2 research outputs found
Ga0.35In0.65 N0.02As0.08/GaAs bidirectional light-emitting and light-absorbing heterojunction operating at 1.3 μm
The Top-Hat hot electron light emission and lasing in semiconductor heterostructure (HELLISH)-vertical-cavity semiconductor optical amplifier (THH-VCSOA) is a bidirectional light-emitting and light-absorbing heterojunction device.
The device contains 11 Ga0.35In0.65 N0.02As0.08/GaAs MQWs in its intrinsic active region which is enclosed between six pairs of AlAs/GaAs top distributed Bragg reflectors (DBRs) and 20.5 pairs of AlAs/GaAs bottom DBR mirrors. The THH-VCSOA is fabricated using a four-contact configuration. The wavelength conversion with amplification is achieved by the appropriate biasing of the absorption and emission regions within the device. Absorption and emission regions may be reversed by changing the polarity of the applied voltage. Emission wavelength is about 1,300 nm and a maximum gain at this wavelength is around 5 dB at T = 300 K
Efficient Targeting of Head and Neck Squamous Cell Carcinoma by Systemic Administration of a Dual uPA and MMP-Activated Engineered Anthrax Toxin
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. Although considerable progress has been made in elucidating the etiology of the disease, the prognosis for individuals diagnosed with HNSCC remains poor, underscoring the need for development of additional treatment modalities. HNSCC is characterized by the upregulation of a large number of proteolytic enzymes, including urokinase plasminogen activator (uPA) and an assortment of matrix metalloproteinases (MMPs) that may be expressed by tumor cells, by tumor-supporting stromal cells or by both. Here we explored the use of an intercomplementing anthrax toxin that requires combined cell surface uPA and MMP activities for cellular intoxication and specifically targets the ERK/MAPK pathway for the treatment of HNSCC. We found that this toxin displayed strong systemic anti-tumor activity towards a variety of xenografted human HNSCC cell lines by inducing apoptotic and necrotic tumor cell death, and by impairing tumor cell proliferation and angiogenesis. Interestingly, the human HNSCC cell lines were insensitive to the intercomplementing toxin when cultured ex vivo, suggesting that either the toxin targets the tumor-supporting stromal cell compartment or that the tumor cell requirement for ERK/MAPK signaling differs in vivo and ex vivo. This intercomplementing toxin warrants further investigation as an anti-HNSCC agent