Chao-Yu Miao

The α7 nicotinic acetylcholine receptor (α7nAChR) has been studied for many years since its discovery.Although many functions and characteristics of brain α7nAChR are widely understood, much remains to be elucidated.The α7nAChR is widely expressed in the central nervous system, not only in neurons but also in astrocytes, microglia, and endothelial cells.α7nAChR can be activated by endogenous agonist like acetylcholine or exogenous agonists like nicotine and PNU282987.Its agonists can be divided into selective agonists and non-selective agonists.The activation of α7nAChR results in a series of physiological processes which have both short-term and long-term effects on cells, for example, calcium influx, neurotransmitter release, synaptic plasticity, and excitatory transmission.It also induces other downstream events, such as inflammation, autophagy, necrosis, transcription, and apoptosis.The cellular responses to α7nAChR activation vary according to cell types and conditions.For example, α7nAChR activation in pyramidal neurons leads to long-term potentiation, while α7nAChR activation in GABAergic interneurons leads to long-term depression.Studies have also shown some contradictory phenomena, which requires further study for clarification.Herein, the cellular responses of α7nAChR activation are summarized, and the functions of α7nAChR in neurons and non-neuronal cells are discussed.We also summarized contradictory conclusions to show where we stand and where to go for future studies.

The in-vivo non-human primate animal and in-vitro cell disease models play a crucial part in the study of the mechanisms underlying the occurrence and development of pancreatic diseases, but with increasingly prominent limitations with in-depth research. Organoids derived from human pluripotent and adult stem cells resemble human in-vivo organs in their cellular composition, spatial tissue structure and physiological function, making them as an advantageous research tool. Up until now, numerous human organoids, including pancreas, have been effectively developed, demonstrating significant potential for research in organ development, disease modeling, drug screening, and regenerative medicine. However, different from intestine, liver and other organs, the pancreas is the only special organ in the human body, consisting of an exocrine gland and an endocrine gland. Thus, the development of pancreatic organoid technology faces greater challenges, and how to construct a composite pancreatic organoid with exocrine and endocrine gland is still difficult in current research. By reviewing the fundamental architecture and physiological role of the human pancreas, along with the swiftly developing domain of pancreatic organoids, we summarize the method and characteristics of human pancreatic organoids, and its application in modeling pancreatic diseases, as a platform for individualized drug screening and in regenerative medicine study. As the first comprehensive review that focus on the pharmacological study of human pancreatic organoid, the review hopes to help scholars to have a deeper understanding in the study of pancreatic organoid.

Stroke is a devastating disease representing the leading cause of morbidity and mortality worldwide. Stroke can be divided into ischemic stroke, due to blockade of cerebral artery and lack of blood flow perfusion, and hemorrhagic stroke, a nontraumatic intracranial hemorrhage. It has been well established that brain injury in ischemic or hemorrhagic stroke has been attributed to cell necrosis and apoptosis, but recently autophagy has been found to be implicated as well. Autophagy acts as a central regulator of cellular homeostatic processes and plays a critical role in the pathophysiology of neural death during stroke. Moreover, autophagy participates in the poststroke recovery by influencing synaptic growth and plasticity. Here, we will summarize recent evidences for cerebral ischemia or hemorrhage-induced autophagy, and discuss the current understanding of the roles of autophagy in ischemic and hemorrhagic stroke.