12 research outputs found

    Exploring Plausible Patches Using Source Code Embeddings in JavaScript

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    Despite the immense popularity of the Automated Program Repair (APR) field, the question of patch validation is still open. Most of the present-day approaches follow the so-called Generate-and-Validate approach, where first a candidate solution is being generated and after validated against an oracle. The latter, however, might not give a reliable result, because of the imperfections in such oracles; one of which is usually the test suite. Although (re-) running the test suite is right under one's nose, in real life applications the problem of over- and underfitting often occurs, resulting in inadequate patches. Efforts that have been made to tackle with this problem include patch filtering, test suite expansion, careful patch producing and many more. Most approaches to date use post-filtering relying either on test execution traces or make use of some similarity concept measured on the generated patches. Our goal is to investigate the nature of these similarity-based approaches. To do so, we trained a Doc2Vec model on an open-source JavaScript project and generated 465 patches for 10 bugs in it. These plausible patches alongside with the developer fix are then ranked based on their similarity to the original program. We analyzed these similarity lists and found that plain document embeddings may lead to misclassification - it fails to capture nuanced code semantics. Nevertheless, in some cases it also provided useful information, thus helping to better understand the area of Automated Program Repair.Comment: Paper accepted in APR2021 conferenc

    Fine-Tuning GPT-2 to Patch Programs, is it Worth it?

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    Abnormal basement membrane results in increased keratinocyte-derived periostin expression in psoriasis similar to wound healing

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    The psoriatic skin resembles wound healing, and it shows abnormalities at the basement membrane (BM), also in the non-lesional skin. Fibroblast-derived dermal periostin has well-known functions in wound healing and Th2-mediated diseases, such as atopic dermatitis. Here we show that serum periostin level was elevated in psoriatic patients, remarkably in the systemically treated ones. Obvious periostin positivity was detected in basal keratinocytes of the non-lesional, lesional, and previously-lesional psoriatic vs. healthy skin. Ex vivo skin models were generated to examine how different skin injuries affect periostin expression during wound healing. Our newly developed cultured salt-split model demonstrated that BM-injury induced periostin expression in basal keratinocytes, and periostin levels in the supernatant were also increased upon healing. In wound healing models, β1-integrin expression was similarly induced. β1-integrin blocking caused reduced periostin expression in in vitro scratch assay, indicating that β1-integrin can mediate periostin production. In contrast to atopic dermatitis, psoriatic basal keratinocytes are in an activated state and show a stable wound healing-like phenotype with the overexpression of periostin. This abnormal BM-induced wound healing as a potential compensatory mechanism can be initiated already in the non-lesional skin present in the lesion and keratinocytes can remain activated in the healed skin

    Stress-related regulation is abnormal in the psoriatic uninvolved skin

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    Keratinocyte stress-response of the uninvolved psoriatic epidermis is known to be altered compared to healthy cells. Therefore, we aimed to reveal potential mechanisms underlying this alteration. We compared the expression of annotated cell-stress-related proteins between uninvolved psoriatic and healthy skin using the protein array method. Data were analyzed by the Reactome over-representation test. We found that p27/CDKN1B and cytochrome C showed at least a two-fold increase, while cyclooxygenase-2, indolamine-2,3-dioxygenase-1, serum paraoxonase 1, serum paraoxonase 3, serine-46-phosphorylated tumor protein p53, and superoxide-dismutase-2 showed a two-fold decrease in expression in the uninvolved skin. Over-representation analysis suggested the Forkhead-box protein O (FOXO)-mediated transcription as the most significant pathway affected by the differently expressed cell-stress-related proteins (DECSRPs). DECSRPs indicate increased FOXO-mediated transcription of cell-cycle genes and reduced interleukin-signaling in the psoriatic uninvolved skin. Nuclear positivity of the FOXO-signaling-related p27/CDKN1B and FOXO1 are negatively correlated with the disease severity and showed increased expression in the uninvolved epidermis and also in healthy primary keratinocytes, which were grown on cartilage oligomeric matrix protein-coated surfaces. Our results indicate a cell-cycle inhibitory process, as a stress-related compensatory mechanism in the uninvolved epidermis, that could be responsible for blocking keratinocyte hyperproliferation in the psoriatic uninvolved skin, thus maintaining the symptomless skin phenotype
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