29 research outputs found

    The use of fluorescence enhancement to improve the microscopic diagnosis of falciparum malaria-1

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    <p><b>Copyright information:</b></p><p>Taken from "The use of fluorescence enhancement to improve the microscopic diagnosis of falciparum malaria"</p><p>http://www.malariajournal.com/content/6/1/89</p><p>Malaria Journal 2007;6():89-89.</p><p>Published online 6 Jul 2007</p><p>PMCID:PMC1950880.</p><p></p> light microscopy. The left hand side was stained with Giemsa alone and the right hand side was stained with Giemsa followed by SYBR Green 1. Panel B depicts the same field of dual stained infected red blood cells viewed under light (left hand side) or fluorescence (right hand side)

    The use of fluorescence enhancement to improve the microscopic diagnosis of falciparum malaria-3

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    <p><b>Copyright information:</b></p><p>Taken from "The use of fluorescence enhancement to improve the microscopic diagnosis of falciparum malaria"</p><p>http://www.malariajournal.com/content/6/1/89</p><p>Malaria Journal 2007;6():89-89.</p><p>Published online 6 Jul 2007</p><p>PMCID:PMC1950880.</p><p></p>BCs were stained with SYBR Green 1 and were then examined using a Zeiss Axiostar Plus microscope with an LED light source fitted in place of its mercury lamp. Photographs depict fluorescent (left) and white light (right) images of a mature parasite (upper) and a ring stage parasite (lower). Fluorescent intensity of the stained parasites was comparable to that observed with the HBO 50/AC high intensity light source supplied by the manufacturer

    The use of fluorescence enhancement to improve the microscopic diagnosis of falciparum malaria-2

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    <p><b>Copyright information:</b></p><p>Taken from "The use of fluorescence enhancement to improve the microscopic diagnosis of falciparum malaria"</p><p>http://www.malariajournal.com/content/6/1/89</p><p>Malaria Journal 2007;6():89-89.</p><p>Published online 6 Jul 2007</p><p>PMCID:PMC1950880.</p><p></p>esents the same field visualized using fluorescence microscopy

    The experimental protocol.

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    <p>Wt: wild-type, TSA: trichostatin A; I/R: ischemia/reperfusion; DMSO: dimethyl sulfoxide.</p

    Effects of TSA on LV-dP/dt max and LV-dP/dt min.

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    <p>Values represent mean ± SE, *p< 0.05 <i>vs</i> Wt+TSA (n = 4–5 per group).</p

    Effects of TSA on heart rates and coronary effluents in post-ischemic myocardium.

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    <p>CF: coronary effluent; HR: heart rate, values represent mean ± SE (n = 4–5 per group). There were no significance differences among groups.</p

    Post-ischemic ventricular functional recovery.

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    <p>Absence of cardiac functional recovery in MKK3<sup>−/−</sup> and Akit-1<sup>−/−</sup> mice treated with trichostatin A. Left ventricular (LV) function was assessed in isovolumetric hearts. The measured parameters include LV systolic pressure (LVSP), developed pressure (LVDP), and rate pressure product (RPP) where LVDP is systolic pressure minus LV end-diastolic pressure (LVEDP). Values represent mean ± SE (n = 4–5 per group), *p<0.05 <i>vs</i> Wt+TSA.</p

    The effect of TSA on myocardial infarct size in wild-type, MKK3<sup>−/−</sup> and Akt-1<sup>−/−</sup> mice.

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    <p>Note that there is a significant greater viable area in the sections of the heart obtained from TSA-treated wild type mice as compared to wild type vehicle-treated group, TSA+ MKK3<sup>−/−</sup> mice, TSA+Akt-1<sup>−/−</sup> mice. Values represent mean ± SE. *p<0.05 <i>vs</i> wild-type vehicle-treated mice, TSA+ MKK3<sup>−/−</sup> mice and TSA+Akt-1<sup>−/−</sup> mice (n = 4–5 per group).</p

    The presence of HDAC4 and HDAC5 in mouse myocardium.

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    <p>The myocytes were stained with anti-sarcomeric actinin (green), HDAC4 and HDAC5 proteins were stained with anti-HDAC4 and HDAC5 (red). Nuclei were stained with 4′6-diamidino-2-phenylindole (DAPI, blue). Images show an overlay of myocytes, HDAC4 and HDAC5 and nuclei, Bar = 50µm.</p

    The effects of TSA on acetylation and phsophorylation of MKK3 in myocardium.

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    <p>The increased acetylated and phosphorylated MKK3 in myocardium after TSA treatment were observed. (A): TSA treatment increased MKK3 phosphorylation in myocardium; (B): The densitometric signal of phosphorylated MKK3 level, the densitometric signal was normalized to the control group and expressed as a percentage; (C): Immunoprecipitation and Western blot: myocardial tissues were collected at 30 min after TSA treatment. Results are mean ± SE (n = 3/per group), *p<0.05 <i>vs</i> control.</p
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