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Objective This study seeks to explore the impact of fast track surgery (FTS) with three-port in patients treated with laparoscopic radical cystectomy and ileal conduit on postoperative recovery, hospital stay and the complications. Methods This retrospective study analyzed 230 patients with invasive bladder cancer who underwent laparoscopic radical cystectomy at the Second Hospital of Anhui Medical University between December 2011 to January 2023. 50 patients received conventional surgery (CS) and 180 patients received FTS with three-port. Patients were assessed for time to normal diet consumption, time to passing first flatus, number of postoperative recovery days and complications. Trends of serum C-reactive protein levels were monitored preoperatively and on postoperative days 1, 3 and 7. Results Patients who underwent FTS with three-port had a shorter duration to first flatus ( P  < 0.05). And number of postoperative hospital days and the length of hospital stay were notably shorter in contrast to the CS group ( P  < 0.05). Serum CRP levels on postoperative day 7 were markedly reduced in those of the FTS group compared to the CS group ( P  < 0.05). Those of the CS group experienced more frequent rates of complications compared to those of the FTS with three-port group ( P  < 0.05). Conclusion Our findings demonstrate that the FTS with three-port program hastens postoperative recovery and reduces duration of hospital stay. It is safer and more effective than the CS program in the Chinese population undergoing laparoscopic radical cystectomy.

The study included 163 patients with muscle‐invasive bladder cancer (MIBC) from 14 hospitals, categorized into the neoadjuvant immunotherapy‐combined‐modality therapy (Neoimmu‐CMT), trimodal therapy (TMT), and neoadjuvant chemotherapy‐combined‐modality therapy (NAC‐CMT) subgroups. Propensity score matching (PSM) was utilized to mitigate baseline variability. Univariate and multivariate Cox analyses were used to identify potential prognostic factors. Biomarker assessment comprised immunohistochemistry and single‐cell RNA sequencing. After PSM, Neoimmu‐CMT demonstrated superior efficacy over NAC‐CMT and comparability to TMT. A clinical complete response to neoadjuvant treatment and lower clinical T stage were positive prognostic factors for Neoimmu‐CMT. Biomarker analysis showed that the immune phenotype of the tumor microenvironment (TME) was closely associated with bladder preservation outcomes. We assessed the potential relationship between various cell types in the TME and bladder preservation outcomes using single‐cell RNA sequencing. The results showed that the dynamic distribution of fibroblast and NK/T cell subclusters was associated with bladder preservation outcomes. In the future, the development of Neoimmu‐CMT will substantially expand its application in bladder preservation therapies.

Effective task scheduling has become the key to optimizing resource allocation, reducing operation costs, and enhancing the user experience. The complexity and dynamics of cloud computing environments require task scheduling algorithms that can flexibly respond to multiple computing demands and changing resource states. Therefore, we propose an enhanced Red-tailed Hawk algorithm (named ERTH) based on multiple elite policies and chaotic mapping, while applying this approach in conjunction with the proposed scheduling model to optimize the efficiency of task scheduling in cloud computing environments. We apply the ERTH algorithm to a real cloud computing environment and conduct a comparison with the original RTH and other conventional algorithms. The proposed ERTH algorithm has better convergence speed and stability in most cases of small and large-scale tasks and performs better in minimizing the task completion time and system load cost. Specifically, our experiments show that the ERTH algorithm reduces the total system cost by 34.8% and 36.4% relative to the traditional algorithm for tasks of different sizes. Further, evaluations in the IEEE Congress on Evolutionary Computation (CEC) benchmark test sets show that the ERTH algorithm outperforms the traditional or emerging algorithms in several performance metrics such as mean, standard deviation, etc. The proposal and validation of the ERTH algorithm are of great significance in promoting the application of intelligent optimization algorithms in cloud computing.

The edge computing paradigm is becoming increasingly commercialized due to the widespread adoption of wireless communication technologies and the growing demand for compute-intensive mobile applications. Edge computing complements the cloud computing model by deploying computation, storage, and network resources to the edge locations of wireless access networks, empowering end devices to run resource-intensive applications. In order to promote the commercialization of edge computing, it is important to explore effective ways to reduce the cost of edge computing networks. This paper provides a comprehensive review of the research findings in recent years, offering a clear perspective on the research dynamics. This paper first recalls the architectural framework of edge computing. Then, the main optimization objectives and optimization methods are comprehensively described. Mainstream mathematical models for cost reduction are then shown in depth. The paper also discusses the methods used to evaluate the effectiveness. Then, typical examples of typical application scenarios for edge computing networks are examined in depth. Finally, the paper identifies some unresolved issues. We expect future research to make more attempts in these directions.

Purpose The role of cytoreductive nephrectomy (CN) has been controversial with the advent of targeted therapy. Our study was to identify the prognostic value of CN combined with targeted therapy for treatment of metastatic renal cell carcinoma (mRCC) by conducting a meta-analysis based on the existing population-based studies. Methods Research articles published up to September 2015 were searched through PubMed and Embase. A meta-analysis was performed to assess the overall survival (OS) and progression-free survival (PFS) of patients with mRCC undergoing CN combined with targeted therapy compared with targeted therapy alone. Furthermore, analysis was made to evaluate some potential prognostic factors predicting survival. Results Eight studies were included in our analysis with 2688 mRCC patients. A fixed-effect model was performed and found the pooled HR of OS was 0.60 (95 % CI 0.53–0.67, p  < 0.0001). Furthermore, the pooled median survival ratio was elevated (HR 2.11, 95 % CI 1.78–2.49, p  < 0.0001), indicating that patients who received CN combined with targeted therapy yielded a more than twofold prolonged OS compared with those who received targeted therapy alone. Moreover, no significant difference was observed in PFS in the patients undergoing CN combined with targeted therapy (HR 0.82, 95 % CI 0.57–1.19, p  = 0.30). Conclusions Current evidence suggests that CN combined with targeted therapy has a significant OS advantage in patients with mRCC. However, the results should be evaluated in the context of the potential selection biases of the existing evidence. Large prospective cohort studies are required to confirm these findings.

Tumor-associated macrophages (TAMs) are the most abundant inflammatory infiltrates in the tumor microenvironment and contribute to lymph node (LN) metastasis. However, the precise mechanisms of TAMs-induced LN metastasis remain largely unknown. Herein, we identify a long noncoding RNA, termed Lymph Node Metastasis Associated Transcript 1 ( LNMAT1 ), which is upregulated in LN-positive bladder cancer and associated with LN metastasis and prognosis. Through gain and loss of function approaches, we find that LNMAT1 promotes bladder cancer-associated lymphangiogenesis and lymphatic metastasis. Mechanistically, LNMAT1 epigenetically activates CCL2 expression by recruiting hnRNPL to CCL2 promoter, which leads to increased H3K4 tri-methylation that ensures hnRNPL binding and enhances transcription. Furthermore, LNMAT1 -induced upregulation of CCL2 recruits macrophages into the tumor, which promotes lymphatic metastasis via VEGF-C excretion. These findings provide a plausible mechanism for LNMAT1 -modulated tumor microenvironment in lymphatic metastasis and suggest that LNMAT1 may represent a potential therapeutic target for clinical intervention in LN-metastatic bladder cancer. Mechanism of lymph node (LN) metastasis induced by tumor associated macrophages (TAMs) remains unclear. Here they demonstrate that a long noncoding RNA LNMAT1 promotes LN metastasis of bladder cancer via recruitment of TAMs through epigenetic regulation of CCL2 expression.

Background Metastatic prostate cancer is a leading cause of cancer-related death in men. Cancer stem cells (CSCs) are involved in tumor progression and metastasis, including in prostate cancer. There is an obvious and urgent need for effective cancer stem cells specific therapies in metastatic prostate cancer. MicroRNAs (miRNAs) are an important class of pervasive genes that are involved in a variety of biological functions, especially in cancer. The goal of this study was to identify miRNAs involved in prostate cancer metastasis and cancer stem cells. Methods A microarray and qRT-PCR were performed to investigate the miRNA expression profiles in PC-3 sphere cells and adherent cells. A transwell assay was used to evaluate the migration of PC-3 sphere cells and adherent cells. MiR-143 was silenced with antisense oligonucleotides in PC-3, PC-3-M and LNCaP cells. The role of miR-143 in prostate cancer metastasis was measured by wound-healing and transwell assays in vitro and bioluminescence imaging in vivo. Bioinformatics and luciferase report assays were used to identify the target of miR-143. Results The expression of miR-143 and the migration capability were reduced in PC-3 sphere cells and progressively increased during sphere re-adherent culture. Moreover, the down-regulation of miR-143 suppressed prostate cancer cells migration and invasion in vitro and systemically inhibited metastasis in vivo. Fibronectin type III domain containing 3B (FNDC3B), which regulates cell motility, was identified as a target of miR-143. The inhibition of miR-143 increased the expression of FNDC3B protein but not FNDC3B mRNA in vitro and vivo. Conclusions These data demonstrate for the first time that miR-143 was up-regulated during the differentiation of prostate cancer stem cells and promoted prostate cancer metastasis by repressing FNDC3B expression. This sheds a new insight into the post-transcriptional regulation of cancer stem cells differentiation by miRNAs, a potential approach for the treatment of prostate cancer.

The redevelopment/regeneration pattern of amputated limbs from a blastema in salamander suggests that enhanced regeneration might be achieved by mimicking the developmental microenvironment. Inspired by the discovery that the expression of magnesium transporter‐1 (MagT1), a selective magnesium (Mg) transporter, is significantly upregulated in the endochondral ossification region of mouse embryos, a Mg‐enriched 3D culture system is proposed to provide an embryonic‐like environment for stem cells. First, the optimum concentration of Mg ions (Mg2+) for creating the osteogenic microenvironment is screened by evaluating MagT1 expression levels, which correspond to the osteogenic differentiation capacity of stem cells. The results reveal that Mg2+ selectively activates the mitogen‐activated protein kinase/extracellular regulated kinase (MAPK/ERK) pathway to stimulate osteogenic differentiation, and Mg2+ influx via MagT1 is profoundly involved in this process. Then, Mg‐enriched microspheres are fabricated at the appropriate size to ensure the viability of the encapsulated cells. A series of experiments show that the Mg‐enriched microenvironment not only stimulates the osteogenic differentiation of stem cells but also promotes neovascularization. Obvious vascularized bone regeneration is achieved in vivo using these Mg‐enriched cell delivery vehicles. The findings suggest that biomaterials mimicking the developmental microenvironment might be promising tools to enhance tissue regeneration. Inspired by the correlation between MagT1 and embryonic endochondral ossification, an embryonic‐like microenvironment is created for stem cells by fabricating a magnesium‐enriched 3D culture system. Mg2+ via MagT1 not only stimulates osteogenic differentiation through the mitogen‐activated protein kinase/extracellular regulated kinase (MAPK/ERK) pathway, but also promotes neovascularization. An obvious vascularized bone regeneration is achieved in vivo using the magnesium‐enriched cell vehicles.

The prognosis for bladder cancer patients with lymph node (LN) metastasis is dismal and only minimally improved by current treatment modalities. Elucidation of the molecular mechanisms that underlie LN metastasis may provide clinical therapeutic strategies for LN-metastatic bladder cancer. Here, we report that a long noncoding RNA LINC00958, which we have termed bladder cancer-associated transcript 2 (BLACAT2), was markedly upregulated in LN-metastatic bladder cancer and correlated with LN metastasis. Overexpression of BLACAT2 promoted bladder cancer-associated lymphangiogenesis and lymphatic metastasis in both cultured bladder cancer cell lines and mouse models. Furthermore, we demonstrate that BLACAT2 epigenetically upregulated VEGF-C expression by directly associating with WDR5, a core subunit of human H3K4 methyltransferase complexes. Importantly, administration of an anti-VEGF-C antibody inhibited LN metastasis in BLACAT2-overexpressing bladder cancer. Taken together, these findings uncover a molecular mechanism in the lymphatic metastasis of bladder cancer and indicate that BLACAT2 may represent a target for clinical intervention in LN-metastatic bladder cancer.

Hypertension is the leading risk factor of cardiovascular disease and has profound effects on both the structure and function of the microvasculature. Abnormalities of the retinal vasculature may reflect the degree of microvascular damage due to hypertension, and these changes can be detected with fundus photographs. This study aimed to use deep learning technique that can detect subclinical features appearing below the threshold of a human observer to explore the effect of hypertension on morphological features of retinal microvasculature. We collected 2012 retinal photographs which included 1007 from patients with a diagnosis of hypertension and 1005 from normotensive control. By method of vessel segmentation, we removed interference information other than retinal vasculature and contained only morphological information about blood vessels. Using these segmented images, we trained a small convolutional neural networks (CNN) classification model and used a deep learning technique called Gradient-weighted Class Activation Mapping (Grad-CAM) to generate heat maps for the class \"hypertension\". Our model achieved an accuracy of 60.94%, a specificity of 51.54%, a precision of 59.27%, and a recall of 70.48%. The AUC was 0.6506. In the heat maps for the class \"hypertension\", red patchy areas were mainly distributed on or around arterial/venous bifurcations. This indicated that the model has identified these regions as being the most important for predicting hypertension. Our study suggested that the effect of hypertension on retinal microvascular morphology mainly occurred at branching of vessels. The change of the branching pattern of retinal vessels was probably the most significant in response to elevated blood pressure.