Optoelectronic Integration on Silicon II, SPIE 2004

NRC publication: Ye

A 100-channel near-infrared SOI waveguide microspectrometer: Design and fabrication challenges

NRC publication: Ye

Tuning the modal birefringence in waveguide devices

NRC publication: Ye

Silicon-based integrated optics: waveguide technology to microphotonics

Using a waveguide spectrometer chip as an example, we describe how high index contrast waveguides systems such as silicon-on-insulator can be combined with microphotonic design rules to extend the performance of waveguide devices. The challenges arising in the implementation of silicon microphotonic technology are discussed, and recent work addressing the issues of waveguide coupling, polarization sensitivity, waveguide loss and massively parallel data acquisition is reviewed.Peer reviewed: YesNRC publication: Ye

Prospects and challenges for microphotonic waveguide components based on Si and SiGe

NRC publication: Ye

Microphotonic elements for integration on the silicon-on-insulator waveguide platform

NRC publication: Ye

Fabrication of Lithographically-defined Optical Coupling Facets for SOI Waveguides by ICP Etching

NRC publication: Ye

Primary T-cell immunodeficiency with immunodysregulation caused by autosomal recessive LCK deficiency

International audienceSignals emanating from the antigen T-cell receptor (TCR) are required for T-cell development and function. The T lymphocyte-specific protein tyrosine kinase (Lck) is a key component of the TCR signaling machinery. On the basis of its function, we considered LCK a candidate gene in patients with combined immunodeficiency. Objective: We identify and describe a child with a T-cell immunodeficiency caused by a homozygous missense mutation of the LCK gene (c.1022T>C) resulting from uniparental disomy. Methods: Genetic, molecular, and functional analyses were performed to characterize the Lck deficiency, and the associated clinical and immunologic phenotypes are reported. Results: The mutant LCK protein (p.L341P) was weakly expressed with no kinase activity and failed to reconstitute TCR signaling in LCK-deficient T cells. The patient presented with recurrent respiratory tract infections together with predominant early-onset inflammatory and autoimmune manifestations. The patient displayed CD41 T-cell lymphopenia and low levels of CD4 and CD8 expression on the T-cell surface. The residual T lymphocytes had an oligoclonal T-cell repertoire and exhibited a profound TCR signaling defect, with only weak tyrosine phosphorylation signals and no Ca21 mobilization in response to TCR stimulation. Conclusion: We report a new form of T-cell immunodeficiency caused by a LCK gene defect, highlighting the essential role of Lck in human T-cell development and responses. Our results also point out that defects in the TCR signaling cascade often result in abnormal T-cell differentiation and functions, leading to an important risk factor for inflammation and autoimmunit