Miracle-dz/UniFAR-FTUs huggingface dataset:
Mapping worldwide research on the Internet of Things during 2011-2016

Purpose The Internet of Things (IoT) has attracted wide attention from researchers to address the potential of this technology in various industries recently. This study aims to investigate different characteristics of worldwide research on the IoT using bibliometrics, network analysis and altmetrics. Growth of the literature, publication types, languages, publication countries and research subjects are addressed. The scientific and social impact of the journal articles has also been examined using citation and altmetrics scores. Design/methodology/approach The Scopus database was searched for articles indexed under the terms “Internet of Thing*” or “IoT” or “Internet of Everything*” or “Web of Thing*”, and a total of 13,725 articles from 2011 to 2016 were retrieved and analysed. Findings There was a continuous increase in the number of publications per year over the period, with a 6.7-fold rise in the number of publications, with the highest share of research output (4,989) published in 2016. Contribution of authors at the micro, meso and macro levels was analysed. About 89 per cent of total publications were the result of collaborative efforts, and Asia-Pacific was responsible for almost 53 per cent of world scientific production of IoT literature. Generally, the IoT research are found in publications concentrating on computer networks and communications, electrical and electronic engineering and computer science applications. The results also showed that the presence of IoT research on the social web is still low, with 6.8 per cent of total publications presenting some altmetric activity. Research limitations/implications The work reported is limited to only Scopus-indexed publications. While the search methodology aimed to be as inclusive as possible, it may not have captured all scholarly research output in the IoT world. Practical implications The findings of this study may help researchers understand the performance of IoT research from across the world and suggest directions for further research. Originality/value This paper reviews the literature of the IoT in past five years using rigorous bibliometric, altmetric and network analysis tools.
A COMPARISON OF THE OBJECTIVE STRUCTURED CLINICAL EXAMINATION AND THE TRADITIONAL ORAL CLINICAL EXAMINATION IN A NIGERIAN UNIVERSITY.

Background Assessment of clinical skills is essential in medical education. Ideally marks should be based on the student's competence alone. The limitations of the traditional long case examinations such as the patient and examiner variability are well known. The objective structured clinical examination (OSCE) was designed to overcome these limitations. Studies comparing the OSCE and the traditional long case examination in the same group of students are very sparse. Aim To compare the objective structured clinical examination (OSCE) and the traditional long case examination by determining their correlations with other forms of assessment in undergraduate surgery. Setting This study was carried out at the College of Medicine, University of Lagos, Nigeria. Methodology The results of 612 undergraduate students in our medical school of the University of Lagos, Nigeria over a period of 4 years (2012-2015) were analysed. The scores in the long case examination , objective structured clinical examination (OSCE) , multiple choice questions and Essays were analysed and compared using the Pearson's Correlation co-efficient. SPSS version 17 software was used and a P-value < 0.01 was regarded as statistically significant. Results Overall, there was a statistical significant positive correlation among most forms of assessment. The OSCE and the long case examination had a correlation of 0.374. Compared with the long case examination, the OSCE had a higher correlation with all other forms of assessment. The total clinical score (the sum of all long case examination and OSCE) however performed better than the OSCE or the long case examination alone as it had the highest correlation with all other forms of assessment. Conclusion The OSCE has been shown to be better than the long case examination as an indicator of the student overall knowledge of surgery as it had a superior correlation with other forms of assessments. The total clinical score was however the best indicator of the student overall knowledge in Surgery as it had the best correlation with other forms of assessment. We recommend and encourage institutions that presently combine the OSCE and the long case examination to carry out similar analysis such as ours to determine the desirability of combining LCE and OSCE rather than outright replacement of LCE with OSCE.
Neural correlates of speech quality dimensions analyzed using electroencephalography (EEG)

Objective. By means of subjective psychophysical methods, quality of transmitted speech has been decomposed into three perceptual dimensions named ‘discontinuity’ (F), ‘noisiness’ (N) and ‘coloration’ (C). Previous studies using electroencephalography (EEG) already reported effects of perceived intensity of single quality dimensions on electrical brain activity. However, it has not been investigated so far, whether the dimensions themselves are dissociable on a neurophysiological level of analysis. Approach. Pursuing this goal in the present study, a high-quality (HQ) recording of a spoken word was degraded on each dimension at a time, resulting in three quality-impaired stimuli (F, N, C) which were on average described as being equal in perceived degradation intensity. Participants performed a three-stimulus oddball task, involving the serial presentation of different stimulus types: (1) HQ or degraded ‘standard’ stimuli to establish sensory/perceptual quality references. (2) Degraded ‘oddball’ stimuli to cause random, infrequent deviations from those references. EEG was employed to examine the neuro-electrical correlates of speech quality perception. Main results. Emphasis was placed on modulations in temporal and morphological characteristics of the P300 component of the event-related brain potential (ERP), whose subcomponents P3a and P3b are commonly linked to attentional orienting and task relevance categorization, respectively. Electrophysiological data analysis () revealed significant modulations of P300 amplitude and latency by the perceptual dimensions underlying both quality references and oddball stimuli. Significance. The present study exemplifies the utility of physiological methods like EEG for dissociating speech degradations not only based on perceived intensity level, but also their distinctive quality dimension.
Sensitivity of seafloor bathymetry to climate-driven fluctuations in mid-ocean ridge magma supply

Understanding abyssal hill spacing The most prominent topographic features on Earth are abyssal hills found on the bottom of the ocean floor. Olive et al. wanted to understand the spacing and size of these hills. They used a model that combines magma supply and the mechanical response of the crust. The model explains observations of hill spacing around mid-ocean ridges. Crustal topography appears to be a poor recorder of changes in magma supply. However, magma supply changes may be faithfully recorded at the base of the crust. Science, this issue p. 310 Tectonic and magmatic extension under a steady magma input explains variations in abyssal hill fabric with spreading rate. Recent studies have proposed that the bathymetric fabric of the seafloor formed at mid-ocean ridges records rapid (23,000 to 100,000 years) fluctuations in ridge magma supply caused by sealevel changes that modulate melt production in the underlying mantle. Using quantitative models of faulting and magma emplacement, we demonstrate that, in fact, seafloor-shaping processes act as a low-pass filter on variations in magma supply, strongly damping fluctuations shorter than about 100,000 years. We show that the systematic decrease in dominant seafloor wavelengths with increasing spreading rate is best explained by a model of fault growth and abandonment under a steady magma input. This provides a robust framework for deciphering the footprint of mantle melting in the fabric of abyssal hills, the most common topographic feature on Earth.
Non-heritable genetics of human disease: spotlight on post-zygotic genetic variation acquired during lifetime

The heritability of most common, multifactorial diseases is rather modest and known genetic effects account for a small part of it. The remaining portion of disease aetiology has been conventionally ascribed to environmental effects, with an unknown part being stochastic. This review focuses on recent studies highlighting stochastic events of potentially great importance in human disease—the accumulation of post-zygotic structural aberrations with age in phenotypically normal humans. These findings are in agreement with a substantial mutational load predicted to occur during lifetime within the human soma. A major consequence of these results is that the genetic profile of a single tissue collected at one time point should be used with caution as a faithful portrait of other tissues from the same subject or the same tissue throughout life. Thus, the design of studies in human genetics interrogating a single sample per subject or applying lymphoblastoid cell lines may come into question. Sporadic disorders are common in medicine. We wish to stress the non-heritable genetic variation as a potentially important factor behind the development of sporadic diseases. Moreover, associations between post-zygotic mutations, clonal cell expansions and their relation to cancer predisposition are central in this context. Post-zygotic mutations are amenable to robust examination and are likely to explain a sizable part of non-heritable disease causality, which has routinely been thought of as synonymous with environmental factors. In view of the widespread accumulation of genetic aberrations with age and strong predictions of disease risk from such analyses, studies of post-zygotic mutations may be a fruitful approach for delineation of variants that are causative for common human disorders.
Minerva: an alignment- and reference-free approach to deconvolve Linked-Reads for metagenomics

Emerging linked-read technologies (aka read-cloud or barcoded short-reads) have revived interest in standard short-read technology as a viable way to understand large scale structure in genomes and metagenomes. Linked-read technologies, such as the 10X Chromium system, use a microfluidic system and a set of specially designed 3’ barcodes (aka UIDs) to tag short DNA reads which were originally sourced from the same long fragment of DNA; subsequently these specially barcoded reads are sequenced on standard short read platforms. This approach results in interesting compromises. Each long fragment of DNA is covered only sparsely by short reads, no information about the relative ordering of reads from the same fragment is preserved, and typically each 3’ barcode matches reads from 5-20 long fragments of DNA. However, the cost per base to sequence is far lower than single molecule long read sequencing systems, far less input DNA is required, and the error rate is that of standard short-reads. Linked-reads represent a new set of algorithmic challenges. In this paper we formally describe one particular issue common to all applications of linked-read technology: the deconvolution of reads with a single barcode into clusters that correspond to a single long fragment of DNA. We introduce Minerva, A graph-based algorithm which approximately solves the barcode deconvolution problem for metagenomic data (where reference genomes may be incomplete or unavailable). Additionally, we demonstrate that deconvolved barcoded reads significantly improve downstream results by improving the specificity of taxonomic assignments, and by improving the ability of topic models to identify clusters of related sequences.
Does inactivation of USP 14 enhance degradation of proteasomal substrates that are associated with neurodegenerative diseases ?

A common pathological hallmark of age-related neurodegenerative diseases is the intracellular accumulation of protein aggregates such as α-synuclein in Parkinson’s disease, TDP-43 in ALS, and tau in Alzheimer’s disease. Enhancing intracellular clearance of aggregation-prone proteins is a plausible strategy for slowing progression of neurodegenerative diseases and there is great interest in identifying molecular targets that control protein turnover. One of the main routes for protein degradation is through the proteasome, a multisubunit protease that degrades proteins that have been tagged with a polyubiquitin chain by ubiquitin activating and conjugating enzymes. Published data from cellular models indicate that Ubiquitin-specific protease 14 (USP14), a deubiquitinating enzyme (DUB), slows the degradation of tau and TDP-43 by the proteasome and that an inhibitor of USP14 increases the degradation of these substrates. We conducted similar experiments designed to evaluate tau, TDP-43, or α-synuclein levels in cells after overexpressing USP14 or knocking down endogenous expression by siRNA.
Combined BRD4 and CDK9 inhibition as a new therapeutic approach in malignant rhabdoid tumors

Rhabdoid tumors are caused by the deletion of SMARCB1, whose protein encodes the SMARCB1 subunit of the chromatin remodeling complex SWI/SNF that is involved in global chromatin organization and gene expression control. Simultaneously inhibiting the main players involved in the deregulated transcription machinery is a promising option for preventing exaggerated tumor cell proliferation and survival as it may bypass compensatory mechanisms. In support of this hypothesis, we report efficient impairment of cellular proliferation and strong induction of cell death elicited by inhibition of bromodomain protein BRD4 and transcription kinase CDK9 using small molecular compounds. Combination of both compounds efficiently represses antiapoptotic genes and the oncogene MYC. Our results provide a novel approach for the treatment of RT.
Extracellular traps derived from macrophages, mast cells, eosinophils and neutrophils are generated in a time‐dependent manner during atherothrombosis

Extracellular traps generated by neutrophils contribute to thrombus progression in coronary atherosclerotic plaques. It is not known whether other inflammatory cell types in coronary atherosclerotic plaque or thrombus also release extracellular traps. We investigated their formation by macrophages, mast cells, and eosinophils in human coronary atherosclerosis, and in relation to the age of thrombus of myocardial infarction patients. Coronary arteries with thrombosed or intact plaques were retrieved from patients who died from myocardial infarction. In addition, thrombectomy specimens from patients with myocardial infarction were classified histologically as fresh, lytic or organised. Neutrophil and macrophage extracellular traps were identified using sequential triple immunostaining of CD68, myeloperoxidase, and citrullinated histone H3. Eosinophil and mast cell extracellular traps were visualised using double immunostaining for eosinophil major basic protein or tryptase, respectively, and citrullinated histone H3. Single‐ and double‐stained immunopositive cells in the plaque, adjacent adventitia, and thrombus were counted. All types of leucocyte‐derived extracellular traps were present in all thrombosed plaques, and in all types of the in vivo‐derived thrombi, but only to a much lower extent in intact plaques. Neutrophil traps, followed by macrophage traps, were the most prominent types in the autopsy series of atherothrombotic plaques, including the adventitia adjacent to thrombosed plaques. In contrast, macrophage traps were more numerous than neutrophil traps in intact plaques (lipid cores) and organised thrombi. Mast cell and eosinophil extracellular traps were also present, but sparse in all instances. In conclusion, not only neutrophils but also macrophages, eosinophils, and mast cells are sources of etosis involved in evolving coronary thrombosis. Neutrophil traps dominate numerically in early thrombosis and macrophage traps in late (organising) thrombosis, implying that together they span all the stages of thrombus progression and maturation. © 2018 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
Differences in characteristics and outcomes after endovascular therapy: A single-center analysis of patients with vertebrobasilar occlusion due to underlying intracranial atherosclerosis disease and embolism

Background Therapeutic strategies and outcomes vary with stroke subtypes for patients with acute vertebrobasilar occlusion (VBAO). This study aimed to compare characteristics and outcomes of VBAO due to intracranial atherosclerotic disease (ICAD) and embolisms and identify baseline predictors of ICAD. Methods Patients with VBAO who received endovascular therapy (EVT) were retrospectively analyzed. Participants fulfilling the criteria were classified as the ICAD group (focal stenosis of >70%, or fixed stenosis >50% in addition to either flow and perfusion impairment on angiography or an evident reocclusion tendency) and the embolism group (defined as no evidence of focal significant stenosis after thrombolysis or thrombectomy). Baseline characteristics and outcomes after EVT were compared between the two groups, and logistic regression was performed to explore the factors associated with ICAD. Results Among the 133 patients enrolled, 95 (71.4%) patients were categorized in the ICAD group, and 38 (28.6%) in the embolism group. A history of atrial fibrillation (odds ratio (OR) 0.142; 95% confidence interval (CI) (0.028–0.707), p = 0.017), distal basilar artery occlusion (OR 0.107; 95% CI (0.040–0.289), p < 0.001) and V4 segment occlusion (OR 3.423; 95% CI (1.172–9.999), p = 0.024) were independently associated with ICAD. Patients with VBAO due to ICAD had a lower rate of recanalization (81.1% vs 100%, p = 0.004), but the 90-day good clinical outcome was comparable (41.1% vs 50.0%, p = 0.347). Conclusions The occlusion sites and a history of atrial fibrillation might be helpful in predicting ICAD in patients with VBAO. Patients with ICAD who were treated by EVT had a lower rate of recanalization but comparable 90-day good outcomes.
Three-Dimensional Analysis of a Viral RNA Replication Complex Reveals a Virus-Induced Mini-Organelle

Positive-strand RNA viruses are the largest genetic class of viruses and include many serious human pathogens. All positive-strand RNA viruses replicate their genomes in association with intracellular membrane rearrangements such as single- or double-membrane vesicles. However, the exact sites of RNA synthesis and crucial topological relationships between relevant membranes, vesicle interiors, surrounding lumens, and cytoplasm generally are poorly defined. We applied electron microscope tomography and complementary approaches to flock house virus (FHV)–infected Drosophila cells to provide the first 3-D analysis of such replication complexes. The sole FHV RNA replication factor, protein A, and FHV-specific 5-bromouridine 5'-triphosphate incorporation localized between inner and outer mitochondrial membranes inside ∼50-nm vesicles (spherules), which thus are FHV-induced compartments for viral RNA synthesis. All such FHV spherules were outer mitochondrial membrane invaginations with interiors connected to the cytoplasm by a necked channel of ∼10-nm diameter, which is sufficient for ribonucleotide import and product RNA export. Tomographic, biochemical, and other results imply that FHV spherules contain, on average, three RNA replication intermediates and an interior shell of ∼100 membrane-spanning, self-interacting protein As. The results identify spherules as the site of protein A and nascent RNA accumulation and define spherule topology, dimensions, and stoichiometry to reveal the nature and many details of the organization and function of the FHV RNA replication complex. The resulting insights appear relevant to many other positive-strand RNA viruses and support recently proposed structural and likely evolutionary parallels with retrovirus and double-stranded RNA virus virions.
Fine-Grained Distribution of a Non-Native Resource Can Alter the Population Dynamics of a Native Consumer

New interactions with non-native species can alter selection pressures on native species. Here, we examined the effect of the spatial distribution of a non-native species, a factor that determines ecological and evolutionary outcomes but that is poorly understood, particularly on a fine scale. Specifically, we explored a native butterfly population and a non-native plant on which the butterfly oviposits despite the plant’s toxicity to larvae. We developed an individual-based model to describe movement and oviposition behaviors of each butterfly, which were determined by plant distribution and the butterfly's host preference genotype. We estimated the parameter values of the model from rich field data. We simulated various patterns of plant distributions and compared the rates of butterfly population growth and changes in the allele frequency of oviposition preference. Neither the number nor mean area of patches of non-native species affected the butterfly population, whereas plant abundance, patch shape, and distance to the nearest native and non-native patches altered both the population dynamics and genetics. Furthermore, we found a dramatic decrease in population growth rates when we reduced the distance to the nearest native patch from 147 m to 136 m. Thus changes in the non-native resource distribution that are critical to the fate of the native herbivore could only be detected at a fine-grained scale that matched the scale of a female butterfly’s movement. In addition, we found that the native butterfly population was unlikely to be rescued by the exclusion of the allele for acceptance of the non-native plant as a host. This study thus highlights the importance of including both ecological and evolutionary dynamics in analyses of the outcome of species interactions and provides insights into habitat management for non-native species.
YAP Activation Drives Liver Regeneration after Cholestatic Damage Induced by Rbpj Deletion

Liver cholestasis is a chronic liver disease and a major health problem worldwide. Cholestasis is characterised by a decrease in bile flow due to impaired secretion by hepatocytes or by obstruction of bile flow through intra- or extrahepatic bile ducts. Thereby cholestasis can induce ductal proliferation, hepatocyte injury and liver fibrosis. Notch signalling promotes the formation and maturation of bile duct structures. Here we investigated the liver regeneration process in the context of cholestasis induced by disruption of the Notch signalling pathway. Liver-specific deletion of recombination signal binding protein for immunoglobulin kappa j region (Rbpj), which represents a key regulator of Notch signalling, induces severe cholestasis through impaired intra-hepatic bile duct (IHBD) maturation, severe necrosis and increased lethality. Deregulation of the biliary compartment and cholestasis are associated with the change of several signalling pathways including a Kyoto Encyclopedia of Genes and Genomes (KEGG) gene set representing the Hippo pathway, further yes-associated protein (YAP) activation and upregulation of SRY (sex determining region Y)-box 9 (SOX9), which is associated with transdifferentiation of hepatocytes. SOX9 upregulation in cholestatic liver injury in vitro is independent of Notch signalling. We could comprehensively address that in vivo Rbpj depletion is followed by YAP activation, which influences the transdifferentiation of hepatocytes and thereby contributing to liver regeneration.