Sentences with phrase «donor cell age»
Passaging the iPSCs gradually erased those donor cell age - related epigenetic differences, the team found.
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The team also tested nanoparticle absorption for other kinds of human cells, including fibroblasts from donors of older ages and found significant differences.
They received either a saline placebo or plasma — blood from which the red cells have been removed — from blood donors aged 18 — 30.
«We studied human T cells, isolated from blood donors of all ages, to compare mature cytotoxic T cells with naive ones,» said Philip Ansumana Hull, graduate student in Ott's lab and one of the first authors of the study.
In addition, recipients of red blood cells from donors aged 20 - 30 were associated with a six percent increased risk of death per transfused product compared with recipients of red blood cells from donors aged 40 - 50.
Recipients of blood from donors aged 17 - 20 were associated with an eight percent increased risk of death per unit transfused compared with recipients of red blood cells from donors aged 40 - 50.
Inhibition of cell division is also more pronounced with donor age [8].
It is also pointed out that donor age (beyond 45 years in the alkaline phosphatase - linked BrdU assays) may also have limited the human wounding response (cell division) in the corneal periphery.
Would her cells show the age of the donor or of a newborn?
Mehta J, Gordon LI, Tallman MS, et al., Does younger donor age affect the outcome of reduced - intensity allogeneic hematopoietic stem cell transplantation for hematologic malignancies beneficially?
To find out, the researchers examined methylation patterns in iPSCs derived from the peripheral blood mononuclear cells of 16 donors, ages 21 to 100.
Overall, the number of iPSC mutations — which the researchers suspect were present but undetected in donor blood cells — increased linearly with donor age.
V. Lo Sardo et al., «Influence of donor age on induced pluripotent stem cells,» Nature Biotechnology, doi: 10.1038 / nbt.3749, 2016.
In order to study rescue effects following surgery, donor cells were introduced at P21, an age preceding major onset of photoreceptor loss.
To study the effect of ageing on the ability of CMV - specific CD8 (+) T cells to produce type 1 - and type 2 - cytokines, interferon - gamma - and IL -10-producing, CD8 (+) T cell responses in the presence of CMV peptide antigen were measured in CMV - seropositive old and young donors.
We have examined CD8 T cell responses to two persistent herpesvirus infections, CMV and EBV, and to a recurrent virus infection, influenza, in different age cohorts of healthy donors using HLA - peptide tetramers and intracellular cytokine detection.
Upon transfer of aged donor CD4 T cells to young hosts, there was significantly reduced expansion and germinal center (GC) differentiation of the antigen - specific B cell population after immunization.
The present study employed Ighb scid mice reconstituted with normal lymphocytes from young (2 -3-mo-old) and aged (20 -25-mo-old) donors and immunized with a protein conjugate of the hapten (4 - hydroxy -3-nitrophenyl) acetyl (NP) to determine whether the molecular changes in antibody repertoire reflect senescence in the B cells or whether they are mediated by the aging helper T lymphocytes.
When T cells were donated by young mice, the anti-NP response in GC was dominated by the canonical V186.2 gene, even if the responder B cells came from aged donors.
To examine the effect of age on the cognate function of CD4 T cells, we have used a novel adoptive transfer model that allows us to compare identical numbers of antigen - specific naive T cells from young and aged TCR transgenic (Tg) donors.
However, when the mice were reconstituted with T cells from aged donors, the expression of the V186.2 gene by young B cells was diminished and the response was dominated by the C1H4 gene, another member of the V186.2 / V3 family.
The team conducted tests on three different samples of cells aged in different ways: cells taken from aged donors, cells aged in culture in the lab, and those isolated from patients suffering from Hutchinson - Gilford progeria syndrome, a rare genetic disorder that ages sufferers at an accelerated rate.