Focusing On The High-End Or Low-End? Local Attacking With Network Externality

Network externality can encourage adoption when a network is growing in size. Network externality, however, can also encourage abandoning when a network is getting small. Therefore, the challenger’s action focusing on persuading a part of the market can eventually affect the whole market when network externality is at work. This paper discusses two local attacking strategies, namely, “focusing on the high-end” and “focusing on the low-end”, and compares their effects. The conclusions show that the former strategy generally exhibits stronger eventual effects than the latter. Although direct effects are local, the eventual effects could be global when network externality is strong and/or consumers have small differences in their reservation prices. Based on our results, the incumbent should set a price keeping all installed users away from being stranded. If any installed user gives up the incumbent’s technology, he or she may be the fuse to trigger the chain reaction. Thus, a better approach is to “make the fuse wet”. To the challenger, local attacking strategies work better when network externality is strong and/or reservation prices of installed users are nearly the same

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

Pinicolol B from Antrodia cinnamomea induces apoptosis of nasopharyngeal carcinoma cells

Ethnopharmacological relevance: The medicinal mushroom Antrodia cinnamomea possesses anticancer properties but the active compounds responsible for these effects are mostly unknown. Aim of the study: We aimed to identify novel A. cinnamomea compounds that produce cytotoxic effects on cancer cells. Materials and methods: Using ethanol extraction and chromatography, we isolated the lanostanoid compound lanosta-7,9(11),24-trien-3β,15α,21-triol (1) from cultured A. cinnamomea mycelium. Cytotoxicity and pro-apoptotic effects of compound 1 were evaluated using the MTS assay and flow cytometry analysis, respectively. Results: Compound 1 produced cytotoxic effects on the nasopharyngeal carcinoma cell lines TW02 and TW04, with IC50 values of 63.3 and 115.0μM, respectively. On the other hand, no cytotoxic effects were observed on non-tumorigenic nasopharyngeal epithelial cells (NP69). In addition, compound 1 induced apoptosis in TW02 and TW04 cells as revealed by flow cytometry analysis. Conclusions: Our results demonstrate for the first time the presence of pinicolol B in A. cinnamomea mycelium and suggest that this compound may contribute to the anticancer effects of A. cinnamomea. Pinicolol B from Antrodia cinnamomea induces apoptosis of nasopharyngeal carcinoma cells

Genome-wide meta-analysis identifies 127 open-angle glaucoma loci with consistent effect across ancestries

10.1038/s41467-020-20851-4Nature Communications121125

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field