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As an essential task in protein structure and function prediction, protein fold recognition has attracted increasing attention. The majority of the existing machine learning-based protein fold recognition approaches strongly rely on handcrafted features, which depict the characteristics of different protein folds; however, effective feature extraction methods still represent the bottleneck for further performance improvement of protein fold recognition. As a powerful feature extractor, deep convolutional neural network (DCNN) can automatically extract discriminative features for fold recognition without human intervention, which has demonstrated an impressive performance on protein fold recognition. Despite the encouraging progress, DCNN often acts as a black box, and as such, it is challenging for users to understand what really happens in DCNN and why it works well for protein fold recognition. In this study, we explore the intrinsic mechanism of DCNN and explain why it works for protein fold recognition usthe working principle of DCNNs in protein fold recognition and exploring the relationship between the predicted protein contact map and protein tertiary structure. This proposed visualization method is flexible and applicable to address other DCNN-based bioinformatics and computational biology questions. The online web server of VGGfold is freely available at http//csbio.njust.edu.cn/bioinf/vggfold/.In virtually every eukaryotic species, the ends of nuclear chromosomes are protected by telomeres, nucleoprotein structures counteracting the end-replication problem and suppressing recombination and undue DNA repair. Although in most cases, the primary structure of telomeric DNA is conserved, there are several exceptions to this rule. One is represented by the telomeric repeats of ascomycetous yeasts, which encompass a great variety of sequences, whose evolutionary origin has been puzzling for several decades. At present, the key questions concerning the driving force behind their rapid evolution and the means of co-evolution of telomeric repeats and telomere-binding proteins remain largely unanswered. Previously published studies addressed mostly the general concepts of the evolutionary origin of telomeres, key properties of telomeric proteins as well as the molecular mechanisms of telomere maintenance; however, the evolutionary process itself has not been analyzed thoroughly. Here, we aimed to inspect the evolution of telomeres in ascomycetous yeasts from the subphyla Saccharomycotina and Taphrinomycotina, with special focus on the evolutionary origin of species-specific telomeric repeats. We analyzed the sequences of telomeric repeats from 204 yeast species classified into 20 families and as a result, we propose a step-by-step model, which integrates the diversity of telomeric repeats, telomerase RNAs, telomere-binding protein complexes and explains a propensity of certain species to generate the repeat heterogeneity within a single telomeric array.Display technology, especially phage display technology, has been widely applied in many fields. The theoretical core of display technology is the physical linkage between the protein/peptide on the surface of a phage and the coding DNA sequence inside the same phage. Starting from phage-displayed peptide/protein/antibody libraries and taking advantage of the ever-growing power of next-generation sequencing (NGS) for DNA sequencing/decoding, rich protein-related information can easily be obtained in a high-throughput way. Based on this information, many scientific and clinical questions can be readily addressed. In the past few years, aided by the development of NGS, droplet technology, and massive oligonucleotide synthesis, we have witnessed and continue to witness large advances of phage display technology, in both technology development and application. The aim of this review is to summarize and discuss these recent advances.
Aneurysmal subarachnoid hemorrhage (SAH) continues to be associated with significant morbidity and mortality despite treatment advancements. Although high blood pressure (BP) remains a significant risk factor in aneurysmal SAH and re-rupture, the role of BP parameters and fluctuation in prognostication remains unclear.

We sought to define how BP parameters and variability within 24 hours of hospitalization in acute-onset SAH affects patient discharge outcomes.

We retrospectively analyzed a prospectively collected cohort of SAH patients. Hourly BP parameters, including systolic BP, diastolic BP, pulse pressure (PP), and their corresponding variability (delineated by standard deviation) were collected to investigate associations with the primary endpoint of discharge disposition.

174 SAH patients were included in the study. On bivariate analysis, Hunt Hess score, Fisher grade, intraventricular hemorrhage, external ventricular drain placement, and systolic BP and pulse pressure variability were significantly associated with a poor disposition. Poor disposition was significantly associated with age, Hunt Hess score, intraventricular hemorrhage, and PP variability on multivariate analysis. PP variability remained an independent predictor for poor disposition (OR 1.11, 95%CI 1.02-1.21, p = 0.02) when adjusting for potential confounders.

Increased BP and PP variability within the first 24 hours of admission portends a poor discharge disposition for aneurysmal SAH patients.
Increased BP and PP variability within the first 24 hours of admission portends a poor discharge disposition for aneurysmal SAH patients.
Uncontrolled activation of intestinal mononuclear phagocytes (MNPs) drives chronic inflammation in inflammatory bowel disease (IBD). Triggering receptor expressed on myeloid cells 1 (TREM-1) has been implicated in IBD pathogenesis. However, the role of TREM-1 + cell subsets in driving IBD pathology, and the link with clinical parameters, are not understood. Liproxstatin1 We investigated TREM-1 expression in human intestinal MNP subsets and examined blocking TREM-1 as a potential IBD therapy.

TREM-1 gene expression was analysed in intestinal mucosa, enriched epithelial and lamina propria (LP) layers and purified cells from controls and IBD patients. TREM-1 protein on immune cells was assessed by flow cytometry and immunofluorescence microscopy. Blood monocyte activation was examined by large-scale gene expression using a TREM-1 agonist or LP conditioned media (LP-CM) from patients in the presence or absence of TREM-1 and TNF antagonist antibodies.

TREM-1 gene expression increases in intestinal mucosa from IBD patients and correlates with the disease score.
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