine from both the stone and non-stone sides of patients with unilateral CaOx stones, provided insight into the dominant role of urinary dysbiosis in CaOx stones formation. Furthermore, this study also predicted the potential crosstalk among urinary microbiota, immunometabolism, and CaOx stones.

Exosomes are lipid bilayer vesicles with a diameter of 40–100 nm secreted by almost all cells. They have been found play crucial regulatory roles in various diseases. With the development of exosomes engineering technology, exosome-based drug delivery has also rapidly evolved. Bladder cancer is a worldwide disease with high morbidity and recurrence but lack of funding, so it is also called Cinderella. Some explorations have demonstrated that exosomes are important in the development, prognosis, diagnosis and drug delivery of bladder cancer. With the rapid development of Mass spectrometry and next-generation sequencing, increasing numbers of differentially expressed molecules derived from exosomes have been found in bladder cancer. Exosomes and their contents are largely involved in bladder cancer progression, engineering of these exosomes with the targeted genes improves their potential for drug delivery of bladder cancer. Furthermore, exosomes and their contents are relate to many characteristics of bladder cancer. Herein, we briefly search 59 researches to explore the cargoes encapsuled in exosomes of bladder cancer patients. We also summarize the biogenesis, function, expression profiles, engineering approaches and biological mechanisms of exosomes and their contents for the diagnosis, prognosis and drug delivery for bladder cancer. We aim to make it clear whether exosomes are the glass slippers of Cinderella. Graphical Abstract

Androgen receptor (AR) signaling is essential in prostate cancer treatment. For many years, androgen deprivation therapy (ADT) has been primarily applied to manage advanced prostate cancer. However, most individuals with metastatic hormone-sensitive prostate cancer (mHSPC) administered ADT alone are at risk of developing metastatic castration-resistant prostate cancer (mCRPC) in less than two years. New approaches employing novel AR inhibitors (ARi) as intensified upfront systemic treatment in mHSPC have recently demonstrated substantial benefits in delaying disease progression and prolonging overall survival. Administration of novel ARi has become the new standard of care in mHSPC. The new landscape simultaneously makes treatment choice more challenging. This review provides comprehensive data on molecular structure, pharmaceutical properties, and efficacy and safety profiles reported by pivotal clinical trials. We also discuss future directions with ongoing Phase III trials of novel ARi in mHSPC. Considering these biological and clinical insights, this review aimed to provide a comprehensive understanding of differences in the development and applications of novel ARi for mHSPC, which may be helpful in designing strategies for first-line treatment choices.

经皮肾造瘘术和经皮肾镜取石术(percutaneous nephrolithotripsy,PCNL)并发脾脏损伤是一项罕见但可能致命的并发症,国外报道 20 余例[1-3],国内仅2 例报道[4-5].华中科技大学同济医学院附属同济医院收治 2 例经皮肾手术并发脾脏损伤的患者,现报告如下.

Recent studies suggest that cancer stemness drives the acquired drug resistance process in cancer therapy. The complementary information provided by multi-omics data can help us to gain a deeper understanding of this process. This study aims to elucidate the impact of cancer stemness on the frontline treatment of clear cell renal cell carcinoma (ccRCC). Consensus clustering based on stem/progenitor signatures refined 3 subgroups in 1,730 tumor samples. We identified master regulons that regulate cancer stemness phenotypes, including key transcription factors, DNA methyltransferases, and promoter methylation probes. In addition, we compared the clinicopathological traits, genomic heterogeneity, cancer hallmarks, tumor microenvironment (TME), and oncological prognosis of the stemness subgroups. Cancer stemness was correlated with reduced efficiency of immune checkpoint blockade therapy. Cancer stemness profoundly affects the prognosis and treatment outcome of ccRCC by increasing genomic instability, tumor-associated malignant events, and immunosuppressive factors. For clinical application, we established and validated a 243-gene signature from stem/progenitor-related genes to distinguish anti-PD-1 outcomes. Overall, this presented study suggested that cancer stemness leads to adaptive resistance to anti-PD-1 treatment in CD8+ T-infiltrated ccRCC and provides a new reference for strategy development to further improve immunotherapy response rates.

Accumulating evidence has suggested the impact of senescence on tumor progression, but no report has yet described how senescence shapes the tumor microenvironment of clear cell renal cell carcinoma (ccRCC). The objective of this study was to delineate the senescence features of ccRCC and its role in shaping the tumor microenvironment through a comprehensive analysis of multiple datasets, including 2,072 ccRCC samples. Unsupervised consensus clustering identified three senescence subtypes, and we found that the senescence-activated subtype survived the worst, even in the condition of targeted therapy and immunotherapy. The activated senescence program was correlated to increased genomic instability, unbalanced PBMR1/BAP1 mutations, elevated immune cell infiltration, and enhanced immune inhibitory factors (cancer-associated fibroblasts, immune suppression, immune exclusion, and immune exhaustion signaling). A senescence score based on nine senescence-related genes (i.e., P3H1, PROX1, HJURP, HK3, CDKN1A, AR, VENTX, MAGOHB, and MAP2K6) was identified by adaptive lasso regression and showed robust prognostic predictive power in development and external validation cohorts. Notably, we found that the senescence score was correlated to immune suppression, and the low-score subgroup was predicted to respond to anti-PD-1 therapy, whereas the high-score subgroup was predicted to respond to Sunitinib/Everolimus treatment. Collectively, senescence acted as an active cancer hallmark of ccRCC, shaped the immune microenvironment, and profoundly affected tumor prognosis and drug treatment response.

Background:Epithelial-mesenchymal transition (EMT) plays a vital role in tumor metastasis and drug resistance. It has been reported that EMT is regulated by several long noncoding RNAs (lncRNAs). We aimed to identify EMT-related lncRNAs and develop an EMT-related lncRNA prognostic signature in kidney renal clear cell carcinoma (KIRC).Materials and Methods:In total, 530 ccRCC patients with 611 transcriptome profiles were included in this study. We first identified differentially expressed EMT-related lncRNAs. Then, all the samples with transcriptional data and clinical survival information were randomly split into training/test sets at a ratio of 1 : 1. Accordingly, we further developed a twelve differentially expressed EMT-related lncRNA prognostic signature in the training set. Following this, risk analysis, survival analysis, subgroup analysis, and the construction of the ROC curves were applied to verify the efficacy of the signature in the training set, test set, and all patients. Besides, we further investigated the differential immune infiltration, immune checkpoint expression, and immune-related functions between high-risk patients. Finally, we explored the different drug responses to targeted therapy (sunitinib and sorafenib) and immunotherapy (anti-PD1 and anti-CTLA4).Results:A twelve differentially expressed EMT-related lncRNA prognostic signature performed superior in predicting the overall survival of KIRC patients. High-risk patients were observed with a significantly higher immune checkpoint expression and showed better responses to the targeted therapy and immunotherapy.Conclusions:Our study demonstrates that the twelve differentially expressed EMT-related lncRNA prognostic signature could act as an efficient prognostic indicator for KIRC, which also contributes to the decision-making of the further treatment.

Background Calcium oxalate (CaOx) is the most common type of kidney stone, but the mechanism of CaOx stones formation remains unclear. The injury of renal cells such as ferroptosis and autophagy has been considered a basis for stones formation. Methods We conducted transmission electron microscope (TEM), reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), and C11-BODIPY analysis to explore whether CaOx could induce autophagy-dependent ferroptosis in vivo and in vitro. To explore the possible mechanism, we conducted bioinformatic analysis of patients with or without CaOx stones, Western blot and qPCR were used to identify the different genes we found in bioinformatic analysis. Results In our study, we found that CaOx could induce autophagy-dependent ferroptosis no matter in vivo or in vitro, which might finally lead to urolithiasis. Bioinformatic analysis of the GSE73680 dataset indicated that the expression of caveolin-1 (CAV1) was higher in control patients than CaOx stone patients, the STRING database indicated that CAV1 might interact with low density lipoprotein receptro-related protein 6 (LRP6), Gene Set Enrichment Analysis (GSEA) showed that the WNT pathway positively associated with the control group while negatively related to the stone group, and LRP6 was the core gene of the WNT pathway. Western blot found that CAV1, LRP6, and Wnt/β-Catenin were decreased in Human Kidney2 (HK2) cells stimulated with CaOx. Furthermore, the WNT pathway was considered to be involved in autophagy and ferroptosis. Conclusions We presumed that CAV1 could ameliorate autophagy-dependent ferroptosis through the LRP6/Wnt/β-Catenin axis, and finally alleviate CaOx stone formation.

Kidney renal clear cell carcinoma (KIRC) has high morbidity and gradually increased in recent years, and the rate of progression once relapsed is high. At present, owing to lack of effective prognosis predicted markers and post-recurrence drug selection guidelines, the prognosis of KIRC patients is greatly affected. Necroptosis is a regulated form of cell necrosis in a way that is independent of caspase. Induced necroptosis is considered an effective strategy in chemotherapy and targeted drugs, and it can also be used to improve the efficacy of immunotherapy. Herein, we quantified the necroptosis landscape of KIRC patients from The Cancer Genome Atlas (TCGA) database and divided them into two distinct necroptosis-related patterns (C1 and C2) through the non-negative matrix factorization (NMF) algorithm. Multi-analysis revealed the differences in clinicopathological characteristics and tumor immune microenvironment (TIME). Then, we constructed the NRG prognosis signature (NRGscore), which contained 10 NRGs (PLK1, APP, TNFRSF21, CXCL8, MYCN, TNFRSF1A, TRAF2, HSP90AA1, STUB1, and FLT3). We confirmed that NRGscore could be used as an independent prognostic marker for KIRC patients and performed excellent stability and accuracy. A nomogram model was also established to provide a more beneficial prognostic indicator for the clinic. We found that NRGscore was significantly correlated with clinicopathological characteristics, TIME, and tumor mutation burden (TMB) of KIRC patients. Moreover, NRGscore had effective guiding significance for immunotherapy, chemotherapy, and targeted drugs.

Aims: We aimed at exploring the role of nicotinamide adenine dinucleotide phosphate oxidase subunit 4 (Nox4) in the regulation of hypercalciuria-induced renal oxidative damage and crystal depositions.Results: High calcium activated Nox4 expression through protein kinase C (PKC). Downregulation of Nox4 expression attenuated hypercalciuria-induced osteoblast-associated protein expression, oxidative stress injury, and crystal deposition in rat kidneys of 1,25-dihydroxyvitamin D3 (VitD) urolithiasis model. Further, calcium-induced activation of mitogen-activated protein kinase (MAPK), overexpression of osteoblast-associated protein, oxidative stress injury, apoptosis, and calcium salt deposition in normal rat kidney epithelial-like (NRK-52E) cells were reversed by downregulating Nox4 expression but were enhanced by upregulating Nox4 expression in vitro. Moreover, calcium-induced increases of osteoblast-associated protein expression were attenuated by the c-Jun-N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) inhibitors.Innovation: Our results demonstrated the effect of Nox4 in the pathological process of kidney stones in in vitro and in vivo studies for the first time. Calcium aggravates renal oxidative stress injury and crystal deposition by activating the Nox4-related reactive oxygen species (ROS)-ERK/JNK pathway in the rat kidney. This study is expected to provide a new theoretical basis for the prevention and treatment of kidney stones.Conclusion: Nox4-derived ROS induced by calcium through PKC caused oxidative stress damage and apoptosis in renal tubular epithelial cells; in addition, Nox4-derived ROS induced by calcium mediated abnormal activation of the bone morphogenetic protein 2 (BMP2) signaling pathway through the MAPK signaling pathway, which induced renal tubular epithelial cells to transdifferentiate into osteoblast-like cells, resulting in the formation of a kidney stone.

Background: To evaluate the safety, efficacy and cost of paravertebral block anesthesia for ureteral stones patients undergoing ureteroscopic lithotripsy. Methods: Four hundred and eighty-two patients who underwent ureteroscopy for unilateral ureteral stones were incorporated into our retrospective study. A propensity-matched comparison in patients with paravertebral nerve block anesthesia (PVB) group and general anesthesia (GA) group was performed. Intraoperative hemodynamic parameters, operative time, visual analog scale for pain, stone-free rate, anesthetic cost and postoperative hospital stay were compared between the two groups. Results: Sixty-one GA cases were propensity matched to 61 PVB cases. In the PVB group, all the procedures were completed successfully without anesthesia conversion. Significantly less intraoperative severe hypotensive (P = 0.002) and arrhythmia (P < 0.001) episodes in PVB group. There were no significant differences in operative time (p = 0.702), initial stone-free rate (p = 0.686), and total stone-free rate (p = 0.794) between the two groups. The PVB group had lower postoperative pain and prolonged analgesia (p = 0.007). The postoperative hospital stay in the PVB group was significantly shorter (3.20 +/- 0.73 vs 3.84 +/- 1.32 d, p = 0.001). And the cost of anesthesia was lower in the PVB group (195.47 +/- 13.01 vs 396.31 +/- 36.45 US dollars, p < 0.001). Conclusion: Under PVB anesthesia, URS can be successfully completed without anesthetic transformation, and its efficacy and safety have been demonstrated. When economic aspects are taken into consideration, PVB seems to be a more economical and effective anesthetic method of URS. (c) 2021 Asian Surgical Association and Taiwan Robotic Surgery Association. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).

Ubiquitin modification is the most common protein post-translational modification (PTM) process in organisms, and 1332 ubiquitin regulators have been identified in humans. Ubiquitin regulators, especially E3 ligases and deubiquitinases, are widely involved in immune processes. This study aims to explore the ubiquitin modification features of clear cell renal cell carcinoma (ccRCC) and to elucidate the role of such ubiquitin modifications in shaping anti-tumor immunity and individual benefits from immune checkpoint blockade (ICB). A comprehensive analysis was performed in the TCGA cohort ( n = 530) and GEO cohort ( n = 682). RNA sequencing data of 758 differentially expressed regulators, which was validated by the proteomics data, was used for k-means unsupervised consensus clustering and three ubiquitin patterns of ccRCC were identified. Then, we focused on the ubiquitin modification and tumor progression signatures, immune infiltration characteristics, and prognostic value. The three patterns with different ubiquitin modification signatures correspond to “immune desert phenotype,” “immune resistance phenotype,” and “immune-inflammatory phenotype,” respectively. To facilitate clinical application, we constructed a ubiquitin score to evaluate individual patients’ ubiquitination outcome, and it was demonstrated to be an independent risk factor for overall survival (OS) in multivariate Cox analysis. It was found that the high score group was correlated to higher immune cells infiltrating level and PD-1/PD-L1/CTLA-4 expression. More importantly, we found that the high score group was predicted to be sensitive to anti-PD-1 treatment, while the low-score group showed lower predicted IC50 values in treatment with Pazopanib and Axitinib. In summary, this study elucidated the potential link between ubiquitin modification and immune infiltration landscape of ccRCC for the first time and provided a new assessment protocol for the precise selection of treatment strategies for patients with advanced ccRCC.

Idiopathic hypercalciuria is an important risk factor for the formation of calcium-containing kidney stones. Matrix metalloproteinase-9 (MMP-9) is closely related to cell and tissue remodeling and is involved in ectopic tissue calcification. However, little is known about its role in kidney stone formation. In this study, we found that the expression of MMP-9 and that of osteoblastic-related proteins was increased in normal rat kidney epithelial-like (NRK-52E) cells following treatment with a high concentration of calcium, while the knockout or overexpression of MMP-9 could, respectively, significantly inhibit or upregulate the expression of osteoblastic-related proteins and calcium crystal deposition. In addition, apoptosis and calcium crystal deposition were significantly reduced in Sprague–Dawley rats with 1,25(OH)2D3-induced hypercalciuria following MMP-9 inhibitor I treatment. Furthermore, inhibiting reactive oxygen species (ROS) production or the nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) pathway significantly reduced calcium-induced MMP-9 expression and calcium crystal deposition. In summary, our results suggested that a high calcium concentration promotes epithelial–osteoblastic transformation and calcium crystal deposition in renal tubule cells by regulating the ROS/NF-κB/MMP-9 axis and identified a novel role for MMP-9 in regulating calcium-induced calcium crystal deposition in renal tubules.

The oxidative injury of renal tubular epithelial cells caused by inflammation and oxidative stress induced by hyperoxaluria is an important factor in the kidney calcium oxalate (CaOx) stone formation. Resveratrol (RSV) has been reported to reduce oxidative injury to renal tubular epithelial cells, and autophagy is critical for the protective effect of resveratrol. However, the protective mechanism of RSV in oxalate-induced oxidative injury of renal tubular cells and the role of autophagy in this process are still unclear. In our study, glyoxylic acid monohydrate-induced rats were treated with or without resveratrol, and it was detected that the overexpression of oxidant species, CaOx crystal deposition, apoptosis level, inflammatory cytokines and osteoblastic-associated protein expression were reversed by resveratrol. Additionally, Resveratrol pretreatment significantly reversed oxalate -induced decline in cell viability, cell damage, oxidant species overexpression, and osteogenic transformation in normal rat kidney epithelial-like (NRK-52E) cells. Furthermore, we found that RSV pretreatment promoted intracellular LC3II upregulation, p62 downregulation, and autophagosome formation, whereas 3-methyladenine treatment reduced this effect. Moreover, RSV induced the expression of transcription factor EB (TFEB) in the nucleus of NRK-52E cells in a concentration-dependent manner. After transfection of NRK-52E cells with TFEB siRNA, we showed that the RSV-induced increase in TFEB expression and autophagosome formation were inhibited. Simultaneously, RSV-induced NRK-52E cells protection was partially reversed. These results suggested that RSV regulates oxalate-induced renal inflammation, oxidative injury, and CaOx crystal deposition in vitro and in vivo through the activation of a TFEB-induced autophagy.

目的 总结机器人辅助腹腔镜根治性膀胱切除(RARC)+体腔内原位回肠新膀胱术的初步经验及手术要点,分析其可行性和安全性.方法 对华中科技大学同济医学院附属同济医院泌尿外科收治的10例膀胱癌患者行RARC+体腔内原位回肠新膀胱术.对患者的临床病理资料、围手术期情况、手术要点进行回顾性分析总结.结果 本组10例膀胱癌患者均为男性,年龄39～67岁,中位年龄57岁,美国麻醉医师协会(ASA)评分2～3分,术前均行经尿道膀胱肿瘤电切术,术后病理诊断均为高级别浸润性尿路上皮癌.手术时间330～540 min,术中出血量150～600 ml,术后住院时间10～19 d,术后病理报告双侧输尿管、尿道残端切缘均为阴性,除1例患者外,其余9例患者均未发现淋巴结转移.最初治疗的2例患者术后因营养状况不良出现肠瘘,需进一步手术治疗.结论 本组研究数据初步表明,RARC+体腔内原位回肠新膀胱术在技术上具有可行性和安全性.通过严格把握患者适应证、围手术期全面管理、术中精细操作,在开展机器人辅助技术比较成熟的中心能使患者达到较满意的效果.

Objectives Coronavirus disease 2019 (COVID-19) is rapidly spreading worldwide. Lianhua Qingwen capsule (LQC) has shown therapeutic effects in patients with COVID-19. This study is aimed to discover its molecular mechanism and provide potential drug targets. Materials and Methods An LQC target and COVID-19-related gene set was established using the Traditional Chinese Medicine Systems Pharmacology database and seven disease-gene databases. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis and protein-protein interaction (PPI) network were performed to discover the potential mechanism. Molecular docking was performed to visualize the patterns of interactions between the effective molecule and targeted protein. Results A gene set of 65 genes was generated. We then constructed a compound-target network that contained 234 nodes of active compounds and 916 edges of compound-target pairs. The GO and KEGG indicated that LQC can act by regulating immune response, apoptosis and virus infection. PPI network and subnetworks identified nine hub genes. The molecular docking was conducted on the most significant gene Akt1, which is involved in lung injury, lung fibrogenesis and virus infection. Six active compounds of LQC can enter the active pocket of Akt1, namely beta-carotene, kaempferol, luteolin, naringenin, quercetin and wogonin, thereby exerting potential therapeutic effects in COVID-19. Conclusions The network pharmacological strategy integrates molecular docking to unravel the molecular mechanism of LQC. Akt1 is a promising drug target to reduce tissue damage and help eliminate virus infection.

目的 比较上尿路尿路上皮癌(UTUC)患者术前输尿管镜活检与术后病检的相符情况,探讨输尿管镜活检在UTUC术前诊断中的价值.方法 统计符合入组标准的55例患者数据,比较术前活检与术后病理结果在肿瘤类型、级别、浸润性等指标的一致性.结果 55例患者中52例经病理证实为尿路上皮癌.27例活检考虑高级别,96.3％(26/27)的患者术后病理符合高级别;21例活检考虑低级别,52.4％(11/21)的患者术后病理符合低级别,总体符合率为72.7％.51.9％(27/52)的患者在活检标本中可见上皮下结缔组织,32.7％(17/52)明确有浸润;5.8％(3/52)的患者镜下可见肌层,仅1例明确有肌层浸润.结论 输尿管镜活检能为大多数UTUC患者提供术前病理诊断,其对高级别肿瘤患者的诊断一致性更高,对于低级别肿瘤患者有可能被低估.输尿管镜活检对肿瘤浸润性及分期的诊断存在明显局限性.

2019年12月以来,湖北省武汉市发现了多例新型冠状病毒感染的肺炎(NCP)患者,随着疫情的蔓延,我国其他地区及境外也相继发现了相关病例,该病通过基因测序确定为一种新的冠状病毒,世界卫生组织(WHO)将其命名为2019冠状病毒病(Corona Virus Disease 2019,COVID-19).该病毒传染性极强,主要通过飞沫和密切接触的途径传播,泌尿外科老年患者居多,往往伴有不同程度的基础疾病或免疫功能低下,这些特点导致感染NCP机会明显增加,且易发展为重症患者.本文从泌尿外科日常防控工作出发,结合NCP疫情相关国家政策方案及最新研究进展,制定了泌尿外科诊疗防控工作建议.