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.