ABSTRACT
Pt-based electrochemical ammonia-nitrogen sensors played a significance role in real-time monitoring the ammonia-nitrogen concentration. The alloying of Pt and transition metals was one of the effective ways to increase the detectability of the sensitive electrode. In this paper, a self-supported electrochemical electrode for the detection of ammonia nitrogen was obtained by the electrodeposition of PtNi alloy nanoleaves on a carbon cloth (PtNi-CC). Experimental results showed that the PtNi-CC electrode exhibited enhanced detection performance with a wide linear range from 0.5 to 500 µM, high sensitivity (7.83 µA µM-1 cm-2 from 0.5 to 150 µM and 0.945 µA µM-1 cm-2 from 150 to 500 µM) and lower detection limit (24 nM). The synergistic effect between Pt and Ni and the smaller lattice spacing of the PtNi alloy were the main reasons for the excellent performance of the electrode. This work showed the great potential of Pt-based alloy electrodes for the detection of ammonia-nitrogen.
ABSTRACT
Prostate cancer (PCa) is a major health problem in males. Metastasis-associated with lung adenocarcinoma transcript-1 (MALAT1), which is overexpressed in PCa tissue, is associated with physiological and pathological conditions of PCa. M2 macrophages are major immune cells abundant in the tumor microenvironment. However, it remains unknown whether M2 macrophages are involved in the effects or not, and molecular mechanisms of MALAT1 on PCa progression have not yet been comprehensively explored. Here we reported that, M2 macrophages (PMA/IL-4 treated THP1) induced MALAT1 expression in PCa cell lines. Knockdown MALAT1 expression level in PCa cell lines inhibited cellular proliferation, invasion, and tumor formation. Further mechanistic dissection revealed that M2 macrophages secreted IL-8 was sufficient to drive up MALAT1 expression level via activating STAT3 signaling pathway. Additional chromatin immunoprecipitation (ChIP) and luciferase reporter assays displayed that STAT3 could bind to the MALAT1 promoter region and transcriptionally stimulate the MALAT1 expression. In summary, our present study identified the IL-8/STAT3/MALAT1 axis as key regulators during prostate tumorigenesis and therefore demonstrated a new mechanism for the MALAT1 transcriptional regulation.
Subject(s)
Interleukin-8/metabolism , RNA, Long Noncoding/metabolism , STAT3 Transcription Factor/metabolism , Antibodies/immunology , Antibodies/pharmacology , Binding Sites , Cell Line, Tumor , Cell Survival/drug effects , Humans , Interleukin-8/immunology , Macrophages/cytology , Macrophages/metabolism , Male , Phosphatidylinositol 3-Kinases/metabolism , Phosphorylation , Promoter Regions, Genetic , Prostatic Neoplasms/metabolism , Prostatic Neoplasms/pathology , Protein Binding , Proto-Oncogene Proteins c-akt/metabolism , RNA Interference , RNA, Long Noncoding/antagonists & inhibitors , RNA, Long Noncoding/genetics , RNA, Small Interfering/metabolism , STAT3 Transcription Factor/chemistry , STAT3 Transcription Factor/genetics , Signal TransductionABSTRACT
Prostate cancer (PCa) is the second lethal disease for men in western countries. Although androgen receptor (AR) signaling has been widely investigated, noncoding RNAs (ncRNAs), deficient of open reading frame, have also received considerable attention. Growing studies showed that the aberrant ncRNAs expression contributed to cell proliferation, metastasis and drug resistance in PCa. Therefore, therapeutically targeting ncRNAs may synergize androgen deprivation therapy (ADT) to have a better effect to fight against PCa, especially castration-resistant prostate cancer (CRPC). This review would systematically summarize the multicellular events controlled by ncRNAs and give a snapshot of future scientific activities and clinical applications.
ABSTRACT
Stroke is usually treated by systemic thrombolytic therapy if the patient presents within an appropriate time window. There is also widespread interest in the development of thrombolytic agents that can be used in cases of delayed presentation. Current agents that can be used in cases of delayed presentation of nerve damage by thrombus. Current systemic thrombolytic therapy is associated with adverse effects such as fibrinogenolysis and bleeding. In an attempt to increase the efficacy, safety, and specificity of thrombolytic therapy, a number of targeted thrombolytic agents have been studied in recent years. This review focuses on the concepts underlying targeted thrombolytic therapy and describes recent drug developments in this field.
