Information-Theoretic Limits of Integrated Sensing and Communication with Correlated Sensing and Channel States for Vehicular Networks

In connected vehicular networks, it is vital to have vehicular nodes that are capable of sensing about surrounding environments and exchanging messages with each other for automating and coordinating purpose. Towards this end, integrated sensing and communication (ISAC), combining both sensing and communication systems to jointly utilize their resources and to pursue mutual benefits, emerges as a new cost-effective solution. In ISAC, the hardware and spectrum co-sharing leads to a fundamental tradeoff between sensing and communication performance, which is not well understood except for very simple cases with the same sensing and channel states, and perfect channel state information at the receiver (CSIR). In this paper, a general point-to-point ISAC model is proposed to account for the scenarios that the sensing state is different from but correlated with the channel state, and the CSIR is not necessarily perfect. For the model considered, the optimal tradeoff is characterized by a capacity-distortion function that quantifies the best communication rate for a given sensing distortion constraint requirement. An iterative algorithm is proposed to compute such tradeoff, and a few non-trivial examples are constructed to demonstrate the benefits of ISAC as compared to the separation-based approach

Paxillin facilitates timely neurite initiation on soft-substrate environments by interacting with the endocytic machinery.

Neurite initiation is the first step in neuronal development and occurs spontaneously in soft tissue environments. Although the mechanisms regulating the morphology of migratory cells on rigid substrates in cell culture are widely known, how soft environments modulate neurite initiation remains elusive. Using hydrogel cultures, pharmacologic inhibition, and genetic approaches, we reveal that paxillin-linked endocytosis and adhesion are components of a bistable switch controlling neurite initiation in a substrate modulus-dependent manner. On soft substrates, most paxillin binds to endocytic factors and facilitates vesicle invagination, elevating neuritogenic Rac1 activity and expression of genes encoding the endocytic machinery. By contrast, on rigid substrates, cells develop extensive adhesions, increase RhoA activity and sequester paxillin from the endocytic machinery, thereby delaying neurite initiation. Our results highlight paxillin as a core molecule in substrate modulus-controlled morphogenesis and define a mechanism whereby neuronal cells respond to environments exhibiting varying mechanical properties

Systematics of g factors of 2_1^+ states in even-even nuclei from Gd to Pt: A microscopic description by the projected shell model

The systematics of g factor of first excited 2^+ state vs neutron number N is studied by the projected shell model. The study covers the even-even nuclei of all isotopic chains from Gd to Pt. g factors are calculated by using the many-body wavefunctions that reproduces well the energy levels and B(E2)'s of the ground-state bands. For Gd to W isotopes the characteristic feature of the g factor data along an isotopic chain is described by the present model. Deficiency of the model in the g factor description for the heavier Os and Pt isotopes is discussed.Comment: 9 pages, 5 figure