ESRO: Experience Assisted Service Reliability against Outages

Modern cloud services are prone to failures due to their complex architecture, making diagnosis a critical process. Site Reliability Engineers (SREs) spend hours leveraging multiple sources of data, including the alerts, error logs, and domain expertise through past experiences to locate the root cause(s). These experiences are documented as natural language text in outage reports for previous outages. However, utilizing the raw yet rich semi-structured information in the reports systematically is time-consuming. Structured information, on the other hand, such as alerts that are often used during fault diagnosis, is voluminous and requires expert knowledge to discern. Several strategies have been proposed to use each source of data separately for root cause analysis. In this work, we build a diagnostic service called ESRO that recommends root causes and remediation for failures by utilizing structured as well as semi-structured sources of data systematically. ESRO constructs a causal graph using alerts and a knowledge graph using outage reports, and merges them in a novel way to form a unified graph during training. A retrieval-based mechanism is then used to search the unified graph and rank the likely root causes and remediation techniques based on the alerts fired during an outage at inference time. Not only the individual alerts, but their respective importance in predicting an outage group is taken into account during recommendation. We evaluated our model on several cloud service outages of a large SaaS enterprise over the course of ~2 years, and obtained an average improvement of 27% in rouge scores after comparing the likely root causes against the ground truth over state-of-the-art baselines. We further establish the effectiveness of ESRO through qualitative analysis on multiple real outage examples.Comment: Accepted to 38th IEEE/ACM International Conference on Automated Software Engineering (ASE 2023

Deletion of GPIHBP1 causing severe chylomicronemia

Lipoprotein lipase (LPL) is a hydrolase that cleaves circulating triglycerides to release fatty acids to the surrounding tissues. The enzyme is synthesized in parenchymal cells and is transported to its site of action on the capillary endothelium by glycophosphatidylinositol (GPI)-anchored high-density lipoprotein-binding protein 1 (GPIHBP1). Inactivating mutations in LPL; in its cofactor, apolipoprotein (Apo) C2; or in GPIHBP1 cause severe hypertriglyceridemia. Here we describe an individual with complete deficiency of GPIHBP1. The proband was an Asian Indian boy who had severe chylomicronemia at 2 months of age. Array-based copy-number analysis of his genomic DNA revealed homozygosity for a 17.5-kb deletion that included GPIHBP1. A 44-year-old aunt with a history of hypertriglyceridemia and pancreatitis was also homozygous for the deletion. A bolus of intravenously administered heparin caused a rapid increase in circulating LPL and decreased plasma triglyceride levels in control individuals but not in two GPIHBP1-deficient patients. Thus, short-term treatment with heparin failed to attenuate the hypertriglyceridemia in patients with GPIHBP1 deficiency. The increasing resolution of copy number microarrays and their widespread adoption for routine cytogenetic analysis is likely to reveal a greater role for submicroscopic deletions in Mendelian conditions. We describe the first neonate with complete GPIHBP1 deficiency due to homozygosity for a deletion of GPIHBP1

Heterogeneous photocatalysis of imidacloprid the effect of reaction parameters

The heterogeneous photocatalytic transformation of a harmful neonicotinoide insecticide, imidacloprid using TiO2 photocatalyst was the aim of the present work. The optimal TiO2 concentrations in oxygenated, aerated and oxygen-free suspensions were determined. However the dissolved oxygen enhanced the transformation rate of imidacloprid that was occurred in oxygen-free suspensions too. This can be explained by the relative high reactivity of imidacloprid towards hydrated electron, thus the relative contribution of direct charge can be significant. The effect of different additives was investigated to prove this assumption: NaF, methanol, t-butanol, chloroform, EDTA and KI. The pH and ionic strength of the solution have also significant effect, most likely by modifying the surface properties of TiO2. The results showed, that beside HO• based reaction the direct charge transfer must have significant role in the transformation of imidaclopride

Approach to diagnosing a pediatric patient with severe insulin resistance in low- or middle-income countries

Diabetes mellitus (DM) in children is most often caused by impaired insulin secretion (type 1 DM). In some children, the underlying mechanism for DM is increased insulin resistance, which can have different underlying causes. While the majority of these children require insulin dosages less than 2.0 U/kg/day to achieve normoglycemia, higher insulin requirements indicate severe insulin resistance. Considering the therapeutic challenges in patients with severe insulin resistance, early diagnosis of the underlying cause is essential in order to consider targeted therapies and to prevent diabetic complications. Although rare, several disorders can attribute to severe insulin resistance in pediatric patients. Most of these disorders are diagnosed through advanced diagnostic tests, which are not commonly available in low- or middle-income countries. Based on a case of DM with severe insulin resistance in a Surinamese adolescent who was later confirmed to have autosomal recessive congenital generalized lipodystrophy, type 1 (Berardinelli–Seip syndrome), we provide a systematic approach to the differential diagnosis and work-up. We show that a thorough review of medical history and physical examination generally provide sufficient information to diagnose a child with insulin-resistant DM correctly, and, therefore, our approach is especially applicable to low- or middle-income countries

Seipin is required for converting nascent to mature lipid droplets

How proteins control the biogenesis of cellular lipid droplets (LDs) is poorly understood. Using Drosophila and human cells, we show here that seipin, an ER protein implicated in LD biology, mediates a discrete step in LD formation—the conversion of small, nascent LDs to larger, mature LDs. Seipin forms discrete and dynamic foci in the ER that interact with nascent LDs to enable their growth. In the absence of seipin, numerous small, nascent LDs accumulate near the ER and most often fail to grow. Those that do grow prematurely acquire lipid synthesis enzymes and undergo expansion, eventually leading to the giant LDs characteristic of seipin deficiency. Our studies identify a discrete step of LD formation, namely the conversion of nascent LDs to mature LDs, and define a molecular role for seipin in this process, most likely by acting at ER-LD contact sites to enable lipid transfer to nascent LDs. DOI: http://dx.doi.org/10.7554/eLife.16582.00