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After 12 months follow-up, the ORR remained at 65%. We also found that SRL treatment exhibited higher efficacy in achieving CR in ITP patients who were younger than 40 years old or steroid dependent by univariate analysis. Importantly, in patients who responded, SRL treatment was associated with a reduction in the percentage of Th2, Th17 cells, and increase in the percentage of M-MDSCs and Tregs, indicating that SRL may reestablish peripheral tolerance. Taken together, Sirolimus demonstrated efficacy as a second-line agent for R/R ITP. Copyright © 2020 Feng, Xiao, Yan, Wang, Zhu, Cassady, Zou, Wang, Chen, Quan, Wang, Yang, Wang, Li, Gao, Zhang, Liu, Kong, Gao and Zhang.Metabolic profiling studies have recently indicated dysfunctional mitochondria in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This includes an impaired function of pyruvate dehydrogenase complex (PDC), possibly driven by serum factor(s), which leads to inadequate adenosine triphosphate generation and excessive lactate accumulation. A reminiscent energy blockade is likely to occur in primary biliary cholangitis (PBC), caused by anti-PDC autoantibodies, as recently proposed. PBC is associated with fatigue and post-exertional malaise, also signifying ME/CFS. We herein have investigated whether ME/CFS patients have autoreactive antibodies that could interfere with mitochondrial function. We found that only 1 of 161 examined ME/CFS patients was positive for anti-PDC, while all PBC patients (15/15) presented significant IgM, IgG, and IgA anti-PDC reactivity, as previously shown. None of fibromyalgia patients (0/14), multiple sclerosis patients (0/29), and healthy blood donors (0/44) controls showed reactivities. Anti-mitochondrial autoantibodies (inner and outer membrane) were negative in ME/CFS cohort. Anti-cardiolipin antibody levels in patients did not differ significantly from healthy blood donors. In conclusion, the impaired mitochondrial/metabolic dysfunction, observed in ME/CFS, cannot be explained by presence of circulating autoantibodies against the tested mitochondrial epitopes. Copyright © 2020 Nilsson, Palmer, Apostolou, Gottfries, Rizwan, Dahle and Rosén.Objective Systemic hypoperfusion is intricately involved in neurohormone secretion, vascular calcification (VC) related impaired vasodilation, and luminal stenosis. We aimed to conduct a joint evaluation of vasopressin-neurophysin II-copeptin peptide (VP) and advanced aortic arch calcification (AAC) on all-cause and cardiovascular (CV) mortality in maintenance hemodialysis (MHD) patients. Methods Unadjusted and adjusted hazard ratios (aHRs) of mortality risks were analyzed for different groups of VP and AAC in 167 MHD patients. The modification effect between higher VP and advanced AAC on mortality risk was examined using an interaction product term. Results Interactions between VP and AAC with respect to all-cause and CV mortality were statistically significant. In multivariable analysis, higher VP predicted all-cause and CV mortality [aHR 2.2 (95% confidence interval (CI) 1.1-4.5)] and 2.6 (95% CI 1.1-4.6), respectively. Advanced AAC was associated with incremental risks of all-cause and CV mortality [aHR 2.1 (95% CI 1.1-4.0)and 2.5 (95% CI 1.0-4.3), respectively]. Patients with combined higher VP (>101.5 ng/mL) and advanced AAC were at the greatest risk of all-cause and CV mortality [aHR 4.7 (95% CI 1.2-16.2)and 4.9 (95% CI 1.1-18.9), respectively]. Conclusion Combined VP and advanced AAC predict not only all-cause but also CV death in MHD patients, and a joint evaluation is more comprehensive than single marker. In light of hypoperfusion and ischemic events in vital organs, VP and AAC could act as more robust dual marker for prognostic assessment. Copyright © 2020 Chang, Chou, Wu, Chen, Ko, Liou, Hsieh, Lin, Wen, Chang, Tung and Wang.Artificial intelligence (AI) has become a progressively prevalent Research Topic in medicine and is increasingly being applied to dermatology. There is a need to understand this technology's progress to help guide and shape the future for medical care providers and recipients. We reviewed the literature to evaluate the types of publications on the subject, the specific dermatological topics addressed by AI, and the most challenging barriers to its implementation. A substantial number of original articles and commentaries have been published to date and only few detailed reviews exist. Most AI applications focus on differentiating between benign and malignant skin lesions, however; others exist pertaining to ulcers, inflammatory skin diseases, allergen exposure, dermatopathology, and gene expression profiling. Applications commonly analyze and classify images, however, other tools such as risk assessment calculators are becoming increasingly available. Although many applications are technologically feasible, important implementation barriers have been identified including systematic biases, difficulty of standardization, interpretability, and acceptance by physicians and patients alike. This review provides insight into future research needs and possibilities. There is a strong need for clinical investigation in dermatology providing evidence of success overcoming the identified barriers. With these research goals in mind, an appropriate role for AI in dermatology may be achieved in not so distant future. Copyright © 2020 Gomolin, Netchiporouk, Gniadecki and Litvinov.Asthma is a frequent heterogeneous multifactorial chronic disease whose severe forms remain largely uncontrolled despite the availability of many drugs and educational therapy. Autophagy inhibitor Several phenotypes and endotypes of severe asthma have been described over the last two decades. Typical type-2-immunity-driven asthma remains the most frequent phenotype, and several targeted therapies have been developed and are now available. On the contrary, non-type-2 immunity-driven severe asthma is less understood and still requires efficient innovative therapies. A personalized approach would allow improving asthma control with the help of robust biomarkers able to predict phenotypes/endotypes, exacerbations, response to targeted treatments and, in the future, possible curative options. Some data from large multicenter cohorts have emerged in recent years, especially in transcriptomics. These data have to be integrated and reproduced longitudinally to provide a systems approach for asthma care. In this focused review, the needs for such an approach and the available data will be reviewed as well as the next steps for achieving personalized medicine in asthma.