Zhihong Liu

Background: Urinary tract reconstruction is a key technical barrier in murine kidney transplantation due to the tiny ureteral caliber. Conventional methods are technically demanding with high morbidity. This study assesses a refined intraluminal stenting approach for better surgical stability, fewer complications, and preserved anti-reflux structural anatomy of the ureterovesical junction. We performed 88 orthotopic mouse kidney transplantations using three distinct reconstruction modalities: bladder patch ( n = 31), ureter implantation ( n = 28), and intraluminal stenting ( n = 29). The stenting protocol utilized a micro-polyethylene (PE) stent to achieve end-to-end ureteral alignment. Outcomes included operative efficiency, learning curve trajectories, postoperative survival, and urinary-related morbidity. Results: The stenting cohort achieved a 14-day survival rate of 96.6% (28/29), significantly higher than the bladder patch group (67.7%, 21/31; p = 0.006), while the difference compared with the ureter implantation group (82.1%, 23/28) did not reach statistical significance ( p = 0.102). Intraluminal stenting markedly reduced reconstruction time (8‘22’‘±0’41’’, p < 0.05 vs. both control groups) and was associated with an accelerated proficiency acquisition curve. The overall urological morbidity in the stenting group was 10.3% (3/29), consisting of 1 case of mild urinary leakage and 2 cases of mild hydronephrosis, which was significantly lower than in the bladder patch (58.1%, 18/31) and ureter implantation (42.9%, 12/28) cohorts ( p < 0.05 for morbidity comparison). Notably, this approach effectively precluded severe complications including ischemic necrosis, ureteral dislodgement, and obstruction, with no urinary tract reconstruction-related deaths observed. Conclusions: This retrospective study shows that the intraluminal stenting technique offers a reliable and highly reproducible approach for urinary tract reconstruction in murine kidney transplantation. This modality significantly minimizes technical complexity and postoperative morbidity, and maintains the intact ureterovesical anatomy that provides the structural foundation for physiological anti-reflux function. It provides an optimized surgical platform for short-term experimental protocols, particularly in acute rejection research.

Dysregulation of chromatin is considered one of the root causes of tumor occurrence and progression. In the past two decades, the SWItch/Sucrose Non-Fermentable (SWI/SNF) complex, a crucial player in chromatin remodeling, has emerged as a significant focus of cancer research and has been found to play a pivotal role in cancer development and progression through the regulation of the expression of cancer-related genes. Notably, studies have unveiled that genetic mutations and functional alterations in the SWI/SNF complex subunits, such as ARID1A, are prevalent across a broad spectrum of cancers, but the role of this complex in genitourinary neoplasms has not been systematically summarized yet. Therefore, in this review, we have summarized the mechanisms of SWI/SNF complex components in the occurrence and development of urological tumors. In addition, we have also discussed its clinical value and presented treatment strategies that target the SWI/SNF complex in order to provide a comprehensive overview of the status of current research and future areas of clinical focus in this field.

Introduction: Previous research has shown that laminin α5 ( LAMA5 ) is es­sential for a variety of biological processes, including cellular adhesion, cell differentiation, migration, and metastasis. However, the role of LAMA5 in bladder cancer (BC) has not been explored before. Therefore, we...

Background: The cardiotoxicity of doxorubicin (DOX) limits its use in cancer treatment. To address this limitation, we developed a novel animal model that uses beagle dogs to investigate DOX-induced cardiac disorders. Unfortunately, the lack of effective cardioprotection strategies against DOX-induced cardiotoxicity poses a significant challenge. To establish a canine model for low-mortality DOX-induced cardiac dysfunction and explore the relationship between inflammatory reprogramming and DOX-related cardiotoxicity. Methods: Twenty male beagle dogs aged two years were randomly assigned into the DOX (N = 10) and control (CON) (N = 10) groups. DOX was infused (1.5 mg/kg) every two weeks until doses cumulatively reached 12 mg/kg. Serum biomarkers and myocardial pathology were evaluated, while real-time fluorescence-based quantitative polymerase chain reaction (RTFQ-PCR), two- and three-dimensional echocardiography (2DE and RT3DE), functional enrichment, and matrix correlation were also performed. Results: In the DOX group, high-sensitive cardiac troponin T (hs cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were significantly increased. Myocardial pathology indicated early to medium myocardial degeneration via a decreased cardiomyocyte cross-sectional area (CSA). Increased levels of inflammatory gene transcripts (interleukin 6 (IL6), tumor necrosis factor (TNF), transforming growth factor β (TGFβ), intercellular adhesion molecule 1 (ICAM1), interleukin 1 (IL1), interleukin 1β (IL1β), and interleukin 8 (IL8)), of collagen metabolism and deposition regulatory genes (matrix metalloproteinase (MMP) family and tissue inhibitor of matrix metalloproteinase (TIMP) family), and the natriuretic peptide family (NPS) (natriuretic peptide A, B and C (NPPA, NPPB, and NPPC)) were observed. Strain abnormalities in the right ventricular longitudinal septal strain (RVLSS), right ventricular longitudinal free-wall strain (RVLFS), left ventricular global longitudinal strain (LVGLS), and left ventricular global circumferential strain (LVGCS) were detected at week 28 (vs. week 0 or CON group, p < 0.05, respectively). A significant decline in RVLSS and RVLFS occurred at week 16, which was earlier than in the corresponding left ventricular areas. A significant right ventricular ejection fraction (RVEF) decline was noted at week 16 (vs. week 0, 33.92 ± 3.59% vs. 38.58 ± 3.58%, p < 0.05), which was 12 weeks earlier than for the left ventricular ejection fraction (LVEF), which occurred at week 28 (vs. week 0, 49.02 ± 2.07% vs. 54.26 ± 4.38%, p < 0.01). The right ventricular strain and functional damages correlated stronger with inflammatory reprogramming (most R from 0.60 to 0.90) than the left ones (most R from 0.30 to 0.65), thereby indicating a more pronounced correlation. Conclusions: Inflammatory reprogramming mediated disorders of strain capacity and cardiac function predominantly in the right side of the heart in the newly established DOX-related cardiomyopathy beagle dog model.

Renal cell carcinoma (RCC) accounts for about 2% of cancer diagnoses and deaths worldwide. Recent studies emphasized the critical involvement of microbial populations in RCC from oncogenesis, tumor growth, and response to anticancer therapy. Microorganisms have been shown to be involved in various renal physiological and pathological processes by influencing the immune system function, metabolism of the host and pharmaceutical reactions. These findings have extended our understanding and provided more possibilities for the diagnostic or therapeutic development of microbiota, which could function as screening, prognostic, and predictive biomarkers, or be manipulated to prevent RCC progression, boost anticancer drug efficacy and lessen the side effects of therapy. This review aims to present an overview of the roles of microbiota in RCC, including pertinent mechanisms in microbiota-related carcinogenesis, the potential use of the microbiota as RCC biomarkers, and the possibility of modifying the microbiota for RCC prevention or treatment. According to these scientific findings, the clinical translation of microbiota is expected to improve the diagnosis and treatment of RCC.

Muscle‐invasive bladder cancer (MIBC) is characterized by a highly complex immune environment, which is not well understood. Interleukin‐6 (IL‐6) is generated and secreted by multifarious types of cells, including tumor cells. This study was aimed at demonstrating that the levels of IL‐6 and the number of myeloid‐derived suppressor cells (MDSCs), with a positive correlation between them, increased in MIBC tissues, promoting MIBC cell proliferation, especially in patients with recurrence. In coculture analysis, MDSCs, with the stimulation of IL‐6, could significantly lower the proliferation ability of CD4⁺ or CD8⁺ T lymphocytes. Further, this study demonstrated that IL‐6 could upregulate the mitogen‐activated protein kinase (MAPK) signaling pathway in MDSCs. The MAPK signaling inhibitor, aloesin, partially reversed the effects of IL‐6 on MDSCs. These data suggested that IL‐6 promoted MIBC progression by not only accelerating proliferation but also improving the immune suppression ability of MDSCs through activating the MAPK signaling pathway.

Renal cell carcinoma (RCC) is among the most common cancers of the genitourinary system. Once RCC has progressed to a high tumor stage, surgery is no longer the optimal option, and treatment with drugs is more suitable. However, a proportion of patients with advanced RCC (aRCC) experience accelerated progression following targeted therapy or immunotherapy, a condition known as hyperprogressive disease (HPD). There is a growing body of literature that recognizes the importance of HPD. In the present review, thousands of studies that describe a variety of treatments for aRCC were identified in PubMed, Web of Science, and Cochrane Library and analyzed to establish the severity of clinical outcomes. Therefore, we managed to perform a review related to HPD of aRCC in these databases. It was found that 7~74% of patients advanced into progressive disease, 0~45% of patients died during post-treatment assessment, possibly due to fatal HPD. However, risk factors, mechanisms, and predictive factors are still not entirely clear. It is suggested that combination therapies might play a pivotal role in preventing HPD. Additional light needs to be shed on customization of therapies for aRCC after more data is collected and analyzed for HPD.