Ferroptosis is a new type of cell death that was discovered in recent years and is usually accompanied by a large amount of iron accumulation and lipid peroxidation during the cell death process; the occurrence of ferroptosis is iron-dependent. Ferroptosis-inducing factors can directly or indirectly affect glutathione peroxidase through different pathways, resulting in a decrease in antioxidant capacity and accumulation of lipid reactive oxygen species (ROS) in cells, ultimately leading to oxidative cell death. Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. How to intervene in the occurrence and development of related diseases by regulating cell ferroptosis has become a hotspot and focus of etiological research and treatment, but the functional changes and specific molecular mechanisms of ferroptosis still need to be further explored. This paper systematically summarizes the latest progress in ferroptosis research, with a focus on providing references for further understanding of its pathogenesis and for proposing new targets for the treatment of related diseases. Facts Ferroptosis is a new type of programmed cell death, which occurs with iron dependence. Ferroptosis plays an important regulatory role in the occurrence and development of many diseases, such as tumors, neurological diseases, acute kidney injury, ischemia/reperfusion, etc. Activating or blocking the ferroptosis pathway to alleviate the progression of the disease, which provides a promising therapeutic strategy for many diseases. Open questions What is the relationship between ferroptosis and other types of cell death? Is it synergy or antagonism? Is iron necessary to promote the production of lipid peroxides, or can other substances take the place of iron in ferroptosis? What is the downstream regulation mechanism of iron in ferroptosis? How can ferroptosis promote the development of inflammation?

There is often a considerable delay between the discovery of a vulnerability and the issue of a patch. One way to mitigate this window of vulnerability is to use a configuration workaround, which prevents the vulnerable code from being executed at the cost of some lost functionality -but only if one is available. Since application configurations are not specifically designed to mitigate software vulnerabilities, we find that they only cover 25.2% of vulnerabilities.To minimize patch delay vulnerabilities and address the limitations of configuration workarounds, we propose Security Workarounds for Rapid Response (SWRRs), which are designed to neutralize security vulnerabilities in a timely, secure, and unobtrusive manner. Similar to configuration workarounds, SWRRs neutralize vulnerabilities by preventing vulnerable code from being executed at the cost of some lost functionality. However, the key difference is that SWRRs use existing error-handling code within applications, which enables them to be mechanically inserted with minimal knowledge of the application and minimal developer effort. This allows SWRRs to achieve high coverage while still being fast and easy to deploy.We have designed and implemented Talos, a system that mechanically instruments SWRRs into a given application, and evaluate it on five popular Linux server applications. We run exploits against 11 real-world software vulnerabilities and show that SWRRs neutralize the vulnerabilities in all cases. Quantitative measurements on 320 SWRRs indicate that SWRRs instrumented by Talos can neutralize 75.1% of all potential vulnerabilities and incur a loss of functionality similar to configuration workarounds in 71.3% of those cases. Our overall conclusion is that automatically generated SWRRs can safely mitigate 2.1× more vulnerabilities, while only incurring a loss of functionality comparable to that of traditional configuration workarounds.

Neuropeptides function in animals to modulate most, if not all, complex behaviors. In invertebrates, neuropeptides can function as the primary neurotransmitter of a neuron, but more generally they co-localize with a small molecule neurotransmitter, as is commonly seen in vertebrates. Because a single neuron can express multiple neuropeptides and because neuropeptides can bind to multiple G protein-coupled receptors, neuropeptide actions increase the complexity by which the neural connectome can be activated or inhibited. Humans are estimated to have 90 plus neuropeptide genes; by contrast, nematodes, a relatively simple organism, have a slightly larger complement of neuropeptide genes. For instance, the nematode Caenorhabditis elegans has over 100 neuropeptide-encoding genes, of which at least 31 genes encode peptides of the FMRFamide family. To understand the function of this large FMRFamide peptide family, we isolated knockouts of different FMRFamide-encoding genes and generated transgenic animals in which the peptides are overexpressed. We assayed these animals on two basic behaviors: locomotion and reproduction. Modulating levels of different neuropeptides have strong as well as subtle effects on these behaviors. These data suggest that neuropeptides play critical roles in C. elegans to fine tune neural circuits controlling locomotion and reproduction.

Modern smartphone operating systems (OSs) have been developed with a greater emphasis on security and protecting privacy. One of the mechanisms these systems use to protect users is a permission system, which requires developers to declare what sensitive resources their applications will use, has users agree with this request when they install the application and constrains the application to the requested resources during runtime. As these permission systems become more common, questions have risen about their design and implementation. In this paper, we perform an analysis of the permission system of the Android smartphone OS in an attempt to begin answering some of these questions. Because the documentation of Android's permission system is incomplete and because we wanted to be able to analyze several versions of Android, we developed PScout, a tool that extracts the permission specification from the Android OS source code using static analysis. PScout overcomes several challenges, such as scalability due to Android's 3.4 million line code base, accounting for permission enforcement across processes due to Android's use of IPC, and abstracting Android's diverse permission checking mechanisms into a single primitive for analysis.We use PScout to analyze 4 versions of Android spanning version 2.2 up to the recently released Android 4.0. Our main findings are that while Android has over 75 permissions, there is little redundancy in the permission specification. However, if applications could be constrained to only use documented APIs, then about 22% of the non-system permissions are actually unnecessary. Finally, we find that a trade-off exists between enabling least-privilege security with fine-grained permissions and maintaining stability of the permission specification as the Android OS evolves.

Scope: Autophagy plays an important role in alleviating alcoholic liver disease (ALD). In this study, it is discovered that a dimer procyanidin (DPC) significantly prevented ALD by promoting hepatic autophagy. Methods and results: Both cell and animal disease models stimulated by excessive ethanol are employed to evaluate the protective actions of DPC. Specifically, in vitro, DPC significantly decreased intracellular lipid deposition, diminished reactive oxygen species (ROS) formation, and elevated the level of mitochondrial membrane potential. These beneficial effects can be remarkably blocked by 3-methyladenine, a potent autophagy inhibitor, suggesting the autophagy-dependent protective role of DPC. In vivo, DPC pretreatment can also significantly reduce lipid accumulation, ROS overproduction, and elevated GSH content in the liver. Similarly, these protective effects of DPC can be partially reversed by chloroquine, a lysosomal inhibitor used to block the late-stage autophagy flux. Moreover, the determinations of LC3 and p62 protein expressions, autophagic flux assessments, and transmission electron microscopy observation further demonstrate the pro-autophagic effect of DPC. Conclusions: DPC may activate hepatic autophagy to eliminate lipid droplets and damaged mitochondria, thereby reducing hepatic lipid disposition and ROS overproduction. This study demonstrates that DPC is a protective reagent on ALD, providing a novel strategy of fighting ALD.

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Efficient regulation of thermal radiation is an effective way to conserve energy consumption of buildings. Because windows are the least energy-efficient part of buildings, their thermal radiation regulation is highly demanded, especially in the changing environment, but is still a challenge. Here, by employing a kirigami structure, we design a variable-angle thermal reflector as a transparent envelope of windows for their thermal radiation modulation. The envelope can be easily switched between heating and cooling modes by loading different pre-stresses, which endow the envelope windows with the ability of temperature regulation, and the interior temperature of a building model can be reduced by ~3.3 °C under cooling mode and increased by ~3.9 °C under heating mode in the outdoor test. The improved thermal management of windows by the adaptive envelope provides an extra heating, ventilation, and air-conditioning energy savings percentage of 13% to 29% per year for buildings located in different climate zones around the world, making the kirigami envelope windows a promising way for energy-saving utilization.

Security vulnerabilities are among the most critical software defects in existence. When identified, programmers aim to produce patches that prevent the vulnerability as quickly as possible, motivating the need for automatic program repair (APR) methods to generate patches automatically. Unfortunately, most current APR methods fall short because they approximate the properties necessary to prevent the vulnerability using examples. Approximations result in patches that either do not fix the vulnerability comprehensively, or may even introduce new bugs. Instead, we propose property-based APR, which uses human-specified, program-independent and vulnerability-specific safety properties to derive source code patches for security vulnerabilities. Unlike properties that are approximated by observing the execution of test cases, such safety properties are precise and complete. The primary challenge lies in mapping such safety properties into source code patches that can be instantiated into an existing program.To address these challenges, we propose Senx, which, given a set of safety properties and a single input that triggers the vulnerability, detects the safety property violated by the vulnerability input and generates a corresponding patch that enforces the safety property and thus, removes the vulnerability. Senx solves several challenges with property-based APR: it identifies the program expressions and variables that must be evaluated to check safety properties and identifies the program scopes where they can be evaluated, it generates new code to selectively compute the values it needs if calling existing program code would cause unwanted side effects, and it uses a novel access range analysis technique to avoid placing patches inside loops where it could incur performance overhead. Our evaluation shows that the patches generated by Senx successfully fix 32 of 42 real-world vulnerabilities from 11 applications including various tools or libraries for manipulating graphics/media files, a programming language interpreter, a relational database engine, a collection of programming tools for creating and managing binary programs, and a collection of basic file, shell, and text manipulation tools.