aboutsummaryrefslogtreecommitdiff
path: root/gnqa/paper2_eval/data/dataset/gpt4o/intermediate_files/gpt4o_de_aging_19
blob: 82e1f47c01af7c47898b9a265e971d054a5e1f15 (plain)
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
{
  "titles": [
    "2008 - GENETIC REGULATION OF HEMATOPOIETIC STEM CELL AGING (3).pdf",
    "2011 - Genome-wide promoter DNA methylation dynamics of human hematopoietic.pdf",
    "2009 - Aging and Replicative Senescence Have Related Effects.pdf",
    "2010 - Age-related molecular genetic changes of murine.pdf",
    "2007 - Aging Hematopoietic Stem Cells Decline in Function and Exhibit Epigenetic Dysregulation.pdf",
    "2009 - Aging and Replicative Senescence Have Related Effects.pdf",
    "2013 - Age-associated epigenetic drift implications.pdf",
    "2007 - Two faces of p53 aging and tumor suppression.pdf",
    "2013 - Effects_of_age_and_strain_on_cell_prolif.pdf",
    "2010 - Age-related molecular genetic changes of murine.pdf"
  ],
  "extraction_id": [
    "fca849bb-6e08-5200-8c66-5250e902dca3",
    "3be2a7fa-1d97-5280-ba37-cc3d311cfb75",
    "f5b29cc7-fe8b-5230-adb1-0531fb1c3187",
    "d39327b0-59b1-5e24-813d-099a48a8de85",
    "188bdad0-f63b-5e4c-8eed-73cd01b8d66f",
    "23921b67-8911-5086-a2e4-a909394a6df4",
    "24500f0a-0e60-574e-9039-e9dd3b5be569",
    "270c5516-f5b2-54d3-8865-b84d8a9506c1",
    "b0fb2185-a2ee-5174-94d0-877ad2d87158",
    "d39327b0-59b1-5e24-813d-099a48a8de85"
  ],
  "document_id": [
    "7412a162-ee3b-5f09-9886-8e9172dd3ee8",
    "30081f4e-7189-5c9f-abf2-895250c0173e",
    "0703ba80-b7a5-5873-9ab0-5d66d57f4750",
    "a69ce6db-4a5e-58a5-9dc5-d529768edcb1",
    "a6fabf0c-e4a5-59f6-82c5-ebabce24fd0a",
    "0703ba80-b7a5-5873-9ab0-5d66d57f4750",
    "8513121f-71f3-5bb0-9433-feece9fd9fbc",
    "b1ef905a-c145-5270-9110-ae6954ea3d72",
    "d7e861e7-cdee-5145-9403-ef05e2d532c0",
    "a69ce6db-4a5e-58a5-9dc5-d529768edcb1"
  ],
  "id": [
    "chatcmpl-AIHYWWczI6kl71Lbbg4Wx4xLfOmE6",
    "cade861a-f60d-51fd-bfac-edce8860b395",
    "7fcd630b-0f09-5947-8a28-f72d4418d8f8",
    "8f53ce05-7527-52f2-8a25-9c3ee9a38861",
    "ccf7dace-b7d8-576f-bb59-c6707e5180f5",
    "f8e0e878-451b-519d-b6e5-e9834d5d3b77",
    "de67cf90-712a-5c28-9f6b-404d84a06d22",
    "e6bb4c40-7fe8-5ff7-af36-1c2b749ed1fb",
    "01740a78-e141-56f0-8f34-7c02c5602344",
    "ae2ad88f-6e02-5541-b6be-966fef7712f1",
    "1dffbbdb-f76d-581b-8384-751ce5f41e90"
  ],
  "contexts": [
    "into old versus young recipients (Liang et al., 2005 ).  Further experiments demonstrated that the muscle stem cell niche adversely effects stem cell function as evidenced by the restoration of old stem cell regenerative potential upon  expos ure to a young systemic microenvironment (Conboy et al., 2005; Conboy and Rando, 2005).  It has also been reported that the spermatogoni al stem cell niche deteriorates with age, causing the failure to suppor t an appropriate balance between stem cell self-renewal and",
    "matopoietic stem cells is regulated by the stemcell niche. Exp Gerontol. 2008;43(11):974-980. 18. Geiger H, Rudolph KL. Aging in the lympho- hematopoietic stem cell compartment. Trends Immunol. 2009;30(7):360-365. 19. Muller-Sieburg C, Sieburg HB. Stem cell aging: survival of the laziest? Cell Cycle. 2008;7(24): 3798-3804. 20. Beerman I, Maloney WJ, Weissmann IL, Rossi DJ. Stem cells and the aging hematopoieticsystem. Curr Opin Immunol. 2010;22(4):500-506. 21. Teschendorff AE, Menon U, Gentry-Maharaj A,",
    "Abstract The regenerative potential diminishes with age and this has been ascribed to functional impairments of adult stem cells. Cells in culture undergo senescence after a certain number of cell divisions whereby the cells enlarge and finally stop proliferation. This observation of replicative senescence has been extrapolated to somatic stem cells in vivo and might",
    "Because of their plasticity and accessibility these cells are also prime candidates for regenerative medicine. The  contribution of stem cell aging to organismal aging is un der debate and one theory is that reparative processes  deteriorate as a consequence of stem cell aging and/or de crease in number. Age has been linked with changes in  osteogenic and adipogen ic potential of MSCs. Results: Here we report on changes in global gene expression of cultured MSCs isolated from the bone marrow of",
    "suggesting that stem cells are not likely to be a factor limiting hematopoietic regeneration with age. However, their func-tional decits do show that HSCs are impacted by the forces of aging in a manner similar to that of differentiated cells [3134]. In our molecular analysis, we identied global age-related changes in gene expression in murine HSCs, with a view to identifying mechanisms that could be responsible for these age-associated declines in HSC function. Genes involved in",
    "Discussion The deterioration of the regenerative potential upon aging might be due to functional changes in adult stem cells. To test this hypothesis we have investigated differential gene expression in primary, human MSC and HPC derived from different agegroups. In this study, we demonstrate for the first time age-related gene expression changes in human MSC and HPC and that there",
    "cells, which may explain the observed decline of stem cell function with age. Age-associated increases inDNAm target developmental genes, overlapping those associated with environmental disease risk factors and with disease itself, notably cancer. In particular, cancers and precursor cancer lesions exhibit aggravated",
    "tion associated with age: loss of stem cell pool division potential (loss of regenerative capacity) and loss ofdierentiated somatic cell function, which directly leads to loss of organ function. Loss of dierentiated somatic cell function can additionally indirectly aect adult stem and progenitor cells by altering the tissue microenviron- ment that is essential for stem cell support (the stem cellniche). In general, loss of stem cell pool division potential",
    "1. Introduction Stem cell aging is regarded as one of the contributors to several degenerative conditions af icting the elderly because it underlies the physiological decline in tissue maintenance and regenerative capacity of many organs ( Rossi et al., 2008 ). The brain is one such organ that contains discrete populations of stem cells and their precursors (collectively referred to as neural progenitor cells [NPCs]) that continue to generate new neurons throughout life",
    "spective of tissue regeneration and repair because there isevidence that these beneficial functions may becomehandicapped with age. Age-related decline in the numberof MSCs in the bone marrows of rodents, monkeys, andhumans have been reported [26-33]. Most studies to datefocused on the effects of aging on the ability of MSCs toenter osteogenic, chondrogenic and adipogenic pro-grams. Some, but not all studies suggest that agingreduces osteogenesis and chondrogenesis while enhanc-"
  ],
  "answer": "Age-related shifts in stem cell niche composition and function have significant implications for tissue regeneration capacity. As individuals age, the stem cell niche, which is crucial for maintaining stem cell function, undergoes changes that can adversely affect the regenerative potential of stem cells. Here are some key implications based on the provided context:  1. **Deterioration of the Stem Cell Niche**: The aging process leads to the deterioration of the stem cell niche, which can result in a failure to support the balance between stem cell self-renewal and differentiation. This is evident in the spermatogonial stem cell niche, which deteriorates with age, affecting its ability to maintain stem cell function [1].  2. **Functional Impairments of Stem Cells**: The regenerative potential diminishes with age due to functional impairments in adult stem cells. This is linked to the phenomenon of replicative senescence, where cells lose their ability to proliferate after a certain number of divisions [3].  3. **Changes in Gene Expression**: Age-related changes in gene expression have been observed in stem cells, such as mesenchymal stem cells (MSCs) and hematopoietic progenitor cells (HPCs). These changes can lead to declines in stem cell function and, consequently, a reduction in tissue regeneration capacity [6].  4. **Loss of Stem Cell Pool Division Potential**: Aging is associated with a loss of stem cell pool division potential, which directly impacts the regenerative capacity of tissues. This loss can also indirectly affect adult stem and progenitor cells by altering the tissue microenvironment essential for stem cell support [8].  5. **Reduction in Stem Cell Numbers**: There is evidence of a decline in the number of MSCs in the bone marrow with age, which can further hinder the ability of these cells to participate in tissue regeneration processes such as osteogenesis and chondrogenesis [10].  Overall, these age-related shifts in stem cell niche composition and function contribute to a decline in the body's ability to repair and regenerate tissues, which is a hallmark of aging and is linked to various degenerative conditions [9].",
  "question": "What are the implications of age-related shifts in stem cell niche composition and function for tissue regeneration capacity?"
}