Miracle-dz/UniFAR-FTUs huggingface dataset:
Automatic classication of pulmonary function in COPD patients using trachea analysis in chest CT scans

Chronic Obstructive Pulmonary Disease (COPD) is a chronic lung disease that is characterized by airflow limitation. COPD is clinically diagnosed and monitored using pulmonary function testing (PFT), which measures global inspiration and expiration capabilities of patients and is time-consuming and labor-intensive. It is becoming standard practice to obtain paired inspiration-expiration CT scans of COPD patients. Predicting the PFT results from the CT scans would alleviate the need for PFT testing. It is hypothesized that the change of the trachea during breathing might be an indicator of tracheomalacia in COPD patients and correlate with COPD severity. In this paper, we propose to automatically measure morphological changes in the trachea from paired inspiration and expiration CT scans and investigate the influence on COPD GOLD stage classification. The trachea is automatically segmented and the trachea shape is encoded using the lengths of rays cast from the center of gravity of the trachea. These features are used in a classifier, combined with emphysema scoring, to attempt to classify subjects into their COPD stage. A database of 187 subjects, well distributed over the COPD GOLD stages 0 through 4 was used for this study. The data was randomly divided into training and test set. Using the training scans, a nearest mean classifier was trained to classify the subjects into their correct GOLD stage using either emphysema score, tracheal shape features, or a combination. Combining the proposed trachea shape features with emphysema score, the classification performance into GOLD stages improved with 11% to 51%. In addition, an 80% accuracy was achieved in distinguishing healthy subjects from COPD patients.
Platinum Priority – Prostate Cancer Prostate Cancer Death After Radiotherapy or Radical Prostatectomy : A Nationwide Population-based Observational Study

Department of Urology, Ryhov Hospital, Jönköping, Sweden; Regional Cancer Centre Uppsala Örebro, Uppsala University Hospital, Uppsala, Sweden; Cancer Epidemiology Group, Division of Cancer Studies, School of Medicine, King's College London, London, UK; Department of Oncology, Institute of Clinical Sciences, The Sahlgrenska Academy, University of Gothenburg, Sweden; Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden; Department of Medicine Solna, Clinical Epidemiology Unit, Karolinska Institutet, Stockholm, Sweden; Department of Oncology and Radiation Physics, Skåne University Hospital, Lund University, Lund, Sweden; Department of Clinical Science, Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm, Sweden; Division of Urological Cancers, Department of Translational Medicine, Lund University, Lund, Sweden; Department of Urology/CamPARI Clinic, Cambridge University Hospitals, Cambridge, UK; Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
Complete assembly of a dengue virus type 3 genome from a recent genotype III clade by metagenomic sequencing of serum

Background Mosquito-borne flaviviruses causing diseases such as dengue and Japanese encephalitis are devastating, particularly in the tropics. Although, multiple flaviviruses are known to co-circulate in India, when a patient presents with febrile illness, testing is usually limited to specific pathogens. Unbiased metagenomic sequencing of febrile cases can reveal the presence of multiple pathogens and provide complete genome information. Sequence information, a cornerstone for tracing virus evolution, is relevant for the design of vaccines and therapeutics. In order to assess the usefulness of unbiased metagenomic sequencing for the identification of viruses associated with febrile illness, we sequenced serum from four individuals and plasma from one individual, all hospitalized at a tertiary care centre in South India with severe or prolonged febrile illnesses, together with one healthy control in 2014. Results We identified and assembled a complete dengue virus type 3 (DENV3) sequence from the serum of a case classified as severe dengue. We also found a small number of Japanese encephalitis virus (JEV) sequences in the serum of two adults with febrile illness, including the one who had dengue. Phylogenetic analysis of the dengue sequence indicates that it belongs to a predominantly Asian, DENV3, genotype III clade. It had an estimated divergence time of 13.86 years (95% Highest Posterior Densities 12.94 - 14.83 years) with the closest Indian strain. Amino acid substitutions were present throughout the sequenced genome, including 11 substitutions in the antigenic envelope protein compared to the strain used for the development of the first commercial dengue vaccine. Of these one substitution (E361D) was unique and six were in critical antigenic sites. Conclusions We demonstrate that both genome assembly and detection of a low number of viral sequences are possible by unbiased sequencing of clinical material. Complete dengue virus sequence analysis places the sequenced genome in a recent, predominantly Asian clade within genotype III of DENV3. The detection of JEV, an agent not routinely tested in febrile illness in India, warrants further analysis and highlights the need to study co-circulating flaviviruses in parallel.
The Greenland shark Somniosus microcephalus—Hemoglobins and ligand-binding properties

A large amount of data is currently available on the adaptive mechanisms of polar bony fish hemoglobins, but structural information on those of cartilaginous species is scarce. This study presents the first characterisation of the hemoglobin system of one of the longest-living vertebrate species (392 ± 120 years), the Arctic shark Somniosus microcephalus. Three major hemoglobins are found in its red blood cells and are made of two copies of the same α globin combined with two copies of three very similar β subunits. The three hemoglobins show very similar oxygenation and carbonylation properties, which are unaffected by urea, a very important compound in marine elasmobranch physiology. They display identical electronic absorption and resonance Raman spectra, indicating that their heme-pocket structures are identical or highly similar. The quaternary transition equilibrium between the relaxed (R) and the tense (T) states is more dependent on physiological allosteric effectors than in human hemoglobin, as also demonstrated in polar teleost hemoglobins. Similar to other cartilaginous fishes, we found no evidence for functional differentiation among the three isoforms. The very similar ligand-binding properties suggest that regulatory control of O2 transport may be at the cellular level and that it may involve changes in the cellular concentrations of allosteric effectors and/or variations of other systemic factors. The hemoglobins of this polar shark have evolved adaptive decreases in O2 affinity in comparison to temperate sharks.
Interleukin-32 plays an essential role in human calcified aortic valve cells

Interleukin-32 (IL-32) is an inflammatory cytokine produced mainly by T, natural killer, and epithelial cells. Previous studies on IL-32 have primarily investigated its proinflammatory properties. The IL-32 also has been described as an activator of the p38 mitogen-activated protein kinase (MAPK) and NF-κB, and induces several cytokines. In this study, we hypothesized that the inflammatory regulators NF-κB, MAP kinase, STAT1, and STAT3 are associated with the expression of the IL-32 protein in human calcified aortic valve cells. This study comprised aortic valve sclerotic patients and control group patients without calcified aortic valve. Increased IL-32 expression in calcified aortic valvular tissue was shown by immunohistochemical staining and western blotting. There was an increase in NF-κB p65 level, p-ERK, p-JNK, and p-p38 MAPK activation underlying IL-32 expression in the study. The level of p-STAT3 but not p-STAT1 was found to be increased in calcified aortic valve tissue. In cultured primary human aortic valve interstitial cells, inhibition of NF-κB or MAPK kinase pathways results in a decrease of IL-32 expression. Treatment of recombinant IL-32 induced the levels of TNF-α, IL-6, IL-1β, and IL-8. Our findings demonstrate that IL-32 may be an important pro-inflammatory molecule involved in calcific aortic valve disease.
MUTE Directly Orchestrates Cell State Switch and the Single Symmetric Division to Create Stomata

Precise cell division control is critical for developmental patterning. For the differentiation of a functional stoma, a cellular valve for efficient gas exchange, the single symmetric division of an immediate precursor is absolutely essential. Yet, the mechanism governing the single division event remains unclear. Here we report the complete inventories of gene expression by the Arabidopsis bHLH protein MUTE, a potent inducer of stomatal differentiation. MUTE switches the gene expression program initiated by its sister bHLH, SPEECHLESS. MUTE directly induces a suite of cell-cycle genes, including CYCD5;1, and their transcriptional repressors, FAMA and FOUR LIPS. The architecture of the regulatory network initiated by MUTE represents an Incoherent Type 1 Feed-Forward Loop. Our mathematical modeling and experimental perturbations support a notion that MUTE orchestrates a transcriptional cascade leading to the tightly-restricted, robust pulse of cell-cycle gene expression, thereby ensuring the single cell division to create functional stomata. Highlights Complete inventories of gene expression in stomatal differentiation state are elucidated MUTE switches stomatal patterning program initiated by its sister bHLH, SPEECHLESS MUTE directly induces cell-cycle genes and their direct transcriptional repressors Incoherent feed-forward loop by MUTE ensures the single division of a stomatal precursor
Application of the CALIOP layer product to evaluate the vertical distribution of aerosols estimated by global models: AeroCom phase I results

[1] The CALIOP (Cloud-Aerosol Lidar with Orthogonal Polarization) layer product is used for a multimodel evaluation of the vertical distribution of aerosols. Annual and seasonal aerosol extinction profiles are analyzed over 13 sub-continental regions representative of industrial, dust, and biomass burning pollution, from CALIOP 2007–2009 observations and from AeroCom (Aerosol Comparisons between Observations and Models) 2000 simulations. An extinction mean height diagnostic (Za) is defined to quantitatively assess the models’ performance. It is calculated over the 0–6 km and 0–10 km altitude ranges by weighting the altitude of each 100 m altitude layer by its aerosol extinction coefficient. The mean extinction profiles derived from CALIOP layer products provide consistent regional and seasonal specificities and a low inter-annual variability. While the outputs from most models are significantly correlated with the observed Za climatologies, some do better than others, and 2 of the 12 models perform particularly well in all seasons. Over industrial and maritime regions, most models show higher Za than observed by CALIOP, whereas over the African and Chinese dust source regions, Za is underestimated during Northern Hemisphere Spring and Summer. The positive model bias in Za is mainly due to an overestimate of the extinction above 6 km. Potential CALIOP and model limitations, and methodological factors that might contribute to the differences are discussed.
Identification of genes and pathways associated with multiple organ dysfunction syndrome by microarray analysis

Multiple organ dysfunction syndrome (MODS) is characterized by the development of progressive physiological dysfunction of ≥2 organs or organ systems and is responsible for the majority of the morbidity and mortality among patients in intensive care units. The aim of the present study was to investigate the potential genes and pathways associated with MODS. The microarray dataset GSE60088 was downloaded from the Gene Expression Omnibus and used to identify differentially expressed genes (DEGs) between organ tissues (lung, liver and kidney) obtained from a murine model of MODS and healthy controls. The interactions between DEGs in lungs, liver and kidneys were revealed by Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. Furthermore, protein-protein interaction (PPI) data for DEGs were obtained from the Search Tool for the Retrieval of Interacting Genes and a PPI network was constructed. Additionally, DEGs that were common among the three organs were screened and transcription factors that regulated them were predicted using the iRegulon plugin. A total of 943, 267 and 227 DEGs were identified in lung, liver and kidney samples, respectively, between mice with MODS and healthy controls. In lung and liver samples, two pathways that were enriched with DEGs were identified and were common between lung and liver samples, including ‘cytokine-cytokine receptor interaction’ and ‘Jnk-STAT signaling pathway’, and examples of DEGs associated with these pathways include C-X-C motif chemokine ligand (Cxcl)1 and Cxcl10, and signal transducer and activator of transcription (Stat)1, respectively. Furthermore, two common pathways were identified in liver and kidney samples, which included ‘MAPK signaling pathway’ and ‘p53 signaling pathway’, and DEGs associated with these pathways included growth arrest and DNA damage-inducible α. A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin-like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.
MicroRNA Targeted Therapeutic Approach for Pancreatic Cancer

Pancreatic cancer remains the fourth leading cause of cancer-related death in the US and is expected to be the second leading cause of cancer-related death by 2030. Therefore, it is important to better understand the molecular pathogenesis, phenotypes and features of pancreatic cancer in order to design novel molecularly targeted therapies for achieving better therapeutic outcome of patients with pancreatic cancer. Recently, the roles of microRNAs (miRNAs) in the development and progression of pancreatic cancer became a hot topic in the scientific community of pancreatic cancer research. By conducting miRNA expression profiling, the aberrant expression of miRNAs was revealed in the serum and in cancer tissues from patients with pancreatic cancer. These aberrantly expressed miRNAs are critically correlated with the disease stage, drug resistance, and survival of pancreatic cancer patients. Hence, targeting these tiny molecules, the specific miRNAs, could provide an efficient and optimal approach in the therapy of pancreatic cancer. Indeed, the pre-clinical and in vivo experiments showed that nanoparticle delivery of synthetic oligonucleotides or treatment with natural agents could be useful to modulate the expression of miRNAs and thereby inhibit pancreatic cancer growth and progression, suggesting that targeting miRNAs combined with conventional anti-cancer therapeutics could be a novel therapeutic strategy for increasing drug sensitivity and achieving better therapeutic outcome of patients diagnosed with pancreatic cancer.
Biochemical Characterization of AGMO Variants Implicated in Relapses in Visceral Leishmaniasis

Head1=Head2=Head1=Head2/Head1 Head2=Head3=Head2=Head3/Head2 © The Author(s) 2018. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com. DOI: 10.1093/infdis/jiy051 Correspondence: F. Sicre de Fontbrune, MD, Hematology Transplant, Hôpital Saint Louis, APHP, Paris, France (flore.sicre-de-fontbrune@aphp.fr).
Vaccine hesitancy in the French population in 2016, and its association with vaccine uptake and perceived vaccine risk–benefit balance

Background Vaccine hesitancy (VH) is prominent in France. Objectives: This study aimed to estimate the prevalence and socio-demographic correlates of VH in sub-groups of the French population and to investigate the association of VH with both vaccine uptake and perceived risk–benefit balance (RBB) for four vaccines. Methods: During the 2016 Health Barometer – a national cross-sectional telephone survey in a representative sample of the French population – parents of 1–15 year-old children, parents of 11–15 year-old girls and elderly people aged 65–75 years were asked about VH (using three questions adapted from the World Health Organization definition), vaccine uptake and perceived RBB for measles and hepatitis B (children’s parents), human papillomavirus (girls’ parents) and seasonal influenza (elderly people) vaccines. Results: A total of 3,938 parents including 959 girls' parents – and 2,418 elderly people were interviewed. VH prevalence estimates were 46% (95% confidence interval (CI): 44–48) among parents, 48% (95%CI: 45–51) among girls’ parents and 35% (95% CI: 33–36) among elderly people, with higher estimates associated with high education level, children’s age (10–15 years), and, for the elderly, poor perception of health status. VH was associated with uncertainty about and/or an unfavourable perception of vaccines’ RBB for the four vaccines and with lower self-reported vaccine uptake, except for human papillomavirus vaccine in girls. Results were confirmed by multivariable analysis. Conclusion: Further research is needed to study the association between VH and vaccine uptake for other vaccines, and to design and validate measurement tools to monitor VH over time.
PtdIns4KIIα generates endosomal PtdIns(4)P and is required for receptor sorting at early endosomes

PtdIns4KIIα has been implicated in the regulation of endosomal traffic, but the role of its enzymatic activity and the site of its action have not been elucidated. Depletion of PtdIns4KIIα significantly reduced the amount of vesicular PtdIns(4)P on early endosomes, leaving cells with an impaired ability to sort molecules from early endosomes.
Pravastatin therapy attenuates left ventricular dysfunction and improves remodeling after myocardial infarction

Objective: The purpose of this study was to investigate the effect of pravastatin on cardiac function with myocardial infarction (MI) and reveal the possible mechanism involved in it. Methods: In the patients assay, 30 consecutive patients with MI (16 males and 14 females) were enrolled. Brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), and left ventricular ejection fraction (LVEF) function before and after pravastatin usage were compared. In the animal assay, two groups of rats were subjected to permanent coronary occlusion. Group II (n = 14) received oral pravastatin (10 mg/kg/d) daily at 3 wk before and 4 wk after MI, while group I (n = 12) received equivalent doses of vehicle. Results: The percentage of patients with high BNP level (BNP > 20 pg/mL) significantly decreased, from 2 D to 24 W in the pravastatin group, but not in the control group. Similar results occurred with respect to the ANP level (ANP > 40 pg/mL). LVEF in pravastatin group was significantly higher than that of the control group at 3 W and 24 W. In the animal assay, compared with group I, echocardiographic LVEF and fractional area change (FAC) were higher while left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic and end-diastolic diameters (LVESD and LVEDD) were lower in treated rats. Conclusion: Both patients and animal assays showed that pravastatin therapy during peri-infarct period significantly improved left ventricular (LV) function and limited adverse LV remodeling following MI independent of a reduction in infarct size.
Output‐feedback control of a class of stochastic nonlinear systems with linearly bounded unmeasurable states

In this paper, the problems of stochastic disturbance attenuation and asymptotic stabilization via output feedback are investigated for a class of stochastic nonlinear systems with linearly bounded unmeasurable states. For the first problem, under the condition that the stochastic inverse dynamics are generalized stochastic input‐to‐state stable, a linear output‐feedback controller is explicitly constructed to make the closed‐loop system noise‐to‐state stable. For the second problem, under the conditions that the stochastic inverse dynamics are stochastic input‐to‐state stable and the intensity of noise is known to be a unit matrix, a linear output‐feedback controller is explicitly constructed to make the closed‐loop system globally asymptotically stable in probability. Using a feedback domination design method, we construct these two controllers in a unified way. Copyright © 2007 John Wiley & Sons, Ltd.
A Rapidly Cooling Neutron Star Astrophysicists have found the first direct evidence for the fastest neutrino-emission mechanism by which neutron stars can cool

N eutron stars are formed in supernova explosions of stars too massive to become white dwarfs. In such supernovae, the hot remnant formed by the collapse of the stellar core is so dense that most protons and electrons combine to make neutrons. By observing how neutron stars cool, researchers hope to understand how matter behaves under extreme conditions—densities exceeding those of atomic nuclei and temperatures that can reach hundreds of billions of kelvin. Now, Edward Brown at Michigan State University, East Lansing, and co-workers have investigated the cooling history of a neutron star that is part of a binary system in our Galaxy. By analyzing the star’s x-ray emissions in the quiescent periods that followed two periods of x-ray outbursts ending in 2001 and 2016, the team found evidence of a particularly fast neutrino cooling mechanism, called the direct Urca process [1]. This process is believed to occur early in the lives of all neutron stars and may operate in later stages of a few neutron stars, but it has never been directly observed.
The diffusion of the United Nations Convention on the Rights of the Child (UNCRC) more than the African Charter on the Rights and Welfare of the Child (ACRWC) in Africa: The influence of coercion and emulation

In 1989, the United Nations adopted the Convention on the Rights of the Child (UNCRC), a seminal instrument in protecting the rights of children. Uniquely, this convention was the only one to receive near universal ratification, with African countries comprising half of the first 20 to sign the convention. Ghana was first among these countries to ratify the convention. This set off a bandwagon effect of other African countries quickly ratifying the convention. However, a year later, African governments reacted to their low involvement in the drafting process of the UNCRC and also to what they thought to be an inadequate representation of the real experience of the African child in the UNCRC. Consequently, this group adopted their own version of the convention – the African Charter on the Rights and Welfare of the Child (ACRWC). However, unlike the experience with the UNCRC, African nations were not quick to ratify their own Charter; the ACRWC is hardly discussed in public and policy forums in Africa, and its use among those charged with the protection of children is minimal. Using the lenses of policy diffusion, I assess the influence of coercion and emulation mechanisms on privileging the UNCRC which is used as the main organizing framework for child rights in most African countries. Additionally, I look at how Ghana’s political reputation influenced other African adopters, an effect which was not replicated with the ratification of the ACRWC. Implications for social work research, policy and practice are discussed.