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Träfflista för sökning "WFRF:(Zidek M) "

Sökning: WFRF:(Zidek M)

  • Resultat 1-7 av 7
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1.
  • 2017
  • swepub:Mat__t
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3.
  • Abdelmagid, N., et al. (författare)
  • Von Willebrand Factor Gene Variants Associate with Herpes simplex Encephalitis
  • 2016
  • Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 11:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Herpes simplex encephalitis (HSE) is a rare complication of Herpes simplex virus type-1 infection. It results in severe parenchymal damage in the brain. Although viral latency in neurons is very common in the population, it remains unclear why certain individuals develop HSE. Here we explore potential host genetic variants predisposing to HSE. In order to investigate this we used a rat HSE model comparing the HSE susceptible SHR (Spontaneously Hypertensive Rats) with the asymptomatic infection of BN (Brown Norway). Notably, both strains have HSV-1 spread to the CNS at four days after infection. A genome wide linkage analysis of 29 infected HXB/BXH RILs (recombinant inbred lines-generated from the prior two strains), displayed variable susceptibility to HSE enabling the definition of a significant QTL (quantitative trait locus) named Hse6 towards the end of chromosome 4 (160.89-174Mb) containing the Vwf (von Willebrand factor) gene. This was the only gene in the QTL with both cis-regulation in the brain and included several non-synonymous SNPs (single nucleotide polymorphism). Intriguingly, in human chromosome 12 several SNPs within the intronic region between exon 43 and 44 of the VWF gene were associated with human HSE pathogenesis. In particular, rs917859 is nominally associated with an odds ratio of 1.5 (95% CI 1.11-2.02; p-value = 0.008) after genotyping in 115 HSE cases and 428 controls. Although there are possibly several genetic and environmental factors involved in development of HSE, our study identifies variants of the VWF gene as candidates for susceptibility in experimental and human HSE.
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4.
  • Christensson, Niklas, et al. (författare)
  • Origin of the Bathochromic Shift of Astaxanthin in Lobster Protein: 2D Electronic Spectroscopy Investigation of beta-Crustacyanin
  • 2013
  • Ingår i: The Journal of Physical Chemistry Part B. - : American Chemical Society (ACS). - 1520-5207 .- 1520-6106. ; 117:38, s. 11209-11219
  • Tidskriftsartikel (refereegranskat)abstract
    • We report on ultrafast spectroscopy study of beta-crustacyanin, the carotenoprotein responsible for the coloration of the lobster shell. beta-Crustacyanin is formed by two closely positioned astaxanthin molecules encapsulated in protein. The 2D electronic spectroscopy together with two-color pump-probe was applied to investigate the electronic structure, the excited-state dynamics, and the influence of the excitonic interaction between the two carotenoids in beta-crustacyanin. By using the similar to 20 Is laser pulses tuned to absorption bands of the S-0-S-2 and S-1-S-n transitions of carotenoids, we were able to trace full excitation relaxation dynamics, starting with S-2-S-1 relaxation on the similar to 30 fs time scale and finishing with the ground-state recovery of 3.2 ps. Superimposed on the relaxation dynamics in the 2D spectra, we observed long-lived beating signals at the characteristic frequencies of astaxanthin vibrational modes. We assign these oscillations to the ground-state vibrational wavepacket dynamics. All major features of the 2ll spectra, including amplitude and phase maps of the long-lived oscillations, were reproduced by employing the exciton-vibronic model. Consistent modeling of all optical properties of beta-crustacyanin (including absorption and circular dichroism spectra) points to the relatively weak coupling between the two astaxanthin molecules (similar to 250 cm(-1)). This implies that the excitonic coupling provides insignificant contribution to the bathochromic shift in beta-crustacyanin. We discuss the origin of the shift and propose that it is caused by two major effects: conformational changes of astaxanthin molecules (increase in effective conjugation length) together with increased charge-transfer character of the S-2 state. We put the bathochromic shift in the broad perspective of other "blue" carotenoids properties.
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5.
  • Jankowski, V, et al. (författare)
  • Detection of angiotensin II in supernatants of stimulated mononuclear leukocytes by MALDI-TOF-TOF-mass spectrometric analysis
  • 2005
  • Ingår i: Hypertension. - 1524-4563. ; 46:3, s. 591-597
  • Tidskriftsartikel (refereegranskat)abstract
    • Angiotensin II ( Ang II) is the major vasoactive component of the renin- angiotensin system. Several components of the renin- angiotensin system have been demonstrated in different tissues. Whereas the roles of tissue and renal renin- angiotensin system have been studied in detail, much less is known on whether the corpuscular elements of circulating blood contribute to Ang II production. Here we examined whether, in addition to vasculature, blood cells also contribute to the circulating Ang II levels. Mononuclear leukocytes were obtained from healthy subjects and were incubated. The resulting supernatant was chromatographed using different chromatographic methods. The vasoconstrictive effects of aliquots of the resulting fractions were tested. Each fraction with a vasoconstrictive effect was analyzed by mass spectrometry. In one fraction with a strong vasoconstrictive effect, Ang II was identified. Mononuclear lymphocytes produced Ang II in amounts sufficient to stimulate Ang II type 1 receptors. Moreover, in mononuclear leukocytes, renin as well as angiotensin- converting enzyme mRNA expression was detectable by RT- PCR. These findings demonstrate that mononuclear leukocytes are a source of Ang II. Ang II secretion by these cells may play a significant role in humoral vascular regulation. In conclusion, the isolation of Ang II in supernatants of mononuclear leukocytes adds a further physiological source of Ang II to the current view of angiotensin metabolism. The quantitative role of lymphocyte- derived Ang II secretion compared with the other sources of Ang II should be defined further, but the release found under the present conditions is at least sufficient to elicit vasoconstrictive effects
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6.
  • Liska, F, et al. (författare)
  • Chromosome assignment of Cd36 transgenes in two rat SHR lines by FISH and linkage mapping of transgenic insert in the SHR-TG19 line.
  • 2002
  • Ingår i: Folia biologica. - 0015-5500. ; 48:4, s. 139-44
  • Tidskriftsartikel (refereegranskat)abstract
    • The chromosome position of the Cd36 insert was determined by FISH in two rat transgenic lines (SHR/Ola-TgN(EF1aCd36)10Ipcv (SHR-TG10) and SHR/Ola-TgN(EF1aCd36)19Ipcv (SHR-TG19). The Cd36 transgene construct labelled with digoxigenin-11-dNTP was used as a probe in the FISH analysis. In accord with the previous finding that the SHR-TG10 harbours 6-8 copies of the transgene, the signals from both metaphase and interphase nuclei of SHR-TG10 preparations were rather strong and the probe hybridized to both copies of chromosome 1 at band q55. The probe hybridization to SHR-TG19 metaphase preparations also showed homozygosity of the transgene with localization of both copies to chromosome 11 at band q11. The signals were distinct but much weaker compared to the SHR-TG10, which again is in accord with the fact that the SHR-TG19 line harbours only a single copy of the transgene. In order to look for a possible impact of the insertion site neighbourhood upon the transgene phenotypic effect, we performed linkage mapping of the transgene in the SHR-TG19 line. By linkage mapping, the placement of the transgene to the proximal part of RNO11 was confirmed, the critical interval being 4 cM between D11Rat20 and D11Rat21, in good agreement with the RH map. Within the close neighbourhood of the inserted Cd36 transgene, there are several genes known to be expressed in kidney, and so the influence of some regulatory sequences enhancing kidney expression of the Cd36 transgene can be envisaged.
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