Miracle-dz/UniFAR-FTUs huggingface dataset:
Monophyly of Endosymbiont Containing Trypanosomatids: Phylogeny versus Taxonomy

To obtain additional information on the phylogenetic relationships within the family Trypanosomatidae (order Kinetoplastida), we have sequenced the small subunit ribosomal RNA genes from the endosymbiont containing species Herpetomonas roitmani TCC080, Herpetomonas sp. TCC263, Crithidia oncopelti ATCC 12982 and a partial large subunit rRNA gene from H. roitmani. The small subunit sequences in the two isolates of Herpetomonas are very similar but not identical, and so are their restriction digest profiles of kinetoplast DNA. The size of minicircles in both isolates is 4.2 kilobases. The inferred ribosomal RNA phylogenetic trees shows the genera Herpetomonas and Crithidia as polyphyletic. Endosymbiont‐bearing herpetomonads cluster with the endosymbiont‐bearing crithidias and a blastocrithidia to form a monophyletic clade, whereas the endosymbiont‐free members of these genera are found elsewhere in the tree. These data support the hypothesis of a monophyletic origin of endosymbiosis in trypanosomatid evolution and also suggest that a taxonomic revision is needed in order to better describe the natural affinities in this family.
A flow graph-based test model for OWL-S web services

OWL-S is a standard for specifying the ontology of web services. It enables web services to be discovered, invoked, and composed automatically. However, OWSL-S web service is difficult to analyze and test as XML-based OWL-S description is hard to understand. In addition, OWL-S introduces various control constructs to compose multiple services and allows describing the preconditions and expected effects of the services, which further complicates the analysis and testing of web services. This paper proposes a flow graph-based test model for OWL-S web services. In particular, the model abstracts the structural test artifacts of OWL-S web services. It can facilitate testers to understand and analyze the control flow of OWL-S web services. Based on the test model, test paths can be derived to ensure the correctness of OWL-S web services.
An alternative measures for detecting stealthy aircraft using monostatic radars

Stealthy aircraft detection attracted a substantial attention in the recent years. The paper proposes an alternative measures for detecting stealthy aircraft using the operating monostatic radar parameters. This technique is used for detecting and tracking the small cross section area and stealthy aircrafts. The proposed measures are studied with different radar parameters to extend the detection coverage over the monostatic radar used for air surveillance. The simulation is done using Computer Aided Radar Performance Evaluation Tool (CARPET). It is a comprehensive computer program which alleviates the difficult task of designing and evaluating surface based radar systems. The studied parameters are the operating frequency, the transmitted power, pulse width, pulse repetition frequency, antenna polarization and tilt angle. The results show that the optimized parameters achieve a range extension of 100 Km and 50% detection probability over the worst case parameters for detecting and tracking stealthy aircraft.
A Novel Dictionary Learning Model with PT-HLBP for Palmprint Recognition

A novel projective dictionary pair learning PDPL model with statistical local features for palmprint recognition is proposed. Pooling technique is used to enhance the invariance of hierarchical local binary pattern PT-HLBP for palmprint feature extraction. PDPL is employed to learn an analysis dictionary and a synthesis dictionary which are utilized for image discrimination and representation. The proposed algorithm has been tested by the Hong Kong Polytechnic University PolyU database v2 and ideal recognition accuracy can be achieved. Experimental results indicate that the algorithm not only greatly reduces the time complexity in training and testing phase, but also exhibits good robustness for image rotation and corrosion.
Exploring integrated thinking in integrated reporting – an exploratory study in Australia

Purpose Integrated thinking is central to the International Integrated Reporting Council’s (IIRC’s) integrated reporting (IR) framework, which is in turn is related to a potential resurgence of intellectual capital (IC) reporting. However, it remains unclear how key IR stakeholders understand this concept in theory or practice. The purpose of this paper is to explore how key stakeholders interpret integrated thinking; and how pilot organizations are applying integrated thinking in practice. Design/methodology/approach The study involved in-depth semi-structured interviews with key IR stakeholders in Australia, including two IR pilot organizations, one professional association, an accounting professional body, an accounting firm and two IIRC officials. Findings First, the IIRC has not fully defined and articulated the concept of integrated thinking, and there is no shared consensus among practitioners. Second, there is evidence of an evolving understanding of integrated thinking within practice. What remains unclear is how this understanding will develop over time. Research limitations/implications Since interviews were conducted with a relatively small sample of participants in Australia, the results may not be generalizable across different contexts. The study emphasizes the need to interpret carefully IR’s potential contribution to organizational practice through either reporting in general, or IC reporting in particular. Originality/value Despite the centrality of integrated thinking to IR, there has been limited research to date on the concept. Clarifying what integrated thinking means in practice can improve our understanding of a key IR concept, and can advance our understanding of IR’s potential to improve IC reporting and research.
Anti-Inflammatory and Immunosuppressive Effects of the A2A Adenosine Receptor

The production of adenosine represents a critical endogenous mechanism for regulating immune and inflammatory responses during conditions of stress, injury, or infection. Adenosine exerts predominantly protective effects through activation of four 7-transmembrane receptor subtypes termed A1, A2A, A2B, and A3, of which the A2A adenosine receptor (A2AAR) is recognised as a major mediator of anti-inflammatory responses. The A2AAR is widely expressed on cells of the immune system and numerous in vitro studies have identified its role in suppressing key stages of the inflammatory process, including leukocyte recruitment, phagocytosis, cytokine production, and immune cell proliferation. The majority of actions produced by A2AAR activation appear to be mediated by cAMP, but downstream events have not yet been well characterised. In this article, we review the current evidence for the anti-inflammatory effects of the A2AAR in different cell types and discuss possible molecular mechanisms mediating these effects, including the potential for generalised suppression of inflammatory gene expression through inhibition of the NF-κB and JAK/STAT proinflammatory signalling pathways. We also evaluate findings from in vivo studies investigating the role of the A2AAR in different tissues in animal models of inflammatory disease and briefly discuss the potential for development of selective A2AAR agonists for use in the clinic to treat specific inflammatory conditions.
Herpes simplex encephalitis as a potential cause of anti-N-methyl-D-aspartate receptor antibody encephalitis: report of 2 cases.

IMPORTANCE Encephalitis mediated by anti-N-methyl-D-aspartate (NMDA) receptor antibodies and herpes simplex (HS) encephalitis are seemingly separate causes of encephalopathy in adults and children. Herpes simplex encephalitis is infectious, and anti-NMDA receptor antibody encephalitis is autoimmune in origin. Both can cause seizures and encephalopathy, although the latter can also cause psychiatric symptoms and movement disorders. Owing to the rarity of these 2 diseases, patients with co-occurrence are important because they alert clinicians to possible links between 2 seemingly separate processes. OBSERVATIONS In a case series of 2 patients observed at our center, we describe an infant and an adult who had confirmed HS encephalitis and then developed confirmed anti-NMDA receptor antibody encephalitis. Polymerase chain reaction testing for HS virus was performed. Testing for NMDA receptor antibodies was performed by Associated Regional and University Pathologists Laboratory in Salt Lake City, Utah. CONCLUSIONS AND RELEVANCE We conclude that atypical cases of HS or other viral encephalitides should be investigated for concomitance of an autoimmune encephalitis. We suspect that the pathophysiologic mechanisms by which HS virus infects neurons produce a higher likelihood of contracting anti-NMDA receptor antibody encephalitis.
Are children and adolescents with psychiatric illness at risk for increased future body weight? A systematic review

The aim of this paper was to review the longitudinal relationship between early‐onset depression and disruptive behaviour and adult body weight. A systematic review of prospective longitudinal studies was conducted of articles in which (1) initial assessment occurred during childhood or adolescence (<18y); and (2) the primary outcome reported as body mass index (BMI), overweight (BMI>25–<30kg/m2), obesity (BMI≥30kg/m2), or depression; and (3) validated assessment measures for assessment of depressive symptoms or disruptive behaviour problems were employed. A total number of 16 articles were identified for review. Obese adolescent females are more likely to develop depressive illness in adulthood than their non‐obese peers. Conversely, depressed adolescent females, and possibly males, are more likely to become overweight adults than non‐depressed adolescents. There are insufficient data addressing future depression risk among overweight, non‐obese, adolescents to evaluate the potentially interactive nature of this relationship. Studies to date are consistent in reporting that children with behaviour problems are at increased risk of future overweight, though whether this risk is conferred by conduct symptoms, ADHD symptoms, or both, is less clear. Care providers of children with disruptive behaviour problems and depressed adolescents should monitor weight gain. Among obese adolescent females, mood should be followed.
Do Goodwill Impairments by European Firms Provide Useful Information to Investors?

Abstract In 2004, the IASB adopted the mandatory annual impairment-test-only of goodwill (IAS 36) instead of amortization of goodwill. We present and discuss the academic literature regarding the association between the goodwill impairment, under this new standard, and the revision of investors’ expectations about a company’s future cash flows. The academic literature highlights that, in some specific cases, IAS 36 may help investors to revise their expectations. More precisely, goodwill impairment seems relevant when: (a) there is strong asymmetry of information between managers and investors, (b) managers disclose detailed information in the notes regarding their own assumptions about future cash flows, and (c) managers do not manage earnings and provide reliable information to investors. In many cases, goodwill impairment is probably useless for investors because they are able to revise their expectations based on public information, or because they cannot trust the accounting numbers and additional information in the notes about the impairment test, which are provided by (undisciplined) managers. More research is, however, needed to understand in which circumstances impairment-test-only is more useful, as well in which cases it is less adequate. Our analysis relates to the current post-implementation review and should be useful to standard-setters. Before any modification, we argue that standard-setters should carefully consider the economic and the institutional contexts when issuing a new accounting standard.
Development and Characterization of NEX-Pten, a Novel Forebrain Excitatory Neuron-Specific Knockout Mouse

The phosphatase and tensin homolog located on chromosome 10 (PTEN) suppresses the activity of the phosphoinositide-3-kinase/Akt/mammalian target of rapamycin (mTOR) pathway, a signaling cascade critically involved in the regulation of cell proliferation and growth. Human patients carrying germ line PTEN mutations have an increased predisposition to tumors, and also display a variety of neurological symptoms and increased risk of epilepsy and autism, implicating PTEN in neuronal development and function. Consistently, loss of Pten in mouse neural cells results in ataxia, seizures, cognitive abnormalities, increased soma size and synaptic abnormalities. To better understand how Pten regulates the excitability of principal forebrain neurons, a factor that is likely to be altered in cognitive disorders, epilepsy and autism, we generated a novel conditional knockout mouse line (NEX-Pten) in which Cre, under the control of the NEX promoter, drives the deletion of Pten specifically in early postmitotic, excitatory neurons of the developing forebrain. Homozygous mutant mice exhibited a massive enlargement of the forebrain, and died shortly after birth due to excessive mTOR activation. Analysis of the neonatal cerebral cortex further identified molecular defects resulting from Pten deletion that likely affect several aspects of neuronal development and excitability.
Thrombopoietin activates a STAT5‐like factor in hematopoietic cells.

Thrombopoietin (TPO) is a newly cloned cytokine which is the major regulator of circulating platelet levels, acting on both proliferation and differentiation of megakaryocytes. We have investigated the ability of TPO to activate the JAK/STAT pathway in megakaryocytic cell lines. We used either the granulocyte‐macrophage colony‐stimulating factor (GM‐CSF)‐ and/or erythropoietin (EPO)‐dependent UT7 cell line in which the murine TPO receptor (mumpl) had been transfected (mumpl‐UT7 transfectants) or the MO7E and DAMI cells which express endogenous human TPO receptors. We demonstrated that TPO activates the kinase JAK2 and a STAT5‐like transcriptional factor but not STAT1, STAT2, STAT3 or STAT4, in a very rapid and transient manner. In order to better ascertain the specificity of the activation of STAT5‐related factor by TPO, we investigated the effect of other cytokines/growth factors. Both GM‐CSF and EPO activated the STAT5‐like factor. In contrast, neither interferon (IFN)‐gamma nor the mitogenic stem cell factor (SCF) activated STAT5, although IFN‐gamma did activate STAT1 in those cells. The hematopoietic DNA binding activity related to STAT5 was identified as a p97 tyrosine‐phosphorylated protein band which exhibited identical gel mobility to the mammary STAT5. Because v‐mpl, a truncated form of the TPO receptor c‐mpl, was shown to be oncogenic, we tested the activity of v‐mpl on STAT5 and found STAT5 constitutively activated in two different v‐mpl‐expressing cells, the transiently transfected Cos7 cells and the stable v‐mpl‐UT7 transfectants. Overall, our data indicate that STAT5 is widely expressed in hematopoietic cells and activated by a number of cytokines, including TPO, GM‐CSF and EPO, but not by IFN‐gamma or SCF.
Profit Optimization under Risk in Cognitive Radio Networks

Radio spectrum is scarce in wireless communication. While there is an increasing demand for spectrum due to the substantial growth of wireless communication systems, extensive measurements observe that conventional static spectrum allocation policies introduce significant inefficiency in spectrum utilization. To achieve higher spectrum efficiency, cognitive radio networks have emerged as a revolutionary technology by allowing unlicensed (secondary) users to utilize licensed bands opportunistically without harming licensed (primary) users. In this thesis, we seek to design a new framework that addresses three important issues in cognitive radio networks simultaneously: protection of primary users, incentives for primary networks to share their spectrum and the performance guarantee for secondary users. Leveraging the idea of Value at Risk from economics, in our solution, primary networks maximize their profits by charging secondary users for opportunistic spectrum access, while in the meantime secondary users impose utility constraints to manage the risks and guarantee performance probabilistically. ii
[Expression of glycogen synthase kinase-3B in pancreatic tissue of acute edematous pancreatitis rats].

OBJECTIVE To investigate the expression of apoptosis related gene glycogen synthase kinase-3B (GSK-3B) in acute edematous pancreatitis (AEP), and the relationship between GSK-3B and AEP. METHODS The AEP rat model was established by the injection of caerulein [50 microg/(kg x h)] intraperitoneally per hour for 4 times. There were total 36 rats, every 6 rats were sacrificed at 0 h, 1 h, 3 h, 6 h, 12 h and 18 h after the injection of caerulein. Blood samples were taken from portal vein for ELISA examination of pancreatic amylase and lipase, pancreatic mRNA was extracted for RT-PCR analysis of GSK-3B, caspase-3, 9. The expression of GSK-3B protein was examed by Western blot, and acinar cell apoptosis was measured by TUNEL assay. RESULTS AEP was successfully induced and pancreatic lesions were most severe at 6 h after the injection of caerulein. Immunohistochemistry assay showed that GSK-3B protein located in cytoplasm of pancreatic acinar cells and endothelial cells, but not in islet cells. The mRNA levels of GSK-3B, caspase-3, 9, the protein level of GSK-3B, as well as cell apoptotic index in AEP rats were significantly increased when compared with the control rats received normal saline. Acinar cell apoptosis index was positively correlated with serum amylase, lipase, ratio of dry/wet of pancreas and GSK-3B mRNA expression, while GSK-3B mRNA level was positively correlated with caspase-3, 9 mRNA expression. CONCLUSION The expression levels of GSK-3B mRNA and protein were related to the severity of AEP and acinar cell apoptotic index.
A review of the newer aromatase inhibitors in the management of metastatic breast cancer

Background: Breast cancer remains a major cause of morbidity and mortality world‐wide. While aminoglutethimide, a first‐generation aromatase inhibitor, has equivalent efficacy to first‐line tamoxifen in the palliative treatment of metastatic breast cancer, its toxicity profile has relegated this drug to a second‐ or third‐line agent in this setting. Recently, several aromatase inhibitors have been released onto the market while others are in phase II and III clinical trials
Mammary gland, limb and yolk sac defects in mice lacking Tbx3, the gene mutated in human ulnar mammary syndrome

Spontanteous mutations in the T-box gene TBX3, result in the human ulnar-mammary syndrome, a dominant developmental disorder characterized by abnormal forelimb and apocrine gland development. In order to develop a mouse model to study the role of this gene during development and disease, we produced a mutation in the mouse ortholog, Tbx3. The phenotype of the mutant mice verifies the role of this gene in limb and mammary gland development, and, in addition, reveals a previously unknown role for the gene in the yolk sac, a fetal membrane that is the site of hematopoiesis and is essential for survival during gestation. In homozygous mutant embryos, the yolk sac undergoes cell death and degeneration at midgestation and the fetuses die over a range of several days; none survive to birth. Tbx3 is the first T-box gene implicated in yolk sac development. Homozygous embryos show a deficiency of mammary gland induction, and exhibit both forelimb and hindlimb abnormalities. Although heterozygous mice, unlike their heterozygous human counterparts, have no apparent phenotype in limb or mammary gland, the homozygous defects in the development of these organs represent more severe manifestations of the defects characteristic of the ulnar-mammary syndrome.
Genetic Variation and Evolutionary Origin of the Direct Repeat Locus of Mycobacterium tuberculosis Complex Bacteria

ABSTRACT The direct repeat region in Mycobacterium tuberculosiscomplex strains is composed of multiple direct variant repeats (DVRs), each of which is composed of a 36-bp direct repeat (DR) plus a nonrepetitive spacer sequence of similar size. It has been shown previously that clinical isolates show extensive polymorphism in the DR region by the variable presence of DVRs, and this polymorphism has been used in the epidemiology of tuberculosis. In an attempt to better understand the evolutionary scenario leading to polymorphic DR loci and to improve strain differentiation by spoligotyping, we characterized and compared the DNA sequences of the complete DR region and its flanking DNA of M. tuberculosis complex strains. We identified 94 different spacer sequences among 26 M. tuberculosis complex strains. No sequence homology was found between any of these spacers and M. tuberculosis DNA outside of the DR region or with any other known bacterial sequence. Although strains differed extensively in the presence or absence of DVRs, the order of the spacers in the DR locus was found to be well conserved. The data strongly suggest that the polymorphism in clinical isolates is the result of successive deletions of single discrete DVRs or of multiple contiguous DVRs from a primordial DR region containing many more DVRs than seen in present day isolates and that virtually no scrambling of DVRs took place during evolution. Because the majority of the novel spacer sequences identified in this study were confined to isolates of the rare Mycobacterium canettii taxon, the use of the novel spacers in spoligotyping led only to a slight improvement of strain differentiation by spoligotyping.
Functional coupling of calcineurin and protein kinase A in mouse ventricular myocytes

We examined the role of the Ca2+‐regulated protein phosphatase calcineurin in controlling Ca2+ signalling in mouse ventricular myocytes. Membrane currents and voltage were measured in single myocytes using the patch‐clamp technique. Cytoplasmic Ca2+ concentration ([Ca2+]i) was measured in cells loaded with the fluorescent Ca2+ indicators fluo‐4 or fura‐2 using a confocal or epifluorescence microscope. Inhibition of calcineurin with cyclosporin A (CsA, 100 nm) or the calcineurin auto‐inhibitory peptide (CiP, 100 μM), increased the amplitude and rate of decay of the evoked [Ca2+]i transient and also prolonged the action potential (AP) of ventricular myocytes to a similar extent. The effects of CsA (100 nm) and 100 μM CiP on the [Ca2+]i transient and AP were not additive. Calcineurin inhibition did not modify the K+ currents responsible for repolarisation of the mouse ventricle. Instead, inhibition of calcineurin increased the amplitude of the Ca2+ current (ICa) and the evoked calcium transient normalized to the ICa. Calcium sparks, which underlie the [Ca2+]i transient, had a higher frequency and amplitude, suggesting an elevation of SR calcium load. Inhibition of protein kinase A (PKA) prevented the effects of calcineurin inhibition, indicating that calcineurin opposes the actions of PKA. Finally, immunofluorescence images suggest that calcineurin and PKA co‐localize near the T‐tubules of ventricular myocytes. We propose that calcineurin and PKA are co‐localized to control Ca2+ influx through calcium channels and calcium release through ryanodine receptors.