Singletonhuffman3293

The emergence of visual saliency has been widely studied in the primary visual cortex and the superior colliculus (SC) in mammals. There are fewer studies on the pop-out response to motion direction contrasting stimuli taken in the optic tectum (OT, homologous to mammalian SC), and these are mainly of owls and fish. To our knowledge the influence of spatial luminance has not been reported. In this study, we have recorded multi-units in pigeon OT and analyzed the tectal response to spatial luminance contrasting, motion direction contrasting, and contrasting stimuli from both feature dimensions. The comparison results showed that 1) the tectal response would pop-out in either motion direction or spatial luminance contrasting conditions. 2) The modulation from motion direction contrasting was independent of the temporal luminance variation of the visual stimuli. 3) When both spatial luminance and motion direction were salient, the response of tectal neurons was modulated more intensely by motion direction than by spatial luminance. The phenomenon was consistent with the innate instinct of avians in their natural environment. This study will help to deepen the understanding of mechanisms involved in bottom-up visual information processing and selective attention in the avian.

Acrylamide (AC) is a carcinogenic substance which is formed during the heating of starchy foods at high temperatures and constitutes an important risk for human health. see more Therefore, reducing the detrimental effects of AC has become an important research topic. This study was performed to evaluate the protective effect of morin against the testicular toxicity induced by AC in male rats.

Testicular damage was evaluated after the rats were treated orally with AC (38.27mg/kg body weight) alone or with morin (50 and 100mg/kg body weight) for 10 consecutive days.

Our results showed that treatment with morin could significantly decrease MDA level and considerably increase the activity of antioxidant enzymes (SOD, CAT, GPx) and GSH level in the testicular tissue of the AC-treated rats. Morin supplementation also suppressed the activation of inflammatory, apoptotic and autophagic pathways by increasing Bcl-2 and decreasing p38α MAPK, TNF-α, NF-κB, IL-1β, IL-6, COX-2, cytochrome c, Bax, caspase-3, LC3A, LC3B and beclin-1 protein levels. Morin also alleviated the side effects caused by AC by regulating the PI3K/Akt/mTOR signaling pathway.

Collectively, our results have shown the possible protective mechanism of morin, a potential therapeutic agent for AC-induced testicular toxicity.

Collectively, our results have shown the possible protective mechanism of morin, a potential therapeutic agent for AC-induced testicular toxicity.

Triple-negative breast cancer (TNBC) is not sensitive to current endocrine treatments, so new treatment strategies need to be explored. Based on previous antitumour studies on anti-TNFα nanobody, we designed a novel fusion nanobody to enhance antitumour activity of the anti-TNFα nanobody in TNBC.

The RGD4C contains RGD sequence, which is the smallest recognition unit binding to the αvβ3 receptor on tumour cell membranes and involved in tumour cell adhesion, proliferation, and metastasis. RGD4C was fused to anti-TNFα nanobody to investigate the antitumour activity in vitro and in vivo.

The antitumour effects of fusion nanobody V-L-R-H could effectively bind to αvβ3 and inhibit cell migration and proliferation of MDA-MB-231, which had satisfying purification efficiency and approving antigen or receptor binding activity. V-L-R-H could inhibit the TNFα-mediated PI3K/AKT/NF-κB signal pathway and integrin αvβ3 correlative FAK focal adhesion signal pathway. Mouse xenograft tumour experiments showed that the V-L-R-H could inhibit tumour proliferation and metastasis; reduce the TNFα, HIFα, Ki67, and CD31 concentrations in tumour; and inhibit the process of epithelial-mesenchymal transition.

The fusion nanobody enhanced antitumour activity of the anti-TNFα nanobody on TNBC. It provided a reference for the design of dual functional fusion proteins and development of tumour treatment strategies of antagonistic TNFα and αvβ3, and a new therapeutic strategy and research direction for the treatment of TNBC.

The fusion nanobody enhanced antitumour activity of the anti-TNFα nanobody on TNBC. It provided a reference for the design of dual functional fusion proteins and development of tumour treatment strategies of antagonistic TNFα and αvβ3, and a new therapeutic strategy and research direction for the treatment of TNBC.

The study aims to investigate the roles of LncRNA and miRNA in ferroptosis in brain ischemia/reperfusion (I/R) in vivo and in vitro.

qPCR assay was used to analyze lncRNA PVT1 and miR-214 expressions in acute ischemic stroke (AIS) patients. Then, we established brain I/R mice models and OGD/R PC12 cell models to analyze the mechanism of ferroptosis. I/R mice were treated by lncRNA PVT silencing or miR-214 overexpressing lentivirus via lateral ventricles. Infarct size was analyzed by TTC staining, accompanied by the detection of ferroptosis indicators through Perls'Prussian blue staining, iron kit, MDA kit, glutathione kit, GPx activities kit and Western blotting (WB). Dual luciferase reporter assay was used to assess whether miR-214 bound to PVT1, TP53 or TFR1. Co-IP analyzed the interplay of p53 with SLC7A11.

We found that the levels of PVT1 were upregulated and miR-214 levels were downregulated in plasma of AIS patients. NIHSS score was positively correlated with PVT1 levels but was negatively with miR-214 levels. PVT1 silencing or miR-214 overexpression significantly reduced infarct size and suppressed ferroptosis in vivo. miR-214 overexpression markedly decreased PVT1 levels. Specifically, miR-214 could bind to 3'untranslated region (3'UTR) of PVT1, TP53 or TFR1. PVT1 overexpression or miR-214 silencing markedly abolished the effects of Ferrostatin-1 on ferroptosis indicators except for TFR1 expression. Besides, miR-214 silencing counteracted the effects of PVT1 knockdown on the ferroptosis-related proteins.

PVT1 regulated ferroptosis through miR-214-mediated TFR1 and TP53 expression. There was a positive feedback loop of lncRNA PVT1/miR-214/p53 possibly.

PVT1 regulated ferroptosis through miR-214-mediated TFR1 and TP53 expression. There was a positive feedback loop of lncRNA PVT1/miR-214/p53 possibly.