| 1. |
|
|
| 2. |
- Maeda, Y., et al.
(författare)
-
Differential cross section and analyzing power measurements for (n)over-right-arrowd elastic scattering at 248 MeV
- 2007
-
Ingår i: Physical Review C. Nuclear Physics. - 0556-2813 .- 1089-490X. ; 76:1, s. 014004-
-
Tidskriftsartikel (refereegranskat)abstract
- The differential cross sections and vector analyzing powers for nd elastic scattering at E-n=248 MeV were measured for 10 degrees-180 degrees in the center-of-mass (c.m.) system. To cover the wide angular range, the experiments were performed separately by using two different setups for forward and backward angles. The data are compared with theoretical results based on Faddeev calculations with realistic nucleon-nucleon (NN) forces such as AV18, CD Bonn, and Nijmegen I and II, and their combinations with the three-nucleon forces (3NFs), such as Tucson-Melbourne 99 (TM99), Urbana IX, and the coupled-channel potential with Delta-isobar excitation. Large discrepancies are found between the experimental cross sections and theory with only 2N forces for theta(c.m.)>90 degrees. The inclusion of 3NFs brings the theoretical cross sections closer to the data but only partially explains this discrepancy. For the analyzing power, no significant improvement is found when 3NFs are included. Relativistic corrections are shown to be small for both the cross sections and the analyzing powers at this energy. For the cross sections, these effects are mostly seen in the very backward angles. Compared with the pd cross section data, quite significant differences are observed at all scattering angles that cannot be explained only by the Coulomb interaction, which is usually significant at small angles.
|
|
| 3. |
- Aoyama, K., et al.
(författare)
-
Cleavage of integrin by mu-calpain during hypoxia in human endometrial cells
- 2004
-
Ingår i: Am J Reprod Immunol. - 1046-7408. ; 52:6, s. 362-9
-
Tidskriftsartikel (refereegranskat)abstract
- PROBLEM: The distribution and activation of mu-calpain and possible cleavage of integrin in human endometrial cells under hypoxic condition were investigated. METHOD OF STUDY: Human endometrial epithelial and stromal cells were subjected to hypoxia, and subsequently used for immunostaining and western blot analysis. RESULTS: The proform of mu-calpain was detected in the cytoplasm of normal cells, and displayed a substantial decrease after hypoxia. Conversely, the active form of mu-calpain was not detected in normal cells, but was abundant after hypoxia. The cytoplasmic domain of integrin beta3 was also detected in the cytoplasm of endometrial cells. Western blot analysis confirmed that both the proform of mu-calpain and the integrin beta3 cytoplasmic domain decreased during hypoxia. CONCLUSIONS: Mu-calpain is activated in human endometrial cells during hypoxia and that subsequent cleavage of the integrin beta3 cytoplasmic domain may give some adverse effects to the function of human endometrium.
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
- Zhou, K., et al.
(författare)
-
An overlooked subset of Cx3cr1(wt/wt) microglia in the Cx3cr1(CreER-Eyfp/wt) mouse has a repopulation advantage over Cx3cr1(CreER-Eyfp/wt) microglia following microglial depletion
- 2022
-
Ingår i: Journal of Neuroinflammation. - : Springer Science and Business Media LLC. - 1742-2094. ; 19:1
-
Tidskriftsartikel (refereegranskat)abstract
- Background Fluorescent reporter labeling and promoter-driven Cre-recombinant technologies have facilitated cellular investigations of physiological and pathological processes, including the widespread use of the Cx3cr1(CreER-Eyfp/wt) mouse strain for studies of microglia. Methods Immunohistochemistry, Flow Cytometry, RNA sequencing and whole-genome sequencing were used to identify the subpopulation of microglia in Cx3cr1(CreER-Eyfp/wt) mouse brains. Genetically mediated microglia depletion using Cx3cr1(CreER-Eyfp/wt)Rosa26(DTA/wt) mice and CSF1 receptor inhibitor PLX3397 were used to deplete microglia. Primary microglia proliferation and migration assay were used for in vitro studies. Results We unexpectedly identified a subpopulation of microglia devoid of genetic modification, exhibiting higher Cx3cr1 and CX3CR1 expression than Cx3cr1(CreER-Eyfp/wt)Cre(+)Eyfp(+) microglia in Cx3cr1(CreER-Eyfp/wt) mouse brains, thus termed Cx3cr1(high)Cre(-)Eyfp(-) microglia. This subpopulation constituted less than 1% of all microglia under homeostatic conditions, but after Cre-driven DTA-mediated microglial depletion, Cx3cr1(high)Cre(-)Eyfp(-) microglia escaped depletion and proliferated extensively, eventually occupying one-third of the total microglial pool. We further demonstrated that the Cx3cr1(high)Cre(-)Eyfp(-) microglia had lost their genetic heterozygosity and become homozygous for wild-type Cx3cr1. Therefore, Cx3cr1(high)Cre(-)Eyfp(-) microglia are Cx3cr1(wt/wt)Cre(-)Eyfp(-). Finally, we demonstrated that CX3CL1-CX3CR1 signaling regulates microglial repopulation both in vivo and in vitro. Conclusions Our results raise a cautionary note regarding the use of Cx3cr1(CreER-Eyfp/wt) mouse strains, particularly when interpreting the results of fate mapping, and microglial depletion and repopulation studies.
|
|
| 7. |
- Jaderstrom, H., et al.
(författare)
-
200 and 300 MeV/nucleon nuclear reactions responsible for single-event effects in microelectronics
- 2008
-
Ingår i: Physical Review C. Nuclear Physics. - 0556-2813 .- 1089-490X. ; 77:4, s. 44601-
-
Tidskriftsartikel (refereegranskat)abstract
- An experimental study of nuclear reactions between Si-28 nuclei at 200 and 300 MeV/nucleon and hydrogen or deuterium target nuclei was performed at the CELSIUS storage ring in Uppsala, Sweden, to collect information about the reactions responsible for single-event effects in microelectronics. Inclusive data on Si-28 fragmentation, as well as data on correlations between recoils and spectator protons or alpha particles are compared to predictions from the Dubna cascade model and the Japan Atomic Energy Research Institute version of the quantum molecular dynamics model. The comparison shows satisfactory agreement for inclusive data except for He fragments where low-energy sub-barrier fragments and recoiling fragments with very large momenta are produced much more frequently than predicted. The yield of exclusive data are also severely underestimated by the models whereas the charge distributions of recoils in these correlations compare well. The observed enhancement in He emission, which may well be important for the description of single-event effects, is most likely to be attributed to alpha clustering in Si-28 nuclei.
|
|
| 8. |
|
|
| 9. |
- Ringbom, A, et al.
(författare)
-
The B-10,B-11(n, p)Be-10,Be-11 reactions at E-n=96 MeV
- 2001
-
Ingår i: NUCLEAR PHYSICS A. - : ELSEVIER SCIENCE BV. - 0375-9474. ; 679:3-4, s. 231-250
-
Tidskriftsartikel (refereegranskat)abstract
- Double-differential cross sections of the B-10,B-11(n,p)Be-10,Be-11 reactions have been measured at 96 MeV in the angular range 0 degrees -30 degrees for excitation energies up to 35 MeV. The spectra have been decomposed into different multipolarities usi
|
|
| 10. |
- Saliba-Gustafsson, P., et al.
(författare)
-
Subclinical atherosclerosis and its progression are modulated by PLIN2 through a feed-forward loop between LXR and autophagy
- 2019
-
Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 286:6, s. 660-675
-
Tidskriftsartikel (refereegranskat)abstract
- Background Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin-2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development. Objective We sought to delineate putative beneficial effects of the Pro251 variant of perlipin-2 on subclinical atherosclerosis and the mechanism by which it acts. Methods A pan-European cohort of high-risk individuals where carotid intima-media thickness has been assessed was adopted. Human primary monocyte-derived macrophages were prepared from whole blood from individuals recruited by perilipin-2 genotype or from buffy coats from the Karolinska University hospital blood central. Results The Pro251 variant of perilipin-2 is associated with decreased intima-media thickness at baseline and over 30 months of follow-up. Using human primary monocyte-derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver-X-receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed-forward loop, regulated by CYP27A1 and 27OH-cholesterol. Conclusions For the first time, we show that perilipin-2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin-2 modulates levels of the LXR ligand 27OH-cholesterol and initiates a feed-forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin-2 exerts its beneficial effects on subclinical atherosclerosis.
|
|
