Nonlinear Set Membership Filter with State Estimation Constraints via Consensus-ADMM

This paper considers the state estimation problem for nonlinear dynamic systems with unknown but bounded noises. Set membership filter (SMF) is a popular algorithm to solve this problem. In the set membership setting, we investigate the filter problem where the state estimation requires to be constrained by a linear or nonlinear equality. We propose a consensus alternating direction method of multipliers (ADMM) based SMF algorithm for nonlinear dynamic systems. To deal with the difficulty of nonlinearity, instead of linearizing the nonlinear system, a semi-infinite programming (SIP) approach is used to transform the nonlinear system into a linear one, which allows us to obtain a more accurate estimation ellipsoid. For the solution of the SIP, an ADMM algorithm is proposed to handle the state estimation constraints, and each iteration of the algorithm can be solved efficiently. Finally, the proposed filter is applied to typical numerical examples to demonstrate its effectiveness

Preventive Effects of the Intestine Function Recovery Decoction, a Traditional Chinese Medicine, on Postoperative Intra-Abdominal Adhesion Formation in a Rat Model

The intestine function recovery decoction (IFRD) is a traditional Chinese medicine that has been used for the treatment of adhesive intestinal obstruction. In this study, the preventative effects and probable mechanism of the IFRD were investigated in a rat model. We randomly assigned rats to five groups: normal, model, control, low dose IFRD, and high dose IFRD. In the animal model, the caecum wall and parietal peritoneum were abraded to induce intra-abdominal adhesion formation. Seven days after surgery, adhesion scores were assessed using a visual scoring system, and histopathological samples were examined. The levels of serum interleukin-6 (IL-6) and transforming growth factor beta-1 (TGF-β1) were analysed by an enzyme-linked immunosorbent assay (ELISA). The results showed that a high dose of IFRD reduced the grade of intra-abdominal adhesion in rats. Furthermore, the grades of inflammation, fibrosis, and neovascularization in the high dose IFRD group were significantly lower than those in the control group. The results indicate that the IFRD can prevent intra-abdominal adhesion formation in a rat model. These data suggest that the IFRD may be an effective antiadhesion agent

Effect of Emodin on Preventing Postoperative Intra-Abdominal Adhesion Formation

Background. Postoperative intra-abdominal adhesions are a major complication after abdominal surgery. Although various methods have been used to prevent and treat adhesions, the effects have not been satisfactory. Emodin, a naturally occurring anthraquinone derivative and an active ingredient in traditional Chinese herbs, exhibits a variety of pharmacological effects. In our study, we demonstrated the effect of emodin treatment on preventing postoperative adhesion formation. Materials and Methods. A total of 48 rats were divided into six groups. Abdominal adhesions were created by abrasion of the cecum and its opposite abdominal wall. In the experimental groups, the rats were administered daily oral doses of emodin. On the seventh day after operation, the rats were euthanized, and blood and pathological specimens were collected. Abdominal adhesion formation was evaluated by necropsy, pathology, immunohistochemistry, Western blot, and enzyme-linked immunosorbent assay analyses. Results. Abdominal adhesions were markedly reduced by emodin treatment. Compared with the control group, collagen deposition was reduced and the peritoneal mesothelial completeness rate was higher in the emodin-treated groups. Emodin had anti-inflammatory effects, reduced oxidative stress, and promoted the movement of the intestinal tract (P<0.05). Conclusion. Emodin significantly reduced intra-abdominal adhesion formation in a rat model

Activation of Nrf2 by Sulforaphane Inhibits High Glucose-Induced Progression of Pancreatic Cancer via AMPK Dependent Signaling

Background/Aims: Sulforaphane (SFN) is known for its potent bioactive properties, such as anti-inflammatory and anti-tumor effects. However, its anti-tumor effect on pancreatic cancer is still poorly understood. In the present study, we explored the therapeutic potential of SFN for pancreatic cancer and disclosed the underlying mechanism. Methods: Panc-1 and MiaPaca-2 cell lines were used in vitro. The biological function of SFN in pancreatic cancer was measured using EdU staining, colony formation, apoptosis, migration and invasion assays. Reactive oxygen species (ROS) production was measured using 2’-7’-Dichlorofluorescein diacetate (DCF-DA) fluorometric analysis. Western blotting and immunofluorescence were used to measure the protein levels of p-AMPK and epithelial-mesenchymal transition (EMT) pathway-related proteins, and cellular translocation of nuclear factor erythroid 2-related factor 2 (Nrf2). Nude mice and transgenic pancreatic cancer mouse model were used to measure the therapeutic potential of SFN on pancreatic cancer. Results: SFN can inhibit pancreatic cancer cell growth， promote apoptosis, curb colony formation and temper the migratory and invasion ability of pancreatic cancer cells. Mechanistically, excessive ROS production induced by SFN activated AMPK signaling and promoted the translocation of Nrf2, resulting in cell viability inhibition of pancreatic cancer. Pretreatment with compound C, a small molecular inhibitor of AMPK signaling, reversed the subcellular translocation of Nrf2 and rescued cell invasion ability. With nude mice and pancreatic cancer transgenic mouse, we identified SFN could inhibit tumor progression, with smaller tumor size and slower tumor progression in SFN treatment group. Conclusion: Our study not only elucidates the mechanism of SFN-induced inhibition of pancreatic cancer in both normal and high glucose condition, but also testifies the dual-role of ROS in pancreatic cancer progression. Collectively, our research suggests that SFN may serve as a potential therapeutic choice for pancreatic cancer

SIRT1 mediated gastric cancer progression under glucose deprivation through the FoxO1-Rab7-autophagy axis

PurposeSilent mating type information regulator 2 homolog 1 (SIRT1) and autophagy have a two-way action (promoting cell death or survival) on the progression and treatment of gastric cancer (GC) under different conditions or environments. This study aimed to investigate the effects and underlying mechanism of SIRT1 on autophagy and the malignant biological behavior of GC cells under conditions of glucose deprivation (GD).Materials and methodsHuman immortalized gastric mucosal cell GES-1 and GC cell lines SGC-7901, BGC-823, MKN-45 and MKN-28 were utilized. A sugar-free or low-sugar (glucose concentration, 2.5 mmol/L) DMEM medium was used to simulate GD. Additionally, CCK8, colony formation, scratches, transwell, siRNA interference, mRFP-GFP-LC3 adenovirus infection, flow cytometry and western blot assays were performed to investigate the role of SIRT1 in autophagy and malignant biological behaviors (proliferation, migration, invasion, apoptosis and cell cycle) of GC under GD and the underlying mechanism.ResultsSGC-7901 cells had the longest tolerance time to GD culture conditions, which had the highest expression of SIRT1 protein and the level of basal autophagy. With the extension of GD time, the autophagy activity in SGC-7901 cells also increased. Under GD conditions, we found a close relationship between SIRT1, FoxO1 and Rab7 in SGC-7901 cells. SIRT1 regulated the activity of FoxO1 and upregulated the expression of Rab7 through deacetylation, which ultimately affected autophagy in GC cells. In addition, changing the expression of FoxO1 provided feedback on the expression of SIRT1 in the cell. Reducing SIRT1, FoxO1 or Rab7 expression significantly inhibited the autophagy levels of GC cells under GD conditions, decreased the tolerance of GC cells to GD, enhanced the inhibition of GD in GC cell proliferation, migration and invasion and increased apoptosis induced by GD.ConclusionThe SIRT1-FoxO1-Rab7 pathway is crucial for the autophagy and malignant biological behaviors of GC cells under GD conditions, which could be a new target for the treatment of GC

XX Sex Chromosome Complement Promotes Atherosclerosis in Mice

Men and women differ in circulating lipids and coronary artery disease (CAD). While sex hormones such as estrogens decrease CAD risk, hormone replacement therapy increases risk. Biological sex is determined by sex hormones and chromosomes, but effects of sex chromosomes on circulating lipids and atherosclerosis are unknown. Here, we use mouse models to separate effects of sex chromosomes and hormones on atherosclerosis, circulating lipids and intestinal fat metabolism. We assess atherosclerosis in multiple models and experimental paradigms that distinguish effects of sex chromosomes, and male or female gonads. Pro-atherogenic lipids and atherosclerosis are greater in XX than XY mice, indicating a primary effect of sex chromosomes. Small intestine expression of enzymes involved in lipid absorption and chylomicron assembly are greater in XX male and female mice with higher intestinal lipids. Together, our results show that an XX sex chromosome complement promotes the bioavailability of dietary fat to accelerate atherosclerosis

The Road

My topic words is traffic, and I put that topic in my game by using the main item, car, in my gam

The Road

My topic words is traffic, and I put that topic in my game by using the main item, car, in my gam

Beta

Our team designed this game based on the theme word Traffic. The main reason about this is that Traffic could be an easy theme to create game. It is a simple game, but we actually met lots of difficulties during the process. The final project actually has huge differences with what I thought. For example, at the beginning, to best express the theme word we chose, we decided to use elements like little cars and a highway to construct it. In our game, players just need to use arrow keys to control. In my mind, the motion of our little red car should be regular. There are 4 lanes in the highway. When player press left or right bottom, the red car should only move one lane and also the same distance. We tried to let it move like 50 on the X coordination, but it’s seems stupid when the car moves and has some conflict with other settings. Therefore, we finally changed to the way that move as much as players want. There are some other kind of vehicles like police cars and some other color ones as well, these are what players need to avoid in our game. We used to put them on arranged places on a long highway which used to provide extent playable time. The difficulty change will increase or decrease those arranged cars. However, I thought that’s boring if someone want to play it again, so we changed the background to a loop and randomly create vehicles on highway. Difficulties will increase with time goes on and reach a maximum. Also, we used to have an end point on the highway, we removed it when we decided to loop the background. Under this circumstance, there is no winning condition and no way to win this game. We just set a limit life and a score based on time. In other words, players need to do their best to survive on this highway. When we tested the game, I found our game is more playable then the initial goal. The red car used to be only allowed to drive on 4 lanes, but now I can control it avoid other vehicles with a very close distance. Also, sometimes it seems surrounded by other vehicles, but they will destroy themselves by collisions. These elements make our game more playable. Xuqi and Kaisen usually say our game looks like drive on highway 17, but I don’t agree with them. Highway 17 is dangerous because of its winding topography, but in our game is dangerous because of those rude vehicles. We set those 3 different vehicles with three different speed. When two of them collide with each other, both will be destroyed and explosive. We hope people will know how dangerous it is when driving rude. We played lots of examples in construct 3 and see how it works to make our game better and innovative. The initial long highway is a typical example. We didn’t know how to make a highway at the beginning until we played the game Glokar. It uses several repeated backgrounds to make the playable time long enough. So we make our game just like it, but unfortunately we found this method is not suitable for our game. All of those games are awesome whatever on graph or entertainment. We try to learn how to make a game through their eventsheets, but some of them are too difficult to understand and some function are not free. In this case, we asked Tas and try to make our idea possible in our own way. For example, we want to make our car be unbeatable after one collision and flash. We made our car unable to touch and disappear a while and appear a while to create a flash scene. However, suddenly we found that there is a flash function, then we had to modify it. Finally, we successfully make a playable endless which brings more possibility to players. We overcome some difficulties and avoid some difficulties. We set random vehicles, which could give the game more possibilities like survive from besiege after enemies collide with others. We create a loop background to make the game have long enough play time. We give the red car a smooth control to give player chance to find gap to avoid their surround. I believe all of these elements could make our game innovative. Although there were so many problem and difficulties, we believe we did our best to create a good playable game.   Xuqi and I made lots of changes in our game on July 26, when Kaisen is on flight back to China, so there maybe some differences between his statement and our game