The design and performance of a compact WR3-band 2-bit phase shifter manufactured in a 35-nm InGaAs technology are described. To compensate the loss of the phase shifting networks, active single-pole ...double-throw switches are embedded. The 180° and 90° phase shifting networks are based on a broadside-coupled 1:1 magnetic transformer and a hybrid edge-coupled tandem coupler, respectively. Measurements show a maximum gain of 0.22 dB with a 3-dB bandwidth of 44 GHz ranging from 235 to 279 GHz. Root-mean-square gain and phase errors are below 0.18 dB and 2.8°, respectively.
An experiment (E166) at the Stanford Linear Accelerator Center has demonstrated a scheme in which a multi-GeV electron beam passed through a helical undulator to generate multi-MeV, circularly ...polarized photons which were then converted in a thin target to produce positrons (and electrons) with longitudinal polarization above 80% at 6 MeV. The results are in agreement with GEANT4 simulations that include the dominant polarization-dependent interactions of electrons, positrons, and photons in matter.
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A millimeter-wave monolithic integrated circuit power amplifier operating in the frequency range between 186 and 212 GHz is presented. The amplifier, dedicated to high-resolution imaging radar and ...communication systems, is realized in a 100 nm gate length metamorphic high electron mobility transistor technology. The three-stage design with four parallel transistors in the output stage achieves a linear gain of more than 12 dB and provides a saturated output power of more than 9 dBm and 7 dBm at 192 and 200 GHz, respectively.
Peroxiredoxin (Prx) is an important antioxidant defense enzyme that reduces hydrogen peroxide to molecular oxygen by using reducing equivalents from thioredoxin. We report that lung Prx I messenger ...RNA (mRNA) is specifically upregulated by oxygen. Throughout the third trimester, mRNA for Prx I was expressed constitutively at low levels in fetal baboon lung. However, after premature birth (125 or 140 d gestation), lung Prx I mRNA increased rapidly with the onset of oxygen exposure. Premature animals (140 d) breathing 100% O(2) developed chronic lung disease within 7 to 14 d. These animals had greater lung Prx I mRNA after 1, 6, or 10 d of life than did fetal controls. In 140-d animals given lesser O(2) concentrations (as needed) that did not develop chronic lung disease, lung Prx I mRNA also was increased on Days 1 and 6, but not Day 10. In fetal distal lung explant culture, Prx I mRNA was elevated in 95% O(2), relative to 1% oxygen, and remained elevated at 24 h. Prx protein activity increased in 140-d premature baboons exposed to as-needed oxygen. By contrast, there was a decrease in Prx activity in 140-d premature baboons exposed to 100% oxygen. In the lung explants from prematures (140 d), there was no significant increase in Prx activity in response to 24 h exposure to hyperoxia, whereas exposure of explants to 48 h hyperoxia caused a nonsignificant decrease in Prx activity. Treatment of lung explants with actinomycin D inhibited Prx mRNA increases in 95% oxygen, indicating transcriptional regulation. In cellular signaling studies we demonstrated that protein kinase (PK) C activity increased when A549 cells were exposed to 95% oxygen, compared with 21% oxygen exposure. In lung explant cultures, specific PKC inhibitors calphostin C or GF109203X inhibited the increase in Prx I mRNA with 95% oxygen exposure, indicating PKC-mediated signaling. The acute increase in gene expression of Prx I in response to oxygen suggests an important role for this protein during the transition from relatively anaerobic fetal life to oxygen-breathing at birth.
A major goal of cancer chemotherapy is the identification of cytotoxic compounds that are highly selective for cancer cells. We describe here one such compound - a novel iron chelator, ...desferri-exochelin 772SM. This desferri-exochelin has unique chemical and pharmacological properties, including extremely high iron binding affinity, the capacity to block iron-mediated redox reactions, and lipid solubility which enables it to enter cells rapidly. At low concentrations, this desferri-exochelin kills T47D-YB and MCF-7 human breast cancer cells by inducing apoptosis, but only reversibly arrests the growth of normal human mammary epithelial cells without cytotoxicity. Since iron-loaded exochelin is ineffective, iron chelation accounts for the efficacy of desferri-exochelin. For both the killing of breast cancer cells and the growth arrest of normal breast epithelial cells, desferri-exochelin was effective at much lower concentrations than the lipid-insoluble iron chelator deferoxamine, which has shown only limited potential as an anti-cancer agent. Growth arrest of progesterone receptor positive T47D-YB cells with the progestin R5020 transiently protects them from the cytotoxic effects of desferri-exochelin, but the cells are killed after cell growth resumes. Similarly, MCF-7 cells arrested with the estrogen antagonist ICI182780 are transiently resistant to killing by desferri-exochelin. Thus the desferri-exochelin is cytotoxic only to actively growing tumor cells. Since desferri-exochelin 772SM can selectively and efficiently destroy proliferating cancer cells without damaging normal cells, it may prove useful for the treatment of cancer.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
mcm5/cdc46-bob1 bypasses the requirement for the S phase activator Cdc7p Hardy, C.F.J. (Washington University School of Medicine, St. Louis, MO.); Dryga, O; Seematter, S ...
Proceedings of the National Academy of Sciences - PNAS,
(1 Apr 1997), 19970401, 1997-04-01, 1997-Apr-01, 1997-04-00, Volume:
94, Issue:
7
Journal Article
Peer reviewed
Open access
Cdc7p is a protein kinase that is G1/S transition and initiation of DNA replication in Saccharomyces cerevisiae. The mechanisms whereby Cdc7p and its substrates exerts their effects are unknown. We ...report bite the characterization in S. cerevisiae of a recessive mutation in a member of the MCM family MCM5/CDC46, which bypasses the requirement for Cdc7p and its interacting factor Dbf4p. Because the MCM family of evolutionarily conserved proteins have been implicated in restricting DNA replication to once per cell cycle, our studies suggest that Cdc7p is required late in G1 because in its absence the Mcm5p/Cdc46p blocks the initiation of DNA replication. Moreover, Mcm5p/Cdc46p may have both positive and negative effects on the ability of cell to initiate replication
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