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Brillouin lasers, with their unique properties, offer an intriguing solution for many applications, yet bringing their performance to integrated platforms has remained questionable. We present a theoretical framework to describe Brillouin lasing in integrated ring microcavities. Specifically, a general case of a mismatch between the Brillouin shift and the microresonator inter-mode spacing is considered. We show that although the lasing threshold is increased with the frequency detuning, a significant enhancement of the laser power in comparison with the pure resonant interaction could be achieved. Moreover, there is an optimal pump frequency detuning from the resonant mode frequency, when the effect is most pronounced. An increase of the Brillouin threshold with the pump frequency detuning is accompanied by narrowing the pump frequency range available for lasing. Importantly, at the optimal value of the pump frequency detuning when the Brillouin signal is maximal, Brillouin signal noise level is minimal. Analytical results obtained in the steady-state approach are in quantitative agreement with the results of numerical simulations.

Peptide toxins of arthropods are one of the potential sources of bioactive substances. Toxins are able to bind to calcium channels and block them. Ca 2+ ions play an important role in many cell processes, in particular, in apoptosis. In this work, we study the effect of some arthropod toxins on intracellular processes associated with the induction of apoptosis. Synthetic analogs of U 5-scytotoxin-Sth1a, ω-hexatoxin-Hv1a, ω-theraphotoxin-Hhn2a, and μ-agatoxin-Aa1a toxins-inhibitors of calcium L, P, and Q channels and sodium channels were used in the study. Apoptosis was induced by AC-1001 H3 peptide. We study the effect of toxins on the level of apoptosis, ROS, mitochondrial potential, GSH, and ATP in CHO-K1 cells. We show that all the tested toxins are able to dose dependently block the induction of apoptosis triggered by AC-1001 H3 and reduce the level of natural apoptosis in CHO-K1 cells. Cell incubation with apoptosis inducer AC-1001 H3 in the presence and absence of toxins causes an increase in the intracellular concentrations of ROS, ATP, and mitochondrial potential and decreases the GSH concentration. The present study reveals the antiapoptotic effect of a number of arthropod peptide toxins. The toxins studied can represent a novel approach used in the treatment of pathologies associated with the activation of apoptotic mechanisms.