27 research outputs found

    Electrochemical method of controlling thiolate coverage on a conductive substrate such as gold

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    An electrochemical method for forming a partial monomolecular layer of a predetermined extent of coverage of a thiolate of the formula, XRS--, therein R can be a linear or branched chain hydrocarbon or an aromatic or the like and X can be any compatible end group, e.g., OH, COOH, CH.sub.3 or the like, upon a substrate such as gold, which involves applying in an electrochemical system a constant voltage preselected to yield the desired predetermined extent of coverage

    A systematic survey in Arabidopsis thaliana of transcription factors that modulate circadian parameters

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    <p>Abstract</p> <p>Background</p> <p>Plant circadian systems regulate various biological processes in harmony with daily environmental changes. In <it>Arabidopsis thaliana</it>, the underlying clock mechanism is comprised of multiple integrated transcriptional feedbacks, which collectively lead to global patterns of rhythmic gene expression. The transcriptional networks are essential within the clock itself and in its output pathway.</p> <p>Results</p> <p>Here, to expand understanding of transcriptional networks within and associated to the clock, we performed both an <it>in silico </it>analysis of transcript rhythmicity of transcription factor genes, and a pilot assessment of functional phenomics on the <it>MYB</it>, <it>bHLH</it>, and <it>bZIP </it>families. In our <it>in silico </it>analysis, we defined which members of these families express a circadian waveform of transcript abundance. Up to 20% of these families were over-represented as clock-controlled genes. To detect members that contribute to proper oscillator function, we systematically measured rhythmic growth <it>via </it>an imaging system in hundreds of misexpression lines targeting members of the transcription-factor families. Three transcription factors were found that conferred aberrant circadian rhythms when misexpressed: <it>MYB3R2</it>, <it>bHLH69</it>, and <it>bHLH92</it>.</p> <p>Conclusion</p> <p>Transcript abundance of many transcription factors in Arabidopsis oscillates in a circadian manner. Further, a developed pipeline assessed phenotypic contribution of a panel of transcriptional regulators in the circadian system.</p

    High Th2 cytokine levels and upper airway inflammation in human inherited T-bet deficiency

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    We have described a child suffering from Mendelian susceptibility to mycobacterial disease (MSMD) due to autosomal recessive, complete T-bet deficiency, which impairs IFN-γ production by innate and innate-like adaptive, but not mycobacterial-reactive purely adaptive, lymphocytes. Here, we explore the persistent upper airway inflammation (UAI) and blood eosinophilia of this patient. Unlike wild-type (WT) T-bet, the mutant form of T-bet from this patient did not inhibit the production of Th2 cytokines, including IL-4, IL-5, IL-9, and IL-13, when overexpressed in T helper 2 (Th2) cells. Moreover, Herpesvirus saimiri–immortalized T cells from the patient produced abnormally large amounts of Th2 cytokines, and the patient had markedly high plasma IL-5 and IL-13 concentrations. Finally, the patient’s CD4+ αβ T cells produced most of the Th2 cytokines in response to chronic stimulation, regardless of their antigen specificities, a phenotype reversed by the expression of WT T-bet. T-bet deficiency thus underlies the excessive production of Th2 cytokines, particularly IL-5 and IL-13, by CD4+ αβ T cells, causing blood eosinophilia and UAI. The MSMD of this patient results from defective IFN-γ production by innate and innate-like adaptive lymphocytes, whereas the UAI and eosinophilia result from excessive Th2 cytokine production by adaptive CD4+ αβ T lymphocytes.ISSN:0022-1007ISSN:1540-0069ISSN:1540-953

    TT2, TT8, and TTG1 synergistically specify the expression of BANYULS and proanthocyanidin biosynthesis in Arabidopsis thaliana

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    Baudry A, Heim MA, Dubreucq B, Caboche M, Weisshaar B, Lepiniec L. TT2, TT8, and TTG1 synergistically specify the expression of BANYULS and proanthocyanidin biosynthesis in Arabidopsis thaliana. The Plant Journal. 2004;39(3):366-380.Genetic analyses have demonstrated that together with TTG1, a WD-repeat (WDR) protein, TT2 (MYB), and TT8 (bHLH) are necessary for the correct expression of BANYULS (BAN). This gene codes for the core enzyme of proanthocyanidin biosynthesis in Arabidopsis thaliana seed coat. The interplays of TT2, TT8, and their closest MYB/bHLH relatives, with TTG1 and the BAN promoter have been investigated using a combination of genetic and molecular approaches, both in yeast and in planta. The results obtained using glucocorticoid receptor fusion proteins in planta strongly suggest that TT2, TT8, and TTG1 can directly activate BAN expression. Experiments using yeast two- and three-hybrid clearly demonstrated that TT2, TT8, and TTG1 can form a stable ternary complex. Furthermore, although TT2 and TT8 were able to bind to the BAN promoter when simultaneously expressed in yeast, the activity of the complex correlated with the level of TTG1 expression in A. thaliana protoplasts. In addition, transient expression experiments revealed that TTG1 acts mainly through the bHLH partner (i.e. TT8 or related proteins) and that TT2 cannot be replaced by any other related A. thaliana MYB proteins to activate BAN. Finally and consistent with these results, the ectopic expression of TT2 was sufficient to trigger BAN activation in vegetative parts, but only where TTG1 was expressed. Taken together, these results indicate that TT2, TT8, and TTG1 can form a ternary complex directly regulating BAN expression in planta

    A systematic survey in Arabidopsis thaliana of transcription factors that modulate circadian parameters

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    Hanano S, Stracke R, Jakoby M, et al. A systematic survey in Arabidopsis thaliana of transcription factors that modulate circadian parameters. BMC Genomics. 2008;9(1): 182

    Baclofen intoxication: a fun drug causing deep coma and nonconvulsive status epilepticus-a case report and review of the literature

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    The number of reports on baclofen intoxication has increased in recent years. We report a 15-year-old boy who was referred in a state of deep coma (Glasgow Coma Scale = 3). On clinical examination, he showed sinus bradycardia with normal blood pressure. On admission to the hospital, he presented intermittent short episodes of generalized tonic-clonic seizures. While results of imaging procedures and initial toxicological screening (including standard HPLC analysis and urine test) were negative, a nonconvulsive status epilepticus was diagnosed by electroencephalography (EEG). Identification of baclofen as causative agent was possible after the boy's father reported abusive baclofen intake. Subsequent toxicological target analysis of blood and urine samples confirmed the excessive intake of baclofen and showed a typical elimination pattern with a secondary release. Following 112 h of mechanical ventilation, the boy rapidly regained consciousness and recovered normal neurological behavior. Conclusions: The present case demonstrates the importance of considering baclofen overdosage in cases of severe coma in combination with an abnormal EEG pattern and sinus bradycardia with normal blood pressure levels, in particular as the substance is popular in internet reports promoting baclofen as a rather harmless fun drug. Furthermore, it underlines the difficulty to identify baclofen as a causative agent without anamnestic information. Nevertheless, by reviewing existing literature on oral baclofen overdosage, it is possible to picture a nearly specific pattern of clinical symptoms in baclofen intoxication

    A systematic survey in of transcription factors that modulate circadian parameters-3

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    �5 days. Representative traces of rhythmic expression of oxplants (pink squares) and wild-type (blue circles) are shown. (, ) -ox, (, ) -ox. (, ) :, (, ) :.<p><b>Copyright information:</b></p><p>Taken from "A systematic survey in of transcription factors that modulate circadian parameters"</p><p>http://www.biomedcentral.com/1471-2164/9/182</p><p>BMC Genomics 2008;9():182-182.</p><p>Published online 21 Apr 2008</p><p>PMCID:PMC2410138.</p><p></p
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