Treating the relationship from the nontarget stick and the outcome allows for subsequent human predictive understanding.

Ancherythroculter nigrocauda is a cyprinid fish endemic of the Upper Reaches of the Yangtze River in China, where it is an important aquaculture and commercial species. On the other hand, A. nigrocauda is a threatened species as a result of overfishing, dam construction, and water pollution. In this study, a chromosome-level genome assembly of A. nigrocauda is reported and built using PacBio sequencing and the Hi-C technology. selleckchem The 1.04 Gb sequenced genome of A. nigrocauda contained 2,403 contigs, with an N50 length of 3.12 Mb. Then, 1,297 contigs, which represented 54.0% of all the numbers of contigs and 97.2% of the whole content of genome nucleotide base, were assembled into 24 chromosomes. Combined with transcriptome data from 10 tissues, 27,042 (78.5%) genes were functionally annotated out of 34,414 predicted protein-coding genes. Interestingly, highly expression of many positively selected genes and expanded gene families in brain suggested that these genes might play important roles in the brain development of A. nigrocauda. Finally, we found tissue-specific expression of 10,732 genes. Functional analyses showed that they were mainly composed of genes related to (i) environmental information processing, (ii) circulatory system and (iii) development, suggesting they might be important for adaptation to different environments and for development of A. nigrocauda. The high-quality genome obtained in this study will not only provide a valuable genomic resource for future studies of A. nigrocauda population and conservation, but also is an important resource for further functional genomics studies of fishes. This article is protected by copyright. All rights reserved.INTRODUCTION To describe cases omental haemorrhage and to review the literature on this topic. METHODS We describe three cases of spontaneous omental haemorrhage and discuss various management strategies, in an attempt to provide direction for similar cases in the future. RESULTS A number of case reports of spontaneous or idiopathic omental haemorrhage exist in the literature. These cases are often attributed to an underlying vasculopathy, such as segmental arterial mediolysis (SAM). Appropriate resuscitation is paramount for best outcome. Severe bleeding may require surgery or transcatheter arterial embolisation, which is best performed early if required. Endovascular management using selective catheterisation of the bleeding vessel and embolisation is a minimally invasive alternative to emergent operative intervention. In the three cases we present, endovascular embolisation was performed in two patients, and surgical ligation in a third. Segmental arterial mediolysis is considered the likely aetiology in at least 2 of the 3 cases, based on imaging findings. No further episodes of haemorrhage occurred at follow-up (ranging from 6 months to 2 years). CONCLUSIONS Acute omental haemorrhage is a rare condition; however, it may be associated with significant morbidity and mortality. CT angiography is the imaging of choice. Management strategies include both endovascular and surgical intervention. © 2020 The Royal Australian and New Zealand College of Radiologists.Acute myeloid leukemia with myelodysplasia-related changes (AML-MRC) are poor outcome leukemias. Its diagnosis is based on clinical, cytogenetic, and cytomorphologic criteria, last criterion being sometimes difficult to assess. A high frequency of ASXL1 mutations have been described in this leukemia. We sequenced ASXL1 gene mutations in 61 patients with AML-MRC and 46 controls with acute myeloid leukemia without other specifications (AML-NOS) to identify clinical, cytomorphologic, and cytogenetic characteristics associated with ASXL1 mutational status. Mutated ASXL1 (ASXL1+) was observed in 31% of patients with AML-MRC compared to 4.3% in AML-NOS. Its presence in AML-MRC was associated with older age, a previous history of myelodysplastic syndrome (MDS) or myelodysplastic/myeloproliferative neoplasms (MDS/MPN), leukocytosis, presence of micromegakaryocytes in bone marrow, lower number of blasts in bone marrow, myelomonocytic/monocytic morphological features and normal karyotype. ASXL1 mutation was not observed in patients with myelodysplastic syndrome-related cytogenetic abnormalities or TP53 mutations. Differences in terms of overall survival were found only in AML-MRC patients without prior MDS or MDS/MPN and with intermediate-risk karyotype, having ASXL1+ patients a worst outcome than ASXL1-. We conclude that the ASXL1 mutation frequency is high in AML-MRC patients being its presence associated with specific characteristics including morphological signs of dysplasia. This association raises the possible role of ASXL1 as a surrogate marker in AML-MRC, which could facilitate the diagnosis of patients within this group when the karyotype is normal, and especially when the assessment of multilineage dysplasia morphologically is difficult. This mutation could be used as a worst outcome marker in de novo AML-MRC with intermediate-risk karyotype. © 2020 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.BACKGROUND Blood levels of endotoxin, uric acid (UA), or lactate (LAC) are associated with type 2 diabetes mellitus (T2DM). Thus, we explored the interactions among blood endotoxin, UA, and LAC levels and the risk of T2DM. METHODS This population-based cross-sectional study included 2520 Chinese adults. Fasting blood endotoxin, UA, and LAC levels were determined and the cut-off values were obtained from the Receiver Operating Characteristic curve analysis. The study population was classified into two or four subgroups based on low or high, or both low and high levels of endotoxin, UA, and LAC, respectively. RESULTS The odds ratios (ORs) for T2DM (all P  less then  0.05) were higher in the high groups than the low groups of endotoxin, UA, or LAC, respectively. Participants in the groups with high levels of both endotoxin and UA, endotoxin and LAC, or UA and LAC, had 4.71 (95% CI 3.01-7.37), 5.13 (95% CI 3.29-7.99), or 3.73 (95% CI 2.34-5.94) times higher risk for T2DM compared to those in groups with low levels of both endotoxin and UA, endotoxin and LAC, or UA and LAC (all P  less then  0.selleckchem