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Load balancing is vital for the efficient and long-term operation of cloud data centers. With virtualization, post (reactive) migration of virtual machines (VMs) after allocation is the traditional way for load balancing and consolidation. However, it is not easy for reactive migration to obtain predefined load balance objectives and it may interrupt services and bring instability. Therefore, we provide a new approach, called Prepartition, for load balancing. It partitions a VM request into a few sub-requests sequentially with start time, end time and capacity demands, and treats each sub-request as a regular VM request. In this way, it can proactively set a bound for each VM request on each physical machine and makes the scheduler get ready before VM migration to obtain the predefined load balancing goal, which supports the resource allocation in a fine-grained manner. Simulations with real-world trace and synthetic data show that our proposed approach with offline version (PrepartitionOff) scheduling has 10%–20% better performance than the existing load balancing baselines under several metrics, including average utilization, imbalance degree, makespan and Capacity_makespan. We also extend Prepartition to online load balancing. Evaluation results show that our proposed approach also outperforms state-of-the-art online algorithms. [ABSTRACT FROM AUTHOR]

Liver steatosis is becoming increasingly common in patients with chronic hepatitis B (CHB), and its effect on liver stiffness measurement (LSM), as assessed by transient elastography, remains controversial. Seven hundred and fifty‐five patients with CHB and normal serum alanine aminotransferase levels, who underwent vibration‐controlled transient elastography and liver biopsy, were included in the study. We examined whether the histological degree of liver steatosis affects the accuracy of transient elastography‐assessed LSM in these patients. Among the 755 CHB patients included in the study, 286 (37.9%) had liver steatosis, of whom 156 had grade S1, 74 had grade S2, and 56 had grade S3 on histology. Presence of liver steatosis was independently associated with greater body mass index (BMI, adjusted‐odds ratio [OR] = 5.786, 95% CI: 3.998–8.373, p = 0.018), and higher serum total cholesterol (adjusted‐OR = 7.944, 95% CI: 4.731–13.339, p < 0.001) and triglyceride levels (adjusted‐OR = 2.777, 95% CI: 2.050–3.761, p < 0.001). There was no significant association between liver steatosis and fibrosis stage (OR = 1.016, 95% CI: 0.905–1.140, p = 0.790). Age (B‐coefficient = 0.020, 95% CI: 0.001–0.040, p = 0.044), BMI (B‐coefficient = 0.060, 95% CI: 0.011–0.127, p = 0.019), serum gamma‐glutamyl‐transpeptidase (GGT, B‐coefficient = 0.015, 95% CI: 0.001–0.029, p = 0.032), positivity for HBeAg (B‐coefficient = −0.816, 95% CI: −1.568 to −0.064, p = 0.034), as well as liver fibrosis stage (B‐coefficient = 2.796, 95% CI: 2.501–3.090, p < 0.001), and inflammation activity grade (B‐coefficient = 0.648, 95% CI: 0.162–1.135, p = 0.009) were all independently associated with higher LSM, while no significant association was found between degree of liver steatosis and LSM. Among patients with the same histological fibrosis stage, LSM values did not show any significant difference among patients with absent, mild, moderate or severe steatosis. We conclude that liver steatosis has no significant effect on transient elastography‐measured LSM in CHB patients with normal serum alanine aminotransferase levels. [ABSTRACT FROM AUTHOR]

Background. Apoptosis signal-regulating kinase 1 (ASK1) has been reported to induce fibrotic signaling in the setting of oxidative stress. However, the role of ASK1 and its mechanism of action in angiotensin II- (Ang II-) induced liver fibrosis remain largely unknown. Methods. Human hepatic LX-2 stellate cells were treated with Ang II alone or cotreated with Ang II plus an ASK1 inhibitor (GS-4997) or siRNA-targeting ASK1. Immunofluorescent staining, real-time PCR, and western blotting were used to determine the expressionof α-SMA, Col I, and Col III expression. Cell viability was assessed by the CCK-8 assay. The concentrations of IL-1β, IL-18, and TNF-α in conditioned medium were determined by ELISA. The levels of intracellular ROS in LX-2 cells were analyzed using a ROS assay kit. Exosome size was determined by electron microscopy. Results. Ang II markedly increased the expression of extracellular matrix (ECM) proteins (α-SMA, Col I, and Col III) and proinflammatory cytokines (IL-1β, IL-18, and TNF-α). Ang II also increased the expression of endoplasmic reticulum stress (ERS) markers (GRP78, p-PERK, and CHOP) and p-ASK1. Results also showed that pretreatment with GS-4997 or siRNA could abolish all the abovementioned effects on LX-2 cells. Furthermore, we found that exosome release caused by ASK1-mediated ERS was involved in the activation of LX-2 cells by Ang II. The activation of LX-2 cells could be blocked by treating the exosomes with annexin. Conclusions. In summary, we found that ASK1 mediates Ang II-activated ERS in HSCs and the subsequent activation of HSCs, suggesting a promising strategy for treating liver fibrosis. [ABSTRACT FROM AUTHOR]