13 research outputs found
Parameterized Synthesis with Safety Properties
Parameterized synthesis offers a solution to the problem of constructing
correct and verified controllers for parameterized systems. Such systems occur
naturally in practice (e.g., in the form of distributed protocols where the
amount of processes is often unknown at design time and the protocol must work
regardless of the number of processes). In this paper, we present a novel
learning based approach to the synthesis of reactive controllers for
parameterized systems from safety specifications. We use the framework of
regular model checking to model the synthesis problem as an infinite-duration
two-player game and show how one can utilize Angluin's well-known L* algorithm
to learn correct-by-design controllers. This approach results in a synthesis
procedure that is conceptually simpler than existing synthesis methods with a
completeness guarantee, whenever a winning strategy can be expressed by a
regular set. We have implemented our algorithm in a tool called L*-PSynth and
have demonstrated its performance on a range of benchmarks, including robotic
motion planning and distributed protocols. Despite the simplicity of L*-PSynth
it competes well against (and in many cases even outperforms) the
state-of-the-art tools for synthesizing parameterized systems.Comment: 18 page
Chronic interleukin-1 exposure drives haematopoietic stem cells towards precocious myeloid differentiation at the expense of self-renewal
Haematopoietic stem cells (HSCs) maintain lifelong blood production and increase blood cell numbers in response to chronic and acute injury. However, the mechanism(s) by which inflammatory insults are communicated to HSCs and their consequences for HSC activity remain largely unknown. Here, we demonstrate that interleukin-1 (IL-1), which functions as a key pro-inflammatory 'emergency' signal, directly accelerates cell division and myeloid differentiation of HSCs through precocious activation of a PU.1-dependent gene program. Although this effect is essential for rapid myeloid recovery following acute injury to the bone marrow, chronic IL-1 exposure restricts HSC lineage output, severely erodes HSC self-renewal capacity, and primes IL-1-exposed HSCs to fail massive replicative challenges such as transplantation. Importantly, these damaging effects are transient and fully reversible on IL-1 withdrawal. Our results identify a critical regulatory circuit that tailors HSC responses to acute needs, and is likely to underlie deregulated blood homeostasis in chronic inflammation conditions