Predicting catastrophes: the role of criticality

Is prediction feasible in systems at criticality? While conventional scale-invariant arguments suggest a negative answer, evidence from simulation of driven-dissipative systems and real systems such as ruptures in material and crashes in the financial market have suggested otherwise. In this dissertation, I address the question of predictability at criticality by investigating two non-equilibrium systems: a driven-dissipative system called the OFC model which is used to describe earthquakes and damage spreading in the Ising model. Both systems display a phase transition at the critical point. By using machine learning, I show that in the OFC model, scaling events are indistinguishable from one another and only the large, non-scaling events are distinguishable from the small, scaling events. I also show that as the critical point is approached, predictability falls. For damage spreading in the Ising model, the opposite behavior is seen: the accuracy of predicting whether damage will spread or heal increases as the critical point is approached. I will also use machine learning to understand what are the useful precursors to the prediction problem

Glycyrrhizin Attenuates Portal Hypertension and Collateral Shunting via Inhibition of Extrahepatic Angiogenesis in Cirrhotic Rats

Portal hypertension develops along with liver cirrhosis then induces the formation of portal-systemic collaterals and lethal complications. Extrahepatic angiogenesis plays an important role. Glycyrrhizin has been found to exhibit anti-angiogenic features, which leads to its extensive use. However, the relevant effects of glycyrrhizin on liver cirrhosis and portal hypertension have not been evaluated. This study thus aimed to investigate the impact of glycyrrhizin on portal hypertension-related derangements in cirrhotic rats. Male Sprague-Dawley rats received bile duct ligation (BDL) to induce cirrhosis or sham operation as control. The rats were subdivided to receive glycyrrhizin (150 mg/kg/day, oral gavage) or vehicle beginning on the 15th day post operation, when BDL-induced liver fibrosis developed. The effects of glycyrrhizin were determined on the 28th day, the typical timing of BDL-induced cirrhosis. Glycyrrhizin significantly reduced portal pressure (p = 0.004). The splanchnic inflow as measured by superior mesenteric arterial flow decreased by 22% (p = 0.029). The portal-systemic collateral shunting degree reduced by 30% (p = 0.024). The mesenteric angiogenesis and phospho-VEGFR2 protein expression were also downregulated (p = 0.038 and 0.031, respectively). Glycyrrhizin did not significantly influence the liver biochemistry data. Although glycyrrhizin tended to reverse liver fibrosis, statistical significance was not reached (p = 0.069). Consistently, hepatic inflow from portal side, hepatic vascular resistance, and liver fibrosis-related protein expressions were not affected. Glycyrrhizin treatment at the stage of hepatic fibrosis still effectively attenuated portal hypertension and portosystemic collateral shunting. These beneficial effects were attributed to, at least in part, the suppression of mesenteric angiogenesis by VEGF signaling pathway downregulation