A Keck High Resolution Spectroscopic Study of the Orion Nebula Proplyds

We present the results of spectroscopy of four bright proplyds in the Orion Nebula obtained at a velocity resolution of 6 km/s. After careful isolation of the proplyd spectra from the confusing nebular radiation, the emission line profiles are compared with those predicted by realistic dynamic/photoionization models of the objects. The spectral line widths show a clear correlation with ionization potential, which is consistent with the free expansion of a transonic, ionization-stratified, photoevaporating flow. Fitting models of such a flow simultaneously to our spectra and HST emission line imaging provides direct measurements of the proplyd size, ionized density and outflow velocity. These measurements confirm that the ionization front in the proplyds is approximately D-critical and provide the most accurate and robust estimate to date of the proplyd mass loss rate. Values of 0.7E-6 to 1.5E-6 Msun/year are found for our spectroscopic sample, although extrapolating our results to a larger sample of proplyds implies that 0.4E-6 Msun/year is more typical of the proplyds as a whole. In view of the reported limits on the masses of the circumstellar disks within the proplyds, the length of time that they can have been exposed to ionizing radiation should not greatly exceed 10,000 years - a factor of 30 less than the mean age of the proplyd stars. We review the various mechanisms that have been proposed to explain this situation, and conclude that none can plausibly work unless the disk masses are revised upwards by a substantial amount.Comment: 23 pages, 8 figures, uses emulateapj.sty, accepted for publication in The Astronomical Journal (scheduled November 1999

Simulation of Conformal Spiral Slot Antennas on Composite Platforms

During the course of the grant, we wrote and distributed about 12 reports and an equal number of journal papers supported fully or in part by this grant. The list of reports (title & abstract) and papers are given in Appendices A and B. This grant has indeed been instrumental in developing a robust hybrid finite element method for the analysis of complex broadband antennas on doubly curved platforms. Previous to the grant, our capability was limited to simple printed patch antennas on mostly planar platforms. More specifically: (1) mixed element formulations were developed and new edge-based prisms were introduced; (2) these elements were important in permitting flexibility in geometry gridding for most antennas of interest; (3) new perfectly matched absorbers were introduced for mesh truncations associated with highly curved surfaces; (4) fast integral algorithms were introduced for boundary integral truncations reducing CPU time from O(N-2) down to O(N-1.5) or less; (5) frequency extrapolation schemes were developed for efficient broadband performance evaluations. This activity has been successfully continued by NASA researchers; (6) computer codes were developed and extensively tested for several broadband configurations. These include FEMA-CYL, FEMA-PRISM and FEMA-TETRA written by L. Kempel, T. Ozdemir and J. Gong, respectively; (7) a new infinite balun feed was designed nearly constant impedance over the 800-3000 MHz operational band; (8) a complete slot spiral antenna was developed, fabricated and tested at NASA Langley. This new design is a culmination of the projects goals and integrates the computational and experimental efforts. this antenna design resulted in a U.S. patent and was revised three times to achieve the desired bandwidth and gain requirements from 800-3000 MHz

Interhemispheric white matter integrity in young people with bipolar disorder and at high genetic risk

White matter (WM) impairments have been reported in patients with bipolar disorder (BD) and those at high familial risk of developing BD. However, the distribution of these impairments has not been well characterized. Few studies have examined WM integrity in young people early in the course of illness and in individuals at familial risk who have not yet passed the peak age of onset. WM integrity was examined in 63 BD subjects, 150 high-risk (HR) individuals and 111 participants with no family history of mental illness (CON). All subjects were aged 12 to 30 years. This young BD group had significantly lower fractional anisotropy within the genu of the corpus callosum (CC) compared with the CON and HR groups. Moreover, the abnormality in the genu of the CC was also present in HR participants with recurrent major depressive disorder (MDD) (n = 16) compared with CON participants. Our findings provide important validation of interhemispheric abnormalities in BD patients. The novel finding in HR subjects with recurrent MDD – a group at particular risk of future hypo/manic episodes – suggests that this may potentially represent a trait marker for BD, though this will need to be confirmed in longitudinal follow-up studies

Recellularization of auricular cartilage via elastase-generated channels

Decellularized tissue matrices are promising substrates for tissue generation by stem cells to replace poorly regenerating tissues such as cartilage. However, the dense matrix of decellularized cartilage impedes colonisation by stem cells. Here, we show that digestion of elastin fibre bundles traversing auricular cartilage creates channels through which cells can migrate into the matrix. Human chondrocytes and bone marrow-derived mesenchymal stromal cells efficiently colonise elastin-treated scaffolds through these channels, restoring a glycosaminoglycan-rich matrix and improving mechanical properties while maintaining size and shape of the restored tiss

Genome-wide linkage analysis of 972 bipolar pedigrees using single-nucleotide polymorphisms.

Because of the high costs associated with ascertainment of families, most linkage studies of Bipolar I disorder (BPI) have used relatively small samples. Moreover, the genetic information content reported in most studies has been less than 0.6. Although microsatellite markers spaced every 10 cM typically extract most of the genetic information content for larger multiplex families, they can be less informative for smaller pedigrees especially for affected sib pair kindreds. For these reasons we collaborated to pool family resources and carried out higher density genotyping. Approximately 1100 pedigrees of European ancestry were initially selected for study and were genotyped by the Center for Inherited Disease Research using the Illumina Linkage Panel 12 set of 6090 single-nucleotide polymorphisms. Of the ~1100 families, 972 were informative for further analyses, and mean information content was 0.86 after pruning for linkage disequilibrium. The 972 kindreds include 2284 cases of BPI disorder, 498 individuals with bipolar II disorder (BPII) and 702 subjects with recurrent major depression. Three affection status models (ASMs) were considered: ASM1 (BPI and schizoaffective disorder, BP cases (SABP) only), ASM2 (ASM1 cases plus BPII) and ASM3 (ASM2 cases plus recurrent major depression). Both parametric and non-parametric linkage methods were carried out. The strongest findings occurred at 6q21 (non-parametric pairs LOD 3.4 for rs1046943 at 119 cM) and 9q21 (non-parametric pairs logarithm of odds (LOD) 3.4 for rs722642 at 78 cM) using only BPI and schizoaffective (SA), BP cases. Both results met genome-wide significant criteria, although neither was significant after correction for multiple analyses. We also inspected parametric scores for the larger multiplex families to identify possible rare susceptibility loci. In this analysis, we observed 59 parametric LODs of 2 or greater, many of which are likely to be close to maximum possible scores. Although some linkage findings may be false positives, the results could help prioritize the search for rare variants using whole exome or genome sequencing

Recurrent duplications of the annexin A1 gene (ANXA1) in autism spectrum disorders

Validating the potential pathogenicity of copy number variants (CNVs) identified in genome-wide studies of autism spectrum disorders (ASD) requires detailed assessment of case/control frequencies, inheritance patterns, clinical correlations, and functional impact. Here, we characterize a small recurrent duplication in the annexin A1 (ANXA1) gene, identified by the Autism Genome Project (AGP) study

Transcription Factor SP4 Is a Susceptibility Gene for Bipolar Disorder

The Sp4 transcription factor plays a critical role for both development and function of mouse hippocampus. Reduced expression of the mouse Sp4 gene results in a variety of behavioral abnormalities relevant to human psychiatric disorders. The human SP4 gene is therefore examined for its association with both bipolar disorder and schizophrenia in European Caucasian and Chinese populations respectively. Out of ten SNPs selected from human SP4 genomic locus, four displayed significant association with bipolar disorder in European Caucasian families (rs12668354, p = 0.022; rs12673091, p = 0.0005; rs3735440, p = 0.019; rs11974306, p = 0.018). To replicate the genetic association, the same set of SNPs was examined in a Chinese bipolar case control sample. Four SNPs displayed significant association (rs40245, p = 0.009; rs12673091, p = 0.002; rs1018954, p = 0.001; rs3735440, p = 0.029), and two of them (rs12673091, rs3735440) were shared with positive SNPs from European Caucasian families. Considering the genetic overlap between bipolar disorder and schizophrenia, we extended our studies in Chinese trios families for schizophrenia. The SNP7 (rs12673091, p = 0.012) also displayed a significant association. The SNP7 (rs12673091) was therefore significantly associated in all three samples, and shared the same susceptibility allele (A) across all three samples. On the other hand, we found a gene dosage effect for mouse Sp4 gene in the modulation of sensorimotor gating, a putative endophenotype for both schizophrenia and bipolar disorder. The deficient sensorimotor gating in Sp4 hypomorphic mice was partially reversed by the administration of dopamine D2 antagonist or mood stabilizers. Both human genetic and mouse pharmacogenetic studies support Sp4 gene as a susceptibility gene for bipolar disorder or schizophrenia. The studies on the role of Sp4 gene in hippocampal development may provide novel insights for the contribution of hippocampal abnormalities in these psychiatric disorders