SGX Switchless Calls Made Configless

Intel's software guard extensions (SGX) provide hardware enclaves to guarantee confidentiality and integrity for sensitive code and data. However, systems leveraging such security mechanisms must often pay high performance overheads. A major source of this overhead is SGX enclave transitions which induce expensive cross-enclave context switches. The Intel SGX SDK mitigates this with a switchless call mechanism for transitionless cross-enclave calls using worker threads. Intel's SGX switchless call implementation improves performance but provides limited flexibility: developers need to statically fix the system configuration at build time, which is error-prone and misconfigurations lead to performance degradations and waste of CPU resources. ZC-SWITCHLESS is a configless and efficient technique to drive the execution of SGX switchless calls. Its dynamic approach optimises the total switchless worker threads at runtime to minimise CPU waste. The experimental evaluation shows that ZC-SWITCHLESS obviates the performance penalty of misconfigured switchless systems while minimising CPU waste.Comment: 10 pages, 53rd Annual IEEE/IFIP International Conference on Dependable Systems and Networks (DSN

The PRSS3P2 and TRY7 deletion copy number variant modifies risk for chronic pancreatitis

Background PRSS1 and PRSS2 constitute the only functional copies of a tandemly-arranged five-trypsinogen-gene cluster (i.e., PRSS1, PRSS3P1, PRSS3P2, TRY7 and PRSS2) on chromosome 7q35. Variants in PRSS1 and PRSS2, including missense and copy number variants (CNVs), have been reported to predispose to or protect against chronic pancreatitis (CP). We wondered whether a common trypsinogen pseudogene deletion CNV (that removes two of the three trypsinogen pseudogenes, PRSS3P2 and TRY7) might be associated with CP causation/predisposition. Methods We analyzed the common PRSS3P2 and TRY7 deletion CNV in a total of 1536 CP patients and 3506 controls from France, Germany, India and Japan by means of quantitative fluorescent multiplex polymerase chain reaction. Results We demonstrated that the deletion CNV variant was associated with a protective effect against CP in the French, German and Japanese cohorts whilst a trend toward the same association was noted in the Indian cohort. Meta-analysis under a dominant model yielded a pooled odds ratio (OR) of 0.68 (95% confidence interval (CI) 0.52–0.89; p = 0.005) whereas an allele-based meta-analysis yielded a pooled OR of 0.84 (95% CI 0.77–0.92; p = 0.0001). This protective effect is explicable by reference to the recent finding that the still functional PRSS3P2/TRY7 pseudogene enhancers upregulate pancreatic PRSS2 expression. Conclusions The common PRSS3P2 and TRY7 deletion CNV was associated with a reduced risk for CP. This finding provides additional support for the emerging view that dysregulated PRSS2 expression represents a discrete mechanism underlying CP predisposition or protection

The PRSS3P2 and TRY7 deletion copy number variant modifies risk for chronic pancreatitis

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