Compiling Tree Transforms to Operate on Packed Representations

When written idiomatically in most programming languages, programs that traverse and construct trees operate over pointer-based data structures, using one heap object per-leaf and per-node. This representation is efficient for random access and shape-changing modifications, but for traversals, such as compiler passes, that process most or all of a tree in bulk, it can be inefficient. In this work we instead compile tree traversals to operate on pointer-free pre-order serializations of trees. On modern architectures such programs often run significantly faster than their pointer-based counterparts, and additionally are directly suited to storage and transmission without requiring marshaling. We present a prototype compiler, Gibbon, that compiles a small first-order, purely functional language sufficient for tree traversals. The compiler transforms this language into intermediate representation with explicit pointers into input and output buffers for packed data. The key compiler technologies include an effect system for capturing traversal behavior, combined with an algorithm to insert destination cursors. We evaluate our compiler on tree transformations over a real-world dataset of source-code syntax trees. For traversals touching the whole tree, such as maps and folds, packed data allows speedups of over 2x compared to a highly-optimized pointer-based baseline

Rebuilding racket on chez scheme (experience report)

We rebuilt Racket on Chez Scheme, and it works well-as long as we're allowed a few patches to Chez Scheme. DrRacket runs, the Racket distribution can build itself, and nearly all of the core Racket test suite passes. Maintainability and performance of the resulting implementation are good, although some work remains to improve end-to-end performance. The least predictable part of our effort was how big the differences between Racket and Chez Scheme would turn out to be and how we would manage those differences. We expect Racket on Chez Scheme to become the main Racket implementation, and we encourage other language implementers to consider Chez Scheme as a target virtual machine

A missense mutation in the MLKL brace region promotes lethal neonatal inflammation and hematopoietic dysfunction

Necroptosis is a regulated form of inflammatory cell death driven by activated MLKL. Here, the authors identify a mutation in the brace region that confers constitutive activation, leading to lethal inflammation in homozygous mutant mice and providing insight into human mutations in this region

Time to Peak Glucose and Peak C-Peptide During the Progression to Type 1 Diabetes in the Diabetes Prevention Trial and TrialNet Cohorts

OBJECTIVE To assess the progression of type 1 diabetes using time to peak glucose or C-peptide during oral glucose tolerance tests (OGTTs) in autoantibody-positive relatives of people with type 1 diabetes. RESEARCH DESIGN AND METHODS We examined 2-h OGTTs of participants in the Diabetes Prevention Trial Type 1 (DPT-1) and TrialNet Pathway to Prevention (PTP) studies. We included 706 DPT-1 participants (mean ± SD age, 13.84 ± 9.53 years; BMI Z-score, 0.33 ± 1.07; 56.1% male) and 3,720 PTP participants (age, 16.01 ± 12.33 years; BMI Z-score, 0.66 ± 1.3; 49.7% male). Log-rank testing and Cox regression analyses with adjustments (age, sex, race, BMI Z-score, HOMA-insulin resistance, and peak glucose/C-peptide levels, respectively) were performed. RESULTS In each of DPT-1 and PTP, higher 5-year diabetes progression risk was seen in those with time to peak glucose >30 min and time to peak C-peptide >60 min (P < 0.001 for all groups), before and after adjustments. In models examining strength of association with diabetes development, associations were greater for time to peak C-peptide versus peak C-peptide value (DPT-1: χ2 = 25.76 vs. χ2 = 8.62; PTP: χ2 = 149.19 vs. χ2 = 79.98; all P < 0.001). Changes in the percentage of individuals with delayed glucose and/or C-peptide peaks were noted over time. CONCLUSIONS In two independent at-risk populations, we show that those with delayed OGTT peak times for glucose or C-peptide are at higher risk of diabetes development within 5 years, independent of peak levels. Moreover, time to peak C-peptide appears more predictive than the peak level, suggesting its potential use as a specific biomarker for diabetes progression