Computer-Vision-Based Sensing Technologies for Livestock Body Dimension Measurement: A Survey.

Livestock's live body dimensions are a pivotal indicator of economic output. Manual measurement is labor-intensive and time-consuming, often eliciting stress responses in the livestock. With the advancement of computer technology, the techniques for livestock live body dimension measurement have progressed rapidly, yielding significant research achievements. This paper presents a comprehensive review of the recent advancements in livestock live body dimension measurement, emphasizing the crucial role of computer-vision-based sensors. The discussion covers three main aspects: sensing data acquisition, sensing data processing, and sensing data analysis. The common techniques and measurement procedures in, and the current research status of, live body dimension measurement are introduced, along with a comparative analysis of their respective merits and drawbacks. Livestock data acquisition is the initial phase of live body dimension measurement, where sensors are employed as data collection equipment to obtain information conducive to precise measurements. Subsequently, the acquired data undergo processing, leveraging techniques such as 3D vision technology, computer graphics, image processing, and deep learning to calculate the measurements accurately. Lastly, this paper addresses the existing challenges within the domain of livestock live body dimension measurement in the livestock industry, highlighting the potential contributions of computer-vision-based sensors. Moreover, it predicts the potential development trends in the realm of high-throughput live body dimension measurement techniques for livestock.

Histone H3 methyltransferase Ezh2 promotes white adipocytes but inhibits brown and beige adipocyte differentiation in mice.

Obesity is a disease characterized by imbalance between energy intake and expenditure, excessive energy store in white adipocytes, but brown and beige adipocytes consume energy to relieve obesity. In this study, we want to explore the role of the histone H3 methyltransferase Ezh2 in the differentiation of white, brown and beige adipocytes with Ezh2 conditional knockout mice (Ezh2flox/floxPrx1-cre) and mouse embryonic fibroblasts (MEFs). The results showed that Ezh2-deficient mice have a leaner phenotype and less white adipose tissues. The morphological changes in the adipose tissue included smaller white adipose tissue depots, white adipocytes with smaller diameter, smaller lipid droplets inside the brown adipocytes and more beige adipocytes in the Ezh2-deficient mice compared with the control. The differentiation markers of white adipocytes in Ezh2 knockout mice decreased; Ucp1 and other browning markers increased in brown and beige adipocytes. The Ezh2 knockout mice could better tolerate cold stimulation, and they can also resist obesity and insulin resistance induced by a high-fat diet. The Ezh2 inhibitor GSK126 could inhibit the differentiation of MEFs into white adipocytes but promote their differentiation into brown/beige adipocytes. The H3K27me3 demethylase Jmjd3/UTX inhibitor GSKJ4 inhibited MEFs' differentiation into brown/beige adipocytes. These results showed that Ezh2 promotes the differentiation of white adipocytes and inhibits the differentiation of brown and beige adipocytes in vivo and in vitro through its methylase activity and this may represent new knowledge for obesity therapeutic strategy.

GSK126 alleviates the obesity phenotype by promoting the differentiation of thermogenic beige adipocytes in diet-induced obese mice.

A close relationship between epigenetic regulation and obesity has been demonstrated in several recent studies. Histone methyltransferase enhancer of Zeste homolog 2 (Ezh2), which mainly catalyzes trimethylation of histone H3K27 to form H3K27me3 was found to be required for the differentiation of white and brown adipocytes in vitro. Here, we investigated the effects of the Ezh2-specific inhibitor GSK126 in a mouse model of obesity induced by a high-fat diet (HFD). We found that GSK126 treatment reduced body fat, improved glucose tolerance, increased lipolysis and improved cold tolerance in mice by promoting the differentiation of thermogenic beige adipocytes. Moreover, we discovered that GSK126 inhibited the differentiation of white adipocytes, and the decrease of Ezh2 enzymatic activity and H3K27me3 also changed the morphology of brown adipocytes but did not alter the expression of thermogenic genes in these cells. Our results indicated that GSK126 was a novel chemical inducer of beige adipocytes and may be a potential therapeutic agent for the management of obesity. Furthermore, they also prompted that Ezh2 and H3K27me3 play different roles in the differentiation of the white, brown, and beige adipocytes in vivo.