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Acupuncture is a therapeutic treatment that is well recognized in many countries. However, the initiation mechanisms of acupuncture are not well understood. Purinergic signaling has been considered a key signaling pathway in acupuncture in recent years. Acupuncture-induced ATP is mainly produced by mast cells and fibroblasts, and ATP is gradually hydrolyzed into adenosine. ATP and adenosine further participate in the process of acupuncture information transmission to the nervous and immune systems through specific purine receptors. Acupuncture initiates analgesia via the down-regulation of the expression of P2 receptors or up-regulation of the expression of adenosine A₁ receptors on nerve fibers. ATP also promotes the proliferation of immune cells through P2 receptors and A₃ receptors, causing inflammation. In contrast, adenosine activates A₂ receptors, promotes the production and infiltration of immunosuppressive cells, and causes an anti-inflammatory response. In summary, we described the role of purinergic signaling as a general signaling pathway in the initiation of acupuncture and the influence of purinergic signaling on the neuroimmune network to lay the foundation for future systematic research on the mechanisms of acupuncture therapeutics.

The basic cytoskeletal transport in cells is achieved by two oppositely directed processive motor proteins, kinesin and dynein, walking along microtubules. Here, we offer a new view of the mechanism of the transport direction regulation by the intrinsic cell's electric fields that interact with kinks elicited in microtubules.

Calcium (${\mathrm{\text{Ca}}}^{2+}$) signaling is reported as a critical factor in the insulin secretion mechanism of pancreatic $\beta$-cells. Further, calcium signaling also has interactions with other similar signaling systems like adenosine triphosphate (ATP) to achieve the functions of $\beta$-cells. Disturbances in any of these two interactive signaling systems can cause disorders in the secretion mechanism of insulin, leading to the onset of type-2 diabetes. Therefore, this paper presents a one-dimensional spatio-temporal mathematical model designed to explore the dynamic interactions between ATP and ${\mathrm{\text{Ca}}}^{2+}$ within a pancreatic $\beta$-cell. The model under consideration comprises a set of nonlinear reaction–diffusion equations governing the behavior of ${\mathrm{\text{Ca}}}^{2+}$ and ATP. The formulation of the initial and boundary conditions takes into account the physical and physiological factors associated with the $\beta$-cell. Further, the model also incorporates adenosine diphosphate (ADP) production due to the hydrolysis of ATP and ${\mathrm{\text{Ca}}}^{2+}$-dependent insulin secretion of the $\beta$-cell. The numerical results are acquired through the utilization of the finite element method. The time derivative terms are resolved through the utilization of the Crank–Nicolson method. The various glycemic states caused by variational impacts of system parameters are demonstrated.

Most industrialized countries subsidize private sector R&D, even under some circumstances when the firm is owned by foreigners. The present paper, using a simple theoretical analysis of a monopoly firm selling only to the U.S. market, argues that such subsidies are welfare enhancing—as long, of course—as the funding agency chooses the projects it funds wisely. The paper suggests that a subsidy rate of 50% might be warranted under some circumstances.

Myosin V, a two-headed motor protein, moves along actin filaments toward the positive end. Similar to other molecular motors, myosin V hydrolyzes Adenosine tri-phosphate (ATP) and releases its product to produce movement. This study proposes a multiple-paths model that considers the hydrolysis processes of catalytic sites at the two heads of myosin V as independent. The proposed model describes the myosin V transition process by seven states, with one load-dependent transition rate among these states. This model demonstrates how myosin V steps forward at different chemical reaction paths. This study also uses the enzyme kinetics to calculate the mean velocity. Stochastic processes are used to analyze the randomness as well. Analytical results reveal that the theoretical mean velocities, mean movement lengths, and randomness with various ATP concentrations under external load agree with the experimental data.

The cyclical interaction between myosin and the actin filament is responsible for muscle contraction. The myosin cross-bridge, which is the ATPase, binds to actin and then undergoes a conformational change (the power stroke) that “rows” the actin filament along. Protein crystallography of myosin has yielded high-resolution models of the beginning and end of the power stroke, which is driven by ATP hydrolysis. ATP also controls the cross bridge affinity for the actin filament. This is low in the presence of ATP and much higher without nucleotide. Recent high-resolution electron microscopy of the actomyosin complex has yielded atomic models of the actin myosin interaction that show two new myosin conformations. These explain the reciprocal link between actin affinity and ATP affinity. Thus there are four states of the myosin cross bridge. The function of the myosin cross bridge is carried out by regulated interactions between these four states.