Design and performance of a F/#-conversion microlens for Prime Focus Spectrograph at Subaru Telescope

The PFS is a multi-object spectrograph fed by 2394 fibers at the prime focus of Subaru telescope. Since the F/# at the prime focus is too fast for the spectrograph, we designed a small concave-plano negative lens to be attached to the tip of each fiber that converts the telescope beam (F/2.2) to F/2.8. We optimized the lens to maximize the number of rays that can be confined inside F/2.8 while maintaining a 1.28 magnification. The microlenses are manufactured by glass molding, and an ultra-broadband AR coating (<1.5% for lambda=0.38-1.26 um) will be applied to the front surface.Comment: 7 pages, 8 figures, SPIE201

Analysis of an alternative human CD133 promoter reveals the implication of Ras/ERK pathway in tumor stem-like hallmarks

<p>Abstract</p> <p>Background</p> <p>An increasing number of studies support the presence of stem-like cells in human malignancies. These cells are primarily responsible for tumor initiation and thus considered as a potential target to eradicate tumors. CD133 has been identified as an important cell surface marker to enrich the stem-like population in various human tumors. To reveal the molecular machinery underlying the stem-like features in tumor cells, we analyzed a promoter of <it>CD133 </it>gene using human colon carcinoma Caco-2 and synovial sarcoma Fuji cells, which endogenously express <it>CD133 </it>gene.</p> <p>Results</p> <p>A reporter analysis revealed that P5 promoter, located far upstream in a human <it>CD133 </it>gene locus, exhibits the highest activity among the five putative promoters (P1 to P5). Deletion and mutation analysis identified two ETS binding sites in the P5 region as being essential for its promoter activity. Electrophoretic mobility shift assays demonstrated the specific binding between nuclear factors and the ETS binding sequence. Overexpression of dominant-negative forms of Ets2 and Elk1 resulted in the significant decrease of P5 activity. Furthermore, treatment of Fuji cells with a specific MEK/ERK inhibitor, U0126, also markedly decreased CD133 expression, but there was no significant effect in Caco-2 cells, suggesting cell type-specific regulation of CD133 expression. Instead, the side population, another hallmark of TSLCs, was dramatically diminished in Caco-2 cells by U0126. Finally, Ras-mediated oncogenic transformation in normal human astrocytes conferred the stem-like capability to form neurosphere-like colonies with the increase of <it>CD133 </it>mRNA expression.</p> <p>Conclusions</p> <p>In conclusion, the Ras/ERK pathway at least in part contributes to the maintenance and the acquisition of stem-like hallmarks, although the extent of its contribution is varied in a cell type-specific manner. These findings could help our comprehensive understanding of tumor stemness, and also improve the development of eradicative therapies against human malignancies.</p

Identification of hypoxia-inducible factor 1 ancillary sequence and its function in vascular endothelial growth factor gene induction by hypoxia and nitric oxide.

Transcription of hypoxia-inducible genes is regulated by hypoxia response elements (HREs) located in either the promoter or enhancer regions. Analysis of these elements reveals the presence of one or more binding sites for hypoxia-inducible factor 1 (HIF-1). Hypoxia-inducible genes include vascular endothelial growth factor (VEGF), erythropoietin, and glycolytic enzyme genes. Site-directed mutational analysis of the VEGF gene promoter revealed that an HIF-1 binding site (HBS) and its downstream HIF-1 ancillary sequence (HAS) within the HRE are required as cis-elements for the transcriptional activation of VEGF by either hypoxia or nitric oxide (NO). The core sequences of the HBS and the HAS were determined as TACGTG and CAGGT, respectively. These elements form an imperfect inverted repeat, and the spacing between these motifs is crucial for activity of the promoter. Gel shift assays demonstrate that as yet unknown protein complexes constitutively bind to the HAS regardless of the presence of these stimuli in several cell lines, in contrast with hypoxia- or NO-induced activation of HIF-1 binding to the HBS. A common structure of the HRE, which consists of the HBS and the HAS, is seen among several hypoxia-inducible genes, suggesting the presence of a novel mechanism mediated by the HAS for the regulation of these genes

Pair Plasma Dominance in the Parsec-Scale Relativistic Jet of 3C345

We investigate whether a pc-scale jet of 3C345 is dominated by a normal plasma or an electron-positron plasma. We present a general condition that a jet component becomes optically thick for synchrotron self-absorption, by extending the method originally developed by Reynolds et al. The general condition gives a lower limit of the electron number density, with the aid of the surface brightness condition, which enables us to compute the magnetic field density. Comparing the lower limit with another independent constraint for the electron density that is deduced from the kinetic luminosity, we can distinguish the matter content. We apply the procedure to the five components of 3C345 (C2, C3, C4, C5, and C7) of which angular diameters and radio fluxes at the peak frequencies were obtainable from literature. Evaluating the representative values of Doppler beaming factors by their equipartition values, we find that all the five components are likely dominated by an electron-positron plasma. The conclusion does not depend on the lower cutoff energy of the power-law distribution of radiating particles.Comment: 17 page

Suppression of Interferon-induced Oligo-2\u27, 5\u27-adenylate Synthetase Induction in Human Hepatoma Cell Line, Li-7

Induction of oligo-2\u27, 5\u27-adenylate synthetase (2-5AS) activity by interferon (IFN) was investigated in a human hepatoma cell line, Li-7 cells. Little induction of 2-5AS activity by IFN was demonstrated in Li-7 cells in comparison with other types of cell lines including Ramos, NC-37, FL, Co-3. Furthermore, failure to induce 2-5AS was much clearer in old-cultured cells. Cell growth inhibition by IFN was demonstrated in only high titers of IFN (>10? IU/ml), in which the enzyme had one hundred fold higher activity than that of untreated cells. Poor induction of 2-5AS was in part the result of some inhibitor presented in cellular extracts of Li-7 cells and the decreased level of 2-5AS mRNA transcription

Tuberous Sclerosis 2 Gene Is Expressed at High Levels in Specific Types of Neurons in the Mouse Brain

Tuberous sclerosis (TSC) is an autosomal dominant disorder characterized by mental retardation, epilepsy and hamartomatous growth in many tissues. The gene (TSC2) encoding a tumor suppressor protein whose mutations cause TSC, has been demonstrated to be expressed at high levels in the adult and developing brain, raising the question of whether or not the TSC2 gene product has unique roles in differentiation related to cytoskeletal interactions within the central nervous system, in addition to a tumor suppressor function. To determine the expression of TSC2 in functionally distinct neuron types of the mouse brain, we carried out in situ hybridization with digoxigenin-labeled riboprobes for the detection of TSC2 mRNA. High levels of the TSC2 gene were in neurons of the pyramidal and dentate granular layer in the hippocampus, cerebellar Purkinje cells, neurons of the piriform cortex, motor neurons in the medulla and interneurons in the striatum, while intermediate levels were in cortical neurons, striatal neurons, septal neurons, thalamic neurons and neurons in the substantia nigra compacta. Thus, the high expression of the TSC2 gene has restricted distribution in specific neuronal types which are characterized by well-developed dendrites and rich in use-dependent long-term changes in synaptic efficacy. These results suggest that the function of the TSC2 gene product may be involved on a cellular basis in neuronal plasticity and relevant to mental retardation observed in TSC patients