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    MS 056 Guide to Jack R. Hild, MD Papers (1962, 1967)

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    The Jack R. Hild, MD papers contains new clippings, newsletters, correspondence, articles and research data related to the career of Dr. Jack Hild in pediatrics, specifically his work on polio. The collection consists of 1 box equaling 0.5 cubic feet. Materials are in good condition

    MS056: A Personal Feeling Daughter, Son of Dr. Hild Fought Off Polio Attacks

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    This is an article clipped from the Houston Chronicle from Wednesday, January 17, 1962 with the headline reading, “Polio Victim Knows Difficulties Her Special Students Are Facing.” The article is about Lisbeth Hild, daughter of Dr. Jack Hild, who suffered from Polio at age 14 and in 1962 was 27 years old working with children in the Texas Institute for Rehabilitation and Research. See more at finding aid.https://digitalcommons.library.tmc.edu/jack_r_hild/1009/thumbnail.jp

    Abbess Hild.

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    Article on The Abbess Hild

    Eva Hild : inside out

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    Glenn Hild

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    Dr. David Glassman, Glenn Hild, Dr. Blair Lordhttps://thekeep.eiu.edu/retirements_2016/1019/thumbnail.jp

    Charles A. Hild

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    Charles A. Hild, 1944https://researchexchange.iaao.org/presidents/1009/thumbnail.jp

    CRP-cAMP-mediated repression of HilD in mid-logarithmic growth requires the 3’UTR of <i>hilD</i>.

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    (A) hilD transcriptional expression was monitored using three different hilD-lacZ reporter fusions; these comprise either hilD to position +76 (within the hilD ORF), to position +965 (including the full-length hilD ORF), or to position +1,235 (including the hilD ORF and the hilD 3’UTR). Transcriptional studies were performed in the wild-type (WT) and Δcrp derivative strains grown in LB at 37°C up to an OD600nm of 0.4. The transcriptional expression is shown in relative values. In each case the reference (WT) value was set to one. Miller units in WT strains, hilD76-lacZ 63.3 +/- 5.9; hilD965-lacZ 5193.0 +/- 334.6; hilD1235-lacZ 38.3+/- 2.0. (B) Immunodetection of HilD-3xFLAG. Two different genetic constructs were used: one containing the hilD 3’UTR (+UTR) and the other lacking that region (-UTR). Immunodetection was assessed in whole cell extracts from cultures of the WT and Δcrp derivative strains grown as in A. (C) Immunodetection of the SPI-1 encoded SipA-3xFLAG protein was performed on whole cell extracts from two independent cultures of the WT and Δcrp derivative strains, either in the presence (+UTR) or the absence (-UTR) of the hilD 3’UTR. Cultures were grown as in A. In B and C, Coomassie Blue staining of the whole cell extracts serve as loading controls. Full length images of the Western blots, including molecular mass markers, are shown in S12 Fig. (D) sipC transcriptional expression was monitored in cultures grown as in A of the WT and Δcrp derivative strains carrying a hilD native gene or a derivative hilD lacking the 3’UTR. The transcriptional expression is shown in relative values. In each background (+UTR, -UTR) the activity reference of WT was set to one. Miller units in WT strains, UTR+ 73.6 +/- 11.8; UTR- 13783.0 +/- 1142.5. In A and D, the β-galactosidase activity was determined for three independent cultures, average and standard deviation is shown. **, pp< 0.001.</p

    J.-A. Hild

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    Ernault E. J.-A. Hild. In: Revue internationale de l'enseignement, tome 68, Juillet-Décembre 1914. pp. 235-236

    A eukaryotic-like 3′ untranslated region in Salmonella enterica hilD mRNA

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    Long 3' untranslated regions (3'UTRs) are common in eukaryotic mRNAs. In contrast, long 3'UTRs are rare in bacteria, and have not been characterized in detail. We describe a 3'UTR of 310 nucleotides in hilD mRNA, a transcript that encodes a transcriptional activator of Salmonella enterica pathogenicity island 1 (SPI-1). Deletion of the hilD 3'UTR increases the hilD mRNA level, suggesting that the hilD 3'UTR may play a role in hilD mRNA turnover. Cloning of the hilD 3'UTR downstream of the green fluorescent protein (gfp) gene decreases green fluorescent protein (GFP) activity in both Escherichia coli and S. enterica, indicating that the hilD 3'UTR can act as an independent module. S. enterica mutants lacking either ribonuclease E or polynucleotide phosphorylase contain similar amounts of hilD and hilD Δ3'UTR mRNAs, suggesting that the hilD 3'UTR is a target for hilD mRNA degradation by the degradosome. The hilD 3'UTR is also necessary for modulation of hilD and SPI-1 expression by the RNA chaperone Hfq. Overexpression of SPI-1 in the absence of the hilD 3'UTR retards Salmonella growth and causes uncontrolled invasion of epithelial cells. Based on these observations, we propose that the S. enterica hilD 3'UTR is a cis-acting element that contributes to cellular homeostasis by promoting hilD mRNA turnover.Ministerio de Economía y Competitividad BIO2010- 15023 y CSD2008-00013Junta de Andalucía P10-CVI-587
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