A colour preference technique to evaluate acrylamide-induced toxicity in zebrafish

The zebrafish has become a commonly used vertebrate model for toxicity assessment, of particular relevance to the study of toxic effects on the visual system because of the structural similarities shared by zebrafish and human retinae. In this article we present a colour preference-based technique that, by assessing the functionality of photoreceptors, can be used to evaluate the effects of toxicity on behaviour. A digital camera was used to record the locomotor behaviour of individual zebrafish swimming in a water tank consisting of two compartments separated by an opaque perforated wall through which the fish could pass. The colour of the lighting in each compartment could be altered independently (producing distinct but connected environments of white, red or blue) to allow association of the zebrafish's swimming behaviour with its colour preference. The functionality of the photoreceptors was evaluated based on the ability of the zebrafish to sense the different colours and to swim between the compartments. The zebrafish tracking was carried out using our algorithm developed with MATLAB. We found that zebrafish preferred blue illumination to white, and white illumination to red. Acute treatment with acrylamide (2 mM for 36 h) resulted in a marked reduction in locomotion and a concomitant loss of colour-preferential swimming behaviour. Histopathological examination of acrylamide-treated zebrafish eyes showed that acrylamide exposure had caused retinal damage. The colour preference tracking technique has applications in the assessment of neurodegenerative disorders, as a method for preclinical appraisal of drug efficacy and for behavioural evaluation of toxicity

Learning Disentangled Representation Implicitly via Transformer for Occluded Person Re-Identification

Person re-identification (re-ID) under various occlusions has been a long-standing challenge as person images with different types of occlusions often suffer from misalignment in image matching and ranking. Most existing methods tackle this challenge by aligning spatial features of body parts according to external semantic cues or feature similarities but this alignment approach is complicated and sensitive to noises. We design DRL-Net, a disentangled representation learning network that handles occluded re-ID without requiring strict person image alignment or any additional supervision. Leveraging transformer architectures, DRL-Net achieves alignment-free re-ID via global reasoning of local features of occluded person images. It measures image similarity by automatically disentangling the representation of undefined semantic components, e.g., human body parts or obstacles, under the guidance of semantic preference object queries in the transformer. In addition, we design a decorrelation constraint in the transformer decoder and impose it over object queries for better focus on different semantic components. To better eliminate interference from occlusions, we design a contrast feature learning technique (CFL) for better separation of occlusion features and discriminative ID features. Extensive experiments over occluded and holistic re-ID benchmarks (Occluded-DukeMTMC, Market1501 and DukeMTMC) show that the DRL-Net achieves superior re-ID performance consistently and outperforms the state-of-the-art by large margins for Occluded-DukeMTMC

Drosophila Perlecan Regulates Intestinal Stem Cell Activity via Cell-Matrix Attachment

SummaryStem cells require specialized local microenvironments, termed niches, for normal retention, proliferation, and multipotency. Niches are composed of cells together with their associated extracellular matrix (ECM). Currently, the roles of ECM in regulating niche functions are poorly understood. Here, we demonstrate that Perlecan (Pcan), a highly conserved ECM component, controls intestinal stem cell (ISC) activities and ISC-ECM attachment in Drosophila adult posterior midgut. Loss of Pcan from ISCs, but not other surrounding cells, causes ISCs to detach from underlying ECM, lose their identity, and fail to proliferate. These defects are not a result of a loss of epidermal growth factor receptor (EGFR) or Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling activity but partially depend on integrin signaling activity. We propose that Pcan secreted by ISCs confers niche properties to the adjacent ECM that is required for ISC maintenance of stem cell identity, activity, and anchorage to the niche

Portable solar billboard

Public bulletin boards are widely used in various public places, but due to the large size of the billboards, it is not easy to carry, and the traditional billboards are integrated, when the billboards need to be transferred, the limited storage space of the vehicle needs to be occupied It is extremely inconvenient, and at night, the traditional bulletin boards need to install additional light sources to illuminate them, which greatly increases energy consumption. Based on this paper designed a new structure of the bulletin board, this structure can make the bulletin board when not in use completely folded up and easy to carry, and in use can be completely unfolded and in the bottom of the added retractable support leg structure can be placed anywhere, and according to the terrain or human will to adjust the height. A solar panel is placed on the top of the bulletin board, which can store solar energy during the day and supply energy to the LED lights on the top at night for lighting, which saves energy and is very environmentally friendly

Heatwave Events and Mortality Outcomes in Memphis, Tennessee: Testing Effect Modification by Socioeconomic Status and Urbanicity

Heatwave studies typically estimate heat-related mortality and morbidity risks at the city level; few have addressed the heterogeneous risks by socioeconomic status (SES) and location within a city. This study aimed to examine the impacts of heatwaves on mortality outcomes in Memphis, Tennessee, a Mid-South metropolitan area top-ranked in morbidity and poverty rates, and to investigate the effects of SES and urbanicity. Mortality data were retrieved from the death records in 2008–2017, and temperature data from the Applied Climate Information System. Heatwave days were defined based on four temperature metrics. Heatwave effects on daily total-cause, cardiovascular, and respiratory mortality were evaluated using Poisson regression, accounting for temporal trends, sociodemographic factors, urbanicity, and air pollution. We found higher cardiovascular mortality risk (cumulative RR (relative risk) = 1.25, 95% CI (confidence interval): 1.01–1.55) in heatwave days defined as those with maximum daily temperature \u3e95th percentile for more than two consecutive days. The effects of heatwaves on mortality did not differ by SES, race, or urbanicity. The findings of this study provided evidence to support future heatwave planning and studies of heatwave and health impacts at a coarser geographic resolution

A glucagon-like peptide-1 analog, liraglutide, ameliorates endothelial dysfunction through miRNAs to inhibit apoptosis in rats

Background and Aims Many studies have revealed that glucagon-like peptide-1 has vasoprotective effects. In this study, we investigated whether liraglutide suppressed endothelial dysfunction and explored the mechanism involved. Methods Experimental diabetes was induced through combined high-fat diet administration and intraperitoneal streptozotocin injections. Rats were randomly divided into the following four groups: control, diabetes, diabetes + a low liraglutide dose (0.2 mg/kg/d), and diabetes + a high liraglutide dose (0.4 mg/kg/d). Endothelial function and metabolic parameters were measured after 8 weeks of treatment. miRNA arrays were analyzed to identify the differentially expressed miRNAs. Results We found that liraglutide significantly improved aortic endothelial function in diabetic rats. Liraglutide inhibited miR-93-5p, miR-181a-5p and miR-34a-5p expression, and activated miR-26a-5p expression. miRNA mimic transfection experiments indicated negative relationships between miR-93-5p, miR-181a-5p, miR-34a-5p, and miR-26a-5p and Sirt1, Creb, Bcl-2, and Pten expression, respectively. Moreover, liraglutide increased Sirt1, Creb, and Bcl-2 expression levels and reduced Pten expression level. Conclusion Our results demonstrate the role of key miRNAs in the liraglutide-mediated regulation of endothelial cell function in diabetic rats

CERKL regulates autophagy via the NAD-dependent deacetylase SIRT1

<p>Macroautophagy/autophagy is an important intracellular mechanism for the maintenance of cellular homeostasis. Here we show that the <i>CERKL</i> (ceramide kinase like) gene, a retinal degeneration (RD) pathogenic gene, plays a critical role in regulating autophagy by stabilizing SIRT1. <i>In vitro</i> and <i>in vivo</i>, suppressing CERKL results in impaired autophagy. SIRT1 is one of the main regulators of acetylation/deacetylation in autophagy. In CERKL-depleted retinas and cells, SIRT1 is downregulated. ATG5 and ATG7, 2 essential components of autophagy, show a higher degree of acetylation in CERKL-depleted cells. Overexpression of SIRT1 rescues autophagy in CERKL-depleted cells, whereas CERKL loses its function of regulating autophagy in SIRT1-depleted cells, and overexpression of CERKL upregulates SIRT1. Finally, we show that CERKL directly interacts with SIRT1, and may regulate its phosphorylation at Ser27 to stabilize SIRT1. These results show that CERKL is an important regulator of autophagy and it plays this role by stabilizing the deacetylase SIRT1.</p

An update on the functional roles of long non‑coding RNAs in ischemic injury (Review)

Ischemic injuries result from ischemia and hypoxia in cells. Tissues and organs receive an insufficient supply of nutrients and accumulate metabolic waste, which leads to the development of inflammation, fibrosis and a series of other issues. Ischemic injuries in the brain, heart, kidneys, lungs and other organs can cause severe adverse effects. Acute renal ischemia induces acute renal failure, heart ischemia induces myocardial infarction and cerebral ischemia induces cerebrovascular accidents, leading to loss of movement, consciousness and possibly, life-threatening disabilities. Existing evidence suggests that long non-coding RNAs (lncRNAs) are regulatory sequences involved in transcription, post-transcription, epigenetic regulation and multiple physiological processes. lncRNAs have been shown to be differentially expressed following ischemic injury, with the severity of the ischemic injury being affected by the upregulation or downregulation of certain types of lncRNA. The present review article provides an extensive summary of the functional roles of lncRNAs in ischemic injury, with a focus on the brain, heart, kidneys and lungs. The present review mainly summarizes the functional roles of lncRNA MALAT1, lncRNA MEG3, lncRNA H19, lncRNA TUG1, lncRNA NEAT1, lncRNA AK139328 and lncRNA CAREL, among which lncRNA MALAT1, in particular, plays a crucial role in ischemic injury and is currently a hot research topic