Learning adaptive reaching and pushing skills using contact information

In this paper, we propose a deep reinforcement learning-based framework that enables adaptive and continuous control of a robot to push unseen objects from random positions to the target position. Our approach takes into account contact information in the design of the reward function, resulting in improved success rates, generalization for unseen objects, and task efficiency compared to policies that do not consider contact information. Through reinforcement learning using only one object in simulation, we obtain a learned policy for manipulating a single object, which demonstrates good generalization when applied to the task of pushing unseen objects. Finally, we validate the effectiveness of our approach in real-world scenarios

Genetic Susceptibility to Vitiligo: GWAS Approaches for Identifying Vitiligo Susceptibility Genes and Loci

Vitiligo is an autoimmune disease with a strong genetic component, characterized by areas of depigmented skin resulting from loss of epidermal melanocytes. Genetic factors are known to play key roles in vitiligo through discoveries in association studies and family studies. Previously, vitiligo susceptibility genes were mainly revealed through linkage analysis and candidate gene studies. Recently, our understanding of the genetic basis of vitiligo has been rapidly advancing through genome-wide association study (GWAS). More than 40 robust susceptible loci have been identified and confirmed to be associated with vitiligo by using GWAS. Most of these associated genes participate in important pathways involved in the pathogenesis of vitiligo. Many susceptible loci with unknown functions in the pathogenesis of vitiligo have also been identified, indicating that additional molecular mechanisms may contribute to the risk of developing vitiligo. In this review, we summarize the key loci that are of genome-wide significance, which have been shown to influence vitiligo risk. These genetic loci may help build the foundation for genetic diagnosis and personalize treatment for patients with vitiligo in the future. However, substantial additional studies, including gene-targeted and functional studies, are required to confirm the causality of the genetic variants and their biological relevance in the development of vitiligo

Expression of Puroindoline a in Durum Wheat Affects Milling and Pasting Properties

Durum wheat has limited culinary utilizations partly due to its extremely hard kernel texture. Previously, we developed transgenic durum wheat lines with expression of the wildtype Puroindoline a (Pina) and characterized PINA’s effects on kernel hardness, total flour yield and dough mixing properties in durum wheat. The medium-hard kernel texture is potentially useful for exploring culinary applications of durum wheat. In the present study, we examined the milling parameters and flour attributes of the transgenic lines, including particle size distribution, damaged starch and water binding capacity. PINA expression results in increased break and reduction flour yield but decreased shorts. PINA expression also leads to finer flour particles and decreased starch damage. Interestingly, PINA transgenic lines showed increased peak viscosity and breakdown viscosity but leave other flour pasting parameters generally unaltered. PINA transgenic lines were associated with increased small monomeric proteins, appearing to affect gluten aggregation. Our data together with several previous results highlight distinct effects of PINs on pasting properties depending on species and variety. The medium-hard kernel texture together with improved pasting parameters may be valuable for producing a broader range of end-products from durum wheat

Effect of Fluorosis on Liver Cells of VC Deficient and Wild Type Mice

For decades, mouse and other rodents have been used for the study of oxidative or related studies such as the effect of fluoride. It is known that rodents normally synthesize their own vitamin C (VC) due to the presence of a key enzyme in ascorbic acid synthesis, l-gulono-lactone-γ-oxidase (Gulo), while humans do not have the capacity of VC synthesis due to the deletion of most parts of the GULO gene. The spontaneous fracture (sfx) mouse recently emerged as a model for study of VC deficiency. We investigated the effect of fluoride on liver cells from wild type Balb/c and sfx mice. We found that activities of SOD, GPx, and CAT were reduced in both wild type and sfx mice; however, the amount of reduction in the sfx cells is more than that in Balb/c cells. In addition, while both cells increased MDA, the increase in the sfx cells is greater than that in Balb/c cells. Gene networks of Sod, Gpx, and Cat in the liver of humans and mice are also different. Our study suggests that reaction to fluoride in vitamin C deficient mice might be different from that of wild type mice

Effect of Fluorosis on liver cells of VC deficient and wild type mice

ABSTRACT For decades, mouse and other rodents have been used for study of oxidative or related studies such as the effect of fluoride. It is known that rodents normally synthesize their own vitamin C (VC) due to the presence of a key enzyme in ascorbic acid synthesis, lgulono-lactone-γ-oxidase (Gulo), while humans do not have the capacity of VC synthesis due to the deletion of most part of the GULO gene. The spontaneous fracture (sfx) mouse recently emerged as a model for study of VC deficiency. We investigated the effect of fluoride on liver cells from wild type Balb/c and sfx mice. We found that reduction of SOD, GPx and CAT activities were reduced in both wild type and sfx mice; however, the amount of reduction in the sfx cells is more than that in Balb/c cells. In addition, while both cells increased MDA, the increase in the sfx cells is greater than that in Balb/c cells. Gene networks of Sod, Gpx and Cat in the liver of humans and mice are also different. Our study suggests that reaction to fluoride in Vitamin C deficient mice might be different from that of wild type mice

Epigenome-wide association data implicates DNA methylation-mediated genetic risk in psoriasis

Abstract Background Psoriasis is a chronic inflammatory skin disease characterized by epidermal hyperproliferation and altered keratinocyte differentiation and inflammation and is caused by the interplay of genetic and environmental factors. Previous studies have revealed that DNA methylation (DNAm) and genetic makers are closely associated with psoriasis, and strong evidences have shown that DNAm can be controlled by genetic factors, which attracted us to evaluate the relationship among DNAm, genetic makers, and disease status. Methods We utilized the genome-wide methylation data of psoriatic skin (PP, N = 114) and unaffected control skin (NN, N = 62) tissue samples in our previous study, and we performed whole-genome genotyping with peripheral blood of the same samples to evaluate the underlying genetic effect on skin DNA methylation. Causal inference test (CIT) was used to assess whether DNAm regulate genetic variation and gain a better understanding of the epigenetic basis of psoriasis susceptibility. Results We identified 129 SNP-CpG pairs achieving the significant association threshold, which constituted 28 unique methylation quantitative trait loci (MethQTL) and 34 unique CpGs. There are 18 SNPs were associated with psoriasis at a Bonferoni-corrected P < 0.05, and these 18 SNPs formed 93 SNP-CpG pairs with 17 unique CpG sites. We found that 11 of 93 SNP-CpG pairs, composed of 5 unique SNPs and 3 CpG sites, presented a methylation-mediated relationship between SNPs and psoriasis. The 3 CpG sites were located on the body of C1orf106, the TSS1500 promoter region of DMBX1 and the body of SIK3. Conclusions This study revealed that DNAm of some genes can be controlled by genetic factors and also mediate risk variation for psoriasis in Chinese Han population and provided novel molecular insights into the pathogenesis of psoriasis