Social networks in the single cell

Plant mitochondrial DNA (mtDNA) can become damaged in many ways. A major repair mechanism is homologous recombination, which requires an undamaged DNA template. Presumably, this template comes from a different mitochondrion in the same cell. Plant mitochondria undergo fission and fusion to form transient networks which could allow the exchange of genetic information. To test this hypothesis, Chustecki et al. (2022) used msh1 mutants with defective DNA repair, and showed that mitochondrial interactions increased, revealing a link between the physical and genetic behavior of mitochondria

Anisotropic correlation functions as tracers of central galaxy alignments in simulations

Motivated by observational results, we use IllustrisTNG hydrodynamical numerical simulations to study the alignment of the central galaxies in groups with the surrounding structures. This approach allows us to analyse galaxy and group properties not available in observations. To perform this analysis, we use a modified version of the two-point cross-correlation function and a measure of the angle between the semi-major axes of the central galaxies and the larger structures. Overall, our results reproduce observational ones, as we find large-scale anisotropy, which is dominated by the red central galaxies. In addition, the latter is noticeably more aligned with their group than the blue ones. In contrast to the observations, we find a strong dependence of the anisotropy on the central galaxy with mass, probably associated with the inability of observational methods to determine them. This result allows us to link the alignment to the process of halo assembly and the well-known dependence of halo anisotropy on mass. When we include the dark matter distribution in our analysis, we conclude that the galaxy alignment found in simulations (and observations) can be explained by a combination of physical processes at different scales: the central galaxy aligns with the dark matter halo it inhabits, and this, in turn, aligns with the surrounding structures at large scales.Comment: 9 pages, 11 figures, Accepted by MNRA

Meter- to Millimeter Emission from Cool Stellar Systems : Latest Results, Synergies Across the Spectrum, and Outlook for the Next Decade

Splinter session summary, to appear in the proceedings of the 20th Cambridge Workshop on Cool Stars, Stellar Systems, and the Sun (ed. S. J. Wolk)Radio observations of cool stellar systems provide unique information on their magnetic fields, high-energy processes, and chemistry. Buoyed by powerful new instruments (e.g. ALMA, JVLA, LOFAR), advances in related fields (e.g., the Gaia astrometric revolution), and above all a renewed interest in the relevant stellar astrophysics, stellar radio astronomy is experiencing a renaissance. In this splinter session, participants took stock of the present state of stellar radio astronomy to chart a course for the field's future

Stability of childhood anxiety disorder diagnoses: a follow-up naturalistic study in psychiatric care

Few studies have examined the stability of major psychiatric disorders in pediatric psychiatric clinical populations. The objective of this study was to examine the long-term stability of anxiety diagnoses starting with pre-school age children through adolescence evaluated at multiple time points. Prospective cohort study was conducted of all children and adolescents receiving psychiatric care at all pediatric psychiatric clinics belonging to two catchment areas in Madrid, Spain, between 1 January, 1992 and 30 April, 2006. Patients were selected from among 24,163 children and adolescents who received psychiatric care. Patients had to have a diagnosis of an ICD-10 anxiety disorder during at least one of the consultations and had to have received psychiatric care for the anxiety disorder. We grouped anxiety disorder diagnoses according to the following categories: phobic disorders, social anxiety disorders, obsessive–compulsive disorder (OCD), stress-related disorders, and "other" anxiety disorders which, among others, included generalized anxiety disorder, and panic disorder. Complementary indices of diagnostic stability were calculated. As much as 1,869 subjects were included and had 27,945 psychiatric/ psychological consultations. The stability of all ICD-10 anxiety disorder categories studied was high regardless of the measure of diagnostic stability used. Phobic and social anxiety disorders showed the highest diagnostic stability, whereas OCD and "other" anxiety disorders showed the lowest diagnostic stability. No significant sex differences were observed on the diagnostic stability of the anxiety disorder categories studied. Diagnostic stability measures for phobic, social anxiety, and "other" anxiety disorder diagnoses varied depending on the age at first evaluation. In this clinical pediatric outpatient sample it appears that phobic, social anxiety, and stress-related disorder diagnoses in children and adolescents treated in community outpatient services may have high diagnostic stability

Premature polyadenylation-mediated loss of stathmin-2 is a hallmark of TDP-43-dependent neurodegeneration.

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are associated with loss of nuclear transactive response DNA-binding protein 43 (TDP-43). Here we identify that TDP-43 regulates expression of the neuronal growth-associated factor stathmin-2. Lowered TDP-43 levels, which reduce its binding to sites within the first intron of stathmin-2 pre-messenger RNA, uncover a cryptic polyadenylation site whose utilization produces a truncated, non-functional mRNA. Reduced stathmin-2 expression is found in neurons trans-differentiated from patient fibroblasts expressing an ALS-causing TDP-43 mutation, in motor cortex and spinal motor neurons from patients with sporadic ALS and familial ALS with GGGGCC repeat expansion in the C9orf72 gene, and in induced pluripotent stem cell (iPSC)-derived motor neurons depleted of TDP-43. Remarkably, while reduction in TDP-43 is shown to inhibit axonal regeneration of iPSC-derived motor neurons, rescue of stathmin-2 expression restores axonal regenerative capacity. Thus, premature polyadenylation-mediated reduction in stathmin-2 is a hallmark of ALS-FTD that functionally links reduced nuclear TDP-43 function to enhanced neuronal vulnerability

Bridging the gap between research, policy, and practice: Lessons learned from academic-public partnerships in the CTSA network.

A primary barrier to translation of clinical research discoveries into care delivery and population health is the lack of sustainable infrastructure bringing researchers, policymakers, practitioners, and communities together to reduce silos in knowledge and action. As National Institutes of Health's (NIH) mechanism to advance translational research, Clinical and Translational Science Award (CTSA) awardees are uniquely positioned to bridge this gap. Delivering on this promise requires sustained collaboration and alignment between research institutions and public health and healthcare programs and services. We describe the collaboration of seven CTSA hubs with city, county, and state healthcare and public health organizations striving to realize this vision together. Partnership representatives convened monthly to identify key components, common and unique themes, and barriers in academic-public collaborations. All partnerships aligned the activities of the CTSA programs with the needs of the city/county/state partners, by sharing resources, responding to real-time policy questions and training needs, promoting best practices, and advancing community-engaged research, and dissemination and implementation science to narrow the knowledge-to-practice gap. Barriers included competing priorities, differing timelines, bureaucratic hurdles, and unstable funding. Academic-public health/health system partnerships represent a unique and underutilized model with potential to enhance community and population health

Hypoxia drives murine neutrophil protein scavenging to maintain central carbon metabolism

Limiting dysfunctional neutrophilic inflammation while preserving effective immunity requires a better understanding of the processes that dictate neutrophil function in the tissues. Quantitative mass-spectrometry identified how inflammatory murine neutrophils regulated expression of cell surface receptors, signal transduction networks, and metabolic machinery to shape neutrophil phenotypes in response to hypoxia. Through the tracing of labeled amino acids into metabolic enzymes, proinflammatory mediators, and granule proteins, we demonstrated that ongoing protein synthesis shapes the neutrophil proteome. To maintain energy supplies in the tissues, neutrophils consumed extracellular proteins to fuel central carbon metabolism. The physiological stresses of hypoxia and hypoglycemia, characteristic of inflamed tissues, promoted this extracellular protein scavenging with activation of the lysosomal compartment, further driving exploitation of the protein-rich inflammatory milieu. This study provides a comprehensive map of neutrophil proteomes, analysis of which has led to the identification of active catabolic and anabolic pathways that enable neutrophils to sustain synthetic and effector functions in the tissues

Cerebral hypomyelination associated with biallelic variants of FIG4

The lipid phosphatase gene FIG4 is responsible for Yunisâ Varón syndrome and Charcotâ Marieâ Tooth disease Type 4J, a peripheral neuropathy. We now describe four families with FIG4 variants and prominent abnormalities of central nervous system (CNS) white matter (leukoencephalopathy), with onset in early childhood, ranging from severe hypomyelination to mild undermyelination, in addition to peripheral neuropathy. Affected individuals inherited biallelic FIG4 variants from heterozygous parents. Cultured fibroblasts exhibit enlarged vacuoles characteristic of FIG4 dysfunction. Two unrelated families segregate the same Gâ >â A variant in the +1 position of intron 21 in the homozygous state in one family and compound heterozygous in the other. This mutation in the splice donor site of exon 21 results in readâ through from exon 20 into intron 20 and truncation of the final 115 Câ terminal amino acids of FIG4, with retention of partial function. The observed CNS white matter disorder in these families is consistent with the myelination defects in the FIG4 null mouse and the known role of FIG4 in oligodendrocyte maturation. The families described here the expanded clinical spectrum of FIG4 deficiency to include leukoencephalopathy.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149294/1/humu23720-sup-0001-Supp_Mat_Lenk_2018.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149294/2/humu23720.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149294/3/humu23720_am.pd