Dynamics Analysis and Simulation of the Swiss Lever Escapement Mechanism

Swiss lever escapement is almost always used in all mechanical watches, which is one of the most critical com- ponents in a mechanical watch. However, its dynamics has not been fully studied. This paper presents a method for dy- namics analysis and simulation of the Swiss level escapement. First, the Swiss lever escapement mechanism is introduced and its motion in a half-period is divided into four sections. Then the dynamics model is developed using impulsive differ- ential equations and the simulation result is obtained by MATIAB. A watch called Seiko7OO9a is taken as an example. The simulation result shows the dynamic behavior in terms of the relationship among displacement, angle and time. The spring constant and balance wheel inertia that governed the timekeeping accuracy are also discussed.

Role of chemokines and their receptors in viral persistence and liver damage during chronic hepatitis C virus infection

Chemokines produced in the liver during hepatitis C virus(HCV) infection induce migration of activated T cells from the periphery to infected parenchyma.The milieu of chemokines secreted by infected hepatocytes is predominantly associated with the T-helper cell/Tc1 T cell(Th1/Tc1) response.These chemokines consist of CCL3(macrophage inflammatory protein-1α;MIP-1α),CCL4(MIP-1β),CCL5(regulated on activation normal T cell expressed and secreted;RANTES),CXCL10(interferon-γ-inducible protein-10;IP-10),CXCL11(interferon-inducible T-cell α chemoattractant;I-TAC),and CXCL9(monokine induced by interferon γ;Mig) and they recruit T cells expressing either CCR5 or CXCR3 chemokine receptors.Intrahepatic and peripheral blood levels of these chemokines are increased during chronic hepatitis C.The interaction between chemokines and their receptors is essential in recruiting HCV-specific T cells to control the infection.When the adaptive immune response fails in this task,non-specific T cells without the capacity to control the infection are also recruited to the liver,and these are ultimately responsible for the persistent hepatic damage.The modulation of chemokine receptor expression and chemokine secretion could be a viral escape mechanism to avoid specific T cell migration to the liver during the early phase of infection,and to maintain liver viability during the chronic phase,by impairing non-specific T cell migration.Some chemokines and their receptors correlate with liver damage,and CXCL10(IP-10) and CXCR3 levels have shown a clinical utility as predictors of treatment response outcome.The regulation of chemokines and their receptors could be a future potential therapeutic target to decrease liver inflammation and to increase specific T cell migration to the infected liver.

Interaction of hepatitis C virus with the type I interferon system

Hepatitis C virus （HCV） needs to tightly manipulate host defences in order to establish infection. The innate immune response slows down viral replication by activating cytokines such as the type Ⅰ interferons （IFN-α/ β）, which trigger the synthesis of antiviral proteins and modulate the adaptive immune system. HCV has therefore developed a number of countermeasures to stay ahead of the IFN system. Here, I will attempt to summarize the current state of research regarding IFN responses against HCV and the viral escape strategies. Particular emphasis will be put on the newly discovered mechanisms HCV employs to avoid the induction of IFN in infected cells.

Spontaneous escape behavior of silver from graphite-like carbon coating and its inhibition mechanism

A series of silver-doped graphite-like carbon coatings was prepared on the surface of aluminum alloy using the magnetron sputtering method. The spontaneous escape behavior and inhibition mechanism of silver from graphite-like carbon coating were studied. The results showed that when the sample prepared with a 0.01-A current on the silver target was placed in an atmospheric environment for 0.5 h, an apparent silver escape phenomenon could be observed. However, the silver escape phenomenon was not observed for samples prepared with a 0.05-A current on the silver target if the sample was retained in a 10^（-1） Pa vacuum environment, even after 48 h. Compared with the sample placed in the atmospheric environment immediately after an ion plating process, the silver escape time lagged for 6 h. Nanometer-thick pure carbon coating coverage could effectively suppress silver escape. When the coating thickness reached700 nm, permanent retention of silver could be achieved in the silver-doped graphite-like carbon coating.As the silver residue content in the graphite-like carbon coating increased from 2.27 at.% to 5.35 at.%, the interfacial contact resistance of the coating decreased from 51mΩcm^2 to 6 mΩcm^2.

Current immune therapeutic strategies in advanced or metastatic non-small cell lung cancer

Immune escape mechanisms in non-small cell lung cancer(NSCLC)can disrupt every step of the anti-cancer immune response.In recent years,an increased understanding of the specific mechanisms fueling immune escape has allowed for the development of numerous immunotherapeutic treatments that have been introduced into the clinical practice.The advent of immunotherapy has dramatically changed the current treatment landscape of advanced or metastatic NSCLC because of its durable efficacy and manageable toxicity.In this review,we will first present a brief overview of recent evidence on immune escape mechanisms in NSCLC.We will then discuss the current promising immunotherapeutic strategies in advanced or metastatic NSCLC tumors.