Despite the capability in successfully fixing more and more real-world bugs, existing
Automated Program Repair (APR)
techniques are still challenged by the long-standing overfitting problem (i.e., a generated patch that passes all tests is actually incorrect). Plenty of approaches have been proposed for
automated patch correctness assessment (APCA
). Nonetheless, dynamic ones (i.e., those that needed to execute tests) are time-consuming while static ones (i.e., those built on top of static code features) are less precise. Therefore, embedding techniques have been proposed recently, which assess patch correctness via embedding token sequences extracted from the changed code of a generated patch. However, existing techniques rarely considered the context information and program structures of a generated patch, which are crucial for patch correctness assessment as revealed by existing studies. In this study, we explore the idea of context-aware code change embedding considering program structures for patch correctness assessment. Specifically, given a patch, we not only focus on the changed code but also take the correlated unchanged part into consideration, through which the context information can be extracted and leveraged. We then utilize the
AST path
technique for representation where the structure information from AST node can be captured. Finally, based on several pre-defined heuristics, we build a deep learning based classifier to predict the correctness of the patch. We implemented this idea as
Cache
and performed extensive experiments to assess its effectiveness. Our results demonstrate that
Cache
can (1) perform better than previous representation learning based techniques (e.g.,
Cache
relatively outperforms existing techniques by
\( \approx \)
6%,
\( \approx \)
3%, and
\( \approx \)
16%, respectively under three diverse experiment settings), and (2) achieve overall higher performance than existing APCA techniques while even being more precise than certain dynamic ones including PATCH-SIM (92.9% vs. 83.0%). Further results reveal that the context information and program structures leveraged by
Cache
contributed significantly to its outstanding performance.
Health benefits, flavour quality indicators and physical properties were analysed after feeding grass carp graded concentrations of soybean isoflavones (SIF) (0, 25, 50, 75, 100 and 125 mg/kg) for 60 days. The results demonstrated that optimal dietary SIF supplementation improved the protein and total PUFA content, especially healthcare n-3 PUFA (C18: 3n-3, EPA and DHA), and increased the flavour-related free amino acid [especially umami amino acid] and 5'-inosine monophosphate content, improving the health benefits and flavour quality indicators in the muscle of grass carp. In addition, optimal dietary SIF supplementation (25 or 50 mg SIF/kg diet) enhanced some physical properties [water-holding capacity and tenderness] and increased the collagen content; however, it reduced cathepsin activity and apoptosis. SIF supplementation enhanced the glutathione content and the activity of antioxidant enzymes (except CuZnSOD) by regulating their gene expression. The gene expression could be regulated by NF-E2-related factor 2 (Nrf2) signalling in the muscle of grass carp. We demonstrated that optimal dietary SIF supplementation elevated the health benefits, flavour quality indicators and physical properties of fish muscle.
Zearalenone (ZEA) is a prevalent mycotoxin with high toxicity in animals. In order to study its effect on juvenile grass carp (Ctenopharyngodon idella), six diets supplemented with different levels of ZEA (0, 535, 1041, 1548, 2002, and 2507 μg/kg diet) for 10 weeks were studied to assess its toxicity on intestinal structural integrity and potential mechanisms of action. Our report firstly proved that ZEA led to growth retardation and body deformity, and impaired the intestinal structural integrity of juvenile grass carp, as revealed by the following findings: (1) ZEA accumulated in the intestine and caused histopathological lesions; (2) ZEA resulted in oxidative injury, apoptosis, and breached tight junctions in the fish intestine, which were probably associated with Nuclear factor-erythroid 2-related factor 2 (Nrf2), p38 mitogen activated protein kinases (p38MAPK), and myosin light chain kinase (MLCK) signaling pathways, respectively. ZEA had no influence on the antioxidant gene levels of Kelch-like ECH associating protein 1 (Keap1)b (rather than Keap1a), glutathione-S-transferase (GST)P1, GSTP2 (not in the distal intestine (DI)), tight junctions occludin, claudin-c (not in the proximal intestine (PI)), or claudin-3c (not in the mid intestine (MI) or DI).
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