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Background Observational studies suggest that hepatorenal syndrome (HRS) patients who receive pharmacological therapy before orthotopic liver transplantation display a post-transplant outcome similar to those without HRS. The aim of this study was to comprehensively compare and rank the pharmacological therapies for HRS. Methods We reviewed PubMed, Elsevier, Medline, and the Cochrane Central Register of Controlled Trials (CENTRAL) for studies that were published between 1 January 1999 and 24 February 2018. The primary endpoint was reversal of HRS. The secondary endpoints were the changes in serum creatinine (Scr) and serum sodium. We evaluated the different therapeutic strategies using network meta-analysis on the basis of Bayesian methodology. Results The study included 24 articles with 1,419 participants evaluating seven different therapeutic strategies for HRS. The most effective treatments to induce reversal of HRS were terlipressin plus albumin, noradrenaline plus albumin, and terlipressin, which had a surface under the cumulative ranking curve (SUCRA) of 0.086, 0.151, and 0.451, respectively. The top two treatments for decreasing Scr were dopamine plus furosemide plus albumin (rank probability: 0.620) and terlipressin plus albumin (rank probability: 0.570). For increasing serum sodium, the optimal treatment was octreotide plus midodrine plus albumin (rank probability: 0.800), followed by terlipressin plus albumin (rank probability: 0.544). Conclusions Terlipressin plus albumin and dopamine plus furosemide plus albumin should be prioritized for decreasing Scr in HRS, and octreotide plus midodrine plus albumin was the most effective at increasing serum sodium. Terlipressin plus albumin showed a comprehensive effect in both decreasing Scr and increasing serum sodium.

Video super-resolution has recently become one of the most important mobile-related problems due to the rise of video communication and streaming services. While many solutions have been proposed for this task, the majority of them are too computationally expensive to run on portable devices with limited hardware resources. To address this problem, we introduce the first Mobile AI challenge, where the target is to develop an end-to-end deep learning-based video super-resolution solutions that can achieve a real-time performance on mobile GPUs. The participants were provided with the REDS dataset and trained their models to do an efficient 4X video upscaling. The runtime of all models was evaluated on the OPPO Find X2 smartphone with the Snapdragon 865 SoC capable of accelerating floating-point networks on its Adreno GPU. The proposed solutions are fully compatible with any mobile GPU and can upscale videos to HD resolution at up to 80 FPS while demonstrating high fidelity results. A detailed description of all models developed in the challenge is provided in this paper., Comment: Mobile AI 2021 Workshop and Challenges: https://ai-benchmark.com/workshops/mai/2021/. arXiv admin note: substantial text overlap with arXiv:2105.07825. substantial text overlap with arXiv:2105.08629, arXiv:2105.07809, arXiv:2105.08630

Additional file 10. HE staining of human left internal mammary arteries and atherosclerotic plaques

Additional file 3. The epigenome-wide signature of DNA methylome in atherosclerotic plaques and LIMAs.

Additional file 6. The biological function of the genes differentially methylated in atherosclerotic plaques and LIMAs

Additional file 9. Expression of Lp-PLA2 mRNA treated with different concentration of 5-aza-CdR

Si Gao,1,2,* Jialin Hu,3,* Yong Li4 1Department of Haematology and Rheumatology, Wuhan Fourth Hospital, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 2The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430014, People’s Republic of China; 3Department of General Medicine, Wuhan Fourth Hospital, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 4Department of Pharmacy, Wuhan Fourth Hospital; Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jialin Hu; Yong LiWuhan Fourth Hospital; Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Qiaokou District, Wuhan, Hubei 430033, People’s Republic of ChinaEmail 13476207218@163.com; yonglig@126.comIntroduction: Chronic myeloid leukemia (CML) is a myeloid malignancy characterized by the oncogene BCR-ABL. CML responds well to therapy targeting BCR-ABL in the chronic phase but is resistant to treatment when it progresses to the blast phase (BP). This study attempted to address whether arachidonate 12-lipoxygenase (Alox12) confers to CML drug resistance.Materials and Methods: We analyzed the expression of Alox12 using Western blotting, ELISA, and RT-PCR methods. Loss of functional analysis was performed using cellular activity assays on CML and normal hematopoietic stem/progenitor cells (HSPCs).Results: Alox12 and 12-Hydroxyeicosatetraenoic acid (12-HETE) are overexpressed in BP-CML but not HSPCs, and that Alox12-12-HETE axis is regulated by BCR-ABL. The Alox12-12-HETE axis is required for CML. Specific Alox12 inhibitor inhibits colony formation, survival, and self-renewal capacity in BP-CML HSPCs, and to a significantly greater extent than in normal HSPCs. Of note, the Alox12 inhibitor significantly augments dasatinib’s efficacy in BP-CML HSPCs. Mechanism studies show that Alox12 inhibition does not affect activities of essential signaling pathways involved in maintaining stem cell function, such as Wnt, p53, and bone morphogenetic protein (BMP). In contrast, we show that Alox12 inhibition disrupts nicotinamide adenine dinucleotide phosphate (NADPH) homeostasis and induces oxidative stress and damage in CML HSPCs and committed cells.Conclusion: Alox12-12-HETE axis is a specific and critical regulator of BP-CML HSPCs functions. Pharmacological inhibition of Alox12 may be useful in BP-CML.Keywords: chronic myeloid leukemia, Alox12, Bcr-Abl, resistance, stem cell