The calculated electronic properties (e.g, gap energy, electron affinity, and electronegativity) of aripiprazole and its iodinated form reveal the higher reactivity of iodinated aripiprazole compared with aripiprazole. CONCLUSION This may explain the higher affinity of iodinated aripiprazole and the increase of its radiochemical yield. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Emerging studies have indicated that circular RNAs (circRNAs) play important roles in the development of many tumors. CircRNA-scavenger receptor class B member 1 (Circ-SCARB1) was consistently reported as an elevated circRNA in RCC tissues. This study focused on examining the biological function and molecular mechanism of circSCARB1 in RCC progression. METHODS Expression of Circ-SCARB1, microRNA (miR)-510-5p and syndecan 3 (SDC3) were detected using quantitative real-time polymerase chain reaction (RT-PCR) and/or western blot. Cell proliferation and apoptosis were measured by 3-(4, 5)-dimethylthiahiazo (-z-y1)-3, 5-diphenytetrazoliumromide and flow cytometry, respectively. Cell migration and invasion were measured using Transwell assays. The interaction between miR-510-5p and Circ-SCARB1 or SDC3 was verified using dual-luciferase reporter assays. RESULTS Circ-SCARB1 was elevated in 30 pairs of RCC tissues and multiple RCC cell lines. Knockdown of Circ-SCARB1 inhibited cell proliferation, migration and invasion, while inducing cell apoptosis. MiR-510-5p was confirmed to be a target of Circ-SCARB1; inhibition of cell progression by silencing Circ-SCARB1 was mediated by a direct interaction between Circ-SCARB1 and miR-510-5p. SDC3 was verified to be a gene target of miR-510-5p; transfection of miR-510-5p mimic not only suppressed the expression of SDC3 but also the cell proliferation and a SDC3 cotransfection partially restored cell proliferation. Additionally, genetic knockdown of Circ-SCARB1 reduced the expression SDC3, and the addition of anti-miR-510-5p could partially re-elevate SDC3 expression. CONCLUSION Circ-SCARB1 promotes RCC progression via sequestering miR-510-5p and indirectly up-regulating SDC3 expression. This provides a novel perspective for the pathogenesis of RCC and potential therapeutic targets for the treatment of RCC. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Amyotrophic lateral sclerosis (ALS) is a neurological disorder clinically characterized by motor system dysfunction, with intraneuronal accumulation of the TAR DNA-binding protein 43 (TDP-43) being a pathological hallmark. Riluzole is a primarily prescribed medicine for ALS patients, while its therapeutical efficacy appears limited. TDP-43 transgenic mice are existing animal models for mechanistic/translational research into ALS. METHODS We developed a transgenic rat model of ALS expressing a mutant human TDP-43 transgene (TDP-43M337V) and evaluated the therapeutic effect of Riluzole on this model. PRT4165 chemical structure Relative to control, rats with TDP-43M337V expression promoted by the neurofilament heavy subunit (NEF) gene or specifically in motor neurons promoted by the choline acetyltransferase (ChAT) gene showed progressive worsening of mobility and grip strength, along with loss of motor neurons, microglial activation, and intraneuronal accumulation of TDP-43 and ubiquitin aggregations in spinal cord. RESULTS Compared to vehicle control, intragastric administration of Riluzole (30mg/kg/d) did not mitigate the behavioral deficits nor alter the neuropathologies in the transgenics. CONCLUSION These findings indicate that transgenic rats recapitulate the basic neurological and neuropathological characteristics of human ALS, while Riluzole treatment can not halt the development of the behavioral and histopathological phenotypes in this new transgenic rodent model of ALS. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Astroglioma, one major form of brain tumors, has remained principally tough to handle for decades, due to the complexity of tumor pathology and the poor response to chemo- and radio-therapies. Our previous study demonstrated that nifurtimox could regulate the signaling axis of AKT-GSK3β in vari ous tumor types including the astroglioma U251 cells. Intriguingly, earlier case studies suggested that nifurtimox could possibly permeate the blood brain barrier and arrest neuroblastoma in the brain. These observations jointly encouraged us to explore whether nifurtimox would hinder the growth of astroglioma in vivo. Our results exhibited that nifurtimox could competently hinder the development of astroglioma in mouse brain as compared to temozolomide, the first line of drug for brain tumors. Meanwhile the surviving rate, as well as the body weight was dramatically upregulated upon nifurtimox treatment, as compared to that of temozolomide. These findings offered nifurtimox as a better alternative drug in treating astroglioma in vivo. Persistently, the manipulation of the signaling axis of AKT-GSK3β in astroglioma was found in line with earlier findings in neuroblastoma when treated with nifurtimox. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Despite technological advancement, there is no 100% effective treatment against metastatic cancer. Increasing resistance of cancer cells towards chemotherapeutic drugs along with detrimental side effects remained a concern. Thus, the urgency in developing new anticancer agents has been raised. Anticancer peptides have been proven to display potent activity against a wide variety of cancer cells. Several mode of actions describing their cytostatic and cytotoxic effect on cancer cells have been proposed which involves cell surface binding leading to membranolysis or internalization to reach their intracellular target. Understanding the mechanism of action of these anticancer peptides is important in achieving full therapeutic success. In the present article, we discuss the anticancer action of peptides accompanied by the mechanisms underpinning their toxicity to cancer cells. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.