163 research outputs found

    Monolithic narrow-linewidth InGaAsP semiconductor laser for coherent optical communications

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    A design for a monolithic narrow-linewidth InGaAsP diode laser has been developed using a multiple-quantum-well (MQW) extended-passive-cavity distributed-Bragg-reflector (DBR) laser design. Theoretical results indicate that this structure has the potential for a linewidth of 100 kHz or less. To realize this device, a number of the fabrication techniques required to integrate low-loss passive waveguides with active regions have been developed using a DBR laser structure. In addition, the MOCVD growth of InGaAs MQW laser structures has been developed, and threshold current densities as low as 1.6 kA/sq cm have been obtained from broad-stripe InGaAs/InGaAsP separate-confinement-heterostructure MQW lasers

    Vapor phase growth technique and system for several 3-5 compound semiconductors Quarterly technical report

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    Vapor phase growth technique and system for group 3A and 5A compound semiconductor

    Vapor phase growth technique and system for several III-V compound semiconductors Interim scientific report

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    Vapor phase growth method for single crystalline preparation of gallium nitride, gallium arsenide alloy, and gallium antimonide allo

    Clonal kinetics and single-cell transcriptional profiling of CAR-T cells in patients undergoing CD19 CAR-T immunotherapy

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    Chimeric antigen receptor (CAR) T-cell therapy has produced remarkable anti-tumor responses in patients with B-cell malignancies. However, clonal kinetics and transcriptional programs that regulate the fate of CAR-T cells after infusion remain poorly understood. Here we perform TCRB sequencing, integration site analysis, and single-cell RNA sequencing (scRNA-seq) to profile CD8+ CAR-T cells from infusion products (IPs) and blood of patients undergoing CD19 CAR-T immunotherapy. TCRB sequencing shows that clonal diversity of CAR-T cells is highest in the IPs and declines following infusion. We observe clones that display distinct patterns of clonal kinetics, making variable contributions to the CAR-T cell pool after infusion. Although integration site does not appear to be a key driver of clonal kinetics, scRNA-seq demonstrates that clones that expand after infusion mainly originate from infused clusters with higher expression of cytotoxicity and proliferation genes. Thus, we uncover transcriptional programs associated with CAR-T cell behavior after infusion.Published versio

    Expression Profiling of Autism Candidate Genes during Human Brain Development Implicates Central Immune Signaling Pathways

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    The Autism Spectrum Disorders (ASD) represent a clinically heterogeneous set of conditions with strong hereditary components. Despite substantial efforts to uncover the genetic basis of ASD, the genomic etiology appears complex and a clear understanding of the molecular mechanisms underlying Autism remains elusive. We hypothesized that focusing gene interaction networks on ASD-implicated genes that are highly expressed in the developing brain may reveal core mechanisms that are otherwise obscured by the genomic heterogeneity of the disorder. Here we report an in silico study of the gene expression profile from ASD-implicated genes in the unaffected developing human brain. By implementing a biologically relevant approach, we identified a subset of highly expressed ASD-candidate genes from which interactome networks were derived. Strikingly, immune signaling through NFκB, Tnf, and Jnk was central to ASD networks at multiple levels of our analysis, and cell-type specific expression suggested glia—in addition to neurons—deserve consideration. This work provides integrated genomic evidence that ASD-implicated genes may converge on central cytokine signaling pathways

    A lack of association between elevated serum levels of S100B protein and autoimmunity in autistic children

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    <p>Abstract</p> <p>Background</p> <p>S100B is a calcium-binding protein that is produced primarily by astrocytes. Increased serum S100B protein levels reflect neurological damage. Autoimmunity may have a role in the pathogenesis of autism in some patients. Autoantibodies may cross the blood-brain barrier and combine with brain tissue antigens, forming immune complexes and resulting in neurological damage. We are the first to investigate the relationship between serum levels of S100B protein, a marker of neuronal damage, and antiribosomal P protein antibodies in autistic children.</p> <p>Methods</p> <p>Serum S100B protein and antiribosomal P antibodies were measured in 64 autistic children in comparison to 46 matched healthy children.</p> <p>Results</p> <p>Autistic children had significantly higher serum S100B protein levels than healthy controls (<it>P </it>< 0.001). Children with severe autism had significantly higher serum S100B protein than patients with mild to moderate autism (<it>P </it>= 0.01). Increased serum levels of antiribosomal P antibodies were found in 40.6% of autistic children. There were no significant correlations between serum levels of S100B protein and antiribosomal P antibodies (<it>P </it>= 0.29).</p> <p>Conclusions</p> <p>S100B protein levels were elevated in autistic children and significantly correlated to autistic severity. This may indicate the presence of an underlying neuropathological condition in autistic patients. Antiribosomal P antibodies may not be a possible contributing factor to the elevated serum levels of S100B protein in some autistic children. However, further research is warranted to investigate the possible link between serum S100B protein levels and other autoantibodies, which are possible indicators of autoimmunity to central nervous system in autism.</p
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