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In this work, we devise a stochastic version of contact Hamiltonian systems and show that the phase flows of these systems preserve contact structures. Moreover, we provide a sufficient condition under which these stochastic contact Hamiltonian systems are completely integrable. This establishes an appropriate framework for investigating stochastic contact Hamiltonian systems.
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This work is to investigate the (top) Lyapunov exponent for a class of Hamiltonian systems under small non-Gaussian Lévy-type noise with bounded jumps. In a suitable moving frame, the linearization of such a system can be regarded as a small perturbation of a nilpotent linear system. The Lyapunov exponent is then estimated by taking a Pinsky-Wihstutz transformation and applying the Khas'minskii formula, under appropriate assumptions on smoothness, ergodicity, and integrability. Finally, two examples are presented to illustrate our results.
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This study was designed to reveal the predictive targets and biological mechanisms of curcumol against interstitial cystitis (IC). By use of available databases and bioinformatic assays, pathogenetic targets of IC and functional targets of curcumol were identified respectively. A network of functional protein-protein interaction (PPI) was produced before screening the main predictive targets, biological processes and signaling pathways of curcumol against IC. In bioinformatic findings, the data of ingenuity pathway analysis (IPA) delineated that curcumol exerted anti-IC benefits through regulating multipronged signaling pathways, including tyrosine protein kinase-2 (PTK2) pathway. Further, optimal 18 biotargets of curcumol against IC were harvested through differential expression analysis. And the predictive targets of receptor tyrosine-protein kinase erbB-2 (ERBB2), epidermal growth factor receptor (EGFR) and PTK2 were the most important molecules. In further validated experiments, PTK2 and phosphorylation PTK2 (p-PTK2) were representatively selected for testing by human and animal IC samples. As results, increased immunoreactive proteins of tumor necrosis factor alpha (TNF-α), PTK2 and p-PTK2Tyr397 in human IC sections were observed, accompanied with altered urinary parameters. Interestingly, curcumol-treated IC mice showed that intracellular expressions of PTK2, p-PTK2Tyr397 in bladder samples were reduced, accompanied with lowered blood inflammatory cytokines of interleukin 6 (IL-6), TNF-α. In conclusion, the current bioinformatic data and preliminary findings unravel that the predominant targets of curcumol against IC may be the potential biological markers for screening and treating IC, such as PTK2 molecule.
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Recently, increasing evidences have suggested that inflammatory stress is markedly occurred in the impaired tissue. Thus, the streptozotocin (STZ)-induced diabetic mice were used to investigate the potential renoprotective effect of ramulus mori polysaccharides (RMP) and to discuss the underlying mechanism. The results from the present study showed that RMP significantly lowered the blood glucose and serum levels of glycosylated protein, cholesterol, urea nitrogen (Urea-N), creatinine (Cr) and 24-hour urine protein, while the albumin content was elevated. Meanwhile, the proinflammatory cytokines such as interleukin-6 (IL-6), interferon-gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α) in renal tissue of STZ-lesioned mice were reduced by RMP treatment. Similarly, pathological examination indicated that STZ-induced renal injury was effectively mitigated. In addition, the protein levels of interleukin-1 (IL-1) and interleukin-1 receptor (IL-1R) in renal tissue were notably decreased. Moreover, the endogenous expressions of phosphorylated-IκB (p-IκB) and nuclear factor-kappa B (NF-κB) were down-regulated, respectively. Together, these findings revealed that RMP treatment effectively attenuated STZ-induced cytotoxicity in renal tissue, in which RMP-exerted renoprotection was associated with intrarenally debilitating inflammation reaction through blocking the IL-1/NF-κB pathway, thereby maintaining the renal homeostasis.