This paper offers a life-course stress process perspective on maternal role strain as a 'pain of imprisonment' by engaging the concept of 'family complexity' in the context of mass incarceration I consider how the living arrangements of minor siblings (i.e., those living apart or together) during maternal incarceration functions as a form of family complexity. When minor children live apart from their siblings, they may experience more isolation which may further serve as a stressor for incarcerated mothers. A positive association between siblings living apart and maternal role strain would support a process of 'stress proliferation' across the prison-family interface. I investigate these connections using survey-based data on mothers with multiple minor children (n = 80) collected in 2011 from a voluntary sample of respondents housed in a federal minimum security prison in the United States. Multivariate logistic regression results indicate that minor siblings living apart during periods of maternal confinement elevates role strain among mothers (odds ratio = 3.66, p < 0.05). This connection is indicative of an 'inter-institutional strain.' Finally, children's age also increases maternal role strain, but this finding is explained by sibling living arrangements during the mother's incarceration.
The US prison boom has resulted in the mass incarceration of parents in the United States. We review recent scholarship on the relationship between parental incarceration and child inequality and social exclusion over the life course. We develop a multilevel social exclusion framework to stimulate future research on the effects of paternal and maternal incarceration. This framework is intergenerational in its focus on incarcerated parents and their children, interinstitutional in its attention to state and school regimes, and intersectional in its consideration of the role of gender and race and ethnic contingencies. It is also systemic in its focus on multiple chosen and overlapping institutional policy domains of exclusion. We address both mediators and moderators of the effects of parental incarceration on child outcomes. We emphasize the underresearched importance of meso-level (e.g., school) and macro-level (e.g., state and cross-national) exclusionary and inclusionary regimes in understanding the effects of parental incarceration. We propose hypotheses to synthesize current research on the impact of maternal and paternal incarceration on children.
The authors discuss social selection, stigmatization, and socialization/strain theoretical explanations for the intergenerational influences of parental incarceration on their children. Results with national survey data reveal that net of selection factors, paternal imprisonment decreases the educational attainment of children in emerging adulthood. While this pattern is found across race/ethnicity, the results in combination with disproportionate minority confinement suggest that parental incarceration is a mechanism of social exclusion of these groups. With data on Texas prisoners, the authors further find that about two-thirds of Hispanic fathers and about half of African American and Anglo fathers expect to live with their children and families when they return to their communities. This last finding suggests a broad foundation across racial/ethnic groups for the investment of resources in supporting the rehabilitation and reunification of these prospective families, for the welfare of the children, their parents, and the communities in which they live.
The authors discuss social selection, stigmatization, and socialization/strain theoretical explanations for the intergenerational influences of parental incarceration on their children. Results with national survey data reveal that net of selection factors, paternal imprisonment decreases the educational attainment of children in emerging adulthood. While this pattern is found across race/ethnicity, the results in combination with disproportionate minority confinement suggest that parental incarceration is a mechanism of social exclusion of these groups. With data on Texas prisoners, the authors further find that about two-thirds of Hispanic fathers and about half of African American and Anglo fathers expect to live with their children and families when they return to their communities. This last finding suggests a broad foundation across racial/ethnic groups for the investment of resources in supporting the rehabilitation and reunification of these prospective families, for the welfare of the children, their parents, and the communities in which they live. [Reprinted by permission of Sage Publications Inc., copyright The American Academy of Political and Social Science.]
Platelet transfusions are a key treatment option for a range of life threatening conditions including cancer, chemotherapy and surgery. Efficient ex vivo systems to generate donor independent platelets in clinically relevant numbers could provide a useful substitute. Large quantities of megakaryocytes (MKs) can be produced from human pluripotent stem cells, but in 2D culture the ratio of platelets harvested from MK cells has been limited and restricts production rate. The development of biomaterial cell supports that replicate vital hematopoietic micro-environment cues are one strategy that may increase in vitro platelet production rates from iPS derived Megakaryocyte cells. In this paper, we present the results obtained generating, simulating and using a novel structurally-graded collagen scaffold within a flow bioreactor system seeded with programmed stem cells. Theoretical analysis of porosity using micro-computed tomography analysis and synthetic micro-particle filtration provided a predictive tool to tailor cell distribution throughout the material. When used with MK programmed stem cells the graded scaffolds influenced cell location while maintaining the ability to continuously release metabolically active CD41 + CD42 + functional platelets. This scaffold design and novel fabrication technique offers a significant advance in understanding the influence of scaffold architectures on cell seeding, retention and platelet production. ; This work was supported by the European Research Council [ERC Advanced Grant 320598 3D-E], EPSRC grant EP/N019938/1 and grants from the NHS Blood and Transplant, the Medical Research Council (MR/L022982/1) and the European Union (SilkFusion: AMD-767309-3).
Hematopoietic stem cells (HSCs) residing in the bone marrow (BM) accumulate during aging but are functionally impaired. However, the role of HSC-intrinsic and -extrinsic aging mechanisms remains debated. Megakaryocytes promote quiescence of neighboring HSCs. Nonetheless, whether megakaryocyte-HSC interactions change during pathological/natural aging is unclear. Premature aging in Hutchinson-Gilford progeria syndrome recapitulates physiological aging features, but whether these arise from altered stem or niche cells is unknown. Here, we show that the BM microenvironment promotes myelopoiesis in premature/physiological aging. During physiological aging, HSC-supporting niches decrease near bone but expand further from bone. Increased BM noradrenergic innervation promotes β2-adrenergic-receptor(AR)-interleukin-6-dependent megakaryopoiesis. Reduced β3-AR-Nos1 activity correlates with decreased endosteal niches and megakaryocyte apposition to sinusoids. However, chronic treatment of progeroid mice with β3-AR agonist decreases premature myeloid and HSC expansion and restores the proximal association of HSCs to megakaryocytes. Therefore, normal/premature aging of BM niches promotes myeloid expansion and can be improved by targeting the microenvironment. ; Y.-H.O. received fellowships from Alborada Scholar-ship (University of Cambridge), Trinity-Henry Barlow Scholarship (Universityof Cambridge), and R.O.C. Government Scholarship to Study Abroad (GSSA). A.G.G. received fellowships from the Ramon Areces Foundationand the LaCaixa Foundation. C.K. was supported by Marie Curie Career Inte-gration (H2020-MSCA-IF-2015-70841). S.M.-F. was supported by Red TerCel (ISCIII-Spanish Cell Therapy Network). V.A. is supported by grants from theSpanish Ministerio de Economıa,Industria y Competitividad (MEIC) with co-funding from the Fondo Europeo de Desarrollo Regional (FEDER, ''Una manerade hacer Europa'') (SAF2016-79490-R), the Instituto de Salud Carlos III (AC16/00091 and AC17/00067), the Fundacio Marato TV3 (122/C/2015), and the Progeria Research Foundation (Established Investigator Award 2014–52). TheCNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia, Innovacion y Universidades (MCIU), and the Pro CNIC Foundation,and is a Severo Ochoa Center of Excellence (SEV-2015-0505). This work wassupported by core support grants from the Wellcome Trust and the MRC to theCambridge Stem Cell Institute, MEIC (SAF-2011-30308), Ramon y Cajal Program Grant (RYC-2009-04703), ConSEPOC-Comunidad de Madrid (S2010/BMD-2542), National Health Service Blood and Transplant (United Kingdom), European Union's Horizon 2020 research (ERC-2014-CoG-64765 and MarieCurie Career Integration grant FP7-PEOPLE-2011-RG-294096), and a Programme Foundation Award from Cancer Research UK to S.M.-F., who wasalso supported in part by an International Early Career Scientist grant fromthe Howard Hughes Medical Institute. ; Sí
Hematopoietic stem cells (HSCs) residing in the bone marrow (BM) accumulate during aging but are functionally impaired. However, the role of HSC-intrinsic and -extrinsic aging mechanisms remains debated. Megakaryocytes promote quiescence of neighboring HSCs. Nonetheless, whether megakaryocyte-HSC interactions change during pathological/natural aging is unclear. Premature aging in Hutchinson-Gilford progeria syndrome recapitulates physiological aging features, but whether these arise from altered stem or niche cells is unknown. Here, we show that the BM microenvironment promotes myelopoiesis in premature/physiological aging. During physiological aging, HSC-supporting niches decrease near bone but expand further from bone. Increased BM noradrenergic innervation promotes β2-adrenergic-receptor(AR)-interleukin-6-dependent megakaryopoiesis. Reduced β3-AR-Nos1 activity correlates with decreased endosteal niches and megakaryocyte apposition to sinusoids. However, chronic treatment of progeroid mice with β3-AR agonist decreases premature myeloid and HSC expansion and restores the proximal association of HSCs to megakaryocytes. Therefore, normal/premature aging of BM niches promotes myeloid expansion and can be improved by targeting the microenvironment. ; We thank A.R. Green for advice and support; M. García-Fernández, C. Fielding, C. Kapeni, X. Langa, and other current and former members of the S.M.-F group for help and discussions; A. Barettino and A. Macías (CNIC), D. Pask, T. Hamilton, the Central Biomedical Services and Cambridge NIHR BRC Cell Phenotyping Hub for technical assistance; H. Jolin and A.N.J. McZenzie (MRC Laboratory of Molecular Biology, Cambridge, UK) for help with milliplex analyses. Y.-H.O. received fellowships from Alborada Scholarship (University of Cambridge), Trinity-Henry Barlow Scholarship (University of Cambridge) and R.O.C. Government Scholarship to Study Abroad (GSSA) A.G.G. received fellowships from Ramón Areces and LaCaixa Foundations. C.K. was supported by Marie Curie Career Integration grant H2020-MSCA-IF-2015-70841. S.M.F., by Red TerCel (ISCIII-Spanish Cell Therapy Network). VA is supported by grants from the Spanish Ministerio de Economía, Industria y Competitividad (MEIC) with cofunding from the Fondo Europeo de Desarrollo Regional (FEDER, "Una manera de hacer Europa") (SAF2016-79490-R), the Instituto de Salud Carlos III (AC16/00091), the Fundació Marató TV3 (122/C/2015), and the Progeria Research Foundation (Established Investigator Award 2014–52). The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia, Innovación y Universidades (MCNU) and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015-0505). This work was supported by core support grants from the Wellcome Trust and the MRC to the Cambridge Stem Cell Institute, the Spanish Ministry of Economy and Competitiveness (SAF-2011-30308), Ramón y Cajal Program grant RYC-2009-04703, ConSEPOC-Comunidad de Madrid S2010/BMD-2542, National 427 Health Service Blood and Transplant (United Kingdom), European Union's Horizon 428 2020 research (ERC-2014-CoG-64765 and Marie Curie Career Integration grant FP7- 429 PEOPLE-2011-RG-294096) and a Programme Foundation Award from Cancer Research 430 UK to S.M.-F., who was also supported in part by an International Early Career Scientist 431 grant of the Howard Hughes Medical Institute.
