With the development of cloud computing technology, the microservice architecture (MSA) has become a prevailing application architecture in cloud-native applications. Many user-oriented services are supported by many microservices, and the dependencies between services are more complicated than those of a traditional monolithic architecture application. In such a situation, if an anomalous change happens in the performance metric of a microservice, it will cause other related services to be downgraded or even to fail, which would probably cause large losses to dependent businesses. Therefore, in the operation and maintenance job of cloud applications, it is critical to mine the causality of the problem and find its root cause as soon as possible. In this paper, we propose an approach for mining causality and diagnosing the root cause that uses knowledge graph technology and a causal search algorithm. We verified the proposed method on a classic cloud-native application and found that the method is effective. After applying our method on most of the services of a cloud-native application, both precision and recall were over 80%.

BackgroundThe aim of this study was investigate the effects of the sesquiterpene lactone, ludartin, on cell proliferation, cell migration, apoptosis, and the cell cycle in osteosarcoma cell lines, compared with a normal osteoblast cell line.Material/MethodsOsteosarcoma cell lines, MG-63 Saos-2 U-2OS, T1-73 143B, and HOS, and normal hFOB 1.19 osteoblasts, were cultured and treated with increasing doses of ludartin, The MTT colorimetric assay was used to measure cell metabolic activity and viability. Apoptosis was studied by fluorescence-activated cell sorting (FACS) using 4′,6-diamidino-2-phenylindole (DAPI) nuclear staining and Annexin-V/propidium iodide (PI) staining. Cell cycle was studied using flow cytometry. Cell migration and invasion were studied using wound healing and Boyden chamber assays. Protein expression was measured by Western blotting.ResultsLudartin inhibited cell viability, cell migration, cell proliferation, and increased cell apoptosis, in all osteosarcoma cell lines, with an IC50 dose ranging from 15–30 μM. The greatest effects were on the Saso-2 osteosarcoma cells, with an IC50 of 15 μM. However, ludartin showed minor cytotoxic effects of the normal hFOB 1.19 osteoblasts (IC50 >100 μM). Ludartin exerted its anti-proliferative effects on Saos-2 cells via induction of apoptosis and cell cycle arrest at the G2/M checkpoint, associated with reduced expression of Cdc25c (Ser216), Cdc25c, pCdc2 (Tyr15), and Cdc2 and increased expression of p21WAF1. Ludartin inhibited cell migration and invasion of the Saos-2 cells.ConclusionsThe dose-dependent effects of ludartin on cell proliferation, migration, apoptosis, cell cycle arrest at the G2/M checkpoint involved p21WAFI in Saos-2 osteosarcoma cells.

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