Safety and efficacy of transcatheter arterial embolization in autosomal dominant polycystic kidney patients with gross hematuria: Six case reports.

BACKGROUND: To retrospectively report the safety and efficacy of renal transcatheter arterial embolization for treating autosomal dominant polycystic kidney disease (ADPKD) patients with gross hematuria. CASE SUMMARY: The purpose of this study is to retrospectively report the safety and efficacy of renal transcatheter arterial embolization for treating ADPKD patients with gross hematuria. Materials and methods: During the period from January 2018 to December 2019, renal transcatheter arterial embolization was carried out on 6 patients with polycystic kidneys and gross hematuria. Renal arteriography was performed first, and then we determined the location of the hemorrhage and performed embolization under digital subtraction angiography monitoring. Improvements in routine blood test results, routine urine test results, urine color and postoperative reactions were observed and analyzed. Results: Renal transcatheter arterial embolization was successfully conducted in 6 patients. The indices of 5 patients and the color of gross hematuria improved after surgery compared with before surgery. No severe complication reactions occurred. CONCLUSION: For autosomal dominant polycystic kidney syndrome patients with gross hematuria, transcatheter arterial embolization was safe and effective.

Long noncoding RNA HOXD-AS1 promotes the progression of pancreatic cancer through miR-664b-3p/PLAC8 axis.

Pancreatic cancer (PC) is one of the most common malignancies worldwide. There are no effective early diagnosis and therapeutic methods for PC. Mounting evidence has shown that lncRNAs promote PC progression. For instance, HOXD-AS1 acts as an oncogenic lncRNA in some digestive tumors. However, its role in PC is unknown. This study aimed to investigate the role of HOXD-AS1 in PC and its underlying mechanisms. Quantitative reverse transcription (qRT­PCR) was used to measure the expression levels of HOXD-AS1, miR-664b-3p, and PLAC8. CCK-8, colony formation, wound healing, and transwell assays were used to assess the effect of HOXD-AS1 on the proliferation, invasion and migration of PC cells. Dual-luciferase reporter and cell function rescue assays were used to verify the regulation relationship of miR-664b-3p and HOXD-AS1 or PLAC8. HOXD-AS1 was significantly upregulated in PC tissues than in paired adjacent tissues. Moreover, HOXD-AS1 was related to the advanced TNM stage. Meanwhile, HOXD-AS1 promoted the proliferation, invasion, and migration of PC cells. Mechanically, HOXD-AS1 upregulated PLAC8 by targeting miR-664b-3p. In conclusion, HOXD-AS1 was upregulated in PC tissues, promoting the proliferation, invasion, and migration of PC cells via the miR-664b-3p/PLAC8 axis.

Clinical significance of changes in AFP, HTATIP2/TIP30, B7-H4 and inflammatory cytokines after transcatheter arterial chemoembolization.

PURPOSE: To explore the clinical significance of changes in alpha-fetoprotein (AFP), HIV-1 TAT interactive protein 2/TAT interactive protein 30 (HTATIP2/TIP30), B7-H4 and inflammatory cytokines after transcatheter arterial chemoembolization (TACE). METHODS: A total of 84 hepatocellular carcinoma (HCC) patients admitted to the Department of Hepatobiliary Surgery and the Department of Interventional Radiology of our hospital from January 1, 2017 to December 31, 2018 were randomly enrolled and divided into an experimental group and a control group according to treatment methods. The expression levels of AFP mRNA, HTATIP2/TIP30, B7-H4 and inflammatory cytokines were detected before and after treatment, the short-term efficacy was followed up and analyzed, and the correlation between the two was statistically analyzed. RESULTS: The AFP expression level in the two groups of patients was lower after treatment than before treatment, this reduction being more obvious in the experimental group (receiving TACE) than in the control group. Although the levels of serum HTATIP2/TIP30 and B7-H4 were decreased after treatment in both groups, and they were lower after treatment than those before treatment in the control group, lower levels were registered in the control group. Both groups of patients had lower expression levels of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) after treatment compared with those before treatment, this decrease being more significant in the experimental group than in the control group. Moreover, the total short-term efficacy rate and the improvement rate of the quality of life were higher in the experimental group than in the control group, although no statistical difference in the survival rate was found between the two groups after 1-year follow-up. The serum level of B7-H4 in the group with good efficacy was lower than in the group with poor efficacy before treatment, and it declined in both groups after treatment, with a lower level in the former than in the latter. Furthermore, the group with good efficacy had a lower level of serum HTATIP2/TIP30 than the group with poor efficacy, while both groups had a decreased level after treatment, with a lower level in the former than in the latter. CONCLUSION: Interventional therapy for primary HCC has good short-term efficacy. It can reduce the levels of serum HTATIP2/TIP30, B7-H4, AFP and inflammation-related indexes, improve the liver function and the patients' quality of life.

MicroRNA-34a negatively regulates anesthesia-induced hippocampal apoptosis and memory impairment through FGFR1.

BACKGROUND: Mounting evidence has shown the toxic effects of anesthesia to neonatal hippocampus. We used an in vivo mouse model to explore the role of microRNA 34a (miR-34a) in regulating anesthesia-induced hippocampal neurotoxicity. METHODS: One-month old C57/BL6 mice received daily intraperitoneal injection of anesthesia (ketamine, 50 mg/kg) for 7 days. One day after, apoptosis was evaluated by TUNEL staining in hippocampal CA1 region, and expression level of miR-34a assessed by real-time quantitative PCR (qPCR). Hippocampal miR-34a was then down-regulated through lentivirus mediated cortical injection prior to anesthesia. The effects of inhibiting hippocampal miR-34a on anesthesia-induced hippocampal apoptosis and memory impairment were further investigated by TUNEL staining and Morris water maze (MWM) test. The predicted molecular target of miR-34a, fibroblast growth factor receptor 1 (FGFR1) was down-regulated in hippocampus through siRNA-mediated cortical injection and its effect on hippocampal apoptosis was also examined. RESULTS: Anesthesia caused severe apoptosis among hippocampal CA1 neurons and upregulated hippocampal miR-34a. On the other hand, lentivirual inhibition of miR-34a protected anesthesia-induced hippocampal apoptosis and memory impairment. Luciferase essay demonstrated FGFR1 was directly regulated by miR-34a in hippocampus. siRNA-induced FGFR1 downregulation further exaggerated anesthesia-induced apoptosis in hippocampus. CONCLUSIONS: Overall, we showed that miR-34a negatively modulated anesthesia-induced hippocampal neurotoxicity.

Blockage of epidermal growth factor receptor by quinazoline tyrosine kinase inhibitors suppresses growth of human hepatocellular carcinoma.

Epidermal growth factor receptor (EGFR) is highly expressed in many human tumors including hepatocellular carcinoma (HCC). Therefore, inhibition of EGF receptors could be a potential target for anticancer therapy. In this study, we investigated the effects of two EGFR tyrosine kinase inhibitors, PD153035 and its analogue 4-[[3-chloro-4-fluorophenyl]amino]-6,7-dimethoxyquinazoline hydrochloride (ANAPD) on human HCC cell lines by cell proliferation assay, flow cytometry and Western blot. Our results demonstrated that both EGFR inhibitors inhibited tumor cell growth in a dose-dependent manner, but ANAPD was more potent than PD153035. These specific inhibitors not only blocked EGF-stimulated EGFR autophosphorylation but also targeted EGFR signaling including MAPK and Akt pathways. Furthermore, EGFR inhibitors induced a delay in cell cycle progression and a G(1) arrest together with a partial G(2)/M block. EGFR inhibitors also induced tumor cells to undergo apoptosis. In conclusion, this study demonstrated that both PD153035 and ANAPD inhibit tumor cell growth in HCC through inhibition of EGFR signaling pathway, and ANAPD is a more potent inhibitor than PD153035. This suggested that blockage of EGF receptors may provide an effective therapeutic approach for human HCC and ANAPD could be a potential drug candidate for the treatment of HCC.