In the ongoing effort to build micro- and nanoscale machines, one of the key approaches is the bio-hybrid approach, which focuses on the use of biological constructs and engineered cells. As a natural extension of this concept to nanoscale communication, molecular communication is an umbrella term encompassing various communication systems that are built based on biological intra- and intercellular communication methods, most of which use molecules and molecular concentration as the information carrier. Compared to other proposed molecular communication systems such as diffusion-based communication and microtubular networks, calcium signaling is expected to provide a faster and more controllable system that is suitable for information dissemination and group behavior in nanoscale sensor networks. In this article, we give a general overview of calcium signaling, a novel communication paradigm that uses intercellular calcium waves in biology as a baseline, explain its capabilities, limitations, and some possible deployment scenarios. We also describe various open issues of this novel communication system and elaborate on some research directions for calcium signaling.

Primary objective: The present study was undertaken to evaluate whether enoant, which is rich in polyphenols, has any effect on electroencephalogram (EEG), oxidative stress and inflammation in ischemia/reperfusion (I/R) injury. Methods: Ischemia was induced by 2-hour occlusion of bilateral common carotid artery. Animals orally received enoant. Group 1 was the ischemic control group. Group 2 was treated with enoant of 1.25 g kg⁻¹ per day for 15 days after I/R. Group 3 received the same concentration of enoant as in group 2 for 15 days before and after I/R. Group 4 was the sham operation group. EEG activities were recorded and the levels of TNF-α, IL-1β and IL-6, TBARS and GSH were measured in the whole brain homogenate. Results: There were significant changes in EEG activity in groups treated with enoant either before or after ischemia when compared with their basal EEG values. TNF-α, IL-6 and IL-1β levels were significantly increased after I/R. GSH levels in group 3 treated with enoant in both pre- and post-ischemic periods were significantly increased and TBARS concentration was decreased compared with the ischemic group. Conclusion: The findings support that both pre-ischemic and post-ischemic administrations of enoant might produce neuroprotective action against cerebral ischemia.

The purpose of this study is to investigate the effect of decorin, a naturally occurring proteoglycan with anti-transforming growth factor beta (TGF-β) activity, on the rat model of Peyronie's disease (PD). Twenty-five adult male Sprague-Dawley rats were divided in three groups: I) TGF-β (0.5 μg) injected (n: 8); II) TGF-β injected and decorin treated (n: 8); and III) controls (n: 9). Decorin (0.5 μg per day) was given with intracavernous injection on the second, third, fourth and fifth day following TGF-β injection. All rats underwent electrical stimulation of the cavernous nerve after 6 weeks. Intracavernosal and arterial blood pressures were measured during this procedure. Cross-sections of the rat penises were examined using Mason trichrome and H&E stains. Statistical analyses were carried out using one-way anova. Histopathological examinations confirmed the Peyronie's-like condition in TGF-β-injected rats, which exhibited a thickening of the tunica albuginea (TA), when compared to controls. Disorganisation of collagen on the TA was also prominent in TGF-β-injected rats, but not in decorin-treated and control rats. Decorin-treated rats showed significantly higher maximal intracavernosal pressure (MIP) responses to cavernous nerve stimulation, when compared to group 1 (P < 0.05). Our results indicate that decorin antagonises the effects of TGF-β in the rat model of PD and prevents diminished erectile response to cavernous nerve stimulation.