MAFG-AS1 is an oncogenic lncRNA in multiple types of cancer. However, its role in bladder cancer (BC) remains unclear. The present study aimed to investigate the function of MAFG-AS1 in BC. BC and paired non-tumor tissues were collected. Two BC cell lines HT01197 and HT-1376 were used. Dual luciferase activity assay, RT-qPCR, western blot, CCK-8, transwell invasion assay, and wound healing assay were performed. We found that MAFG-AS1 was significantly up-regulated in BC tissues and predicted a poor survival rate. MAFG-AS1 interacted with miR-125b-5p. However, the expression levels of MAFG‑AS1 and miR-125b-5p were not obviously correlated in BC tissues, and MAFG‑AS1 and miR-125b-5p did not regulate the expression of each other. Interestingly, we found that SphK1, a downstream target of miR-125b-5p, was negatively correlated with miR-125b-5p, while it was positively correlated with MAFG-AS1 across BC tissues. In addition, overexpression of MAFG‑AS1 upregulated the expression of SphK1 in BC cells, and attenuated the inhibitory effects of miR-125b-5p on the expression of SphK1. Functional assays showed that overexpression of MAFG‑AS1 promoted BC cell proliferation, migration, and invasion, while its effects were attenuated by overexpression of miR-125b-5p. Moreover, overexpression of miR-125b-5p inhibited BC cell proliferation, migration, and invasion, while its effects were alleviated by overexpression of SphK1. Taken together, our findings demonstrated that MAFG-AS1 has an oncogenic role in BC by regulating the miR-125b-5p/SphK1 axis. MAFG-AS1 might serve as a good diagnostic marker and a potential therapeutic target of BC.

Background Population-based analysis for the short-term non-bladder cancer related mortality among patients with non-metastatic bladder cancer is currently lacking. The objective of the current study was to assess and quantify cause of death after bladder cancer diagnosis. Methods The custom Surveillance, Epidemiology, and End Results (SEER) dataset for standardized mortality ratios (SMRs) was utilized to identify 24,074 patients who were diagnosed with nonmetastatic (M0) bladder cancer from 2014 to 2015. SMRs for causes of death were calculated. Risk factors for bladder cancer-specific mortality, competing mortality, second-cancer mortality, and noncancer mortality were determined using either multivariable Cox or competing risk regression models. Results Among all the 4179 (17.4%) deaths occurred during the follow-up period, almost half of them (44.2%) were attributed to non-bladder cancer cause, including second non-bladder cancer (10%) and other non-cancer causes (34.2%). The most common noncancer causes of death were heart diseases followed by chronic obstructive pulmonary disease. Patients had a higher risk of death from second malignancies (SMR, 1.59; 95% CI, 1.47–1.74) compared with death from first malignancies in the US general population, and also had higher risks of death from heart diseases (SMR, 1.29; 95% CI, 1.18–1.40) and chronic obstructive pulmonary disease (SMR, 1.52; 95% CI, 1.29–1.79) compared with the US general population. Additionally, some risk factors for competing second malignancies or noncancer mortality were determined, such as age, gender, marital status and treatment modalities. Conclusions Death from non-bladder cancer cause contributed to almost half of all deaths in bladder cancer survivors during the short-term follow-up period. These findings can inform medical management and assist clinicians in counseling those survivors regarding their short-term health risks.

Rationale: Anatomical variations in aortic arch (AA) branching are not unusual. Generally, these variations are asymptomatic and are diagnosed incidentally. Here, we report a rare case of a middle-aged female patient with an aberrant right subclavian artery (ARSA) associated with anomalous origins of the bilateral vertebral arteries (VAs). Patient concerns: The patient treated for urolithiasis complained of repeated dizziness for several years. Diagnoses: Echocardiography and computed tomography angiography (CTA) confirmed arterial variations. Moreover, mild stenosis was found in the left common carotid artery (LCCA), which was considered to be the cause of dizziness. Interventions: Congenital anomalous arteries were not necessary to intervene urgently, but aspirin and atorvastatin were administered to prevent potential thrombosis attributed to vascular stenosis after completing the operation for urolithiasis. Outcomes: Whether the symptoms will be alleviated or not should be continuously followed up, and the patient may accept interventional therapy in the future if necessary. Lessons: Here, we report the rare variation of AA branches and highlight the importance of preoperative vascular assessment in surgical or interventional procedures for the affected body regions.

Gemcitabine (GEM) is one of the first choice drugs for treating bladder cancer. In this study, we loaded M1 macrophage-derived exosomes (M1-Exo) with GEM by ultrasonication technique to derive an M1-Exo-GEM drug delivery system, and then explored its effects on bladder cancer. After inducing M1 polarization of macrophages in vitro, ultracentrifugation was performed to obtain M1-Exo, followed by construction of M1-Exo-GEM via ultrasonication technique. Mouse bladder cancer MB49 cells were chosen for study. CCK-8, PI staining and flow cytometry (FCM) assays were employed to assess the cell viability and apoptosis level. Inflammatory cytokines were detected by ELISA, while the protein expressions of Bcl-2, Bax and Caspase-3 were examined through Western-Blotting. After injecting M1-Exo-GEM into the tumor-bearing mouse model, the pathological changes were observed by H&E staining, the cancer cell damage was detected by TUNEL staining, and the apoptosis pathway activation was analyzed through immunohistochemical (IHC) staining and protein expression assays for Caspase-3 and Bax. Our results showed that M1-Exo and GEM had cytotoxic effects on MB49 cells, which increased the apoptosis level and the inflammatory cytokine expressions. Compared to M1-Exo and GEM, M1-Exo-GEM was significantly more cytotoxic to MB49 cells while markedly up-regulating the expressions of inflammatory cytokines. In the tumor-bearing mouse model, M1-Exo-GEM significantly inhibited tumor growth and damaged tumor cells, which outperformed GEM. Meanwhile, it also increased the tissue levels of inflammatory cytokines. This study finds that the drug delivery system composed of M1-Exo and GEM can act synergistically with GEM to exert cytotoxicity and induce inflammatory damage of bladder cancer cells.

BackgroundAcute kidney injury (AKI) is the most common major complication of cardiac surgery field. The purpose of this study is to investigate the association between acute kidney injury and the prognoses of cardiac surgery patients in the Medical Information Mart for Intensive Care III (MIMIC-III) database.MethodsClinical data were extracted from the MIMIC-III database. Adult (≥18 years) cardiac surgery patients in the database were enrolled. Multivariable logistic regression analyses were employed to assess the associations between acute kidney injury (AKI) comorbidity and 30-day mortality, 90-day mortality and hospital mortality. Different adjusting models were used to adjust for potential confounders.ResultsA total of 6,002 patients were involved, among which 485 patients (8.08%) had comorbid AKI. Patients with AKI were at higher risks of prolonged ICU stay, hospital mortality, 90-day mortality (all P < 0.001), and 30-day mortality (P = 0.008). AKI was a risk factor for hospital mortality [Model 1, OR (95% CI) = 2.50 (1.45–4.33); Model 2, OR (95% CI) = 2.44 (1.48–4.02)], 30-day mortality [Model 1, OR (95% CI) = 1.84 (1.05–3.24); Model 2, OR (95% CI) = 1.96 (1.13–3.22)] and 90-day mortality [Model 1, OR (95% CI) = 2.05 (1.37–3.01); Model 2, OR (95% CI) = 2.76 (1.93–3.94)]. Higher hospital mortality, 30-day mortality and 90-day mortality was observed in higher KDIGO grade for cardiac surgery patients with AKI (all P < 0.05).ConclusionComorbid AKI increased the risk of hospital mortality, 30-day mortality, and 90-day mortality of cardiac surgery patients in the MIMIC-III database.