Search

Summary: Traditional applications have been developed for decades. Most of the security research around them have focused on the detection of memory corruption vulnerabilities, such as buffer overflow, double fetch, and integer overflow. On the contrary, logic bugs, a kind of flaws caused by unreasonable application logic, attract much less attention. Files are the most common media for programs to persist their data in the system. As the file owners, programs are responsible for protecting their files from malicious users' tampering by leveraging access control mechanisms. However, if a program configures their access control mechanisms in wrong ways and causes evil users to bypass security checks to access files, there exists a file access control vulnerability. As a branch of logic flaws, file access control vulnerabilities are less popular with researchers. Thus, to mitigate the harm of the file access control vulnerabilities on Windows system, our team conducted first‐step research on them. We first classified file access control bugs into two types and codified some bug patterns. Then we formalized file access control vulnerabilities to propose a scalable detection method and implemented a lightweight analysis system StaticFAC. After evaluating StaticFAC in real‐world Windows software, we discovered 15 0‐day bugs. [ABSTRACT FROM AUTHOR]

Intervertebral disc degeneration (IDD) is characterized by the decreased function and number of nucleus pulposus cells (NPCs) caused by excessive intervertebral disc (IVD) pressure. This research aims to provide novel insights into IDD prevention and treatment by clarifying the effect of andrographolide (ANDR) on IDD cell autophagy and oxidative stress under mechanical stress. Human primary NPCs were extracted from the nucleus pulposus tissue of non-IDD trauma patients. An IDD cell model was established by posing mechanical traction on NPCs. Through the construction of an IDD rat model, the influence of ANDR on IDD pathological changes was explored in vivo. The proliferation and autophagy of NPCs were decreased while the apoptosis rate and oxidative stress reaction were increased by mechanical traction. ANDR intervention obviously alleviated this situation. MiR-9 showed upregulated expression in IDD cell model, while FoxO3 and PINK1/Parkin were downregulated. Decreased proliferation and autophagy as well as enhanced apoptosis and oxidative stress response of NPCs were observed following miR-9 mimics and H89 intervention, while the opposite trend was observed after FoxO3 overexpression. FoxO3 is a direct target downstream miR-9. The in vivo experiments revealed that after ANDR intervention, the number of apoptotic cells in rat IVD tissue decreased and the autophagy increased. In conclusion, ANDR improves NPC proliferation, and autophagy, inhibits apoptosis and oxidative stress, and alleviates the pathological changes of IDD via the miR-9/FoxO3/PINK1/Parkin axis, which may be a new and effective treatment for IDD in the future.