| 1. |
- Koptyug, Andrey, 1956-, et al.
(author)
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Spin-locking in concentration-narrowed OD ESR spectra
- 1989
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In: Chemical Physics. - Amsterdam : Elsevier. - 0301-0104 .- 1873-4421. ; 138:1, s. 173-178
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Journal article (peer-reviewed)abstract
- The effect of spin- locking under the action of a resonance rf field of large amplitude has been observed in the optically detected ESR spectra (OD ESR) of radical-ion pairs both in strong and weak magnetic fields. "Hampering" of singlet-tgriplet transitions occurs for concentrations of aromatic acceptors in non polar solutions at room temperature from 10e-4 to 1 M. It is proposed that in spite of strong concentration narrowing OD ESR signals are inhomogeneously broadened. This can be due to neutral molecule- radical-anion aggregate formation.
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| 2. |
- Korhonen, Emilia A., et al.
(author)
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Lymphangiogenesis requires Ang2/Tie/PI3K signaling for VEGFR3 cell-surface expression
- 2022
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In: Journal of Clinical Investigation. - : American Society for Clinical Investigation. - 0021-9738 .- 1558-8238. ; 132:15
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Journal article (peer-reviewed)abstract
- Vascular endothelial growth factor C (VEGF-C) induces lymphangiogenesis via VEGF receptor 3 (VEGFR3), which is encoded by the most frequently mutated gene in human primary lymphedema. Angiopoietins (Angs) and their Tie receptors regulate lymphatic vessel development, and mutations of the ANGPT2 gene were recently found in human primary lymphedema. However, the mechanistic basis of Ang2 activity in lymphangiogenesis is not fully understood. Here, we used gene deletion, blocking Abs, transgene induction, and gene transfer to study how Ang2, its Tie2 receptor, and Tie1 regulate lymphatic vessels. We discovered that VEGF-C???induced Ang2 secretion from lymphatic endothelial cells (LECs) was involved in full Akt activation downstream of phosphoinositide 3 kinase (PI3K). Neonatal deletion of genes encoding the Tie receptors or Ang2 in LECs, or administration of an Ang2-blocking Ab decreased VEGFR3 presentation on LECs and inhibited lymphangiogenesis. A similar effect was observed in LECs upon deletion of the PI3K catalytic p110?? subunit or with small -molecule inhibition of a constitutively active PI3K located downstream of Ang2. Deletion of Tie receptors or blockade of Ang2 decreased VEGF-C???induced lymphangiogenesis also in adult mice. Our results reveal an important crosstalk between the VEGF-C and Ang signaling pathways and suggest new avenues for therapeutic manipulation of lymphangiogenesis by targeting Ang2/Tie/PI3K signaling.
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| 3. |
- Muhl, Lars, et al.
(author)
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The SARS-CoV-2 receptor ACE2 is expressed in mouse pericytes but not endothelial cells : Implications for COVID-19 vascular research
- 2022
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In: Stem Cell Reports. - : Elsevier. - 2213-6711. ; 17:5, s. 1089-1104
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Journal article (peer-reviewed)abstract
- Humanized mouse models and mouse-adapted SARS-CoV-2 virus are increasingly used to study COVID-19 pathogenesis, so it is impor-tant to learn where the SARS-CoV-2 receptor ACE2 is expressed. Here we mapped ACE2 expression during mouse postnatal development and in adulthood. Pericytes in the CNS, heart, and pancreas express ACE2 strongly, as do perineurial and adrenal fibroblasts, whereas endothelial cells do not at any location analyzed. In a number of other organs, pericytes do not express ACE2, including in the lung where ACE2 instead is expressed in bronchial epithelium and alveolar type II cells. The onset of ACE2 expression is organ specific: in bronchial epithelium already at birth, in brain pericytes before, andin heart pericytes after postnatal day 10.5. Establishing the vascular localization of ACE2 expression is central to correctly interpret data from modeling COVID-19 in the mouse and may shed light on the cause of vascular COVID-19 complications.
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| 4. |
- Nilsson, Ingrid, et al.
(author)
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VEGF receptor 2/-3 heterodimers detected in situ by proximity ligation on angiogenic sprouts
- 2010
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In: EMBO Journal. - : Wiley. - 0261-4189 .- 1460-2075. ; 29:8, s. 1377-1388
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Journal article (peer-reviewed)abstract
- The vascular endothelial growth factors VEGFA and VEGFC are crucial regulators of vascular development. They exert their effects by dimerization and activation of the cognate receptors VEGFR2 and VEGFR3. Here, we have used in situ proximity ligation to detect receptor complexes in intact endothelial cells. We show that both VEGFA and VEGFC potently induce formation of VEGFR2/-3 heterodimers. Receptor heterodimers were found in both developing blood vessels and immature lymphatic structures in embryoid bodies. We present evidence that heterodimers frequently localize to tip cell filopodia. Interestingly, in the presence of VEGFC, heterodimers were enriched in the leading tip cells as compared with trailing stalk cells of growing sprouts. Neutralization of VEGFR3 to prevent heterodimer formation in response to VEGFA decreased the extent of angiogenic sprouting. We conclude that VEGFR2/-3 heterodimers on angiogenic sprouts induced by VEGFA or VEGFC may serve to positively regulate angiogenic sprouting.
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| 5. |
- Nowak-Sliwinska, Patrycja, et al.
(author)
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Consensus guidelines for the use and interpretation of angiogenesis assays
- 2018
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In: Angiogenesis. - : Springer. - 0969-6970 .- 1573-7209. ; 21:3, s. 425-532
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Research review (peer-reviewed)abstract
- The formation of new blood vessels, or angiogenesis, is a complex process that plays important roles in growth and development, tissue and organ regeneration, as well as numerous pathological conditions. Angiogenesis undergoes multiple discrete steps that can be individually evaluated and quantified by a large number of bioassays. These independent assessments hold advantages but also have limitations. This article describes in vivo, ex vivo, and in vitro bioassays that are available for the evaluation of angiogenesis and highlights critical aspects that are relevant for their execution and proper interpretation. As such, this collaborative work is the first edition of consensus guidelines on angiogenesis bioassays to serve for current and future reference.
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| 6. |
- Sauge, Sebastien, et al.
(author)
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Controlling an actively-quenched single photon detector with bright light
- 2011
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In: Optics Express. - 1094-4087. ; 19:23, s. 23590-23600
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Journal article (peer-reviewed)abstract
- We control using bright light an actively-quenched avalanche single-photon detector. Actively-quenched detectors are commonly used for quantum key distribution (QKD) in the visible and near-infrared range. This study shows that these detectors are controllable by the same attack used to hack passively-quenched and gated detectors. This demonstrates the generality of our attack and its possible applicability to eavsdropping the full secret key of all QKD systems using avalanche photodiodes (APDs). Moreover, the commercial detector model we tested (Perkin-Elmer SPCM-AQR) exhibits two new blinding mechanisms in addition to the previously observed thermal blinding of the APD, namely: malfunctioning of the bias voltage control circuit, and overload of the DC/DC converter biasing the APD. These two new technical loopholes found just in one detector model suggest that this problem must be solved in general, by incorporating generally imperfect detectors into the security proof for QKD.
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| 7. |
- Yao, Li-Chin, et al.
(author)
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Pulmonary Lymphangiectasia Resulting From Vascular Endothelial Growth Factor-C Overexpression During a Critical Period
- 2014
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In: Circulation Research. - 0009-7330 .- 1524-4571. ; 114:5, s. 806-822
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Journal article (peer-reviewed)abstract
- Rationale: Lymphatic vessels in the respiratory tract normally mature into a functional network during the neonatal period, but under some pathological conditions they can grow as enlarged, dilated sacs that result in the potentially lethal condition of pulmonary lymphangiectasia. Objective: We sought to determine whether overexpression of the lymphangiogenic growth factor (vascular endothelial growth factor-C [VEGF-C]) can promote lymphatic growth and maturation in the respiratory tract. Unexpectedly, perinatal overexpression of VEGF-C in the respiratory epithelium led to a condition resembling human pulmonary lymphangiectasia, a life-threatening disorder of the newborn characterized by respiratory distress and the presence of widely dilated lymphatics. Methods and Results: Administration of doxycycline to Clara cell secretory protein-reverse tetracycline-controlled transactivator/tetracycline operator-VEGF-C double-transgenic mice during a critical period from embryonic day 15.5 to postnatal day 14 was accompanied by respiratory distress, chylothorax, pulmonary lymphangiectasia, and high mortality. Enlarged sac-like lymphatics were abundant near major airways, pulmonary vessels, and visceral pleura. Side-by-side comparison revealed morphological features similar to pulmonary lymphangiectasia in humans. The condition was milder in mice given doxycycline after age postnatal day 14 and did not develop after postnatal day 35. Mechanistic studies revealed that VEGF recptor (VEGFR)-3 alone drove lymphatic growth in adult mice, but both VEGFR-2 and VEGFR-3 were required for the development of lymphangiectasia in neonates. VEGFR-2/VEGFR-3 heterodimers were more abundant in the dilated lymphatics, consistent with the involvement of both receptors. Despite the dependence of lymphangiectasia on VEGFR-2 and VEGFR-3, the condition was not reversed by blocking both receptors together or by withdrawing VEGF-C. Conclusions: The findings indicate that VEGF-C overexpression can induce pulmonary lymphangiectasia during a critical period in perinatal development.
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