Spectrally resolved detection in transient-reflectivity measurements of coherent optical phonons in diamond

Coherent optical phonons in bulk solid system play a crucial role in understanding and designing light-matter interactions and can be detected by the transient-reflectivity measurement. In this paper, we demonstrate spectrally resolved detection of coherent optical phonons in diamond from ultrashort infrared pump-probe measurements using optical band-pass filters. We show that this enhances the sensitivity approximately 35 times in measuring the coherent oscillations in the transient reflectivity compared with the commonly used spectrally integrated measurement. To explain this observation, we discuss its mechanism.Comment: 8 pages, 4 figure

Gamma-secretase inhibitor does not induce cytotoxicity in adult T cell leukemia cell lines despite NOTCH1 overexpression

Abstract Background: Activated mutations in Notch homolog 1, translocation-associated (Drosophila; NOTCH1) are driver oncogenes of T-cell type acute lymphoblastic leukemia/lymphoma. The γ-secretase inhibitor (GSI), which suppresses the function of NOTCH1, is expected to be a molecular-targeted agent. NOTCH1 is also expressed in other malignant neoplasms. We aimed to determine the function of NOTCH1 expression and the effects of GSI on adult T-cell leukemia/lymphoma (ATL) caused by long-term human T-cell leukemia virus type I (HTLV-1) infection. Methods: We analyzed active NOTCH1 in six ATL and HTLV-1-infected cell lines and investigated the influence of activated NOTCH1 together with GSI on cell proliferation. Results: Activated NOTCH1 found in ATL and HTLV-1-infected cell lines was undetectable after incubation with GSI, regardless of whether the contactin gene Tax, which encodes HTLV-1 protein, was expressed. Whole exome sequencing revealed that activated NOTCH1 mutations were undetectable in six cell lines infected with ATL and HTLV-1 regardless of abundant NOTCH1 expression. Moreover, GSI did not suppress the growth of ATL cell lines. Conclusions: These findings suggested that NOTCH1 protein is constitutively activated, but is likely a passenger during NOTCH1 mutation negative ATL cell proliferation.</jats:p