Relative Policy-Transition Optimization for Fast Policy Transfer

We consider the problem of policy transfer between two Markov Decision Processes (MDPs). We introduce a lemma based on existing theoretical results in reinforcement learning to measure the relativity gap between two arbitrary MDPs, that is the difference between any two cumulative expected returns defined on different policies and environment dynamics. Based on this lemma, we propose two new algorithms referred to as Relative Policy Optimization (RPO) and Relative Transition Optimization (RTO), which offer fast policy transfer and dynamics modelling, respectively. RPO transfers the policy evaluated in one environment to maximize the return in another, while RTO updates the parameterized dynamics model to reduce the gap between the dynamics of the two environments. Integrating the two algorithms results in the complete Relative Policy-Transition Optimization (RPTO) algorithm, in which the policy interacts with the two environments simultaneously, such that data collections from two environments, policy and transition updates are completed in one closed loop to form a principled learning framework for policy transfer. We demonstrate the effectiveness of RPTO on a set of MuJoCo continuous control tasks by creating policy transfer problems via variant dynamics.Comment: Accepted by AAAI 202

The lung-gut crosstalk in respiratory and inflammatory bowel disease

Both lung and gut belong to the common mucosal immune system (CMIS), with huge surface areas exposed to the external environment. They are the main defense organs against the invasion of pathogens and play a key role in innate and adaptive immunity. Recently, more and more evidence showed that stimulation of one organ can affect the other, as exemplified by intestinal complications during respiratory disease and vice versa, which is called lung-gut crosstalk. Intestinal microbiota plays an important role in respiratory and intestinal diseases. It is known that intestinal microbial imbalance is related to inflammatory bowel disease (IBD), this imbalance could impact the integrity of the intestinal epithelial barrier and leads to the persistence of inflammation, however, gut microbial disturbances have also been observed in respiratory diseases such as asthma, allergy, chronic obstructive pulmonary disease (COPD), and respiratory infection. It is not fully clarified how these disorders happened. In this review, we summarized the latest examples and possible mechanisms of lung-gut crosstalk in respiratory disease and IBD and discussed the strategy of shaping intestinal flora to treat respiratory diseases

Tumor-suppressor activity of RRIG1 in breast cancer

<p>Abstract</p> <p>Background</p> <p>Retinoid receptor-induced gene-1 (RRIG1) is a novel gene that has been lost in several types of human cancers. The aim of this study was to determine whether RRIG1 plays a role in breast cancer, such as in the suppression of breast cancer cell growth and invasion.</p> <p>Methods</p> <p>Immunohistochemistry was used to detect RRIG1 expression in breast tissue specimens. Gene transfection was used to restore or knock down RRIG1 expression in breast cancer cell lines for analysis of cell viability, colony formation, and migration/invasion potential. Reverse-transcription polymerase chain reaction and western blot assays were used to detect the changes in gene expression. The RhoA activation assay was used to assess RRIG1-induced inhibition of RhoA activity.</p> <p>Results</p> <p>The immunohistochemical data showed that <it>RRIG1 </it>expression was reduced in breast cancer tissues compared with normal and atypical hyperplastic breast tissues. <it>RRIG1 </it>expression was inversely correlated with lymph node metastasis of breast cancer but was not associated with the status of hormone receptors, such as estrogen receptor, progesterone receptor, or HER2. Furthermore, restoration of <it>RRIG1 </it>expression inhibited proliferation, colony formation, migration, and invasion of breast cancer cells. Expression of RRIG1 also reduced phosphorylated Erk1/2 and Akt levels; c-Jun, MMP9, and Akt expressions; and RhoA activity. In contrast, knockdown of RRIG1 expression promoted breast cancer cell proliferation, colony formation, migration, and invasion potential.</p> <p>Conclusion</p> <p>The data from the current study indicated that <it>RRIG1 </it>expression was reduced or lost in breast cancer and that restoration of RRIG1 expression suppressed breast cancer cell growth and invasion capacity. Future studies will determine the underlying molecular mechanisms and define RRIG1 as a tumor-suppressor gene in breast cancer.</p

Analysis of hailstorm (and thunderstorm) activities during the summer of 1985 in Dong Xiang Region, Gansu [Chinese language]

Abstract in Englis

Supercell hailstorm formed by echo mergence [Chinese language]

Includes abstract in Englis