text:
Dick Giordano/Executive Editor, Paris Cullins/Cover Artist, Mike Machlan/Cover Artist,
Dan Mishkin/Writer
Rick Hoberg/Penciler
Mike Gustovich/Inker
Gene D'Angelo/Colourist
John Costanza/Letterer
Alan Gold/Editor
Justice League of America (New Earth)/Appearances
Ralph Dibny (New Earth)/Appearances
Cynthia Reynolds (New Earth)/Appearances
J'onn J'onzz (Earth-One)/Appearances
Paco Ramone (New Earth)/Appearances
Mari McCabe (New Earth)/Appearances
Zatanna Zatara (New Earth)/Appearances
Ronald Raymond (New Earth)/Appearances
Martin Stein (New Earth)/Appearances
Dinah Laurel Lance (New Earth)/Appearances
Oliver Queen (New Earth)/Appearances
Katherine Sutton (New Earth)/Appearances
Kal-El (Earth-One)/Appearances
Outsiders (New Earth)/Appearances
Bruce Wayne (Earth-One)/Appearances
Jefferson Pierce (New Earth)/Appearances
Brion Markov (New Earth)/Appearances
Red Tornado (New Earth)/Appearances
Susan Dearbon (New Earth)/Appearances
Dale Gunn (New Earth)/Appearances
Justice League Satellite I/Appearances
Africa/Appearances
United States of America/Appearances
Michigan/Appearances
Lansing/Appearances
New York/Appearances
California/Appearances
San Francisco/Appearances
Australia/Appearances
Sydney/Appearances
Trick Arrows/Appearances
1985, November
August 7, 1985 (Publication)
1985, August (Publication)
Justice League of America Annual Vol 1
Copper-Age
Justice League of America Annual Vol 1 3
"Force of Nature": The synopsis for this issue has not yet been written.
"Force of Nature"
Part of the "Crisis on Infinite Earths" event.
Justice League of America Annual Vol 1 #3
Paris Cullins
Mike Machlan
Dan Mishkin
Rick Hoberg
Mike Gustovich
Gene D'Angelo
John Costanza
Alan Gold
Justice League of America Annual # 2 —
Justice League of America Annual #3 is an issue of the series Justice League of America Annual (Volume 1) with a cover date of November, 1985. It was published on August 8, 1985.
1 Synopsis for "Force of Nature"
2 Appearing in "Force of Nature"
Synopsis for "Force of Nature"
Appearing in "Force of Nature"
Elongated Man
Zatanna Zatara
Martin Stein
Black Canary (Dinah Laurel Lance)
Green Arrow (Ollie Queen)
Kathy Sutton
Geo-Force
Red Tornado
Sue Dibny
Dale Gunn
Dr. Sarti
Justice League Satellite I (Destroyed)
Kathy Sutton Residence
Trick Arrows
Reprinted in Crisis on Infinite Earths Companion: Deluxe Edition Vol. 3.
This story occurs following and simultaneous to elements of Crisis on Infinite Earths #8.
There are three panels on page 24 where Martian Manhunter is erroneously drawn as a background character standing, with other JLA members, on a dam. As seen on previous and subsequent pages, at that moment he is high in Earth's atmosphere attempting to destroy orbiting satellites.
Cover gallery for the Justice League of America Annual series
Crisis on Infinite Earths Crossover
The events from this issue or series are related to the Crisis on Infinite Earths, a reality-spanning event which led to the destruction of the original Pre-Crisis Multiverse.
This template will categorize articles that include it into the Crisis on Infinite Earths category.
Crisis on Infinite Earths #1 • Crisis on Infinite Earths #2 • Crisis on Infinite Earths #3 • Crisis on Infinite Earths #4 • Crisis on Infinite Earths #5 • Crisis on Infinite Earths #6 • Crisis on Infinite Earths #7 • Crisis on Infinite Earths #8 • Crisis on Infinite Earths #9 • Crisis on Infinite Earths #10 • Crisis on Infinite Earths #11 • Crisis on Infinite Earths #12
Tie-Ins
All-Star Squadron #50 • All-Star Squadron #51 • All-Star Squadron #52 • All-Star Squadron #53 • All-Star Squadron #54 • All-Star Squadron #55 • All-Star Squadron #56 • Amethyst (Volume 2) #13 • Blue Devil #17 • Blue Devil #18 • DC Comics Presents #86 • DC Comics Presents #87 • DC Comics Presents #88 • Firestorm (Volume 2) #41 • Firestorm (Volume 2) #42 • Green Lantern (Volume 2) #194 • Green Lantern (Volume 2) #195 • Green Lantern (Volume 2) #198 • Infinity Inc. #18 • Infinity Inc. #19 • Infinity Inc. #20 • Infinity Inc. #21 • Infinity Inc. #22 • Infinity Inc. #23 • Infinity Inc. #24 • Infinity Inc. Annual #1 • Justice League of America #244 • Justice League of America #245 • Justice League of America Annual #3 • Legion of Super-Heroes (Volume 3) #18 • Losers Special #1 • New Teen Titans (Volume 2) #13 • New Teen Titans (Volume 2) #14 • Omega Men #31 • Superman #414 • Superman #415 • Swamp Thing (Volume 2) #46 • Wonder Woman #327 • Wonder Woman #328 • Wonder Woman #329
Retrieved from "https://dc.fandom.com/wiki/Justice_League_of_America_Annual_Vol_1_3?oldid=2664224"
Paris Cullins/Cover Artist
Mike Machlan/Cover Artist


Lewisham NHS workers took part in a four-hour nationwide strike today in an attempt to secure a 1% pay rise for all NHS staff.
The strike, which was expected to affect NHS services across England and parts of Northern Ireland, had an impressive turnout in the Lewisham borough as ambulance services, midwives and nurses formed picket lines outside their work place.
The strike was called after the government refused to give workers both a promised 1% pay rise and an annual salary increment based on seniority.. Five unions called for a strike in an attempt to force Health Secretary Jeremy Hunt to make more money available to NHS staff.
Health Minister, Jeremy Hunt told the BBC Radio 4 Today programme that hospitals would be forced to lay off staff if the recommended pay award was met in full.
Maggie, also an NHS worker at Lewisham Hospital said: ''We want to get more than 1%. If the MPs can give themselves 11% then why shouldn't we? But we also want to save the NHS from cuts and privatisation and the whole destruction of the health service as we know it, which is what the current government are trying to do.
Len McCluskey, general secretary of Unite, accused the Conservatives of "lying" over their treatment of the NHS.
Under the coalition, NHS staff have seen their earnings cut by 15% in real terms.
According to The Guardian, the five unions involved in the nationwide stoppage represent less than half the 1 million staff in the NHS.
It is thought that the strike affected some non-urgent operations and routine appointments. Ambulance services were the most likely to be affected, and in London patients were warned that they may have to make their own way to hospital.
A man, who asked not to be named, was visiting Lewisham Hosptial during the strikes with his daughter. He said he feared his daughter's appointment with a nurse was going to be cancelled, however it was only rescheduled until later that morning.


It might have been difficult for a Black Metal fan to have heard of these guys, a couple of years ago. Enslaved, a Norwegian Black Metal band that has stepped outside the all too common "let's burn the church down" (Both literally and metaphorically) underground, keeping the same rebellious insightful edge and channeling their anger wisely into their lyrics and Music.
I will not bore you with a summary of how Enslaved came to be, instead I will stick to discussing their recent releases on both the Musical and lyrical levels.
Enslaved has been making their steady ascend towards prominence, becoming a solid figure in the Black Metal underground even though they have followed their own route adopting subtle themes for their lyrics. These guys don't only create Music about their viking heritage, but they also look like grand warriors trapped in the 21st century.
With their last release in 2008, Vertebrae. The band keeps setting itself apart from the rest of the prevalent Black Metal scene in Norway, becoming more international and more "audience friendly" but extremely witty and talented nevertheless.
This last composition by Enslaved is more melodic than its predecessors with more progressive elements. It is this induced variety that makes Vertebrae ever so enjoyable, proving that growth is as important as consistency. If you compare it to their earlier releases, Vertabrae certainly isn't as raw and was forged with a less than an "in your face" approach by the Norwegian Musicians.
Enslaved's fascination with nature and it's mighty force has very well reached its golden era through Vertebrae.
"To the Coast" can be described as "darker" than "Clouds" right from the beginning, the Metal pioneers proceed to deliver a dark song embracing the ambiguous.
Another well delivered and dark melodic track is "Vertebrae" keeping a steady beat first 2:40 minutes of the song. But even in its tranquility and melodic vocals, it maintains the dark atmosphere with cleverly inserted keys.
"New Dawn" starts out with a very promising intro, a promising underground sounding guitar effect that bursts out into a very catchy old-school melody until the chorus hits. That's when things get a little chaotic and one looses grip over instruments' singularity. However, the disappointment doesn't last long, the song kicks back into the intro riff to introduce another well crafted build up with mesmerizing clear vocals. A great track when broken down, but not Enslaved's best as an overall view.
The mellowest track on the record, yet the most haunting of which. "Center" marks Enslaved's new approach to the ominous and vague. Screatchy whispers dominate the song, until it all explodes for a brief moment before the haunting mood settles back again till the end of the song. With the prevalent unsettling atmosphere this song has, I personally find it to be very empowering.
Finally, to bring the journey to an end, comes "The Watcher" (A very subtle title). Another example as to why "Vertebrae" is an all round Epic journey.


text:
Passiflora pergrandis är en passionsblomsväxtart som beskrevs av L.B. Holm-nielsen och J.E. Lawesson. Passiflora pergrandis ingår i släktet passionsblommor, och familjen passionsblomsväxter. Inga underarter finns listade i Catalogue of Life.

Källor

Externa länkar

Passionsblommor
pergrandis

redpajama_set_name: RedPajamaWikipedia


text:
\section{Introduction}
Most living systems have evolved the ability to sense and adapt to environmental fluctuations through several internal biochemical processes. Photoreception is one of the most important signaling processes for several higher organisms. This signaling process starts from activation of the photoreceptor rhodopsin on the membranous disk, which is regulated by negative feedback through activation and repression cascades mediated by several membrane-associated proteins, low-molecular weight signaling molecules, and ions in each rod cell\cite{rod1,rod2,rod3,rod4}.

 Recent studies have demonstrated the phenomenon of the crowding of macromolecules in individual cells, in which the volume fraction of macromolecules is much higher than that observed under typical in vitro conditions \cite{crowd1,crowd2,crowd3,crowd4,crowd5,crowd6,crowd7,crowd8,crowd9,crowd10,crowd11,crowd12,crowd13,crowd14,crowd15,crowd16,crowd17,crowd18,crowd19,crowd20}. Such ``molecular crowding'' is considered to highly suppress the diffusion of molecules\cite{crowd2,crowd3,crowd4,crowd5,crowd6,crowd7,crowd8,crowd9,crowd10,crowd11,crowd12,crowd13,crowd14} ,which ultimately hinders intra-cellular reaction processes but also often enhances protein folding \cite{crowd15,crowd16}, stabilization of the intracellular architecture \cite{crowd17,crowd18}, and processive phosphorylations of ERK mitogen-associated protein kinase and associated gene transcription\cite{crowd19,crowd20,mem1}. In a molecular crowding scenario, the volume fractions of macromolecules on the membranes of cells and in intra-cellular organelles are also considered to be as high as that in the cytoplasm \cite{mem1,mem2,mem3,mem4,mem5,mem6}. Thus, molecular crowding on the cell membrane is expected to have more complex effects for tightly controlled biochemical processes such as the pattern formations of signaling proteins \cite{mem6}.

A high volume fraction of the photoreceptor rhodopsin tends to be maintained in the outer segments of the membranous disks of the rod cells of vertebrates\cite{rod1,rod2,rod3,rod4,rod5,rod6,rod7,rod8}. Indeed, this high packing density of photoreceptors has been proposed to ensure efficient photon capture. On the other hand, recent experimental studies of mouse rod cells showed that activation and relaxation of this signaling pathway in wild type (WT) mouse rod cells was slower than those of mutant cell containing half the amount of rhodopsin on the disk membrane. This fact suggests that the crowding of rhodopsin might actually limit the diffusion of signaling proteins on the disk membrane to slow down the phototransduction processes after rhodopsin activation. \cite{rod4,rod7}.

Recently, theoretical and experimental studies revealed the influence of the crowding of rhodopsin or other molecules on the disk membrane on the activation of the phototransduction process\cite{rod6,rod8,rod9}. Moreover, the influence of the secondary messengers in the cytoplasm, such as $cGMP$, disk membrane shape, and multi-level phosphorylations of rhodopsin on the phototransductions have also been explored with reaction diffusion models\cite{rod7,rod10,rod11,rod12,rod13,rod14}. These studies have successfully depicted the photoresponse behaviors in response to weak light stimuli. However, some of the mechanisms to explain characteristic phenomena observed in experiments have not yet been sufficiently explained yet, including: (i) activation and relaxation of the WT mouse rod cell progresses more slowly than those of mutant cells containing half the amount of rhodopsin on the disk membrane; (ii) the time interval of the photoactive state is drastically prolonged in response to strong light stimuli compared to weak stimuli; (iii) the lifetime of photoactivation exhibits a logarithmic increase with light strength under strong light stimuli.

To address these questions, in this study, we constructed a theoretical model of the whole process of phototransduction occurring in the outer segment of WT and mutant mouse rod cells in order to unveil the characteristics and the mechanism underlying the observed photoresponse behaviors for a wide range of light intensities. Recent experiments have shown that $\sim 20$ types of signaling components such as proteins, low-molecular weight molecules, ions, and their complexes contribute to these processes. Based on these experimental findings, we constructed a rate equation model incorporating the molecular crowding effects of rhodopsin that could hinder the diffusion and reactions of molecules on the disk membrane. We confirmed that the present model can qualitatively reproduce and explain the light intensity-dependent temporal phototransduction behaviors, lifespan of activation, and rhodopsin volume fraction-dependent restrictions of the phototransduction speed in mouse rod cells, as observed in experiments.

\section{Model and methods}
\subsection{Signaling components and reaction network of phototransduction}
The molecular networks of vertebrate phototransduction have been extensively investigated experimentally \cite{rod1,rod2,rod3,rod4}. After activation of rhodopsin ($R$) as $R \to R^*$ ($^*$ indicates the active form) by a light stimulus, the signal goes through a series of activation and relaxation states via the following reactions processes (Fig. 1).

\begin{figure}
\begin{center}
\includegraphics[width=12.0cm]{FIG1r.eps}
\end{center}
\caption{{\bf Illustration of the phototransduction network in the outer segment of a mouse rod cell: } (a) Each circle represents the chemical components of the signaling transduction processes, where red and blue circles indicate chemical components on and outside of the disk membrane, respectively. Arrows represent the reaction process, where red (blue) arrows indicate the transition from the inactive (active) to active (inactive) state of chemical components, such as activation (inactivation), synthesis (degradation), and opening (closing); green arrows indicate the binding and dissociation of chemical components; purple arrows indicate the catalyzations; and black arrows indicate the movement of chemical components. (b) Illustrations of the local part of the outer segment and representation of the relative concentrations of each type of signaling component.}
\end{figure}

Phototransduction starts with the activation of the G-protein transducin ($G$), which diffuses on the disk membrane via collision with photoactivated rhodopsin ($R^*$), as
\begin{eqnarray}
R^* + G \to R^* + G^*,
\end{eqnarray}
where $R^*$ catalyzes the exchange of a GTP for a GDP on $G$.
$G^*$ then diffuses along the membrane surface, and two $G^*$ molecules eventually bind to a single cyclic GMP phosphodiesterase (PDE) to construct a complex, $(2G^* \cdot PDE)$, as
\begin{eqnarray}
2G^* + PDE \rightleftharpoons G^* + (G^* \cdot PDE) \to (2G^* \cdot PDE).
\end{eqnarray}
A membrane-associated regulator of G-protein signaling, $RGS9$, binds to $(2G^* \cdot PDE)$ as
\begin{eqnarray}
(2G^* \cdot PDE) + RGS9 \to (2G^* \cdot PDE \cdot RGS9).
\end{eqnarray}
Then, the G-bound GTP molecules are hydrolyzed and this complex is dissociated as
\begin{eqnarray}
(2G^* \cdot PDE \cdot RGS9) \to 2G +  PDE + RGS9.
\end{eqnarray}

$cGMP$ is synthesized by guanylate-cyclase-activating proteins in the cytoplasm
\begin{eqnarray}
 \to cGMP,
\end{eqnarray}
which opens the $Ca^{2+}$ channel ($Ch$) as
\begin{eqnarray}
n\,cGMP + Ch_c \to n\,cGMP + Ch_o, \,\,\,\,\,\,\,\, Ch_o \to Ch_c.
\end{eqnarray}
Here, $Ch_c$ and $Ch_o$ indicate the closed and open channel, respectively, and $n$ refers to the number of $cGMP$ molecules required to open a channel\cite{rod1,rod2,rod3}. In this study, we assume $n=2$. The hydrolysis of $cGMP$ is accelerated by $(2G^* \cdot PDE)$ as
\begin{eqnarray}
cGMP + (2G^* \cdot PDE) \to (2G^* \cdot PDE) \\
\end{eqnarray}
which results in the closure of $Ca^{2+}$ channels in the membrane.

$Ca^{2+}$ flows into the cytoplasm of the outer segment through the $Ca^{2+}$ channel and is extruded by an $Na^+/Ca^{2+},K^+$ exchanger as
\begin{eqnarray}
Ch_o \to Ch_o + Ca^{2+}, \,\,\,\,\,\,\,\, Ca^{2+} \to .
\end{eqnarray}
If the concentrations of $Ca^{2+}$ become reduced in the outer segment, the rod cell moves into a hyperpolarization state, which can activate the downstream neurons.

Two $Ca^{2+}$s bind to the cytoplasmic protein recoverin ($Rec_c$) as
\begin{eqnarray}
2Ca^{2+} + Rec_c \to Ca^{2+} + (Ca^{2+} \cdot Rec_c) \to 2Ca^{2+} \cdot Rec_c
\end{eqnarray}
and bind to the membrane as
\begin{eqnarray}
 2Ca^{2+} \cdot Rec_c \to 2Ca^{2+} \cdot Rec_m
\end{eqnarray}
($Rec_m$ indicates $Rec$ on membrane.).

Rhodopsin kinase ($RK$) accelerates the inactivation of $R$ through inducing the phospholyration of activated rhodopsin $R^*$ as
\begin{eqnarray}
RK + R^* \to RK + R,
\end{eqnarray}
which triggers the relaxation of this phototransduction. $RK$ is then inactivated by coupling with $(2Ca^{2+} \cdot Rec_m)$ as
\begin{eqnarray}
RK + 2Ca^{2+} \cdot Rec_m \to (2Ca^{2+} \cdot Rec_m \cdot RK),
\end{eqnarray}
and eventually returns to the active form through dissociation of the complex as
\begin{eqnarray}
(2Ca^{2+} \cdot Rec_m \cdot RK) \to 2Ca^{2+} + Rec_c + RK.
\end{eqnarray}

\subsection{Rate equation model}
Recent experiments have mainly focused on the activation and relaxation of cells in response to an instantaneous light stimulus under dark conditions \cite{rod1,rod2,rod3, rod4,rod7}. Thus, we here simulate the same general situations using the following rate equation model.

The density of signaling components $i$ ($[i]$) on the surface of a disk membrane in the outer segment of a rod cell is given as i) $[i]=$ [Number of component $i$ on one surface of the disk membrane] / [Area of the disk membrane] for signaling components on the disk membrane, and ii) $[i]=$ [Half of the number of component $i$ between two neighboring membrane disks] / [Area of the disk membrane] for signaling components in the cytoplasm (Fig. 1(b)). Here, the density of the $Ca^{2+}$ channel is given by [Number of $Ca^{2+}$ channels] / [Area of the cell membrane]. It is noted that each signaling component is assumed to occupy a finite area on the disk membrane. Thus, the total concentration of signaling components on the disk membrane is limited.

Now, for simplicity, we define the concentration of signaling component $i$, $X_i$, as a rescaled  density of signaling component $i$ obeying the limitations
\begin{eqnarray}
\rho = X^t_{R} + X^t_{G} + X^t_{PDE} + X^t_{RGS9} + X^t_{RK}
+ X_{2Ca^{2+}\cdot Rec^m} + X_{2Ca^{2+}\cdot Rec^m\cdot RK} \le 1.
\end{eqnarray}
where $X^t_{i}$ indicates the total concentration of signaling components $i$ (rhodopsin, G-protein, $PDE$, $RGS9$, $RK$, and $Rec$) on the disk membrane.

Based on the reaction processes described in the previous subsection, the rate equations of $X_i$ after instantaneous exposure to a light stimulus are obtained as
\begin{eqnarray}
{\dot X_{R^*}} = -AX_{R^*}X_{RK},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{R}} = AX_{R^*}X_{RK},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{G^*}} = BX_{R^*}X_{G}-C^{+}X_{PDE}X_{G^*}
+C^{-}X_{G^*\cdot PDE}-DX_{G^*}X_{G^*\cdot PDE},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{G^*\cdot PDE}} = C^{+}X_{PDE}X_{G^*}-C^{-}X_{G^*\cdot PDE}
-DX_{G^*}X_{G^*\cdot PDE},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{2G^*\cdot PDE}} = DX_{G^*}X_{G^*\cdot PDE}
-EX_{RGS9*}X_{2G^*\cdot PDE},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{2G^*\cdot PDE \cdot RGS9}} = EX_{RGS9*}X_{2G^*\cdot PDE}
-FX_{2G^*\cdot PDE \cdot RGS9},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{G}} = 2FX_{2G^*\cdot PDE \cdot RGS9}-BX_{R^*}X_{G},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{PDE}} = FX_{2G^*\cdot PDE \cdot RGS9}-C^{+}X_{PDE}X_{G^*}
+C^{-}X_{G^*\cdot PDE},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{RGS9}} = FX_{2G^*\cdot PDE \cdot RGS9}-EX_{RGS9*}X_{2G^*\cdot PDE},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{cGMP}} = G-HX_{2G^*\cdot PDE}X_{cGMP}-IX_{cGMP},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{Ch_o}} = JX_{cGMP}X_{Ch_c} -KX_{Ch_o},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{Ca^{2+}}} = MX_{Ch_o}- NX_{Ca^{2+}}-PX_{Ca^{2+}}X_{Rec^c}  \nonumber \\
-QX_{Ca^{2+}}X_{Ca^{2+}\cdot Rec^c}+2RX_{2Ca^{2+}\cdot Rec^m \cdot RK},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{Ca^{2+}\cdot Rec^c}} = PX_{Ca^{2+}}X_{Rec^c}-QX_{Ca^{2+}}X_{Ca^{2+}\cdot Rec^c},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{2Ca^{2+}\cdot Rec^c}} = QX_{Ca^{2+}}X_{Ca^{2+}\cdot Rec^c}-SX_{2Ca^{2+}\cdot Rec^c},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{2Ca^{2+}\cdot Rec^m}} = SX_{2Ca^{2+}\cdot Rec^c}-TX_{2Ca^{2+}\cdot Rec^m}X_{RK},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{Rec^c}} = RX_{2Ca^{2+}\cdot Rec^m\cdot RK} - PX_{Ca^{2+}}X_{Rec^c},
\end{eqnarray}
\begin{eqnarray}
{\dot X_{RK}} = RX_{2Ca^{2+}\cdot Rec^m\cdot RK} -TX_{2Ca^{2+}\cdot Rec^m}X_{RK},
\end{eqnarray}
and
\begin{eqnarray}
{\dot X_{2Ca^{2+}\cdot Rec^m\cdot RK}} = TX_{2Ca^{2+}\cdot Rec^m}X_{RK}
-RX_{2Ca^{2+}\cdot Rec^m\cdot RK}
\end{eqnarray}
Here, since the time scales of gene expression and protein degradation are much slower than those of the phenomena of focus, we assume conservation of the total concentrations of the following molecules, $X^t_i$, in the outer segment of the rod cell:
\begin{eqnarray}
X^t_{R} = X_{R} + X_{R^*}
\end{eqnarray}
\begin{eqnarray}
X^t_{G} = X_{G}+X_{G^*}+X_{G^*\cdot PDE} + 2X_{2G^*\cdot PDE}
+ 2X_{2G^*\cdot PDE\cdot RGS9},
\end{eqnarray}
\begin{eqnarray}
X^t_{PDE} = X_{PDE} + X_{G^*\cdot PDE} + X_{2G^*\cdot PDE}
+ X_{2G^*\cdot PDE\cdot RGS9},
\end{eqnarray}
\begin{eqnarray}
X^t_{RGS9} = X_{RGS9} + X_{G^*\cdot PDE} + X_{2G^*\cdot PDE\cdot RGS9},
\end{eqnarray}
\begin{eqnarray}
X^t_{RGS9} = X_{RGS9} + X_{G^*\cdot PDE} + X_{2G^*\cdot PDE\cdot RGS9},
\end{eqnarray}
\begin{eqnarray}
X^t_{Ch} = X_{Ch_o} + X_{Ch_c}
\end{eqnarray}
\begin{eqnarray}
X^t_{Rec} = X_{Rec^c} + X_{Ca^{2+}\cdot Rec^c} + X_{2Ca^{2+}\cdot Rec^c}
 + X_{2Ca^{2+}\cdot Rec^m} + X_{2Ca^{2+}\cdot Rec^m\cdot RK},
\end{eqnarray}
and
\begin{eqnarray}
X^t_{RK} = X_{RK} + X_{2Ca^{2+}\cdot Rec^m\cdot RK}.
\end{eqnarray}

\subsection{Implemetation of light stimuli and evaluation of photoactivation of the cell}
In the present arguments, the instantaneous light stimulus is implemented as follows. It is noted that the time course of the presented rate equation model always induces relaxation to a unique stationary state for a given parameter set such as reaction coefficients and $X^t_{i}$, independent of the initial concentrations of the signaling components. Here, the concentrations of signaling components of this stationary state correspond to those of the rod cells kept in darkness for a sufficiently long period of time. Thus, to consider the behaviors of this model in response to an instantaneous light stimulus, we set the state of the system at $t=0$ as follows. First, we make the system relax to the stationary state with long-term simulation. Here, $X_{R^*}$ relaxes to $=0$. Next, after inducing the relaxation, we change the concentration of $X_{R^*}$ from $0$ to $X_{R^*}^0$ ($X_{R}$ from $X_{R}^t$ to $X_{R}^t-X_{R^*}^0$), and set the time as $t=0$. Here, $L = X_{R^*}^0/X_{R}^t$ is considered to be proportional to the intensity of the light stimulus. Then, we define $L$ as the light intensity.

In experiments, the photoactivation of cells was estimated by monitoring the $Ca^{2+}$ flux through $Ca^{2+}$ channels, $\phi$, as $\displaystyle r = 1 - \frac{\phi}{\phi^{dark}}$, where $\phi^{dark}$ indicates the $Ca^{2+}$ flux in the darkness\cite{rod1,rod2,rod3, rod4,rod7}. In the present model, the $Ca^{2+}$ flux is proportional to $X_{Ch_o}(t)$. Thus, we measure
\begin{eqnarray}
r(t) = 1 - \frac{X_{Ch_o}(t)}{X_{CH_o}(0)}
\end{eqnarray}
to estimate the photoactivation of the system.

\subsection{Assumptions of the parameters for WT and mutant models}

The present rate equation model involves a large number of parameters such as the reaction coefficients and the total numbers of chemical components. Now, we assume the following parameter sets for the model to most accurately reproduce and explain several of the experimental results observed in mouse rod cells.

First, we set the total concentration of each signaling component $X^t_{i}$ according to the following assumptions for constructing both the WT model and mutant model of cells. As shown in recent experiments, the area fractions of rhodopsin are expected to be $\sim 0.27$ in WT mouse rod cells, in contrast to $\sim 0.135$ for mutant cells\cite{rod4,rod7}. It is noted that the area fration is restricted to be $\le 1$. In the previous subsection, we set the same restriction for the total concentration of signaling components on the disk membrane. Thus, we assume $X^t_{R} = 0.27$ for the WT model and $X^t_{R} = 0.135$ for the mutant model.

It has also been shown that the expression levels of genes encoding signaling proteins are almost identical between WT and mutant cells, except for rhodopsin\cite{rod4}. Thus, we assume that $X^t_{PDE}$, $X^t_{G}$, $X^t_{RGS9}$, and $X^t_{RK}$ are the same between the WT and mutant models, and their sum obeys $\le 0.4 - X^t_{R}$, since the volume fractions of molecules in normal cells are estimated to be $0.2 \sim 0.4$. In the following arguments, we mainly focus on the cases of $X^t_{G}=0.01$, $X^t_{PDE}=0.1$, $X^t_{RGS9} =0.0005$, and $X^t_{RK}=0.0005$, and the total concentration of $Rec$ in the cytoplasm and that of the channel on the cell membrane are assumed to be $X^t_{Rec}=0.05$ and $X^t_{Ch}=0.05$, respectively.

Next, we consider the reaction coefficients. The reaction coefficients are given as the combinations of the association and/or dissociation rates of molecules and their diffusion constants. However, not all of these values are precisely determined or reported in experiments. Thus, each reaction coefficient is set according to the following naturally assumed facts aiming for simplicity.

A1) In general, the diffusion of molecules on the lipid membrane is slower than that in the cytoplasm, suggesting that two-body reactions occur more frequently in the cytoplasm than on the membrane. Thus, the reaction coefficients for two-body reactions on the disk membrane are considered to be smaller than those in the cytoplasm. In this argument, for simplicity, we assume that the reaction coefficients on both the disk membrane and cytoplasm are respective constant values $k_{mem}$ and $k_{cyt}$, independent of signaling components, when the concentrations of the molecules are diluted.

A2) The diffusion of molecules in cells is restricted by their molecular crowding\cite{crowd2,crowd3,crowd4,crowd5,crowd6,crowd7,crowd8,crowd9,crowd10,crowd11,crowd12,crowd13,crowd14}. Thus, each reaction in a molecularly crowded environment is slower than that in an enviroment with diluted molecules. In this argument, we assume that the effective reaction rate of two-body reactions on the disk membrane and cytoplasm, $k'_{mem}$ and $k'_{cyt}$, obey $k_{mem} : k'_{mem} = 1:(1-\rho)$ and $k_{cyt} : k'_{cyt}= 1:(1-\rho_c)$, where $\rho_c$ refers to the total volume of molecules in the cytoplasm, and is assumed to be constant since the fluctuation of the molecular density in the cytoplasm seems to be small and relax immediately.

Then, the coefficients of the two-body reaction processes on the disk membrane are $A$, $B$, $C^{+}$, $D$, $E$, $S$, $T$ $= k'_{mem} = k_{mem}(1-\rho)$, and $H$, $J$, $P$, $Q$ $= k'_{cyt}$. Here, we regard the degradation of $cGMP$ by $(2G \cdot PDE)$ and the opening of the $Ca^{2+}$ channel by $cGMP$ (reaction (6)) as the representative cytoplasmic reactions, since the diffusion of $cGMP$ in the cytoplasm is an essential determinant of the frequency of these reactions. Moreover, the binding rate of $2Ca^{2+}\cdot Rec^c$ to the disk membrane is assumed to be similar to that of the reactions on the membrane, since this process is also influenced by the molecular concentration on the disk membrane.

A3) The diffusion of $Ca^{2+}$ in the cytoplasm is faster than any other reaction process. Here, we assume that the inflow and outflow rates of $Ca^{2+}$ are the same with $M = N = k_{ion}$, which is set as a large value.

A4) If any $cGMP$ molecules do not bind to the $Ca^{2+}$ channel, this channel is considered to close quickly. Thus, $K =k_c$ is set to be a large value.

A5) The spontaneous reactions are considered to be slower than catalytic reactions. For simplicity, we assume that the coefficients of spontaneous degradation of signaling components are small constant values of $C^{-}$, $F$, $I$, $R$ $=k_{d}$.

A6) The synthesis of molecules is also considered to be a relatively slower reaction. Thus, the production rate of $cGMP$, $G = k_{cG}$, is set to be a small value.

Based on these assumptions, we classify the parameters as follows: L) $k'_{cyt}$, $k_{ion}$, and $k_{c}$ have large values; S) $k_{d}$ and $k_{cG}$ have small values; and M) $k_{mem}$ has an intermediate value. In the following sections, we mainly focus on the results derived in the case of $k'_{cyt} = 1.6 \times 10^5$, $k_{mem} = 8.0 \times 10^4$, $k_{ion}= 1.6 \times 10^5$, $k_{c}= 1.6 \times 10^5$, $k_{d}= 4.0 \times 10^2$, and $k_{cG}= 4.0 \times 10^2$.

\section{Results and discussion}

First, we focus on the time course of $r(t)$ for both the WT and mutant models of mouse rod cells for an appropriately large $L$ (Fig. 2(a,b)). The results showed that the relaxation of the mutant model was faster than that of the WT model for each $L$, which is consistent to experimental observations\cite{rod4,rod7}. Notably, the photoactivated state with large $r(t)$ was prolonged with the appearance of the plateau of $r(t)$ for large $L$ values, a result that has not been obtained in recent theoretical models of the mouse rod cell\cite{rod6,rod7,rod8,rod9,rod10,rod11,rod12,rod13,rod14} but has been observed in experiments\cite{rod1,rod2,rod3,rod4,rod7}.

\begin{figure}
\begin{center}
\includegraphics[width=12.0cm]{FIG2.eps}
\end{center}
\caption{{\bf Time courses of photoactivation of WT and mutant model of mouse rod cell: }  Time courses of the photoactivation, $r(t)$, of the (a) WT and (b) mutant models of the mouse rod cell. The difference of the colors of curves indicate variations in $L$ where purple, green, sky blue, orange, yellow, blue, red, and black curves indicates the cases of $L = 1, 0.75^4, 0.75^8, ... , 0.75^{28}$.}
\end{figure}

Second, the lifespan of the photoactivation of cells, $\tau$, was measured, which is defined as the time interval from the point at which $r(t)$ reaches its maximum $r_{max}$ to the point at which $r(t) = 0.8r_{max}$, based on a recent experiment\cite{rod4} (Fig. 3(a)). For the cases in which $L$ is larger (than $\sim 2.0 \times 10^{-4}$), $\tau$ for the WT model was always longer than that for the mutant model for the same $L$, as observed in the experiment\cite{rod4}. Moreover, in both models, the slope of $\tau$ increased with an increase in $L$, and $tau$ showed a logarithmic increase when $L$ was so large that $r(t)$ reached a plateau. Such phenomena were also observed in the experiment\cite{rod4}. In addition, both the activation and relaxation of the mutant model were faster than those of the WT model in the case of the same $X_{R^*}^0$ ($L=L_w$ for the WT model and $L = 2L_w$ for the mutant model) when $L$ is larger than $\sim 2.0 \times 10^{-4}$ but $X_{R^*}^0$ is small (Fig. 3(d)), as observed in experiments with weak light intensity\cite{rod4,rod7}.

\begin{figure}
\begin{center}
\includegraphics[width=12.0cm]{FIG3.eps}
\end{center}
\caption{{\bf Light intensity dependency of the lifespan of photoactivation time, and time courses of the photoactivation in the WT and mutant models given weak light stimuli: } (a) Lifespan of the photoactivation $\tau$ as a function of light intensity $L$ in the WT (blue) and mutant (red) models, and (b) time courses of $r(t)$ of the WT (blue curve) and mutant (red curve) models for the same small value of $X_{R^*}^0$ ($= 2.41 \times 10^{-4}$).}
\end{figure}

The present model also demonstrated a decrease in $\tau$ for smaller $L$ values (less than $\sim 2.0 \times 10^{-4}$) with an increase in $L$ (Fig. 3(a)). Such behavior has not been reported in any experiments. We speculate that this was due to acceleration in the relaxation of the activation of each rod cell with increasing light intensity within the context of very weak light stimuli. However, this conjecture should be confirmed in future experiments to evaluate the validity of the present model.

\begin{figure}
\begin{center}
\includegraphics[width=12.0cm]{FIG4.eps}
\end{center}
\caption{{\bf Time courses of photoactivation and the light intensity dependency of the lifespan of  photoactivation for the cases of different parameter sets from the ideal case: } The time courses of $r(t)$ of the WT model for the cases of $X^t_{RGS9}$ increase to (a) $0.005$ and (b)$0.05$. The colors of the curves are the same as those described for Fig. 2. (c) Time courses of $r(t)$ of the WT model and (d) the lifespan of the photoactivation $\tau$ as a function of light intensity $L$ in the WT (blue) and mutant (red) models for the case of $X^t_{G}$ increases to $0.05$.}
\end{figure}

Now, we consider the mechanism of the phenomena obtained in the present model. In particular, we focus on the accelerations of the activation and relaxation due to the mutations and the appearances of the plateau of $r(t)$ for large $L$.

The reason for the accelerations in the activation and relaxation in the mutant cell with a reduced rhodopsin density can be easily understood as follows. The limiting steps of the present signaling processes are the two-body reactions on the disk membrane, becauase of the slow diffusion and molecular crowding effects on the membrane. In the mutant model, the concentraton of rhodopsin is half that of the WT model. Thus, the reaction coefficients for the limiting reaction steps of the mutant model are larger than those of the WT model. By this simple fact, the photoactivation and relaxation of mutant cells are more quickly achieved than those of WT cells.

Next, we consider the mechanism of the slow relaxation of $r(t)$ with the appearance of the plateau for large $L$ values. The dominant contribution of the appearance of the plateau is considered to result from the deficiency of $RGS9$; in particular, its concentration is substantially reduced compared to $G$ and $PDE$, which slows down the degradation of $(2G^* \cdot PDE)$ to $2G + PDE$. If $L$ is small, the concentration of $G^*$ is not so large, so that the concentration of $(2G^* \cdot PDE)$ is similar or less than that of $RGS9$. In this case, $(2G^* \cdot PDE)$ is rapidly transformed to $(2G^* \cdot PDE \cdot RGS9)$ and the degradation of $cGMP$ is immediately suppressed. On the other hand, if $L$ becomes large, the concentration of $G^*$ becomes so large that the concentration of $(2G^* \cdot PDE)$ becomes larger than that of $RGS9$. Consequently, most of the $RGS9$ becomes involved in $(2G^* \cdot PDE \cdot RGS9)$, and $cGMP$ continues to be degraded by the remaining $(2G^* \cdot PDE)$. Thus, the transformation from $(2G^* \cdot PDE)$ to $(2G^* \cdot PDE \cdot RGS9)$ is hindered by the conflict of $RGS9$, which induces the observed plateau of $r(t)$ for large $L$

These arguments were confirmed by simulations of the model using larger values of $X^t_{RGS9}$ than $0.0005$ (Fig. 4(a, b)) where the length of the plateau, the range of $L$ with which the plateau appears, was changed. Moreover, the maximum $r(t)$ was reduced with an increase in $RGS9$. Thus, the deficiency of $RGS9$ has a dominant contribution to the amplification and reduction in the rate of relaxation of photoactivation of rod cells.

Finally, we show the typical behaviors obtained by the present model when the parameters are changed from the previously considered ideal cases. If $X^t_{G}$ ($X^t_{PDE}$) becomes so large (small) to approach $X^t_{PDE}$ ($X^t_{G}$) or $X^t_{RK}$ becomes larger, a slow increase in $\tau$ with an increase in $L$ appeared again for larger $L$ values (Fig. 4(c,d)). Similar results were obtained when some reaction coefficients were randomly changed. However, these behaviors have not yet been reported experimentally.

\section{Conclusion}
In this study, we investigated the mouse rod phototransduction process through the development of rate equation models consisting of the chemical components that contribute to the signaling processes into and around the membranous disks in the outer segments of rod cells. By considering the effects of the molecular crowding of rhodopsin on the disk membrane, we could explain the mechanism observed both experimentally and theoretically by which photoactivation and relaxation in the WT mouse rod cell are slower than those of the mutant cell containing half the amount of rhodopsin. We also clarified that the deficiency of $RGS9$ compared to the other molecules on the disk membrane is primarily responsible for inducing prolongation of the photoactivated state of rod cells in response to strong light stimuli; these observations and explanations have not previously been obtained in recent theoretical models.

The present model includes a large number of parameters, and only a portion of these parameters are experimentally derived. Thus, in the presented arguments, we have adopted simple but reasonably appropriate assumptions for estimating the unknown parameters. The accumulation of further experimental data for several of the relevant parameters in the future would allow us to address quantitative considerations and derive several predictions for the realistic behaviors of mouse rod cells. Moreover, the reduction and mathematical analysis of a few effective valuables and their rate equations from the presented model should be conducted in the future in order to unveil more detail properties and mechanisms of these signaling processes.

\section*{Acknowledgment}
The author is grateful to M. Fujii, T. Yamashita, and M. Yanagawa for fruitful discussions. This research is partially supported by the Platform Project for Supporting in Drug Discovery and Life Science Research Platform for Dynamic Approaches to Living System from the Ministry of Education, Culture, Sports, Science (MEXT), the Japan Agency for Medical Research and development (AMED), and the Grant-in-Aid for Scientific Research on Innovative Areas ``Spying minority in biological phenomena (No.3306) (24115515)'' and ``Initiative for High-Dimensional Data-Driven Science through Deepening of Sparse Modeling (No.4503)(26120525)'' of MEXT of Japan.

redpajama_set_name: RedPajamaArXiv


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Departments Character Licensing Catherine Aguilar
In her early career Catherine worked as an in-house designer for the Art Group, a London based card and poster publisher. When she left the company to set up on her own, it was a natural transition to create designs and illustrations for products that she liked and was familiar with, so designs for cards, gift wraps, tableware and stationery items have become her bread and butter.
However, Catherine also creates book covers for several large publishers and takes on graphic design and artworking projects for a variety of companies. Catherine's clients include Vanity Fair, Woman & Home magazine, Tescos, John Lewis and German book publisher Rowholt.
Catherine is an excellent designer to commission. Her ability to understand a complicated brief and her dedication to get the job done to the very best standard mean that she has a 100% success rate for commissions.
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Our Network and Partners
Psychedelia: Love is in the Air!
About Mental Health
Online Resources Promoting Mental Health
Bob Bilodeau
Robert (Bob) Bilodeau, 1948 – 2018
The Our Harbour community has been saddened by the death of Bob Bilodeau, a long-term resident who recently moved to an assisted living facility in Longueuil. We extend our condolences to his large extended family.
His passing particularly affects the residents, staff and volunteers charmed by his special grace and humble manner.
Bob prospered within Our Harbour's protective envelope. His warm, endearing ways and quick smile belied his ongoing struggles with medical issues. Despite being a man of few words, he was known for his epigrams. Asked how he was feeling, he usually deflected concern with a characteristic, "Not too bad."
On June 22nd, Our Harbour hosted a lovely memorial service for Bob officiated by Reverend Jennifer Mountain of the Saint Lambert United Church. Several of the over thirty participants told of Bob's impact on their lives. He will be missed.
His sister, Jocelyn Bilodeau, has asked that, in lieu of flowers, donations be made to Our Harbour.
info@ourharbour.org
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Q: Generate a PDF document and open it in a new window with java bean I'm trying to generate a PDF document and open it in a new window. I create a Servlet to create the PDF and in my backing bean I have this code:
public void viewReport(){
        try {
            FacesContext.getCurrentInstance()
               .getExternalContext().redirect("/app/report.pdf?type=sb");
            return;
        } catch (IOException e) {
            // TODO Auto-generated catch block
            e.printStackTrace();
        }
}

and in my page I have this:
<h:form target="_blank">
<h:commandButton action="#{clientBean.viewReport}" value="#{msgs['button.view']}"/>
</h:form>

The PDF is ok but it opens in the same window. How can I open the PDF in a new window from bean?

A: What about you do it with plain HTML, instead of doing hacks with the bean the server-side?
#{msgs['button.view']}

A: See this example
<h:form target="_blank">
    <h:commandButton value="Download PDF" action="#{myBean.downloadPDF}" />
</h:form>

It uses the same code as your example, the difference is in the backing bean code which does not perform a redirect but instead directly creates and returns a PDF document in the response stream.

redpajama_set_name: RedPajamaStackExchange


text:
Q: Bochner's Theorem for Periodic Functions It's fairly straightforward to prove the following, which seem like special cases of Bochner's Theorem for periodic functions, but don't quite match the statements of Bochner's Theorem that I've seen, because they give a specific form for the nonnegative measure. (To my knowledge Bochner's just states that there exists a certain nonnegative measure.) Are the following stated and proven somewhere in the literature? I've Googled around, but haven't found anything.

*

*Let $f:\mathbb{Z}\to\mathbb{R}$ be an even function with integer period $s$. Then $f$ is positive semidefinite if and only if the discrete Fourier transform $c_0,\ldots,c_{s-1}$ of the sequence $f(0),\ldots,f(s-1)$ satisfies $c_k\geq 0$ for all $k$.

*Let $f:\mathbb{R}\to\mathbb{R}$ be an even function with period $s$ whose Fourier series converge on $[0,s]$. Then $f$ is positive semidefinite if and only if its Fourier series coefficients are all nonnegative.

In (2) above I refer to the exponential form of the Fourier series, i.e. the Fourier series coefficients $c_k$ satisfy
$$ f(x) = \sum_{k=-\infty}^{\infty} c_k \exp(\imath 2 \pi k x / s). $$


text:
Which Came First, Breakfast or the Egg?
America's obsession with eggs is a long-standing tradition, and it shows no signs of slowing down. We take a look at its evolution.
While eggs have been consumed by humans for millennia, it was those inimitable French chefs who realized the incredible functionality of this humble gift of nature. Patrons were delighted with soufflés that mysteriously rose high above the pan rim; creamy mayonnaise that emulsified right before their eyes; and pâte á choux—the divine pastry used for cream puffs, profiteroles and eclairs.
Legend has it that the traditional tall chef toque has 100 pleats to signify 100 ways an accomplished chef can prepare eggs. Today, there would likely be at least one thousand pleats, since chefs now put eggs atop and within countless menu items at all dayparts. It would be difficult to name a food item with more beneficial attributes. Eggs are inexpensive, nutritious, readily available and versatile. They are also a fantastic carrier for other ingredients.
According to the American Egg Board, the United States produces 75 billion eggs each year, about 10 percent of the world's supply. Sixty percent of that 75 billion are used by consumers, nine percent by the foodservice industry, and the remainder is turned into egg products used in foodservice and food manufacturing.
While trailblazing chefs across the country are revolutionizing breakfast, eggs still play a major role. Breakfast is no longer just a daypart; in some operations, it has moved into all dayparts. Ingredients for breakfast dishes are becoming more and more sophisticated, with ancient grains, seafood, specialty meats, fancy fruits and vegetables and all manner of savories and sweets. But today's breakfast menus are still peppered with eggs and egg-based dishes, both classic and contemporary.
At the Atlanta Breakfast Club in Georgia, the zesty Spanish frittata is loaded with three eggs, chorizo sausage, tomatoes, scallions and cheddar cheese. The Terrace Room in the Omni William Penn Hotel in Pittsburgh serves a croque-monsieur for breakfast. It is a sandwich on sourdough that features grilled country ham, gruyere cheese and fried egg (which technically makes it a croque-madame). The hotel's Baltimore Benedict is made with poached eggs, a jumbo lump crab cake and hollandaise.
The lobster hash at New York's tony Oceana is topped with poached eggs and lobster bearnaise. And Oceana's Italian fried eggs come with cured sardines and cherry tomatoes, served with a potato-tomato-onion gratin.
Brennan's, that New Orleans bastion of breakfast, uses more than 450,000 eggs a year in dishes such as eggs Hussarde (Benedict with marchand de vin sauce); eggs Sardou (crispy artichokes, parmesan creamed spinach); and eggs a la Turk (soft scrambled eggs with roasted foie gras).
"We're very particular about our eggs," says Christian Pendleton, Brennan's general manager, "because our reputation depends on them. The yolks are sunset orange, and the flavor is rich and luxurious. We procure them from a local co-op, and spend about $80,000 per year over regular eggs. It's that important."
According to the American Egg Board, the United States produces 75 billion eggs each year.
10% of the world's supply
60% are used by consumers
9% is used by the foodservice industry
The rest is turned into egg product.
Author: Mary Dagget
Categories: Food & Beverage Spotlight, VOL 7 - ISSUE 1 • WINTER 2019


text:
Home Los Angeles Public Library Photo Collection Behind the finish line at Culver City Speedway
Behind the finish line at Culver City Speedway
Title Behind the finish line at Culver City Speedway
Location/Accession Sports-Automobiles-Racing-Culver City.; N-002-497 5x7
Historical Data Jack Prince and Art Pillsbury built the Beverly Hills Speedway in 1919 on 275 acres of land, at a cost of $500,000. The 1.25-mile wood oval, which featured 45-degree banked turns, was funded by a group of actors and others in the industry known as the Beverly Hills Speedway Syndicate. The track was inaugurated on February 28, 1920, but after only four years the 70,000-seat stadium was disassembled to make room for other improvements in the newly incorporated city of Beverly Hills, holding its last race on February 24, 1924 before a crowd of 85,000. The developers eventually moved the racetrack to Culver City, and it was located at the intersection of Culver Blvd and Overland Blvd, right across the street from MGM Studios. It was at this "new" location and "new" track where Red Cariens was involved in a fatal crash on November 29, 1925. It was also at this location where Mickey Rooney's classic racing movie "The Big Wheel" (1949) was shot. This speedway was built at a time when car races were popular, so popular in fact, that there were radio broadcasts from the speedways. California had approximately six wooden track speedways, also known as "toothpick track" speedways. Culver City Speedway operated from December 14, 1924 to March 6, 1927; it was eventually removed to make way for movie studios.
Description Aerial view of the Culver City Speedway, which was in existence as an auto racing venue from December 14, 1924, until March 6, 1927. A cluster of cars are neatly aligned behind a white "hash mark" that is most likely the finish line. The large structure with multi-color tile is the grand stand and the smaller building to the right of it might be a clubhouse or restaurant under construction. The adjacent parking lot is full of cars.
Subject Culver City Speedway.
Racetracks (Automobile racing)--California--Culver City.
Automobile racing--California--Culver City.
Automobiles--California--Culver City.
Parking lots--California--Culver City.
Prince, Jack.
Pillsbury, Art.
Culver City (Calif.).
Internal Notes An additional print is in photograph sleeve.


One family's 'desire for power' cost the nation, says Modi as Congress general secretary visits Varanasi.
NEW DELHI: Prime Minister Narendra Modi launched a scathing attack on the Nehru-Gandhi dynasty on Wednesday just as Congress general secretary Priyanka Gandhi Vadra undertook her first tour of Varanasi, his Lok Sabha constituency.
The PM did so through a detailed blog in which he held the Nehru-Gandhi family responsible for insulting institutions. Vadra, who is Congress in-charge for East Uttar Pradesh, later sought to counter the PM with a similar charge.
"From the press to Parliament. From soldiers to free speech. From the Constitution to the courts. Institutional insult is the Congress way. Everyone is wrong, only the Congress is correct," wrote Modi in a sharp attack on the Congress's first family.
Modi brought up former PM Indira Gandhi for promulgating Emergency and interfering with the judiciary.
"The Emergency made the nation a prison overnight. Even to express was to commit sin…It was Mrs. Indira Gandhi who called for a 'committed judiciary', which seeks to make the courts more loyal to a family than to the Constitution," wrote the PM.
He also recalled how Rajiv Gandhi once called the Planning Commission, then led by Manmohan Singh, "a bunch of jokers".
The response over PM's attack came from Vadra who was in Varanasi as a part of her threeday Ganga Yatra from Prayagraj to Varanasi. "BJP has systematically attacked every institution in last 5 years including the media. PM should stop thinking people are fools and understand that they see through this," she said.
In her yatra over the past three days, Vadra has kept her focus on directly taking on the PM. Now with the PM responding, a shoots of a new contest between PM Modi and Priyanka Gandhi Vadra are set to spice up the 2019 elections.
PM Modi in his speeches makes a constant reference to pre-dominant Congress rule of 70 years in a bid to compare his performance of the last five years.
Will Karthi Chidambaram open his poll account this time?


The AlphaLISA® immunoassay kit for human Alpha-synuclein enables the quantitative determination of Alpha-synuclein in biological fluids such as serum, plasma, cerebrospinal fluid and cell culture supernatants using a homogeneous AlphaLISA assay (no wash steps).
Alpha-synuclein is a 140 amino acids protein primarily expressed in the mammalian brain. It is mainly located at the synaptic end of neurons, where it plays a role in the binding of neurotransmitter-containing vesicles to the membrane and their release outside the cell. It also plays a role in controlling energy production in neural mitochondria. The normal form of the protein is a monomer. However, this protein can form pathological oligomers in diseases such as Parkinson's disease or Lewis body atrophy coupled with neurotransmitters deregulation and inhibition of mitochondrial function. The presence of alpha-synuclein in blood raises the possibility of using the protein as a marker for disease states and to test the effect of drugs on neuronal activity. This kit has been designed for the detection and quantification of alpha-synuclein in serum, plasma, and cell culture supernatants.
This manual explains how to run the AlphaLISA no-wash human a-synuclein detection assay.


There was a great response to our first ever 'Peoples Choice' Indie Games Award at Play Expo. It was a close call, but the winner was Fully Illustrated's awesome historical old school beat'em up Wulverblade.
You can check out an excellent blog post from Fully Illustrated's Michael Heald.


text:
Optical/IP / VoIP Systems
Ericsson Sells PBX Business
Ray Le Maistre, Editor-in-Chief
Ericsson AB (Nasdaq: ERIC) is selling its enterprise PBX business to Canadian firm Aastra Technologies Ltd. for 650 million Swedish Kroner ($103 million) as part of its efforts to focus exclusively on carrier customers. (See Ericsson Sells PBX Biz.)
"Ericsson has a strategic focus on telecommunication operators and service providers, hence considers its enterprise PBX solutions business to be outside its core focus," noted the Swedish giant in its official statement Monday morning.
An Ericsson spokeswoman said the PBX products and associated applications are all sold through partners, and that the Swedish giant is "getting out of the indirect channels business."
She added that the giant vendor does not have any other similar business units to divest.
Aastra generates the vast majority of its sales in Europe and has grown significantly in the region during the past few years following a number of acquisitions. It will take on about 630 staff, of which 360 are based in Sweden. (See Aastra Ups Its Euro Telephony Assault.)
Ericsson's enterprise PBX business, which includes products such as its MX-ONE range of IP PBXs and its SIP-based Enterprise Multimedia Server, generated SEK3 billion ($473 million) in revenues in 2007 from customers in Western and Eastern Europe, the Middle East, Africa, Asia/Pacific, and Latin America.
The sale will slice only about 1.6 percent off Ericsson's annual revenues. The company recently announced 2007 revenues of SEK187.8 billion ($29.6 billion). (See Ericsson Cuts Jobs as H2 Bites.)
The deal will make a significant impact on Aastra's business though, as the revenues from the Ericsson business will add about 75 percent to Aastra's top line.
Aastra, which competes with the likes of Alcatel-Lucent (NYSE: ALU), Avaya Inc. , Cisco Systems Inc. (Nasdaq: CSCO), Nortel Networks Ltd. , and Siemens AG (NYSE: SI; Frankfurt: SIE) in the IP PBX market, generates revenues of around $600 million a year. The Canadian firm is set to report its 2007 financial results on February 20.
The acquisition will give Aastra greater scale in a sector that's set to grow by more than 20 percent during the next three years, from less than $10 billion in 2007 to about $12 billion in 2010, according to Infonetics Research Inc. .
The move doesn't mean Ericsson is abandoning the enterprise space completely, though, as it is still pushing what it calls "enterprise applications" directly to operators. These applications include push email, which is hosted by the carrier but provides service for enterprise customers. Ericsson noted it will be retaining "strategic products from the acquisition of Netwise," a Swedish developer of IP applications acquired in 2006. (See Ericsson Launches Netwise Takeover.)
The sale is expected to close in April 2008, once the deal receives regulatory approval from various competition authorities.
Ericsson's share price is hardly unchanged Monday at SEK14.00 on the Stockholm exchange.
— Ray Le Maistre, International News Editor, Light Reading
douaibei
re: Ericsson Sells PBX Business
Ericsson is focused on the carrier market, but the PBX businss is too small compare to they core business; PBX market need more on the software support which ericsson do not have, so the best option is to spin off the business.
Astra will be ale to develop a competitive UC story in the market
Doesn't size come into this?
I don't know how big the Avaya biz was when it was spun out, but I bet it was WAY bigger than the minnow Ericsson is selling off.
I am sure Ericsson had to make the call between investing heavily to try to make a bigger impression in a market where Cisco, Avaya and Nortel and strong, or back off.
FbytF
Remember Lucent abondoned the Enterprise PBX space by spinning off Avaya to focus on the Carrier space exclusively. A market with too many competitors and not enough customers. See how well it worked out for Lucent. Go Ericsson, you deserve it.
jasanz
What about Alcatel-Lucent? Can the OmniPCX present battle to Cisco Unifed Communications Manager?


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Alex Paul is the award winning author of Arken Freeth and the Adventure of the Neanderthals books series, and co-author of They're Mine and I'm Keeping Them.
Alex Paul lives with his wife Laura Ross-Paul (co-author of They're Mine and I'm Keeping Them), and two faithful dogs, in Portland Oregon in the winter, and the Oregon Coast in the summer.
He trained as an Industrial Engineer at Oregon State University, working in a variety of fields before settling into a career as a real estate developer.
Alex Paul has been a life long outdoors enthusiast, having a wealth of knowledge and experience to draw on for his epic fantasy Arken Freeth series.


Interoperable DOM Events are a core part of delivering the promise of HTML5's "same markup." With DOM Events support in IE9, web developers can write more interoperable code using an event model that is more robust and offers additional functionality not possible in IE's previous model.
With IE9, you can write the same markup and script and have it work across browsers without sacrificing functionality or performance. Please follow best practices to ensure your standards-based event processing runs in IE9. The Platform Preview will let you begin to see how your code will run in IE9. We encourage you to report issues you find. Since IE9 is still in development, the Release Notes and Connect bug database will help you understand if the issue you found is known.
Today developers can't have the same markup run across browsers. IE9's support of DOM Level 3 Events is a huge step forward but doesn't entirely solve the problem. That's why we're working in the W3C to create a high-quality spec and create a test suite to help browsers converge on interoperable behavior.
For several years now, we have been working with the W3C standards organization to provide input and feedback on this latest version of DOM Events. When finished, this "Level 3" version will supersede its nearly 10-year old predecessor, DOM L2 Events. It's been a pleasure to work regularly with members of that working group, representatives from industry, and other browser vendors to ensure that the specification is implementable, meets web developer scenarios, and raises the bar on interoperability.
There are two specific parts of the DOM Level 3 Events specification that I'm particularly excited about from the perspective of interoperability. The first is that IE's "mouseenter/mouseleave" and "focusin/focusout" events have been recently adopted based on their utility and wide-use on the web.
The second is the Keyboard event interface. Did you know that the ubiquitous "keydown" "keyup" and "keypress" events (present in all browsers) were never standardized? This is an example of one of the reasons that web developers don't have the "same markup" (script) running across browsers with regard to the keyboard.
The IE9 platform preview is the first implementation of the Keyboard event interface from the DOM Level 3 Events specification. The Keyboard event interface defines a Keyboard-interaction model that solves longstanding internationalization issues as well as provides a convenient high-level keyboard abstraction (based on Unicode). Naturally, we expect that previous low-level keyboard APIs (e.g., "keyCode"), despite not being 100% interoperable, will coexist in browsers for backwards compatibility. We welcome feedback on this interface, and for those interested in providing feedback directly to the working group, please email www-dom@w3.org.
In our continued efforts to drive interoperability, we have contributed an initial set of tests for the DOM Level 3 Events specification and plan to contribute more in future updates to the Test Center. As the specification evolves toward recommendation status, these tests may also need to evolve. We look forward to feedback on these tests, and welcome test contributions from the community and other implementations to establish a DOM Level 3 test suite that meets the high interoperability goals of the specification.
A "catch-all" listener can be registered on a DOM subtree for an event which does not bubble (requires capture phase).
Guaranteed firing order for multiple listeners on a single node.
Ability to tell which node the event flow is currently on (currentTarget).
The bubble/cancel defaults for many events have changed to match the standard.
Event listener registration for legacy events supported in the new model (using attachEvent/detachEvent) use the same event-firing order as addEventListener.
Registration using the HTML event attributes (and their properties) will simultaneously enable the MSEventObj (legacy event object) through the window.event property as well as the new DOM event via the event handler parameter. We do this because the HTML event attribute registration technique is ambiguous—e.g., did the web developer expect the new DOM Events model or the old IE one?
We built an interactive demo to showcase some of the features of the DOM Events model. Check it out on the IE9 Test Drive site. We also show a simple example of one way in which DOM Events can be used in practice. View it in the IE9 platform preview then view it in another browser; the key takeaway is that the DOM Events model works the same way across browsers—"same markup" in action.
We're still in development so there's more to come. Here are a few top things you may find missing that will be available in a future update to the platform preview. Please read the Release Notes for further information.
Mutation events. The mutation events allow web pages to react to changes in the structure of an HTML document such as changes in attributes, text content, element removals and additions, etc. The DOM Level 2 Events specification defines the mutation events. Note, however, that not all the mutation events are implemented across all browsers.
DOMContentLoaded. The DOM Level 3 Events specification defines the generic event framework and a core set of events, but does not define all the events that are relevant for a web browser to support. HTML5 defines many additional events, most notably DOMContentLoaded and other events related to parsing and loading a webpage.
Compatible event properties. While not standardized, many event properties like "keyCode", "cancelBubble", etc. are widely implemented by other browsers and many web pages depend on their functionality for purposes of interoperability.
We encourage web developers everywhere to start coding primarily to the DOM Event model. Check out the test drive demo and interactive events demo, the DOM Level 3 Events test cases, and send us feedback.


If you are in the habit of listening to your flowers speak, you will hear Monarda's gentle whispers, barely audible between the wind and the crickets, telling you to fly, and to remember. This is a plant of my childhood, a favorite of my mother who would swoon over the beautiful, raggedy fuchsia and purple flowers, and then pull them out by the roots. Both a hardy and prolific grower, Monarda just loves to take over. They do not, in my experience, have a bad growing spot outside of deep shade. As are all members of the Lamiaceae family (think mint, thyme and sage), they are able to adapt and spread in just about any growing condition. I have two types of Monarda in my garden, M.fistulosa, otherwise known as wild bergamot, and M. didyma, which my mother called 'Beebalm.' They do tend to mildew if they get too wet in shade, but mom would cut them to the ground and they would still come back, year after year. It was M. didyma that my mom loved, but the wild bergamot is famous for its medicinal qualities, and was used by Native Americans long before European botanists fell in love. Medicinally, Monarda is a nervine, inspiring both calmness and joy. Herbalists have used her to stimulate renewed hope in those who are experiencing grief. She is often used in poultices and tinctures to treat skin infections and wounds of all types, a use first discovered by the Blackfoot Indians. Monarda is high in thymol, an ingredient often found in mouthwashes and a powerful antimicrobial and antioxidant. A strong tea of the leaves and flowers can be brewed to treat headaches and fevers, a common usage in my household.
We are a group of individuals who feel drawn to an earth-based spirituality who gather to celebrate the cycles of the moon and sun, passages of life and death and to work for positive change within our own lives as well as the lives of those around us. We strive to live in harmony with nature, and its cycles guided by the strength and enduring qualities of the Oak tree and the resilient, nurturing energies of the Willow.
Enjoy a select writing from one of our members. More available on our Tumblr.


It has now become imperative in political discourse to analyze the new meanings of the terms "terror" and "terrorism," as well as their implications in international politics. To a certain extent (and according to the needs of the moment, i.e. the needs of the powerful), the old and traditional meaning of these terms is still being used for conflicts and situations that are considered local and, globally, harmless or lacking any global range or dimension.
Following the paranoia created by the re-established momentum of 9/11 in contemporary history, the recoined use and recent meanings that are devoted to these terms are nowadays applied in the undetermined complex called "Arabic-place-ethnicity-religion-and/or Islam."
State terror is now exclusively considered defensive and preliminarily justified. However, it still includes para-state terror and international "anti-terrorist strategies," along with wars, torture, extraordinary interpretations, extraterritoriality and extra-legality of pre-trial detention, secret detention, man-made droughts, pollution, climate change, famine, etc. Language is not only a means for overcoming conflicts through necessary and welcome negotiations, but also provides a potential space for conflict. Language can (but should not) be as much a weapon as anything else. Therefore, the language "policy" must be researched, as the political (but not politics) "precedes" the language. This is not just a matter of freedom of speech, but also a question: "Who, for what purposes and under what conditions sets these rights and that freedom or that which causes violence?"
And, here comes again a sad drama for humanity, and sustenance for politics. It's about the latest or last event that took place in a country so far from us – in New Zealand. History is filled with such events, and scriptures have shown the true face of infidelity and the danger coming out of it. But then punishments were somehow proof of the abuse of belief and believers. And what to do with man? He likes to be deceived; he has fallen in love with Darwin's animalistic "origin" – wants to be turned into a monkey again. Politics has, as its main sustenance, terrorism, while religion has love and guidance that is why the greatest pain and problem is why have we, heavenly religions, allowed to be subjugated to dangerous, scary games, which are only consuming man. We fell prey to the Sept. 11 games. Imagine, in our time, when everything is somewhat under our control, this expression has been transformed into a myth, for which today the innocent are paying the price, instead of the guilty ones, those who should be punished.
Without going into the depths of history, I want to say that from this century, which is becoming famous for its history filled with blood and corps, we are not taking any lessons. "Why?" is a very important question to be asked in this regard. History without God has been depicted by all religions as very dangerous and one that doesn't do a thing, except for crime and punishment. Such history, knowing where the danger is coming from, relied on power, once of materialism and now of the material, or as a great Serbian chauvinist Dragosh Kalajic has put it, on the power of the dollar, which has become a god. Everyone is bowing before this little god, this god of paper, except the true believer.
Sept. 11, was a spectacle that witnessed something great and scary. Instead of those who organized, planned and executed it to come out, they hid so as to become a myth, a permanent power of punishment and fear. In their stead, those who were not supposed to, came out: The church and the mosque, heavenly religions, although their duty was to sit down, to purify themselves, to submit to God with their prayers. But, what did they do? They rushed toward the myth, which was forbidden to them by God, because religion within itself has never had, has not and will not have violence, and hence allowed themselves to admit that there is violence in religion. Who gave this right to the representatives of heavenly religions!? Were they the holy scriptures and believers? No! Yet, are we believers innocent for that? No, we are equally guilty, because we are giving support to our representatives, who have no spirit or imaan, but only outward look and power, which is no more than a deception.
What was the fault of the Christian people, in this case of New Zealand, to experience the sin of a devilish-terrorist man!? We must be aware that we live in this world where both good and evil, peace and war have existed and continue to exist. Unfortunately, I cannot find the sibling to this terror: Is it terrorism or what? Or, maybe, it is anti-terrorism? It seems that both are terrorism. This kind of acting has become ridiculous: As soon as an incident takes place, instead of shutting it down, it is turned into an exclusivity, and instantly those millions and millions of homeless, starving, expelled, persecuted are forgotten, not to speak about the pain and punishment they suffer. Today, innocent people are being punished each day at airports all around the world. I'm not talking about suspicion, but concretely about their punishment and humiliation. They have made us suspect each other, and that suspicion has become a kind of sustenance, by spying and cheating on each other.
Even the weakest believers have had, and still have, a perception about religion, in the sense that they fear evil, terrorism and especially organized terrorism, which in no case is accidental, and whose beginning and end we are not aware of, because it doesn't stem out of religion, but out of power, out of the desire for power – and politics has such desire. Politics is organizing it; politics has made it a kind of sustenance and has turned us into monkeys; or into players in a football game: Today you will "score," tomorrow I will "score." And what can the masses do – they shout, although there are among them those who understand correctly the game of terrorism. But the masses, at this time when freedom has been taken from them and fear increased in every segment of life, are afraid to drink water, are afraid to feed, because almost everything is out of its wish – not by chance. The issue is why we believers allow ourselves to be deceived, regardless of all good intended sincerity, or the words of New Zealand's Prime Minister Jacinda Ardern, which were deeply humane and wise words, which enable the creation of peace and stability (it was a moment that made me realize that humanity has not died yet); as well as the politeness of the Christians in fighting this terrorism.
There is something else here which deceives us, and my appeal is for us not to fall prey to such filthy games of those who organize and are not "seen." We in fact must fight them: If it's about politics, we should not vote for them; if it's about religious hypocrites, we should not trust them. The best thing that politics can do today is to show the real face of "Sept. 11," and what was really behind it. The war on terrorism has turned into a very dangerous and scary game.
To sum up: I am glad and proud of being a Muslim, of belonging to a religion that has forbidden me to commit crime and punishment; that has allowed me to respect both the believer and the nonbeliever; that has taught me to be cautious toward hypocrisy and the hypocrite; that has obliged me not to vote and support the devil in the form of man and the man in the form of the devil; That has told me to sit "only with the devoted and God-fearful." That demands from me to respect my neighbor, regardless of his religious conviction – as long as he is human; that has made a condition to me not to allow evil to reign and not to support it; that has made imperative for me to believe in God's prophets: Abraham/Ibrahim, Moses/Musa, Jesus/Isa and Muhammad. That is Islam and that is Islam's call. God's religion has God and the scriptures sent to us by Him, which forbid childish deception coming from money and "power."


The Rolex Commodores? Cup enters its final phase tonight with the start of the 24-36 hour long offshore race, the last race of the regatta, starting an hour later than scheduled tonight at 1930BST from the Royal Yacht Squadron line.
Over the last 24 hours the points separating the teams at the top have been jumping up and down thanks to action both on the water and in the protest room.
Points for France Bleu, for example, were reinstated today after the team led by Géry Trentesaux had been disqualified for sailing the wrong course on Wednesday's coastal race. With their reinstatement plus a sound performance in today's final inshore race – where they scored two seconds and a third – France Bleu are now back in the fight in fourth place on 66 points, just half a point behind Ireland Orange and still within striking distance of the lead.
Tonight's offshore race counts for double points – twice that of Wednesday's coastal race and four times the scoring co-efficient for the inshores and thus with 16.5 points separating the first from the fourth-placed teams, France Bleu's three boats between them will need to gain at least eight places on the leaders if Trentesaux and team are to take the trophy for a second time.
Leaders since the opening day of this regatta, Ireland Green continues to top the scoreboard with a slender lead of just under five points. If the second placed team get each of their three boats one place ahead of those in Ireland Green then they will win.
How this will work out given a light forecast for the offshore race remains to be seen. One theory goes that the bigger boats will fair better in lighter conditions as they will see fewer changes in the weather and tide. This could bode well for Colm Barrington's Magic Glove in Ireland Orange and the two Farr 52s Bear of Britain and Chernikeef II. However, Ireland Green's big boat is the smallest in Class 1. At only 40ft long the bigger Farr 52s, for example, must give Tiamat 7.5 minutes an hour.
Her small size and comparatively slower pace should also prevent Tiamat from being taken out? by her competitors as we have witnessed happen to other boats over the last 48 hours.
After a blistering start to the regatta Andrew Allen and Colm Monohan's J/109 No Naked Flames, the Ireland Green small boat, scored a fourth to put them on 14 points total, the second lowest score for an individual boat this week – David Dwyer's Mills 39 marinerscove.ie 2 still holds the lowest series score with just 9 points.
While it will be hard for Tiamat to be threatened in tonight's race due to her size difference, amongst the smaller boats where the racing is closer there will be more vulnerability. "We need to keep our heads over the night. We will see what the course is like. We are hoping the breeze will stay down a little bit, but we have a sail inventory covering it all, so we'll have to go out and see and see what the forecast brings us," continued Monohan, who recounts one of their competitors having interfered with their racing, when they tacked on them 19 times up one beat.
The biggest upset of the day so far has been Ireland Orange losing second place to their compatriots in Ireland White. In this morning's inshore race Magic Glove was late for the start line eventually finishing in 10th place, while Conor and Denise Phelan's Jump Juice scored an eighth.
The forecast for the next 36 hours is for the wind to be mainly light, dropping off this evening and possibly building for a time tomorrow morning. The course for the offshore race will see all yachts heading east out of the Solent before heading out into the English Channel to one of the RORC's offshore marks and then westwards to Poole. The Class 1 (big) boats have a 182 Nm course, the Class 2 (medium) boats have a 164 Nm course while the Class 3 (small) boats will sail 147Nm.
First boats are expected back in Cowes late tomorrow (Saturday) night.


Inferring flight parameters of Mesozoic avians through multivariate analyses of forelimb elements in their living relatives.
Our knowledge of the diversity, ecology, and phylogeny of Mesozoic birds has increased significantly during recent decades, yet our understanding of their flight competence remains poor. Wing loading (WL) and aspect ratio (AR) are two aerodynamically relevant parameters, as they relate to energy costs of aerial locomotion and flight maneuverability. They can be calculated in living birds (i.e., Neornithes) from body mass (BM), wingspan (B), and lift surface (SL). However, the estimates for extinct birds can be subject to biases from statistical issues, phylogeny, locomotor adaptations, and diagenetic compaction. Here we develop a sequential approach for generating reliable multivariate models that allow estimation of measurements necessary to determine WL and AR in the main clades of non-neornithine Mesozoic birds. The strength of our predictions is supported by the use of those variables that show similar scaling patterns in modern and stem taxa (i.e., non-neornithine birds) and the similarity of our predictions with measurements obtained from fossils preserving wing outlines. In addition, although our WL and AR values are based on estimates (BM, B, and SL) that have an associated error, there is no cumulative error in their calculation, and both parameters show low prediction errors. Therefore, we present the first taxonomically broad, error-calibrated estimation of these two important aerodynamic parameters in non-neornithine birds. Such estimates show that the WL and AR of the non-neornithine birds here analyzed fall within the range of variation of modern birds (i.e., Neornithes). Our results indicate that most modern flight modes (e.g., continuous flapping, flap and gliding, flap and bounding, thermal soaring) were possible for the wide range of non-neornithine avian taxa; we found no evidence for the presence of dynamic soaring among these early birds.


This is in response to "Ethical carnivores; An iconic outdoor pursuit," by Barbara Brotman, the Tribune's Outdoor Adviser columnist, and "Ethical carnivores; An urbanite aims for dinner," by Tribune reporter Monica Eng (Perspective, Feb. 27).
As a devoted, avid, lifelong hunter, I thank the Tribune so much for approaching this assignment with an open mind.
You hit a home run, showing how much true hunters and shooters are ethical and are safety-conscience to the nth degree.
It made my day to read pieces that did not bash me and my fellow hunters but celebrated what we believe in and live daily.
— Jamie Phelps, Bloomington, Ill.
The killing of another living being is sad, unnecessary and cruel.
There is an internal logic to the arguments of Barbara Brotman and Monica Eng that can help soothe any doubts they, or others, might have about the true morality of what they are doing.
In fact, however, the logic only holds up because they are working backward.
When we decide we want to engage in a certain behavior, no matter what the real consequences, and then create reasons why this is all right, we can avoid reality.
In this case, the reality is that living creatures, sentient beings, are murdered for no other reason than humans want to.
You can "pretty it up" any way you like, but those animals are bothering no one, they are living their lives, and we confuse the ability to do something, i.e., kill them, with the right to do it.
We're in the food chain, certainly, but it's our hubris that makes us think we are on the top of it.
One pertinent difference between human animals and most non-human animals is that we do have the ability to create a moral structure that is based on empathy and compassion.
We can make decisions beyond our "instinct."
We can also walk in the woods and be mindful through careful observation, using a camera or binoculars.
We need not eat meat and, in fact, are healthier if we do not.
Let's at least be honest.
If they want to hunt, they will hunt.
But perhaps they need to be clear with themselves that there is something about the killing that is enticing to them.
But that doesn't make it ethical or moral.
I would like to applaud Barbara Brotman and Monica Eng for stepping outside of their comfort zones and trying hunting.
I am a deer hunter and I do it as a means to provide healthy food for my family, as an outlet for myself and as a family activity.
While I was unsuccessful this past season, I killed four deer the year before, two with my bow and two with my shotgun.
I made this meat into ground, roast, steaks, pepperoni and jerky.
My whole extended family enjoyed these treats and it was truly a blessing to be able to share the fruits of my labors with them.
I have a wife and two little girls, 4 years and 4 months, and my oldest daughter, Hannah, can't wait to go hunting with Daddy.
She spent a lot of time in my back yard with her great-grandfather and me while we would practice with our bows.
It was a proud day for her when Daddy made her a bow out a stick and some rubber bands and she was able to shoot with us.
She was given a youth compound bow by her great-grandfather on Christmas Eve this year. He passed the next day on Christmas morning and it is very special to her. I recently obtained a bow for my wife and have started her shooting as well with the hope that one day she will hunt with me.
For me, as well as the hunters you talked to, hunting is more than killing an animal.
My non-hunting friends can never understand why I am still so happy after a day hunting although I didn't kill a deer. It is about being at peace with yourself, the sharing and generosity of friends and family, and the quality experiences with your loved ones that you just can't get anywhere else.
As a born-and-bred city kid (from the North Side) and not having been exposed to firearms growing up, it wasn't until I was in my early 30s that I was introduced to putting meat on my own table (that is, as opposed to picking something up shrink-wrapped at a local retailer). I'm of the opinion that until you've attained proficiency with a harvesting tool of choice, stalked, harvested (as expediently and as cleanly as possible), butchered and prepared the game you yourself have harvested, that one simply doesn't have the same levels of respect and/or appreciation of the bounty one consumes. Any time I see meat left on a plate, it irks me no end to witness this lack of basic respect or appreciation of the animal that was harvested for our sustenance.
Along with our thumbs and mental capacities comes a prerequisite not to waste food. Events around the globe regarding food shortages and those going hungry alone should serve to increase our awareness; however, being at the top of the food chain and particularly those of us in urban settings, it's clear that many of us have lost touch with the basic respect for that which we entirely too often take for granted (the food upon our plates).
It is a pity that the humanity of Barbara Brotman and Monica Eng has retrogressed to the level at which killing has become "fun." Although hunters claim that "the kill" is not the major factor in hunting, that appears to be a fallacy. The immersion in nature, understanding the nuances of forest sounds, smelling the Earth and learning the habits of wild creatures may all be experienced without taking life.
Of course there is a predator-prey factor in the wild, but this is a life-or-death balance. The wolf isn't out for fun when it takes down a deer. It is hungry and must sustain life. The hawk isn't seeking titillation when it devours a sparrow. It is surviving.
Hunters excuse their pastime as a remedy for overpopulation of whitetails, etc. Study the elements of "maximum sustained yield" and understand that populations of deer are managed to provide targets for hunting and for economic benefit to wildlife managers and providers.
Eng seeks an alternative to subjecting animals to the horrors of factory farming and the slaughterhouse. She would escape ingestion of chemicals and antibiotics fed to "meat" animals and eliminate the pollution of waterways caused by waste matter disposal. I give her credit for that. But there is another solution to those problems: vegetarianism. It is not only healthy, but contributes to a compassionate mode of life.
Unfortunately, as reporters, Brotman and Eng are not eliciting an appreciation of our natural world. They are glorifying a less-civilized, insensate existence.
— Kathleen Bauer, Bristol, Ind.


Stephen Bate is a British citizen, Chartered Arbitrator, barrister and accredited mediator, with a UK domestic and international commercial arbitration practice carried on through ARBDB, international arbitration chambers in London: www.arbdb.com. His practice background is as a barrister at the English Bar, with over 25 years' experience in a range of civil and commercial matters, specialising in media & entertainment law, latterly at 5RB barristers' chambers until 2017.
Stephen was accredited as a mediator in the UK by the Centre for Effective Dispute Resolution (CEDR) in 2002 and has since mediated approximately 120 cases with values up to £250M in a very wide range of commercial disputes, with a settlement rate of about 70%. His mediation practice is carried out through CEDR Chambers: www.cedr.com. Stephen is listed in the Legal 500 2018/19 as a leading mediator.
Stephen is a member of the Presidential Panel of arbitrators at the Chartered Institute of Arbitrators and is also listed with the Dubai International Arbitration Centre as a qualified arbitrator. He is also a member of the panel of arbitrators maintained by Sport Resolutions and an arbitrator on the panel of arbitrators maintained by Phonographic Performance Ltd., the licensing body.
Dispute over performance of a shareholders' agreement of a telecommunications company, arbitration under UNCITRAL Rules. Award of US$130M (one of three arbitrators).
Dispute over exercise of pre-emption rights over further shares in the same company; arbitration under UNCITRAL Rules. Claim value c. US$80M (one of three arbitrators).
Sole arbitrator in contract dispute concerning the supply of education services to the Middle East, claim value c. £2M.
Sole arbitrator in LLP partnership dispute concerning accountancy business; claims brought by partnership against one partner and cross-claims.
Sole arbitrator in dispute involving claims relating to the sale and re-purchase of fleet motor vehicles.
Sole arbitrator in patent licence dispute.
Sole arbitrator in dispute concerning the supply of advertising services.
Sole arbitrator in contractual loss of profits dispute in the fashion industry.
Sole arbitrator in sale of goods dispute.
Sole arbitrator in disputes concerning partnership retirement and enforceability of restrictive covenants against a leaving partner.
Sole arbitrator in dispute concerning contracts for the provision of facilities for the UK National Health Service.
Sole arbitrator in contract dispute in the soft drinks industry.
Chairman of arbitrators appointed by Sport Resolutions for the English Football Association in disputes between player and player's agent under Rule K procedures.
Chairman of English Football League's Disciplinary Commission (FDC) in arbitration under EFL's Rules and Regulations concerning financial disclosures by former Chairman of Watford FC on behalf of the club, EFL v Raffaele Riva.
FDC Chairman in arbitration between football clubs under EFL's Rules and Regulations over the poaching of a management team, Colchester FC v Norwich FC.
FDC Chairman in dispute between player and club arising from termination of player's contract.
FDC Chairman in dispute between (i) club and youth player over player's registration and (ii) clubs and player over liability to pay 'signing on' fee.
15 ABTA documents-only arbitrations in holiday and travel cases.
2007-2016, legal member of the Licensing Committee of UK horse racing's regulator (the British Horseracing Authority), chairing numerous hearings under 'fit and proper person' jurisdiction of the regulator.
Legal Assessor, sitting with and advising Fitness to Practise Panels for the General Dental Council and Health and Care Professions Tribunal Service in misconduct, performance and health cases; previous experience (2010-2018) sitting as Legal Assessor in GMC (doctors' fitness to practise) and racing corruption cases.
Approximately 70 documents-only adjudications for CISAS under UK Communications Act 2003.
50 expert determinations for Nominet in registration disputes over .co.uk internet domain name registrations.
Fields of work covered include commercial contracts, defamation, ICT (information, communications and technology), intellectual property, leisure and travel, manufacturing, media & entertainment, partnership/shareholder, property, pharmaceutical, NHS, healthcare and other regulatory matters, sport and telecommunications.
The above include/further areas are: sale of goods, supply of services, distribution agreements, licensing agreements in various fields, such as telecommunications, media and entertainment and intellectual property (e.g. patent and trade mark) disputes, copyright infringement; franchise agreements, gas supply contracts, computer contracts, employment contracts, restrictive covenant disputes, insurance claims, guarantee claims, contract disputes in many other different fields, e.g. sale of companies, warranty claims under sale and purchase agreements, joint venture contracts, agency agreements, contracts for advertising services; landlord & tenant, professional negligence (solicitors), competition claims, claims for breach of statutory duty, sponsorship and other sports-related agreements; breach of confidence, privacy and data protection.
1980 – 1981 Passed Bar Finals exams and called to the English Bar.
1979 – 1980 Diploma in Law, City University.
1976 – 1979 Magdalene College, Cambridge; M.A Foreign Languages (French and German).
Interests include a wide variety of sporting activities, reading history and membership of the Royal Geographical Society.
1 The arbitration appointments were by the UK Chartered Institute of Arbitrators, by courts (English High Court, the Federal High Court of Nigeria), the Centre for Effective Dispute Resolution (CEDR) and by appointing bodies in sports matters, such as Sport Resolutions for the English Football Association.