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Memory-corruption attacks such as code-reuse attacks and data-only attacks have been a key threat to systems security. To counter these threats, researchers have proposed a variety of defenses, including control-flow integrity (CFI), codepointer integrity (CPI), and code (re-)randomization. All of them, to be effective, require a security primitive-intra-process protection of confidentiality and/or integrity for sensitive data (such as CFI's shadow stack and CPI's safe region).In this paper, we propose SEIMI, a highly efficient intraprocess memory isolation technique for memory-corruption defenses to protect their sensitive data. The core of SEIMI is to use the efficient Supervisor-mode Access Prevention (SMAP), a hardware feature that is originally used for preventing the kernel from accessing the user space, to achieve intra-process memory isolation. To leverage SMAP, SEIMI creatively executes the user code in the privileged mode. In addition to enabling the new design of the SMAP-based memory isolation, we further develop multiple new techniques to ensure secure escalation of user code, e.g., using the descriptor caches to capture the potential segment operations and configuring the Virtual Machine Control Structure (VMCS) to invalidate the execution result of the control registers related operations. Extensive experimental results show that SEIMI outperforms existing isolation mechanisms, including both the Memory Protection Keys (MPK) based scheme and the Memory Protection Extensions (MPX) based scheme, while providing secure memory isolation.

Facial nerve (FN) injury seriously affects human social viability and causes a heavy economic and social burden. Although mesenchymal stem cell-derived exosomes (MSC-Exos) promise therapeutic benefits for injury repair, there has been no evaluation of the impact of MSC-Exos administration on FN repair. Herein, we explore the function of MSC-Exos in the immunomodulation of macrophages and their effects in repairing FN injury. An ultracentrifugation technique was used to separate exosomes from the MSC supernatant. Administrating MSC-Exos to SD rats via local injection after FN injury promoted axon regeneration and myelination and alleviated local and systemic inflammation. MSC-Exos facilitated M2 polarization and reduced the M1-M2 polarization ratio. miRNA sequencing of MSC-Exos and previous literature showed that the MAPK/NF-κb pathway was a downstream target of macrophage polarization. We confirmed this hypothesis both in vivo and in vitro. Our findings show that MSC-Exos are a potential candidate for treating FN injury because they may have superior benefits for FN injury recovery and can decrease inflammation by controlling the heterogeneity of macrophages, which is regulated by the p38 MAPK/NF-κb pathway.

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