Family Values, Social Capital and Contradictions of American Modernity

Contemporary American social and political discourses have integrated concerns about family values into the realm of debates about the associational life of social capital. In these discussions, theoretical and historical confusions about the relations between family and civil society run rampant. In this article, I first bring theoretical clarity to these social structures and the type of relations upon which they are predicated and, second, briefly historicize the relationships between an American idea of family and civil society. By tracing changes in popular understandings of family and civil society, I demonstrate that the modern family values movement spurns its Victorian roots by maintaining the nostalgic language for a life and family of old built around a Christian home, while embracing means and institutions, and even more importantly, a form of family, which belies the nostalgia. The family has now become an institution or association which can be sustained through instrumental interventions; it is no longer to do with the organic relations of sentiment remaining from some long-faded Gemeinschaft. The family and the Christian home ideal, which were at the center of American critiques of modernization, have ceased to be.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Distinct Requirements for Cranial Ectoderm and Mesenchyme-Derived Wnts in Specification and Differentiation of Osteoblast and Dermal Progenitors

<div><p>The cranial bones and dermis differentiate from mesenchyme beneath the surface ectoderm. Fate selection in cranial mesenchyme requires the canonical Wnt effector molecule β-catenin, but the relative contribution of Wnt ligand sources in this process remains unknown. Here we show Wnt ligands are expressed in cranial surface ectoderm and underlying supraorbital mesenchyme during dermal and osteoblast fate selection. Using conditional genetics, we eliminate secretion of all Wnt ligands from cranial surface ectoderm or undifferentiated mesenchyme, to uncover distinct roles for ectoderm- and mesenchyme-derived Wnts. Ectoderm Wnt ligands induce osteoblast and dermal fibroblast progenitor specification while initiating expression of a subset of mesenchymal Wnts. Mesenchyme Wnt ligands are subsequently essential during differentiation of dermal and osteoblast progenitors. Finally, ectoderm-derived Wnt ligands provide an inductive cue to the cranial mesenchyme for the fate selection of dermal fibroblast and osteoblast lineages. Thus two sources of Wnt ligands perform distinct functions during osteoblast and dermal fibroblast formation.</p></div

Mesenchyme deletion of <i>Wntless</i> leads to diminished differentiation and Wnt responsiveness in the bone lineage.

<p>Indirect immunofluorescence with DAPI-stained (blue) nuclei (A, B, D, F, G, H, J, L, P, T) and immunohistochemistry (M,Q) was performed on coronal mouse embryonic head sections In situ hybridization (C, I, N, O, R, S) or eosin counterstain (E, K), was performed on coronal tissue sections of embryonic murine heads at the indicated stages. Diagram in (A) demonstrates plane of section and region of interest for E11.5-E12.5. Box in (D, J) demonstrate the region of high magnification. (I, S, T) Red arrows highlight changes in marker expression in osteoprogenitor domain. (E,K) vhf: subraorbital vibrissae hair follicle and black bracket indicates the dermal layer. (A,G) Scale bars represent 100 µm.</p

Delayed Union of a Diaphyseal Forearm Fracture Associated With Impaired Osteogenic Differentiation of Prospectively Isolated Human Skeletal Stem Cells

Delayed union or nonunion are relatively rare complications after fracture surgery, but when they do occur, they can result in substantial morbidity for the patient. In many cases, the etiology of impaired fracture healing is uncertain and attempts to determine the molecular basis for delayed union and nonunion formation have been limited. Prospectively isolating skeletal stem cells (SSCs) from fracture tissue samples at the time of surgical intervention represent a feasible methodology to determine a patient's biologic risk for compromised fracture healing. This report details a case in which functional in vitro readouts of SSCs derived from human fracture tissue at time of injury predicted a poor fracture healing outcome. This case suggests that it may be feasible to stratify a patient's fracture healing capacity and predict compromised fracture healing by prospectively isolating and analyzing SSCs during the index fracture surgery. © 2020 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research

Expression of Wnt ligands, Wntless, and Wnt signaling response in cranial ectoderm and mesenchyme.

<p>(A, B) RT-PCR for individual Wnt ligands was performed on cDNA from purified mouse embryonic cranial mesenchyme and surface ectoderm. (C, D G, H) Indirect immunofluorescence with DAPI counterstained nuclei (blue), (E) <i>in situ</i> hybridization, or immunohistochemistry (F, I) was performed on coronal mouse embryonic head sections. (G, H, I) Boxes indicate region in insets at higher magnification. White arrowheads indicate co-expression of (G) Wls/Runx2 or (D,H) Lef1/Runx2, (I) red arrowheads indicate osteoblast progenitors, and blue arrowheads indicate dermal progenitors. (F–I) White hatched lines demarcate ectoderm from mesenchyme. (J) Summary scheme of E12.5 supraorbital cranial mesenchyme. (J) Embryonic axes, figure depicts lateral view of embryonic head, region of interest in sections used in figures are shown. Scale bars represent 100 µm.</p

Deletion of <i>Wntless</i> in the cranial ectoderm and mesenchyme.

<p>(A, C, E, G) β-galactosidase staining with eosin counterstain or (B, D, F, H) indirect immunofluorescence with DAPI-stained nuclei (blue) was performed on coronal mouse E12.5 head sections. (A–H) Box outlines indicate region in inset and white hatched line in insets demarcates cranial ectoderm from mesenchyme. (I–L) Lateral view of whole-mount skeletal preps or gray-scaled bright field images of embryonic mouse heads. Ey, eye. Scale bars for sections represent 100 µm. Scale bar (K) for whole mount pictures (I–L) represents 5 mm. Diagram inset in (D) depicts lateral view of embryonic head with box outlining region of interest.</p

Generation of Wnt responsiveness in the cranial mesenchyme.

<p>In situ hybridization (A–E, H, Q, R), immunohistochemistry (S, T) or indirect immunofluorescence with DAPI-stained nuclei (blue) was performed on coronal mouse embryonic head sections (F, G, I–P). (S, T) White dotted line demarcates ectoderm from mesenchyme. Embryonic head diagram depicts region of interest and plane of section. Embryonic axes for the sections are presented. Scale bars represent 100 µm.</p

Distinct requirements for <i>Wntless</i> in the cranial ectoderm and mesenchyme.

<p>(A, B, C, D, C′, D′) Von Kossa staining, or (E–H) alcian blue staining was performed on coronal mouse embryonic head sections and counterstained with eosin. Br, brain, fb, frontal bone, vhf, supraorbital vibrissae hair follicle, mn, meningeal progenitors. Black arrowheads indicate guard hair follicles (hf), red arrowheads indicate dorsal extent of ossified frontal bone, and open black arrows indicate ectopic cartilage. (C′, D′ C″, D″) Black dotted line demarcates the lower limit of the dermal layer and the black bracket shows dermal thickness. Diagrams inset (B) figure depicts lateral view of E15.5 embryonic head with plane of section and region of interest. Red regions in diagram represent bone primordia. Scale bars (A,E) represent 100 µm.</p

Ectoderm deletion of <i>Wntless</i> leads to loss of cranial bone and dermal lineage markers in the mesenchyme.

<p>Indirect immunofluorescence with DAPI-stained (blue) nuclei was performed on coronal mouse embryonic head sections at E12.5 or as indicated (A,B, F, G, H, I, M, N, P, R, T, V). Alkaline Phosphatase staining (C, J), in situ hybridization (D, E, K, L, O, S), or β-galactosidase staining with eosin counterstain (Q, U) was performed on coronal tissue sections. Diagram in (A) demonstrates plane of section and region of interest for E12.5-E13.5 (A–T). Box and dashed lines in (Q, U) demonstrate the region of high magnification, and β-galactosidase stained sections were included for perspective for (R, V). Diagram inset in high magnification photograph from (Q) shows plane of section and region of interest for E15.5. Red arrows indicate changes in marker expression and black arrows in (U) high magnification indicate ectopic cartilage. Scale bars represent 100 µm.</p