The increasing popularity of virtual reality (VR) in a wide spectrum of applications has generated sensitive personal data such as medical records and credit card information. While protecting such data from unauthorized access is critical, directly applying traditional authentication methods (e.g., PIN) through new VR input modalities such as remote controllers and head navigation would cause security issues. The authentication action can be purposefully observed by attackers to infer the authentication input. Unlike any other mobile devices, VR presents immersive experience via a head-mounted display (HMD) that fully covers users' eye area without public exposure. Leveraging this feature, we explore human visual system (HVS) as a novel biometric authentication tailored for VR platforms. While previous works used eye globe movement (gaze) to authenticate smartphones or PCs, they suffer from a high error rate and low stability since eye gaze is highly dependent on cognitive states. In this paper, we explore the HVS as a whole to consider not just the eye globe movement but also the eyelid, extraocular muscles, cells, and surrounding nerves in the HVS. Exploring HVS biostructure and unique HVS features triggered by immersive VR content can enhance authentication stability. To this end, we present OcuLock, an HVS-based system for reliable and unobservable VR HMD authentication. OcuLock is empowered by an electrooculography (EOG) based HVS sensing framework and a record-comparison driven authentication scheme. Experiments through 70 subjects show that OcuLock is resistant against common types of attacks such as impersonation attack and statistical attack with Equal Error Rates as low as 3.55% and 4.97% respectively. More importantly, OcuLock maintains a stable performance over a 2month period and is preferred by users when compared to other potential approaches.

With the advanced discoveries in the field of pathogenesis, a series of cerebral diseases, such as cerebral ischaemia, Alzheimer's disease, and depression, have been found to have multiple signalling targets in the microenvironment. Only a few existing agents have been shown to have curative effects due to this specific circumstance. In recent decades, active ingredients isolated from natural plants have been shown to be crucial for original drug development. Geniposide, mainly extracted from Gardenia jasminoides Ellis, is representative of these natural products. Geniposide demonstrates various biological activities in the treatment of cerebral, cardiovascular, hepatic, tumorous, and other diseases. The multiple protective effects of geniposide on the brain have especially drawn increasing attention. Thus, this article specifically reviews the characteristics of current models of cerebral ischaemia and illustrates the possible effects of geniposide and its pathogenetic mechanisms on these models. Geniposide has been shown to significantly reduce the area of cerebral infarction and alleviate neuronal damage and necrosis mainly by inhibiting inflammatory signals, including NLRP3, TNF-α, IL-6, and IL-1β. Neuronal protection was also involved in activating the PI3K/Akt and Wnt/catenin pathways. Geniposide was able to increase autophagy and inhibit apoptosis by regulating the function of mTOR in treating Alzheimer's disease. Geniposide has also been shown to act as a glucagon-like peptide-1 receptor (GLP-1R) agonist to reduce amyloid plaques and inhibit oxidative stress to alleviate memory impairment as well as synaptic loss. Moreover, geniposide has been shown to exert antidepressant effects primarily by regulating the hypothalamic–pituitary–adrenal (HPA) axis. Detailed explorations have shown that the biological activities of inhibiting inflammatory cytokine secretion, alleviating oxidative stress, and suppressing mitochondrial damage are also involved in the mechanism of action of geniposide. Therefore, geniposide is a promising agent awaiting further exploration for the treatment of cerebral diseases via various phenotypes or signalling pathways.

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