<?xml version="1.0" encoding="UTF-8"?>
<rss xmlns:dc="http://purl.org/dc/elements/1.1/" version="2.0">
  <channel>
    <title>DSpace Collection: This collection contains the citation and abstract of research publications authored or co-authored by University of Manitoba researchers.</title>
    <link>http://hdl.handle.net/1993/2762</link>
    <description>This collection contains the citation and abstract of research publications authored or co-authored by University of Manitoba researchers.</description>
    <pubDate>Thu, 23 May 2013 22:04:32 GMT</pubDate>
    <dc:date>2013-05-23T22:04:32Z</dc:date>
    <item>
      <title>Dietary zinc deficiency and expression of T lymphocyte signal transduction proteins</title>
      <link>http://hdl.handle.net/1993/2960</link>
      <description>Title: Dietary zinc deficiency and expression of T lymphocyte signal transduction proteins
Authors: Taylor, CG ; Giesbrecht J-AC
Abstract: Impaired immune function in dietary zinc (Zn) deficiency is characterized in part by reduced lymphocyte numbers (lymphopenia) and depressed cell-mediated (T lymphocyte) immune function, however, the causative mechanisms at the molecular level have not been elucidated. This paper will focus on the role of dietary Zn in T lymphocyte signal transduction, and specifically, the early Zn-dependent steps for phosphorylation and the putative Zn-finger proteins or Zn-metalloenzymes that may be part of the molecular mechanism for explaining immune dysfunction in Zn deficiency. One of the major recent findings is that murine splenic T lymphocyte p56(lck) expression is elevated in dietary Zn deficiency and caloric deficiency. Based on the known functions of p56(lck), it is proposed that elevated p56(lck) may contribute to altered thymocyte maturation, apoptosis, and lymphopenia in dietary Zn deficiency and other malnutrition syndromes.</description>
      <pubDate>Fri, 31 Dec 2004 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://hdl.handle.net/1993/2960</guid>
      <dc:date>2004-12-31T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Modulation of ICa-L by alpha(1)-adrenergic stimulation in rat ventricular myocytes</title>
      <link>http://hdl.handle.net/1993/2961</link>
      <description>Title: Modulation of ICa-L by alpha(1)-adrenergic stimulation in rat ventricular myocytes
Authors: Zhang, ST; Lin, JJ; Hirano, YJ; Hiraoka, M
Abstract: We found when L-type calcium current (ICa-L) was recorded with the perforated patch-clamp method in rat ventricular myocytes that bath application of phenylephrine (with propranolol) evoked a biphasic response characterized by an initial transient suppression followed by a sustained potentiation. The transient suppression occurred 30-60 s after phenylephrine perfusion and reached peak inhibition at approximately 2 min. The biphasic modulation of ICa-L was also elicited by methoxamine, and the effects of phenylephrine were blocked by prazosin, indicating that the responses were mediated through alpha(1)-adrenoceptors. Pretreatment of cells with H7 (100 mu mol/L), a broad-spectrum protein kinase inhibitor that inhibits both protein kinase C and A, eliminated potentiation but did not affect transient suppression. The transient suppression occurred concurrently with the acceleration of the fast component of ICa-L inactivation. Depletion of intracellular Ca2+ stores by ryanodine plus caffeine or thapsigargin eliminated the transient suppression. When ICa-L was recorded with whole-cell patch-clamp and with 0.05 mmol/L EGTA in the pipette solution to allow intracellular Ca2+ to fluctuate, phenylephrine evoked a transient suppression as in the perforated patch recordings. Heparin, a specific blocker of IP3 (inositol 1,4,5-trisphosphate) receptors, eliminated the phenylephrine-induced transient suppression of ICa-L when added to the pipette solution. Intensive chelation of intracellular Ca2+ by 5 mmol/L BAPTA (1,2-bis(2aminophenoxy)ethane-N,N,N',N'-tetraacetic acid) in the pipette solution also eliminated the phenylephrine-induced transient suppression of ICa-L We conclude that transient increase in the concentration of intracellular calcium ([Ca2+](i)) caused by Ca2+ release from intracellular stores underlies the transient suppression of ICa-L, whereas the potentiation of ICa-L is a result of activation of protein kinases.</description>
      <pubDate>Wed, 30 Nov 2005 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://hdl.handle.net/1993/2961</guid>
      <dc:date>2005-11-30T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Derivation and comparison of SAR and frequency-wavenumber migration within a common inverse scalar wave problem formulation</title>
      <link>http://hdl.handle.net/1993/2959</link>
      <description>Title: Derivation and comparison of SAR and frequency-wavenumber migration within a common inverse scalar wave problem formulation
Authors: Gilmore, C; Jeffrey, I; LoVetri, J
Abstract: Two common Fourier imaging algorithms used in ground penetrating radar (GPR), synthetic aperture radar (SAR), and frequency-wavenumber (F-K) migration, are reviewed and compared from a theoretical perspective. The two algorithms, while arising from seemingly different physical models: a point-scatterer model for SAR and the exploding source model for F-K migration, result in similar imaging equations. Both algorithms are derived from an integral equation formulation of the inverse scalar wave problem, which allows a clear understanding of the approximations being made in each algorithm and allows a direct comparison. This derivation brings out the similarities of the two techniques which are hidden by the traditional formulations based on physical scattering models. The comparison shows that the approximations required to derive, each technique from the integral equation formulation of the inverse problem are nearly identical, and hence the two imaging algorithms and physical models are making similar assumptions about the solution to the inverse problem, thus clarifying why the imaging equations are so similar. Sample images of landmine-like targets buried in sand are obtained from experimental GPR data. using both algorithms.</description>
      <pubDate>Fri, 30 Jun 2006 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://hdl.handle.net/1993/2959</guid>
      <dc:date>2006-06-30T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Hardware invariant protocol disruptive interference for 100BaseTX Ethernet communications</title>
      <link>http://hdl.handle.net/1993/2958</link>
      <description>Title: Hardware invariant protocol disruptive interference for 100BaseTX Ethernet communications
Authors: Jeffrey, I; Gilmore, C; Siemens, G; LoVetri, J
Abstract: In this paper, we introduce a new concept that we refer to as hardware invariant protocol disruptive interference (HIPDI). Such interference would pose a severe threat as intentional EMI to the corresponding protocol for which it was designed. In this paper, we consider only the 100BaseTX Ethernet protocol over UTP CAT-5 cable which is used extensively in local-area networks. We show that low power, narrowband, differential-mode voltage levels on a 100BaseTX Ethernet twisted-pair can seriously degrade network throughput independent of the physical features of the network or the protocol interpreter hardware. Moreover, we show that the required parameters of disruptive interference can be derived from the protocol itself using a concept we call hardware aperture. The experimental results reported herein indicate that creating such interference is practically feasible and therefore, is a possible threat to existing communication networks.</description>
      <pubDate>Mon, 30 Aug 2004 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://hdl.handle.net/1993/2958</guid>
      <dc:date>2004-08-30T00:00:00Z</dc:date>
    </item>
  </channel>
</rss>

