We present the modeling of a quantum regime for surface plasmon polaritons (SPPs) excited by an electron beam skimming parallel to the surface of a metallic structure. The theoretical approach resembles that used to describe the quantum Cherenkov radiation in which the quantized free electrons interact with a classical radiation field. In this paper, we rephrase the model in a more rigorous way, considering the detrimental effects of losses on coherent light. In the quantum regime of SPPs, each electron emits a single photon due to the transition between two successive momentum states. It is shown that the quantum nature of SPPs is realized in the low beam current limit where the radiation (gain in the field strength) operates in discrete frequency bands with a remarkably narrow linewidth. When losses are negligible, the photon emission occurs in periodic bursts along the interaction length. We show also that the Ohmic loss effects in the SPP process set an intrinsic limit on the coherent production of photons and also have severe detrimental effects on the radiation intensity. The findings of this study can describe recent experimental observations of the surface plasmonic near-field based on the photon-induced near-field electron microscopy.

Delay in wound healing remains one of diabetes's worse side effects, which increases mortality. The proposed study sought to scrutinize the implications of bee gomogenat (BG) on diabetic's wound closure in a streptozotocin-(STZ)-enhanced type-1 diabetes model’s rodents. We used 3 different mice groups: group 1 non-diabetic rodents "serving as control", group 2 diabetic rodents, and group3 BG-treated diabetic rodents. We noticed that diabetic rodents experience a delayed wound closure, which emerged as a significant (*P < 0.05) decline in the deposition of collagen as compared to control non-diabetic animals. We noticed that diabetic rodents have a delayed wound closure characterized by a significant (*P < 0.05) decrease in the CD31 expression (indicator for wound angiogenesis and neovascularization) and an apparent elevation in the expression of such markers of inflammation as MCP-1 and HSP-70 as compared to control animals. Moreover, diabetic animals displayed a significant (*P < 0.05) increase in the expression of gap junction proteins Cx43 and a significant decrease in the expression of Panx3 in the wounded skin tissues when compared to the controls. Intriguingly, topical application with BG on the diabetic wounded skin tissues contributes to a significant (#P < 0.05) enhancing in the collagen deposition, up-regulating the level of CD31 expression and a significant (#P < 0.05) down-regulation in the MCP-1 and HSP-70 expressions as compared to diabetic non-treated animals. The expression's levels of Cx43 and Panx3 were significantly (#P < 0.05) retrieved in diabetic rodents after BG treatment. Taken together, our findings showed for the first time that BG promotes the recovering process and accelerated the closure of diabetic related wounds.

Touch perception is enabled by mechanically activated ion channels, the opening of which excites cutaneous sensory endings to initiate sensation. In this study, we identify ELKIN1 as an ion channel likely gated by mechanical force, necessary for normal touch sensitivity in mice. Touch insensitivity in Elkin1−/− mice was caused by a loss of mechanically activated currents (MA currents) in around half of all sensory neurons activated by light touch (low-threshold mechanoreceptors). Reintroduction of Elkin1 into sensory neurons from Elkin1−/− mice restored MA currents. Additionally, small interfering RNA–mediated knockdown of ELKIN1 from induced human sensory neurons substantially reduced indentation-induced MA currents, supporting a conserved role for ELKIN1 in human touch. Our data identify ELKIN1 as a core component of touch transduction in mice and potentially in humans.

The kinetics of oxidations of caffeine by permanganate ion in both perchloric and sulfuric acids solutions have been investigated spectrophotometrically at a constant ionic strength of 1.0 mol dm-3 and at 25°C. In both acids, the reactiontime curves were obtained with a sigmoid profile suggesting an autocatalytic effect caused by Mn(II) ions formed as a reaction product. Both catalytic and non-catalytic processes were determined to be first order with respect to the permanganate ion and caffeine concentrations, whereas the orders with respect to [H+ ] and [Mn(II)] were found to be less than unity. Variation of either ionic strength or dielectric constant of the medium had no significant effect on the oxidation rates. Spectroscopic studies and Michaelis-Menten plots showed no evidence for the formation of intermediate complexes in both acids suggesting that the reactions point towards the outer-sphere pathway. The reactions mechanism adequately describing the kinetic results was proposed. In both acids, the main oxidation products of caffeine were identified as 1,3,7-trimethyluric acid. Under comparable experimental conditions, the oxidation rate of caffeine in perchloric acid was slightly higher than that in sulfuric acid. The constants involved in the different steps of the reactions mechanism have been evaluated. With admiration to the rate-limiting step of these reactions, the activation parameters have been evaluated and discussed.

The kinetics of oxidation of cadaverine (CAD) by permanganate ion in acidic, neutral and alkaline media has been investigated spectrophtometrically at constant ionic strengths and temperature. The reactions in different media exhibited a first order kinetics in [MnO4 - ] and less than unit order dependences with respect to [CAD]. The oxidation of cadaverine showed less than unit order dependences with respect to [H+ ] and [OH- ] in acidic and alkaline media, respectively. Variation of ionic strengths in both acidic and alkaline media had no significant effect on the oxidation rates. The proposed oxidations mechanisms in all media involve formation of 1:1 intermediate complexes between the kinetically active species of both cadaverine and permanganate ion. The final oxidation products of cadaverine were identified as 5-aminopentanal and ammonia. The appropriate rate laws in all media were deduced. The reaction constants involved in the different steps of the mechanisms were evaluated.