Institutionalized Delinquent and Maladjusted Juveniles: A Psycholegal Systems Analysis

I. Introduction II. The Criminal Justice and Mental Health Systems ... A. Angles A1 and A2 ... B. A1→B1, or A2→B2 … C. Angles B1 and B2 ... D. The Shuffle: A1→C1→A1 or A2; or A2→C2→A2 or A1; or A1→B2 or C1→B2 ... E. The Merger ... F. Prospects for Change ... G. Summary III. The Juvenile Justice System ... A. Legal Rights at Intake in the Juvenile Justice System (Angle A3 ) ... B. Legal Rights during Juvenile Incarceration (A3 to B3) ... C. Controversy over the Goal of Juvenile Justice (Angle B3) ... D. Dumping (Angle C3) and Shuffling (A3→C3→A3 or A1 or A2; or A3→A1 or A2) in the Juvenile Justice System ... E. Merger with the Criminal Justice System ... F. Summary IV. Juveniles in the Mental Health System ... A. Commitment of Juveniles to Mental Health Facilities (Angle A4) ... B. Incipient Legalization at Angle A4 ... C. Prospects for Further Legalization at Angle A4 ... D. Prospects for Treatment Rights (A4→B4) ... E. The Future of the Juvenile Mental Health System ... F. Summary V. Conclusio

Institutionalized Delinquent and Maladjusted Juveniles: A Psycholegal Systems Analysis

I. Introduction II. The Criminal Justice and Mental Health Systems ... A. Angles A1 and A2 ... B. A1→B1, or A2→B2 … C. Angles B1 and B2 ... D. The Shuffle: A1→C1→A1 or A2; or A2→C2→A2 or A1; or A1→B2 or C1→B2 ... E. The Merger ... F. Prospects for Change ... G. Summary III. The Juvenile Justice System ... A. Legal Rights at Intake in the Juvenile Justice System (Angle A3 ) ... B. Legal Rights during Juvenile Incarceration (A3 to B3) ... C. Controversy over the Goal of Juvenile Justice (Angle B3) ... D. Dumping (Angle C3) and Shuffling (A3→C3→A3 or A1 or A2; or A3→A1 or A2) in the Juvenile Justice System ... E. Merger with the Criminal Justice System ... F. Summary IV. Juveniles in the Mental Health System ... A. Commitment of Juveniles to Mental Health Facilities (Angle A4) ... B. Incipient Legalization at Angle A4 ... C. Prospects for Further Legalization at Angle A4 ... D. Prospects for Treatment Rights (A4→B4) ... E. The Future of the Juvenile Mental Health System ... F. Summary V. Conclusio

Public Response to Community Mitigation Measures for Pandemic Influenza

Results from a national survey indicated that most persons would follow public health officials’ guidelines

Zebrafish Numb and Numblike Are Involved in Primitive Erythrocyte Differentiation

BACKGROUND:Notch signaling is an evolutionarily conserved regulatory circuitry implicated in cell fate determination in various developmental processes including hematopoietic stem cell self-renewal and differentiation of blood lineages. Known endogenous inhibitors of Notch activity are Numb-Nb and Numblike-Nbl, which play partially redundant functions in specifying and maintaining neuronal differentiation. Nb and Nbl are expressed in most tissues including embryonic and adult hematopoietic tissues in mice and humans, suggesting possible roles for these proteins in hematopoiesis. METHODOLOGY AND PRINCIPAL FINDINGS:We employed zebrafish to investigate the possible functional role of Numb and Numblike during hematopoiesis, as this system allows a detailed analysis even in embryos with severe defects that would be lethal in other organisms. Here we describe that nb/nbl knockdown results in severe reduction or absence of embryonic erythrocytes in zebrafish. Interestingly, nb/nbl knocked-down embryos present severe downregulation of the erythroid transcription factor gata1. This results in erythroblasts which fail to mature and undergo apoptosis. Our results indicate that Notch activity is increased in embryos injected with nb/nbl morpholino, and we show that inhibition of Notch activation can partially rescue the hematopoietic phenotype. CONCLUSIONS AND SIGNIFICANCE:Our results provide the first in vivo evidence of an involvement of Numb and Numblike in zebrafish erythroid differentiation during primitive hematopoiesis. Furthermore, we found that, at least in part, the nb/nbl morphant phenotype is due to enhanced Notch activation within hematopoietic districts, which in turn results in primitive erythroid differentiation defects

Coe Genes Are Expressed in Differentiating Neurons in the Central Nervous System of Protostomes

Genes of the coe (collier/olfactory/early B-cell factor) family encode Helix-Loop-Helix transcription factors that are widely conserved in metazoans and involved in many developmental processes, neurogenesis in particular. Whereas their functions during vertebrate neural tube formation have been well documented, very little is known about their expression and role during central nervous system (CNS) development in protostomes. Here we characterized the CNS expression of coe genes in the insect Drosophila melanogaster and the polychaete annelid Platynereis dumerilii, which belong to different subgroups of protostomes and show strikingly different modes of development. In the Drosophila ventral nerve cord, we found that the Collier-expressing cells form a subpopulation of interneurons with diverse molecular identities and neurotransmitter phenotypes. We also demonstrate that collier is required for the proper differentiation of some interneurons belonging to the Eve-Lateral cluster. In Platynereis dumerilii, we cloned a single coe gene, Pdu-coe, and found that it is exclusively expressed in post mitotic neural cells. Using an original technique of in silico 3D registration, we show that Pdu-coe is co-expressed with many different neuronal markers and therefore that, like in Drosophila, its expression defines a heterogeneous population of neurons with diverse molecular identities. Our detailed characterization and comparison of coe gene expression in the CNS of two distantly-related protostomes suggest conserved roles of coe genes in neuronal differentiation in this clade. As similar roles have also been observed in vertebrates, this function was probably already established in the last common ancestor of all bilaterians

Single neuron transcriptomics identify SRSF/ SR protein B52 as a regulator of axon growth and Choline acetyltransferase splicing.

We removed single identified neurons from living Drosophila embryos to gain insight into the transcriptional control of developing neuronal networks. The microarray analysis of the transcriptome of two sibling neurons revealed seven differentially expressed transcripts between both neurons (threshold: log(2)1.4). One transcript encodes the RNA splicing factor B52. Loss of B52 increases growth of axon branches. B52 function is also required for Choline acetyltransferase (ChAT ) splicing. At the end of embryogenesis, loss of B52 function impedes splicing of ChAT, reduces acetylcholine synthesis, and extends the period of uncoordinated muscle twitches during larval hatching. ChAT regulation by SRSF proteins may be a conserved feature since changes in SRSF5 expression and increased acetylcholine levels in brains of bipolar disease patients have been reported recently

In Vivo Expression of MHC Class I Genes Depends on the Presence of a Downstream Barrier Element

Regulation of MHC class I gene expression is critical to achieve proper immune surveillance. In this work, we identify elements downstream of the MHC class I promoter that are necessary for appropriate in vivo regulation: a novel barrier element that protects the MHC class I gene from silencing and elements within the first two introns that contribute to tissue specific transcription. The barrier element is located in intergenic sequences 3′ to the polyA addition site. It is necessary for stable expression in vivo, but has no effect in transient transfection assays. Accordingly, in both transgenic mice and stably transfected cell lines, truncation of the barrier resulted in transcriptional gene silencing, increased nucleosomal density and decreased histone H3K9/K14 acetylation and H3K4 di-methylation across the gene. Significantly, distinct sequences within the barrier element govern anti-silencing and chromatin modifications. Thus, this novel barrier element functions to maintain transcriptionally permissive chromatin organization and prevent transcriptional silencing of the MHC class I gene, ensuring it is poised to respond to immune signaling

Control of Neural Daughter Cell Proliferation by Multi-level Notch/Su(H)/E(spl)-HLH Signaling

The Notch pathway controls proliferation during development and in adulthood, and is frequently affected in many disorders. However, the genetic sensitivity and multi-layered transcriptional properties of the Notch pathway has made its molecular decoding challenging. Here, we address the complexity of Notch signaling with respect to proliferation, using the developing Drosophila CNS as model. We find that a Notch/Su(H)/E(spl)-HLH cascade specifically controls daughter, but not progenitor proliferation. Additionally, we find that different E(spl)-HLH genes are required in different neuroblast lineages. The Notch/Su(H)/E(spl)-HLH cascade alters daughter proliferation by regulating four key cell cycle factors: Cyclin E, String/Cdc25, E2f and Dacapo (mammalian p21CIP1/p27KIP1/p57Kip2). ChIP and DamID analysis of Su(H) and E(spl)-HLH indicates direct transcriptional regulation of the cell cycle genes, and of the Notch pathway itself. These results point to a multi-level signaling model and may help shed light on the dichotomous proliferative role of Notch signaling in many other systems

Expression in Aneuploid Drosophila S2 Cells

Analysis of the relationship between gene copy number and gene expression in aneuploid male Drosophila cells reveals a global compensation mechanism in addition to X chromosome-specific dosage compensation