Surnames in adoption: (re)creating identities of belonging

Names are increasingly recognised in sociology as important routes for understanding family relationships, as well as familial and individual identities. In this article, we use qualitative ‘name story’ data to examine the meanings of surnames for adults who were adopted as a child and for adults who have adopted a child. Our findings suggest that adult adoptees and adopters can feel differently about surnames and how these connect them—or otherwise—to familial identities of belonging and to their own individual identities. Especially for adopters, shared surnames are understood as important for ‘family-making’ through the way they cement and display familial belonging. Adult adoptees’ feelings about belonging, birth surnames and adoptive surnames appeared more complicated and often changed over time. For some, adoption enabled a flexibility in the choice and use of different surnames. Cultures of patronymic and patrilineal surnaming meant that women adoptees and women adopters also faced an additional layer of complexity that shaped decisions made about surnames and family belonging. Through examining experiences of and feelings about family names in adoption, our article highlights the complexities of surname praxis in identity construction, adoptive family life and lineages

Human astrocytes and microglia show augmented ingestion of synapses in Alzheimer's disease via MFG-E8

Synapse loss correlates with cognitive decline in Alzheimer's disease (AD). Data from mouse models suggests microglia are important for synapse degeneration, but direct human evidence for any glial involvement in synapse removal in human AD remains to be established. Here we observe astrocytes and microglia from human brains contain greater amounts of synaptic protein in AD compared with non-disease controls, and that proximity to amyloid-β plaques and the APOE4 risk gene exacerbate this effect. In culture, mouse and human astrocytes and primary mouse and human microglia phagocytose AD patient-derived synapses more than synapses from controls. Inhibiting interactions of MFG-E8 rescues the elevated engulfment of AD synapses by astrocytes and microglia without affecting control synapse uptake. Thus, AD promotes increased synapse ingestion by human glial cells at least in part via an MFG-E8 opsonophagocytic mechanism with potential for targeted therapeutic manipulation.</p

Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer’s disease

Synapse loss correlates with cognitive decline in Alzheimer’s disease, and soluble oligomeric amyloid beta (Aβ) is implicated in synaptic dysfunction and loss. An important knowledge gap is the lack of understanding of how Aβ leads to synapse degeneration. In particular, there has been difficulty in determining whether there is a synaptic receptor that binds Aβ and mediates toxicity. While many candidates have been observed in model systems, their relevance to human AD brain remains unknown. This is in part due to methodological limitations preventing visualization of Aβ binding at individual synapses. To overcome this limitation, we combined two high resolution microscopy techniques: array tomography and Förster resonance energy transfer (FRET) to image over 1 million individual synaptic terminals in temporal cortex from AD (n = 11) and control cases (n = 9). Within presynapses and post-synaptic densities, oligomeric Aβ generates a FRET signal with transmembrane protein 97. Further, Aβ generates a FRET signal with cellular prion protein, and post-synaptic density 95 within post synapses. Transmembrane protein 97 is also present in a higher proportion of post synapses in Alzheimer’s brain compared to controls. We inhibited Aβ/transmembrane protein 97 interaction in a mouse model of amyloidopathy by treating with the allosteric modulator CT1812. CT1812 drug concentration correlated negatively with synaptic FRET signal between transmembrane protein 97 and Aβ. In human-induced pluripotent stem cell derived neurons, transmembrane protein 97 is present in synapses and colocalizes with Aβ when neurons are challenged with human Alzheimer’s brain homogenate. Transcriptional changes are induced by Aβ including changes in genes involved in neurodegeneration and neuroinflammation. CT1812 treatment of these neurons caused changes in gene sets involved in synaptic function. These data support a role for transmembrane protein 97 in the synaptic binding of Aβ in human Alzheimer’s disease brain where it may mediate synaptotoxicity

Plasma concentrations of soluble IL-2 receptor α (CD25) are increased in type 1 diabetes and associated with reduced C-peptide levels in young patients.

AIMS/HYPOTHESIS: Type 1 diabetes is a common autoimmune disease that has genetic and environmental determinants. Variations within the IL2 and IL2RA (also known as CD25) gene regions are associated with disease risk, and variation in expression or function of these proteins is likely to be causal. We aimed to investigate if circulating concentrations of the soluble form of CD25, sCD25, an established marker of immune activation and inflammation, were increased in individuals with type 1 diabetes and if this was associated with the concentration of C-peptide, a measure of insulin production that reflects the degree of autoimmune destruction of the insulin-producing beta cells. METHODS: We used immunoassays to measure sCD25 and C-peptide in peripheral blood plasma from patient and control samples. RESULTS: We identified that sCD25 was increased in patients with type 1 diabetes compared with controls and replicated this result in an independent set of 86 adult patient and 80 age-matched control samples (p = 1.17 × 10(-3)). In 230 patients under 20 years of age, with median duration-of-disease of 6.1 years, concentrations of sCD25 were negatively associated with C-peptide concentrations (p = 4.8 × 10(-3)). CONCLUSIONS/INTERPRETATION: The 25% increase in sCD25 in patients, alongside the inverse association between sCD25 and C-peptide, probably reflect the adverse effects of an on-going, actively autoimmune and inflammatory immune system on beta cell function in patients

Size-Dependent Hydrogenation of <i>p-</i>Nitrophenol with Pd Nanoparticles Synthesized with Poly(amido)amine Dendrimer Templates

Monodisperse palladium nanoparticles consisting of 10–200 atoms were prepared using poly­(amido)­amine (PAMAM) dendrimer templates and were evaluated as catalysts using the model reduction of <i>para</i>-nitrophenol. The use of dendrimer templates allows for fine control of the average number of atoms per nanoparticle and systematic investigation of the effect of size on the catalytic activity of nanoparticles less than 2 nm in diameter. The palladium dendrimer-encapsulated nanoparticles (DENs) were found to be highly active for the hydrogenation of <i>para</i>-nitrophenol to <i>para</i>-aminophenol, with surface area-normalized rate constants ranging from 0.87 to 1.65 L s^–1 m^–2 (which is greater than any previously reported system). A near linear dependence of the observed rate constant on the synthetic Pd²⁺:dendrimer ratio was observed, suggesting that, within the size regime studied, most of the atoms lie on the surface of the nanoparticle and contribute to the catalytic activity. Interestingly, for Pd clusters containing between 10 and 50 atoms, the rate constant normalized on a per atom basis shows little variability, supporting the idea that all atoms lie on the surface of these clusters. However, for particles containing between 50 and 200 atoms, a decrease in per-atom activity is observed with increasing particle size, suggesting that in this size regime some atoms are located in the catalytically inactive core. Additionally, the generation of the PAMAM dendrimer template was found to have a significant effect on the observed rate constant due to steric crowding at the periphery (whereas the choice of an amine- or hydroxyl-termination on the dendrimer periphery did not)

A Novel εγδβ-Thalassemia Deletion Associated with Severe Anemia at Birth and a β-Thalassemia Intermedia Phenotype Later in Life in Three Generations of a Greek Family

We describe a novel deletion causing heterozygous εγδβ-thalassemia (εγδβ-thal) across three generations of a Greek family. The Greek deletion is about 72 kb in length, spanning from the hypersensitive site 4 (HS4) in the locus control region (LCR) to the 3&apos; end of the β-globin gene, thus encompassing the entire β-globin gene cluster. The deletion caused severe but transient neonatal anemia and a non transfusion-dependent chronic hemolytic anemia state later in life, resembling mild β-thalassemia intermedia (β-TI) rather than β-thalassemia (β-thal) trait, as had been previously reported. Apart from the presentation of clinical and laboratory characteristics, the challenges involving clinical management are also discussed. © 2019, © 2019 Informa UK Limited, trading as Taylor &amp; Francis Group