191 research outputs found

    SYSTEM AND METHOD FOR PREDICTING HARDWARE FAILURES OF ELECTRONIC DEVICES USING ONBOARD SENSORS AND DEVICE LIFECYCLE DATA

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    Techniques herein provide a capability to predict failures of hardware by using onboard sensors and provide for the ability to move from detection to prediction for hardware failures. In turn, such techniques can help to reduce downtime due to marginal hardware and improves network availability. The techniques can also help to reduce unnecessary maintenance and changes related to replacing hardware that has not failed, which can lead to business efficiencies for both customers and vendors and may become even more important in a Network-As-A-Service (NAAS) context in which both sides are paid by the vendor

    Oral Ornaments: An Overview

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    Nowadays, people desire to look attractive and have become very alert about their appearance and smile. Since the face is most exposed part of our body, and mouth a prominent feature, teeth are getting enormous share of attention. Intraoral jewellery has currently gained popularity and is slowly becoming a craze, but this fashion trend is also associated with some significant health issues. These ornaments though are said to enhance beauty cause problems such as increase pain, infection, scar formation, tooth fractures, metal hyper-sensitivity reactions, localized periodontal disease, speech impediment, and nerve damage. This review draws special attention to the prevalence, complications, and side effects of dental jewellery in humans. Here we suggest people must be aware of all the risks associated with wearing dental jewellery, and they should undergo dental check-ups regularly

    GATA2 Mediates Thyrotropin-Releasing Hormone-Induced Transcriptional Activation of the Thyrotropin Ξ² Gene

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    Thyrotropin-releasing hormone (TRH) activates not only the secretion of thyrotropin (TSH) but also the transcription of TSHΞ² and Ξ±-glycoprotein (Ξ±GSU) subunit genes. TSHΞ² expression is maintained by two transcription factors, Pit1 and GATA2, and is negatively regulated by thyroid hormone (T3). Our prior studies suggest that the main activator of the TSHΞ² gene is GATA2, not Pit1 or unliganded T3 receptor (TR). In previous studies on the mechanism of TRH-induced activation of the TSHΞ² gene, the involvements of Pit1 and TR have been investigated, but the role of GATA2 has not been clarified. Using kidney-derived CV1 cells and pituitary-derived GH3 and TΞ±T1 cells, we demonstrate here that TRH signaling enhances GATA2-dependent activation of the TSHΞ² promoter and that TRH-induced activity is abolished by amino acid substitution in the GATA2-Zn finger domain or mutation of GATA-responsive element in the TSHΞ² gene. In CV1 cells transfected with TRH receptor expression plasmid, GATA2-dependent transactivation of Ξ±GSU and endothelin-1 promoters was enhanced by TRH. In the gel shift assay, TRH signal potentiated the DNA-binding capacity of GATA2. While inhibition by T3 is dominant over TRH-induced activation, unliganded TR or the putative negative T3-responsive element are not required for TRH-induced stimulation. Studies using GH3 cells showed that TRH-induced activity of the TSHΞ² promoter depends on protein kinase C but not the mitogen-activated protein kinase, suggesting that the signaling pathway is different from that in the prolactin gene. These results indicate that GATA2 is the principal mediator of the TRH signaling pathway in TSHΞ² expression

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    Data from experiments 1 and
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