Multi-version concurrency control (MVCC) is currently the most popular transaction management scheme in modern database management systems (DBMSs). Although MVCC was discovered in the late 1970s, it is used in almost every major relational DBMS released in the last decade. Maintaining multiple versions of data potentially increases parallelism without sacrificing serializability when processing transactions. But scaling MVCC in a multi-core and in-memory setting is non-trivial: when there are a large number of threads running in parallel, the synchronization overhead can outweigh the benefits of multi-versioning. To understand how MVCC perform when processing transactions in modern hardware settings, we conduct an extensive study of the scheme's four key design decisions: concurrency control protocol, version storage, garbage collection, and index management. We implemented state-of-the-art variants of all of these in an in-memory DBMS and evaluated them using OLTP workloads. Our analysis identifies the fundamental bottlenecks of each design choice.

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Metabolic regulation has been proven to play a critical role in T cell antitumor immunity. However, cholesterol metabolism as a key component of this regulation remains largely unexplored. Herein, we found that the low-density lipoprotein receptor (LDLR), which has been previously identified as a transporter for cholesterol, plays a pivotal role in regulating CD8+ T cell antitumor activity. Besides the involvement of cholesterol uptake which is mediated by LDLR in T cell priming and clonal expansion, we also found a non-canonical function of LDLR in CD8+ T cells: LDLR interacts with the T-cell receptor (TCR) complex and regulates TCR recycling and signaling, thus facilitating the effector function of cytotoxic T-lymphocytes (CTLs). Furthermore, we found that the tumor microenvironment (TME) downregulates CD8+ T cell LDLR level and TCR signaling via tumor cell-derived proprotein convertase subtilisin/kexin type 9 (PCSK9) which binds to LDLR and prevents the recycling of LDLR and TCR to the plasma membrane thus inhibits the effector function of CTLs. Moreover, genetic deletion or pharmacological inhibition of PCSK9 in tumor cells can enhance the antitumor activity of CD8+ T cells by alleviating the suppressive effect on CD8+ T cells and consequently inhibit tumor progression. While previously established as a hypercholesterolemia target, this study highlights PCSK9/LDLR as a potential target for cancer immunotherapy as well.

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