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Novel Low Cost Ripple Based Controlled Pulse Width Modulator for Fast Transient Response
S.Hirose,K.Ono,T.Sato,T.Nabeshima,K.Nishijima 전력전자학회 2011 ICPE(ISPE)논문집 Vol.2011 No.5
This paper presents novel pulse width modulation circuit for fast transient response. In the proposed modulator, C-MOS logic inverters are used instead of high speed comparators. Four types of new modulator are proposed and operating principle described in detail. The proposed modulator is applied to a buck converter, and steady state characteristics and frequency response of the proposed modulator are measured with the bread board circuit. From the experimental result, it is found that the proposed modulator has the derivative characteristics as hysteretic PWM controller that has good transient performance. Excellent load and line regulation are obtained. By using C-MOS inverter, compared with conventional hysteretic PWM controller with fast comparator, cost is reduced to one-fifth.
Hirose, S.,Iijima, T.,Adachi, I.,Adamczyk, K.,Aihara, H.,Al Said, S.,Asner, D. M.,Atmacan, H.,Aushev, T.,Ayad, R.,Aziz, T.,Babu, V.,Badhrees, I.,Bakich, A. M.,Bansal, V.,Berger, M.,Bhardwaj, V.,Bhuyan American Physical Society 2018 Physical Review D Vol.97 No.1
<P>With the full data sample of 772 x 10(6) B (B) over bar pairs recorded by the Belle detector at the KEKB electron-positron collider, the decay (B) over bar -> D+ tau(-)(nu) over bar (tau) is studied with the hadronic tau decays tau(-) -> pi(-)nu(tau) and tau(-) -> rho(-)nu(tau). The tau polarization P-tau(D*) in two-body hadronic tau decays is measured, as well as the ratio of the branching fractions R(D*) = B((B) over bar -> D*tau(-) (nu) over bar (tau))/B((B) over bar -> D*l(-) (nu) over bar (l),where l(-) denotes an electron or a muon. Our results, P-tau (D*) = - 0.38 +/- 0.51(stat)(+0.21)(-0.16) (syst) and R(D*) = 0.270 +/- 0.035(stat)(+0.028)(-0.025)(syst), are consistent with the theoretical predictions of the standard model. The polarization values of P-tau(D*) > +0.5 are excluded at the 90% confidence level.</P>
K. Hirose,T. Ohtsuki,Y. Shibasaki,N. Iwasa,J. Hori,S. Sekimoto,K. Takamiya,H. Yashima,K. Nishio,Y. Kiyanagi 한국물리학회 2011 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.59 No.23
The cross section for the neutron-induced fission of ^(237)Np was measured in an energy range from 0.1 eV to 2 keV using the lead slowing-down neutron spectrometer at the Research Reactor Institute, Kyoto University. The relative cross sections were obtained from the energy-dependent neutron flux measured using a BF^3 counter. The relative cross section for each (n,f) was normalized to the absolute value which obtained using the reference cross section for ^(235)U(n,f) between 100 eV and 1 keV.
Miyake, N.,Tsukaguchi, H.,Koshimizu, E.,Shono, A.,Matsunaga, S.,Shiina, M.,Mimura, Y.,Imamura, S.,Hirose, T.,Okudela, K.,Nozu, K.,Akioka, Y.,Hattori, M.,Yoshikawa, N.,Kitamura, A.,Cheong, H.,Kagami, S University of Chicago Press [etc.] 2015 American journal of human genetics Vol.97 No.4
The nuclear pore complex (NPC) is a huge protein complex embedded in the nuclear envelope. It has central functions in nucleocytoplasmic transport, nuclear framework, and gene regulation. Nucleoporin 107 kDa (NUP107) is a component of the NPC central scaffold and is an essential protein in all eukaryotic cells. Here, we report on biallelic NUP107 mutations in nine affected individuals who are from five unrelated families and show early-onset steroid-resistant nephrotic syndrome (SRNS). These individuals have pathologically focal segmental glomerulosclerosis, a condition that leads to end-stage renal disease with high frequency. NUP107 is ubiquitously expressed, including in glomerular podocytes. Three of four NUP107 mutations detected in the affected individuals hamper NUP107 binding to NUP133 (nucleoporin 133 kDa) and NUP107 incorporation into NPCs in vitro. Zebrafish with nup107 knockdown generated by morpholino oligonucleotides displayed hypoplastic glomerulus structures and abnormal podocyte foot processes, thereby mimicking the pathological changes seen in the kidneys of the SRNS individuals with NUP107 mutations. Considering the unique properties of the podocyte (highly differentiated foot-process architecture and slit membrane and the inability to regenerate), we propose a ''podocyte-injury model'' as the pathomechanism for SRNS due to biallelic NUP107 mutations.