PDP and OPAP and vinyl pyrimidine:
PDP:
related to digital and phone and human?
Simulation of Drosophila Circadian Oscillations, Mutations, and Light Responses by a Model with VRI, PDP-1, and CLK
Paul Smolen†, Paul E. Hardin*, Brian S. Lo†, Douglas A. Baxter† and John H. Byrne†, Go To Corresponding Author,
† Department of Neurobiology and Anatomy, W. M. Keck Center for the Neurobiology of Learning and Memory, The University of Texas-Houston Medical School, Houston, Texas
* Department of Biology and Biochemistry, University of Houston, Houston, Texas
Address reprint requests to John H. Byrne, Dept. of Neurobiology and Anatomy, W. M. Keck Center for the Neurobiology of Learning and Memory, The University of Texas-Houston Medical School, PO Box 20708, Houston, TX 77225. Tel.: 713-500-5602; Fax: 713-500-0623.
Abstract
A model of Drosophila circadian rhythm generation was developed to represent feedback loops based on transcriptional regulation of per, Clk (dclock), Pdp-1, and vri (vrille). The model postulates that histone acetylation kinetics make transcriptional activation a nonlinear function of [CLK]. Such a nonlinearity is essential to simulate robust circadian oscillations of transcription in our model and in previous models. Simulations suggest that two positive feedback loops involving Clk are not essential for oscillations, because oscillations of [PER] were preserved when Clk, vri, or Pdp-1 expression was fixed. However, eliminating positive feedback by fixing vri expression altered the oscillation period. Eliminating the negative feedback loop in which PER represses per expression abolished oscillations. Simulations of per or Clk null mutations, of per overexpression, and of vri, Clk, or Pdp-1 heterozygous null mutations altered model behavior in ways similar to experimental data. The model simulated a photic phase-response curve resembling experimental curves, and oscillations entrained to simulated light-dark cycles. Temperature compensation of oscillation period could be simulated if temperature elevation slowed PER nuclear entry or PER phosphorylation. The model makes experimental predictions, some of which could be tested in transgenic Drosophila.
www.cell.com/biophysj/abstract/S0006-3495(04)74332-5=========================
Biological clocks are internal mechanisms that control the timing of daily activities in living organisms. In Drosophila melanogaster, these circadian clocks are regulated by a small group of genes including per (period), tim (timeless), dbt (double-time), clk (clock), cyc (cycle), sgg (shaggy), Pdp1 (PAR domain protein 1) and vri (vrille) loci. Mutations in any of these genes can lengthen or shorten the period of behavioral and other circadian rhythms or can abolish the rhythms altogether. The abundance of per, tim, vri, Pdp1 and clk RNA and their encoded proteins changes rhythmically with a circadian period in wild-type flies. Mutations affecting any of these genes have corresponding effects on behavioral and molecular rhythms.
Dr. Young has been studying circadian clocks for nearly three decades with a focus on their cellular and molecular machinery. Research from the Young lab led to the discovery of most of the genes listed above. Two of the genes make key proteins, TIM and PER, that shift their subcellular location in a 24-hour cycle. Dr. Young and his colleagues found that these two proteins accumulate, pair up in the cell’s cytoplasm and then migrate into the nucleus where their presence switches off their production by shutting down the per and tim genes. These events are strictly timed within the cell, as PER and TIM are retained in the cytoplasm for a fixed interval of several hours. This delay promotes RNA and protein rhythms and determines the period of the clock. Another of the Young lab’s discoveries is that the enzyme casein kinase 1 (DBT) regulates the pace of this 24-hour molecular clock by restricting the longevity of the PER protein in this process. Others have recently shown that faulty interactions between casein kinase 1 and PER are responsible for certain heritable sleep disorders in humans.
www.rockefeller.edu/research/abstract.php?id=158Eye recognition, digital TV? and phones?
Phosphors emit light on TV.
Plasma display
A plasma display panel (PDP) is a type of flat panel display common to large TV displays (32" inches or larger). Many tiny cells between two panels of glass hold a mixture of noble gases. The gas in the cells is electrically turned into a plasma which then excites phosphors to emit light. Plasma displays should not be confused with LCDs, another lightweight flatscreen display using different technology.[1][2
en.wikipedia.org/wiki/Plasma_displaydisturbance of retina?
Evaluation of binary-coded light-emission-period schemes forimproving the moving image quality on PDP
Chern-Lin Chen Ching-Te Tseng Shin-Tai Lo Lee, K.
Dept. of Electr. Eng., Nat. Taiwan Univ., Taipei ;
This paper appears in: Information Display, 1999. ASID '99. Proceedings of the 5th Asian Symposium on
Publication Date: 1999
On page(s): 309-313
Meeting Date: 03/17/1999 - 03/19/1999
Location: Hsinchu, Taiwan
ISBN: 957-97347-9-8
References Cited: 7
INSPEC Accession Number: 6429797
Digital Object Identifier: 10.1109/ASID.1999.762769
Current Version Published: 2002-08-06
Abstract
While a moving image is displayed on an AC-PDP, disturbances of gray scales and colors may be observed. Various methods to improve the image quality are quantitatively compared. Motion image disturbance on an AC-PDP has been simulated on a computer by using a simple eye-tracking model to simplify the relation between the moving image on the AC-PDP, light emission from the PDP, and the captured image with disturbance on the retina. From the simulation results, we can easily choose an effective light emission scheme to improve the moving image quality of an AC-PDP
ieeexplore.ieee.org/xpl/freeabs_all.jsp?arnumber=762769skyship