525 research outputs found

    Responses of Periwinkle (Catharanthus roseus) to soil and foliar applications of Haza (Haplophyllum tuberculatum).

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    This study aimed to investigate the responses of Periwinkle plants to soil and foliar applications of Haza plant in two separate tests under the conditions of the nursery at Shambat, Khartoum North, Sudan. The foliar treatments were for boiled water extracts of hand crushed Haza shoots in concentrations: 0.0, 5, 10, 15 and 20 g/l, while the soil dressing test was for powder of dry shoots of Haza applied in doses of: 0.0, 5, 10, 15 and 20 g per plant. The Periwinkle transplants were planted in 18 inch plastic pots containing River Nile sedimentary soil. The study was arranged in complete randomized design and each treatment was replicated 7 times. Data were collected 4 months after applications. The results showed substantial increments in vegetative and reproductive growth parameters coupled with high alkaloids content from soil dressing with 10 g/plant Haza treatment or the foliar application of the 10 g/l Haza extract. These findings elucidated the bio-stimulating potential of Haza applications for enhanced vegetative and reproductive growth beside alkaloids content of Periwinkle. This stimulating potential may be of value for trials on organic production of other horticultural crops

    In-beam fast-timing measurements in 103,105,107Cd

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    Fast-timing measurements were performed recently in the region of the medium-mass 103,105,107Cd isotopes, produced in fusion evaporation reactions. Emitted gamma-rays were detected by eight HPGe and five LaBr3:Ce detectors working in coincidence. Results on new and re-evaluated half-lives are discussed within a systematic of transition rates. The 7/21+7/2_1^+ states in 103,105,107Cd are interpreted as arising from a single-particle excitation. The half-life analysis of the 11/2111/2_1^- states in 103,105,107Cd shows no change in the single-particle transition strength as a function of the neutron number

    Notch signaling during human T cell development

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    Notch signaling is critical during multiple stages of T cell development in both mouse and human. Evidence has emerged in recent years that this pathway might regulate T-lineage differentiation differently between both species. Here, we review our current understanding of how Notch signaling is activated and used during human T cell development. First, we set the stage by describing the developmental steps that make up human T cell development before describing the expression profiles of Notch receptors, ligands, and target genes during this process. To delineate stage-specific roles for Notch signaling during human T cell development, we subsequently try to interpret the functional Notch studies that have been performed in light of these expression profiles and compare this to its suggested role in the mouse

    Differential Regulation of the PGC Family of Genes in a Mouse Model of Staphylococcus aureus Sepsis

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    The PGC family of transcriptional co-activators (PGC-1α [Ppargc1a], PGC-1β [Ppargc1b], and PRC [Pprc]) coordinates the upregulation of mitochondrial biogenesis, and Ppargc1a is known to be activated in response to mitochondrial damage in sepsis. Therefore, we postulated that the PGC family is regulated by the innate immune system. We investigated whether mitochondrial biogenesis and PGC gene expression are disrupted in an established model of Staphylococcus aureus sepsis both in mice with impaired innate immune function (TLR2−/− and TLR4−/−) and in wild-type controls. We found an early up-regulation of Ppargc1a and Ppargc1b post-infection (at 6 h) in WT mice, but the expression of both genes was concordantly dysregulated in TLR2−/− mice (no increase at 6 h) and in TLR4−/− mice (amplified at 6 h). However, the third family member, PRC, was regulated differently, and its expression increased significantly at 24 h in all three mouse strains (WT, TLR2−/−, and TLR4−/−). In silico analyses showed that Ppargc1a and Ppargc1b share binding sites for microRNA mmu-mir-202-3p. Thus, miRNA-mediated post-transcriptional mRNA degradation could account for the failure to increase the expression of both genes in TLR2−/− mice. The expression of mmu-mir-202-3p was measured by real-time PCR and found to be significantly increased in TLR2−/− but not in WT or TLR4−/− mice. In addition, it was found that mir-202-3p functionally decreases Ppargc1a mRNA in vitro. Thus, both innate immune signaling through the TLRs and mir-202-3p-mediated mRNA degradation are implicated in the co-regulation of Ppargc1a and Ppargc1b during inflammation. Moreover, the identification of mir-202-3p as a potential factor for Ppargc1a and Ppargc1b repression in acute inflammation may open new avenues for mitochondrial research and, potentially, therapy

    Fast-timing measurements in 95,96Mo

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    Half-lives of the 19/2+ and 21/2+ states in 95Mo and of the 8+ and 10+ states in 96Mo were measured. Matrix elements for yrast transitions in 95Mo and 96Mo are discussed.Comment: Proceedings of XIX International School on Nuclear Physics, Neutron Physics and Applications, Varna, Bulgaria, 2011, 5 pages, 6 figure

    A Toll-Like Receptor 2 Pathway Regulates the Ppargc1a/b Metabolic Co-Activators in Mice with Staphylococcal aureus Sepsis

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    Activation of the host antibacterial defenses by the toll-like receptors (TLR) also selectively activates energy-sensing and metabolic pathways, but the mechanisms are poorly understood. This includes the metabolic and mitochondrial biogenesis master co-activators, Ppargc1a (PGC-1α) and Ppargc1b (PGC-1β) in Staphylococcus aureus (S. aureus) sepsis. The expression of these genes in the liver is markedly attenuated inTLR2−/− mice and markedly accentuated in TLR4−/− mice compared with wild type (WT) mice. We sought to explain this difference by using specific TLR-pathway knockout mice to test the hypothesis that these co-activator genes are directly regulated through TLR2 signaling. By comparing their responses to S. aureus with WT mice, we found that MyD88-deficient and MAL-deficient mice expressed hepatic Ppargc1a and Ppargc1b normally, but that neither gene was activated in TRAM-deficient mice. Ppargc1a/b activation did not require NF-kβ, but did require an interferon response factor (IRF), because neither gene was activated in IRF-3/7 double-knockout mice in sepsis, but both were activated normally in Unc93b1-deficient (3d) mice. Nuclear IRF-7 levels in TLR2−/− and TLR4−/− mice decreased and increased respectively post-inoculation and IRF-7 DNA-binding at the Ppargc1a promoter was demonstrated by chromatin immunoprecipitation. Also, a TLR2-TLR4-TRAM native hepatic protein complex was detected by immunoprecipitation within 6 h of S. aureus inoculation that could support MyD88-independent signaling to Ppargc1a/b. Overall, these findings disclose a novel MyD88-independent pathway in S. aureus sepsis that links TLR2 and TLR4 signaling in innate immunity to Ppargc1a/b gene regulation in a critical metabolic organ, the liver, by means of TRAM, TRIF, and IRF-7

    Levenberg Marquardt artificial neural network model for self organising networks implementation in wireless sensor network

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    The Wireless Sensor Network needs to become a dynamic and adaptive network to conserve energy stored in the wireless sensor network node battery. This dynamic and adaptive network sometimes are called SON (Self Organizing Network). Several SON concepts have been developed such as routing, clustering, intrusion detection, and other. Although several SON concepts already exist, however, there is no concept for SON in dynamic radio configuration. Therefore, the authors’ contribution to this field would be proposing a dynamic and adaptive Wireless Sensor Network node radio configuration. The significance of their work lies in the modelling of the SON network that builds based on our measurement in the real‐world jungle environment. The authors propose input parameters such as SNR, the distance between the transmitter and receiver, and frequency as the static parameter. For adaptive parameters, we propose bandwidth, spreading factor, and its most important parameter such as power for data transmission. Using the Levenberg Marquardt Artificial Neural Network (LM‐ANN) self‐organise Network model, power reduction and optimisation from 20 dBm to 14.9 dBm for SNR 3, to 11.5 dBm for SNR 6, and to 12.9 dBm for SNR 9 all within a 100‐m range can be achieved. With this result, the authors conclude that we can use LM‐ANN for the wireless sensor network SON model in the jungle environment

    Consensus on the assessment of systemic sclerosis–associated primary heart involvement: World Scleroderma Foundation/Heart Failure Association guidance on screening, diagnosis, and follow-up assessment

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    INTRODUCTION: Heart involvement is a common problem in systemic sclerosis. Recently, a definition of systemic sclerosis primary heart involvement had been proposed. Our aim was to establish consensus guidance on the screening, diagnosis and follow-up of systemic sclerosis primary heart involvement patients. METHODS: A systematic literature review was performed to investigate the tests used to evaluate heart involvement in systemic sclerosis. The extracted data were categorized into relevant domains (conventional radiology, electrocardiography, echocardiography, cardiac magnetic resonance imaging, laboratory, and others) and presented to experts and one patient research partner, who discussed the data and added their opinion. This led to the formulation of overarching principles and guidance statements, then reviewed and voted on for agreement. Consensus was attained when the mean agreement was ⩾7/10 and of ⩾70% of voters. RESULTS: Among 2650 publications, 168 met eligibility criteria; the data extracted were discussed over three meetings. Seven overarching principles and 10 guidance points were created, revised and voted on. The consensus highlighted the importance of patient counseling, differential diagnosis and multidisciplinary team management, as well as defining screening and diagnostic approaches. The initial core evaluation should integrate history, physical examination, rest electrocardiography, trans-thoracic echocardiography and standard serum cardiac biomarkers. Further investigations should be individually tailored and decided through a multidisciplinary management. The overall mean agreement was 9.1/10, with mean 93% of experts voting above 7/10. CONCLUSION: This consensus-based guidance on screening, diagnosis and follow-up of systemic sclerosis primary heart involvement provides a foundation for standard of care and future feasibility studies that are ongoing to support its application in clinical practice

    Progressive resistance of BTK-143 osteosarcoma cells to Apo2L/TRAIL-induced apoptosis is mediated by acquisition of DcR2/TRAIL-R4 expression: resensitisation with chemotherapy

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    © 2003 Cancer Research UKApo2 ligand (Apo2L, also known as TRAIL) is a member of the tumour necrosis factor (TNF) family of cytokines that selectively induces the death of cancer cells, but not of normal cells. We observed that recombinant Apo2L/TRAIL was proapoptotic in early-passage BTK-143 osteogenic sarcoma cells, inducing 80% cell death during a 24 h treatment period. Apo2L/TRAIL-induced apoptosis was blocked by caspase inhibition. With increasing passage in culture, BTK-143 cells became progressively resistant to the apoptotic effects of Apo2L/TRAIL . RNA and flow cytometric analysis demonstrated that resistance to Apo2L/TRAIL was paralleled by progressive acquisition of the decoy receptor, DcR2. Blocking of DcR2 function with a specific anti-DcR2 antibody restored sensitivity to Apo2L/TRAIL in a dose-dependent manner. Importantly, treatment of resistant cells with the chemotherapeutic agents doxorubicin, cisplatin and etoposide reversed the resistance to Apo2L/TRAIL, which was associated with drug-induced upregulation of mRNA encoding the death receptors DR4 and DR5. BTK-143 cells thus represent a useful model system to investigate both the mechanisms of acquisition of resistance of tumour cells to Apo2L/TRAIL and the use of conventional drugs and novel agents to overcome resistance to Apo2L/TRAIL.S Bouralexis, D M Findlay, G J Atkins, A Labrinidis, S Hay & A Evdokio
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